Oxford American Handbook of Physical Medicine & Rehabilitation (Oxford American Handbooks)

Oxford American Handbook of

Physical Medicine and Rehabilitation

Published and Forthcoming Oxford American Handbooks Oxford American Handbook of Clinical Medicine Oxford American Handbook of Anesthesiology Oxford American Handbook of Clinical Dentistry Oxford American Handbook of Clinical Diagnosis Oxford American Handbook of Clinical Pharmacy Oxford American Handbook of Critical Care Oxford American Handbook of Emergency Medicine Oxford American Handbook of Geriatric Medicine Oxford American Handbook of Nephrology and Hypertension Oxford American Handbook of Obstetrics and Gynecology Oxford American Handbook of Oncology Oxford American Handbook of Otolaryngology Oxford American Handbook of Pediatrics Oxford American Handbook of Physical Medicine and Rehabilitation Oxford American Handbook of Psychiatry Oxford American Handbook of Pulmonary Medicine Oxford American Handbook of Rheumatology Oxford American Handbook of Surgery

Oxford American Handbook of

Physical Medicine and Rehabilitation Edited by

Lyn D. Weiss Jay M. Weiss Thomas Pobre

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Oxford University Press, Inc. publishes works that further Oxford University’s objective of excellence in research, scholarship and education. Oxford New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With offices in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland Thailand Turkey Ukraine Vietnam

Copyright © 2010 by Oxford University Press, Inc. Published by Oxford University Press Inc. 198 Madison Avenue, New York, New York 10016 www.oup.com Oxford is a registered trade mark of Oxford University Press First published 2010 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Oxford University Press, Library of Congress Cataloging-in-Publication Data Oxford American handbook of physical medicine and rehabilitation / edited by Lyn D. Weiss, Jay M. Weiss, Thomas Pobre. p. ; cm.—(Oxford American handbooks) Includes bibliographical references and index. ISBN 978–0–19–536777–5 (flexicover : alk. paper) 1. Medicine, Physical—Handbooks, manuals, etc. 2. Medical rehabilitation— Handbooks, manuals, etc. I. Weiss, Lyn D. II. Weiss, Jay, MD. III. Pobre, Thomas. IV. Series: Oxford American handbooks. [DNLM: 1. Physical Medicine—methods—Handbooks. 2. Rehabilitation—methods— Handbooks. WB 39 O9785 2010] RM701.6.O94 2010 617’.03—dc22 2009021103

987654321 Printed in China on acid-free paper

This material is not intended to be, and should not be considered, a substitute for medical or other professional advice. Treatment for the conditions described in this material is highly dependent on the individual circumstances. And, while this material is designed to offer accurate information with respect to the subject matter covered and to be current as of the time it was written, research and knowledge about medical and health issues is constantly evolving and dose schedules for medications are being revised continually, with new side effects recognized and accounted for regularly. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulation. Oxford University Press and the authors make no representations or warranties to readers, express or implied, as to the accuracy or completeness of this material, including without limitation that they make no representation or warranties as to the accuracy or efficacy of the drug dosages mentioned in the material. The authors and the publishers do not accept, and expressly disclaim, any responsibility for any liability, loss or risk that may be claimed or incurred as a consequence of the use and/or application of any of the contents of this material.

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Preface Physical medicine and rehabilitation (PM&R, or physiatry) is a growing, but still misunderstood medical specialty in the United States. Perhaps no field is as broad in the areas it covers as PM&R, as this book attempts to show. By necessity, areas that could fill volumes are limited to a few pages or paragraphs. We have tried to distill the information into as useful a format as possible while attempting to include most of the important points. This book is aimed primarily at medical students rotating through PM&R, and PM&R residents. It is meant to be available for quick reference on a topic when in the hospital or clinic. There is ample space for note taking while on rounds, and its size and layout are meant to encourage this. It is also intended for physiatrists who may encounter conditions or topics that they rarely see or haven’t seen in years. Our residents enter our programs with varied experiences and knowledge of this field. In contrast to fields such as internal medicine or Ob/Gyn, there is no standard exposure to PM&R in medical school. Thus we have to assume that residents and students have no familiarity with PM&R and start with the most basic knowledge of the field. This Handbook should be considered only a first step, and we hope it will help provide a foundation for understanding that can be advanced by further reading and research. Many aspects of the specialty (such as spinal procedures, electromyography, and others) are impossible to learn without a guided preceptorship or fellowship. This book tries to stress an understanding of when, where, and why these procedures fit into the care of patients, but cannot teach how to perform them. In those cases we hope this book serves as an introduction. There are many excellent texts in the field of PM&R that are written by well-respected authors. The reader is encouraged to consult these books for a more detailed discussion of PM&R in general. There are also many excellent books that focus on specific topics. Obviously, the Internet has increased the amount of material available exponentially. The resources chapter at the end of this book lists organizations, journals, and Web sites that serve as resources for the most up-to-date information.

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Acknowledgments The authors have been privileged to work for and with many talented individuals. Students, colleagues, and mentors have all influenced our practice of medicine. We would like to thank all of the contributors to this book. Their enthusiasm for learning and teaching is evident in their work. The editors at Oxford University Press have been wonderful to work with. Special thanks go to Elizabeth Kates and Andrea Seils for their assistance and patience. Of course, we couldn’t do half of the things we do without our coordinator, secretary, and office manager Sheila Slezak. We would like to thank Dr. Yasha Magyar for his outstanding illustrations. We are extremely grateful to have the support and encouragement of our Medical Director and CEO at Nassau University Medical Center. Steve Walerstein, MD, and Arthur Gianelli, CEO, are role models in the practice of medicine and administration. They always put patient care first and strive to provide the best care possible. We have given better care to our patients because of them, and for that we are appreciative. Finally, and most importantly, we would like to thank our spouses, children, and family for their love and support. Jay, Lyn, Ari, Helene, Stefan, Richard, Rhona, and Nicole have been our foundation and the most important part of our lives. This book is dedicated to them, in the hopes that they may always find happiness and fulfillment. Lyn Weiss Jay M. Weiss Thomas Pobre

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Contents Detailed contents xi Contributors xvii Symbols and abbreviations xxi 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

General principles Head and neck Spine Upper extremity Lower extremity Pain syndromes Procedures and medications Neurological disorders Rheumatological disorders Prosthetics and orthotics Spinal cord injury Traumatic brain injury Stroke Pulmonary and cardiac rehabilitation Pediatrics Common complications Rehabilitation issues Index 441

1 15 33 71 121 165 183 227 253 277 305 321

327 343 351 363 401

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Detailed contents 1

General principles Physiatry 2 The physiatric history and physical examination 4 Rehabilitation: the team approach 6 The 75% rule 8 Impairment, disability, and handicap 10

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Head and neck An overview of cervical pain 16 Cervical radiculopathy 18 Myelopathy 22 Cervical spondylosis 24 Cervical sprain and strain and whiplash 26 Cervical myofascial pain 28 Headache 30

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Spine Compression fractures 34 Osteoporosis 36 Scoliosis 42 Thoracic radiculopathy and thoracic intervertebral disc herniations 48 Lumbar sprain, strain 50 Lumbar radiculopathy 54 Lumbar spinal stenosis 58 Cauda equina and conus medullaris syndrome 60 Lumbar spondylosis 62 Spondylolisthesis 64 Spondylolysis 68

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DETAILED CONTENTS

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Upper extremity Shoulder bursitis 72 Shoulder tendonitis 74 Shoulder impingement syndrome 76 Management treatment 80 Rehabilitation after rotator cuff surgery 82 Adhesive capsulitis 86 Rehabilitation of superior labral tears 88 Epicondylitis 90 Bicipital tendonitis 92 Ulnar neuropathy at the elbow and cubital tunnel syndrome 94 Radial tunnel syndrome and supinator syndrome 96 Olecranon bursitis 98 Carpal tunnel syndrome 100 Wrist pain 104 De Quervain’s tenosynovitis 106 Ganglion cyst 108 The hand: hand basics 110 Mallet finger 112 Phalanx dislocations 114 Thumb ligament injuries 116 Trigger finger 118

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Lower extremity Osteoarthritis of the hip 122 Trochanteric bursitis or greater trochanter pain syndrome 126 The knee 128 Knee osteoarthritis 132 Knee bursitis 136 Patellar and quadriceps tendonitis, Osgood Schlatter 140

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DETAILED CONTENTS

Medial and lateral collateral ligament injuries 142 Anterior cruciate ligament injury 144 Meniscal injuries 146 Patellofemoral pain 150 The ankle 152 The foot 160 6

Pain syndromes Fibromyalgia 166 Myofascial pain syndrome 172 Complex regional pain syndrome 176 Postherpetic neuralgia 180

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Procedures and medications Electrodiagnosis 184 Trigger point injection 192 Musculoskeletal injection and aspiration 194 Interventional spinal procedures 202 Physical modalities 212 Pain pharmacology 216

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Neurological disorders Parkinson’s disease 228 Multiple sclerosis 230 Disorders of the motor unit 236 Guillain–Barré syndrome (acute inflammatory demyelinating polyneuropathy) 240 Neuropathy 242 Myopathy 248

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Rheumatological disorders Psoriatic arthritis 254 Rheumatoid arthritis 258

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DETAILED CONTENTS

Juvenile rheumatoid arthritis 262 Ankylosing spondylitis 264 Gout 268 Joint replacement 274 10

Prosthetics and orthotics Amputation 278 Lower extremity prosthetics 282 Upper limb prosthetics (transradial), (transhumeral) 288 Ankle foot orthoses (AFO) 294 Knee ankle foot orthoses (KAFO) 298 Truncal and cervical orthoses 300

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Spinal cord injury General facts: epidemiology and demographics 306 Function by level 310 Management and medications 314 Complications 318

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Traumatic brain injury

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Stroke

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Pulmonary and cardiac rehabilitation Prematurity 344 Cerebral palsy 346

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Pediatrics Prematurity 352 Cerebral palsy 354 Spina bifida 360

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DETAILED CONTENTS

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Common complications Heterotopic ossification 348 Bladder dysfunction 368 Spasticity 374 Pressure ulcers 378 Venous thromboembolism 382 Swallowing disorders 388 Sexuality and the disabled 396 Immobility syndrome 398

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Rehabilitation issues Burns 402 AIDS/HIV-associated conditions 406 Cancer rehabilitation 408 Communication disorders 412 Neuropsychological assessment and treatment 416 Osteopathic manipulation 420 Gait 424 Wheelchair prescriptions 428 Assistive devices 432 Adaptive devices 434 Resources for the physiatrist 438

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Index 441

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Contributors Rafael Abramov, DO

Carol Kave Chamoff, OTR/L

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Occupational Therapy Supervisor Rehabilitation Unit Nassau University Medical Center East Meadow, New York

Maryam Rafael Aghalar, DO

New York College of Osteopathic Medicine Old Westbury, New York

Adjunct Faculty Occupational Therapy Program Stony Brook University Medical Center Stony Brook, New York Adjunct Faculty Occupational Therapy Program Touro College Bay Shore, New York

Rawa Araim, DO

Kenny Chantasi, DO

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Tamir Aldad, DO

John J.W. Asheld III, DO Department of Internal Medicine Stony Brook University Medical Center Stony Brook, New York

Ricardo Cruz, MD

Wilbur J. Asheld, DO

Director of Brain Injury Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

New York College of Osteopathic Medicine Old Westbury, New York

Robert A. Domingo, PhD, CCC-SLP

Shimon Y. Blau, MD Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Christopher Burrei, DO Long Island Physical and Medical Rehabilitation Levittown, New York

Department of Communication Sciences and Disorders Long Island University C.W. Post Campus Brookville, New York Department of Speech–Language Pathology Nassau University Medical Center East Meadow, New York

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CONTRIBUTORS

Dennis J. Dowling, DO, MA, FAAO

Nassau University Medical Center East Meadow, New York

Director of Osteopathic Manipulative Services Department of Physical Medicine and Rehabilitation Nassau University Medical Center East Meadow, New York

Attending Physician Saint Charles Rehabilitation Hospital Port Jefferson, New York

Derek Higgins, DO

Private Practice Osteopathic Manipulative Medicine Associates, PC Syosset, New York

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Chioma Ezeadichie, DO, MPH

Adam C. Isaacson, MD

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Elizabeth Flynn, MA, PT Chief Physical Therapist Nassau University Medical Center East Meadow, New York

Andrew Galmer, DO Internal Medicine North Shore University Hospital Manhasset, New York

Walter J. Gaudino, MD, MSPT

Associate Chairman Associate Professor of Clinical PM&R Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Alexander Knijnikov, DO, BS New York College of Osteopathic Medicine Old Westbury, New York

Shilo Kramer, DO New York College of Osteopathic Medicine Old Westbury, New York

Associate Professor Department of Physical Medicine & Rehabilitation SUNY at Stony Brook, New York Stony Brook, New York

Yasha Magyar, DO

Adjunct Clinical Associate Professor Department of Medicine (PM&R) New York College of Osteopathic Medicine of New York Institute of Technology Old Westbury, New York

Shahab Mahboubian, DO, MPH

Director of Prosthetic and Orthotics Department of Physical Medicine & Rehabilitation

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Department of Physical Medicine & Rehabilitation Nassau University Medical Center. East Meadow, New York

Orthopaedic Surgery Peninsula Hospital Consortium Northshore–LIJ affiliated hospitals of Long Island, New York

Jose Mathew, DO, MPH

CONTRIBUTORS

Sina Menashehoff, DO

Adeel Popalzai, DO

New York College of Osteopathic Medicine Old Westbury, New York

Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Samantha Mendelson, DO Department of Physical Medicine and Rehabilitation North Shore Long Island Jewish Medical Center

Matthew J. Mikosz, CP, LP

Waqaas A. Quraishi, MD Department of Physical Medicine & Rehabilitation Long Island Jewish Medical Center New Hyde Park, New York

Hanger Prosthetics and Orthotics National Upper Extremity Prosthetics Specialist San Antonio, Texas

Nicholas Renaldo, MD

Francine G. Moshkovski, MD, FAAAPMR

Libi Rind, DO

Attending Physician Department of Ambulatory Care New York Harbor Healthcare System Brooklyn VA Medical Center Brooklyn, New York

Adaku Nwachuku, DO, MBA RehabNY Amherst, New York

Thomas Pobre, MD, FAAPMR Director of Outpatient Services Department of Physical Medicine and Rehabilitation Nassau University Medical Center East Meadow, New York Associate Professor of Clinical Physical Medicine and Rehabilitation Stony Brook University School of Medicine Stony Brook, New York Adjunct Associate Professor of Clinical Physical Medicine and Rehabilitation New York College of Osteopathic Medicine Old Westbury, New York

Department of Orthopaedic Surgery Long Island Jewish Medical Center New Hyde Park, New York Columbia University Physical Medicine and Rehabilitation New York, New York

Thomas A. Riolo, DO, BA New York College of Osteopathic Medicine Old Westbury, New York

Charles Ruotolo, MD Chairman of Orthopedics Nassau University Medical Center East Meadow, New York

Vladimir Salomon, DO Spine Technology & Rehabilitation Physical Medicine & Rehabilitation Fort Wayne, IN

Lynn A. Schaefer, PhD, ABPP-CN Chief, Neuropsychology and Medical Psychology Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York Clinical Assistant Professor (Psychiatry) New York College of Osteopathic Medicine Old Westbury, New York

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CONTRIBUTORS

Matthew M. Shatzer, DO Residency Program Director Physical Medicine & Rehabilitation North Shore-Long Island Jewish Healthcare System Chief, Physical Medicine & Rehabilitation North Shore University Hospital Manhasset, New York

Divyajot Sohal, DO Department of Internal Medicine New York Hospital Queens Flushing, New York

Ajendra Sohal, MD Director of Pain Management Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York Assistant Professor of Clinical Physical Medicine and Rehabilitation

Rebecca Trangco-Evans, MD Advanced Minimally Invasive Surgery Morris Plains, New Jersey

Teena Varghese, MD Department of Physical Medicine & Rehabilitation Nassau University Medical Center East Meadow, New York

Albert Villafuerte, MD Medical Director Bronx Rehabilitation and Physical Therapy Physical Medicine and Rehabilitation Bronx, New York

Frederick Weiss, MD, DPT Radiology University of Maryland Medical Center Baltimore, Maryland

Jay M. Weiss, MD, FAAPMR, FAANEM Medical Director Long Island Physical Medicine and Rehabilitation Levittown, New York Associate Professor of Clinical Physical Medicine and Rehabilitation Stony Brook University School of Medicine Stony Brook, New York Adjunct Associate Professor of Clinical Physical Medicine and Rehabilitation New York College of Osteopathic Medicine Old Westbury, New York

Lyn D. Weiss, MD, FAAPMR, FAANEM Chairman and Director of Residency Training Director of Electrodiagnostic Services Department of Physical Medicine & Rehabiliation Nassau University Medical Center East Meadow, New York Professor of Clinical Physical Medicine and Rehabilitation Stony Brook University School of Medicine Stony Brook, New York Adjunct Professor of Clinical Physical Medicine and Rehabilitation New York College of Osteopathic Medicine Old Westbury, New York

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Symbols and abbreviations i d * AACVPR AAOS AAPM&R ABC ABG AC ACL ACTH ADA ADH ADL AED AFO AIDP ALS AMAN AP AROM AS ASIA AST ATFL ATP AV BADL bid BKA BMD BMI BP BPH CBC

increased decreased degree(s) American Association of Cardiovascular and Pulmonary Rehabilitation American Academy of Orthopadeic Surgeons American Academy of Physical Medicine and Rehabilitation airway, breathing, circulation arterial blood gases acromioclavicular anterior cruciate ligament adrenocorticotrophic hormone Americans with Disabilities Act antidiuretic hormone activities of daily living automated external defibrillator ankle foot orthoses acute inflammatory demyelinating polyneuropathy amyotrophic lateral sclerosis acute motor axonal neuropathy anteroposterior active range of motion ankylosing spondylitis American Spinal Injury Association aspartate aminotransferase anterior talofibular ligament adenosine triphosphate arteriovenous basic activities of daily living twice daily below-knee amputation bone mineral density; Becker muscular dystrophy body mass index blood pressure benign prostatic hypertrophy complete blood count

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SYMBOLS AND ABBREVIATIONS

CCP CCU CDC CE CES CFL CHF CM CMAP CMC CMG CMS CNS CON COPD COX CP CPM CPR CRF CRH CRP CRPS CSF CT CTS CVA DBP DBS DIP DM DMARD DMD DVT ECG ECRB ECRL ECSWT EMG

citrulline-containing protein coronary care unit Centers for Disease Control and Prevention cauda equina cauda equina syndrome calcaneofibular ligament congestive heart failure conus medullaris compound muscle action potential carpometacarpal cystometrogram Centers for Medicare and Medicaid Services central nervous system concentric chronic obstructive pulmonary disease cyclooxygenase cerebral palsy continuous passive motion cardiopulmonary resuscitation chronic renal failure corticotropin-releasing hormone C-reactive protein complex regional pain syndrome cerebrospinal fluid computed tomography carpal tunnel disease cerebrovascular accident diastolic blood pressure deep brain stimulation distal interphalangeal diabetes mellitus disease-modifying anti-rheumatic drug Duchenne muscular dystrophy deep venous thrombosis electrocardiogram extensor carpi radialis brevis extensor carpi radialis longus extracorporeal shockwave therapy electromyography

SYMBOLS AND ABBREVIATIONS

ENMG EPB ER ESR ESRD ETD FABER FDA FDP FEES FES FMS FSHMD GCS GERD GFR GI GOAT Hb Hct HIV HO H&P HPA HVLA IADL ICF ICIDH ICP IDEA IGF-1 IM INO IP IR IV IVC

electoneuromyography extensor polaris brevis external rotation erythrocyte sedimentation rate end-stage renal disease electronic terminal device flexion abduction external rotation Food and Drug Administration flexor digitorum profundis fiber-optic endoscopic evaluation of swallowing functional electrical stimulation fibromyalgia syndrome fascioscapulohumeral muscular dystrophy Glasgow Coma Scale gastroesophageal reflux disease glomerular filtration rate gastrointestinal Galveston Orientation and Amnesia Test hemoglobin hematocrit human immunodeficiency virus heterotopic ossification history and physical hypothalamic–pituitary–adrenal high velocity/low amplitude instrumental activities of daily living International Classification of Functioning, Disability, and Health International Classification of Impairments, Disabilities, and Handicaps intracranial pressure Individuals with Disabilities Education Act insulin-like growth factor 1 intramuscular internuclear opthalmoplegia interphalangeal internal rotation intravenous inferior vena cava

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SYMBOLS AND ABBREVIATIONS

JCAHO JIA JRA KAFO LBP LCL LDH LES LFT LMWH LP LS LTR MAO MAP MAS MBS MCL MCP MDR MET MFS MI MLF MMPI MPS MRI MS MSU MVA NCV NDT NG NIHSS NINDS NPO NSAID N/V

Joint Commission on Accreditation of Healthcare Organizations juvenile idiopathic arthritis juvenile rheumatoid arthritis knee ankle foot orthoses lower back pain lateral collateral ligament lactate dehydrogenase lower esophageal sphincter liver function test low-molecular-weight heparin lumbar puncture lumbosacral latent twitch response monoamine oxidase mean arterial pressure macrophage activation syndrome modified barium swallow medial collateral ligament metacarpophalangeal multidisciplinary rehabilitation metabolic equivalent Miller–Fisher syndrome myocardial infarction median longitudinal fasciculus Minnesota Multiphasic Personality Inventory myofascial pain syndrome magnetic resonance imaging multiple sclerosis mid-stream urine sample motor vehicle accident nerve conduction velocity neurodevelopmental treatment nasogastric National Institutes of Health Stroke Scale National Institute of Neurological Disorders and Stroke nothing by mouth (nil per os) nonsteroidal anti-inflammatory drug nausea/vomiting

SYMBOLS AND ABBREVIATIONS

OA OMT PA PCL PE PEG PFP PFT PINS PIP PLS PM&R PNF PO PPI PRICE PROM PSW PT PTA PTH PVL PVR qd qhs qid RA RCL RF RFA ROM RSD RTA rt-PA SACH SAH SAP SBP SC

osteoarthritis osteopathic manipulation posteroanterior posterior cruciate ligament pulmonary embolism percutaneous endoscopic gastrostomy (tube) patellofemoral pain pulmonary function test progressive inhibition of neuromuscular structures proximal interphalangeal posterior leaf spring physical medicine and rehabilitation proprioceptive neuromuscular facilitation by mouth proton pump inhibitor protect, rest, ice, compression, elevation passive range of motion positive sharp wave physical therapy post-traumatic amnesia parathyroid hormone periventricular leukomalacia post-void response every day every night 4 times a day (quarter in die) rheumatoid arthritis radial collateral ligament rheumatoid factor radiofrequency ablation range of motion reflex sympathetic dystrophy renal tubular acidosis recombinant Alteplase solid ankle cushion heel subarachnoid hemorrhage serum alkaline phosphatase systolic blood pressure subcutaneous

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SYMBOLS AND ABBREVIATIONS

SCI SCS SD SEP/SSEP SFEMG SI SLAP SLE SNAP SNRB SPECT SSA SSDI SSI SSRI TBI TCA TENS TFCC TFT TIA tid TLS t-PA TPI TSH TTS UCL UFH UNE UTI VEP V/Q VZV WAD WHO WNL

spinal cord injury spinal cord stimulation standard deviation somatosensory evoked potential single-fiber electromyography sacroiliac superior labrum anterior to posterior systemic lupus erythematosus sensory nerve action potential selective nerve root block single photon emission computer tomography Social Security Administration Social Security disability insurance supplemental security income selective serotonin reuptake inhibitor traumatic brain injury tricyclic antidepressant transcutaneous electrical nerve stimulation triangular fibrocartilage complex thyroid function test transient ischemic attack 4 times daily thoracolumbosacral tissue plasminogen activator trigger point injection thyroid-stimulating hormone transdermal therapeutic system ulnar collateral ligament unfractionated heparin ulnar neuropathy at the elbow urinary tract infection visual evoked potential ventilation–perfusion (scan) varicella-zoster virus whiplash-associated disorder World Health Organization within normal limits

Chapter 1

General principles Lyn Weiss Adam C. Isaacson Physiatry 2 The physiatric history and physical examination 4 Rehabilitation: the team approach 6 The 75% rule 8 Impairment, disability, and handicap 10

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CHAPTER 1

General principles

Physiatry The field of physiatry is over 60 years old, yet I still get confused looks from patients as well as physicians (and relatives!) who do not know what we do. Lay people as well as professionals confuse physiatry with psychiatry, podiatry, physical therapy, and psychology, just to name a few. Physiatry as a global concept is concerned with reducing pain, improving and maintaining function, reducing disability, and improving quality of life. Physiatrists are concerned with improving the patient’s ability to function. More than almost any medical specialty, physiatrists work as members of a team. The physiatrist is the leader of a team that may include physical therapists, occupational therapists, speech pathologists, psychologists, recreational therapists, nurses, prosthetists, orthotists, social workers, discharge planners, and, most importantly, the patient and his or her family. The team can be thought of as a well-tuned orchestra, with the physiatrist as the conductor. The physiatrist is responsible for diagnosis, treatment, patient and family education, coordination of the team, decreasing pain, and prevention of morbidity and disability. The goal is to improve function. Physiatry is also known as physical medicine and rehabilitation (PM&R). The physical medicine refers to primarily neuromusculoskeletal disorders (neck pain, back pain, nerve injuries, knee disorders, shoulder pain, etc.). The rehabilitation aspect of PM&R refers to maximizing functional potential after an injury or illness. Usually, the diagnosis has been established, the patient has been stabilized for his or her acute medical condition, and he or she is then brought to the rehabilitation unit. Disorders that are treated include stroke, brain injury, amputation, spinal cord injury, or trauma, among others. There are many areas of specialization in the field of physiatry. Some physiatrists concentrate on outpatient musculoskeletal conditions, such as back pain, neck pain, or chronic pain. Other physiatrists specialize in interventional pain, electrodiagnostic testing, or work-related injuries. Still other physiatrists may work in an acute inpatient rehabilitation center, a subacute facility, or a nursing home. There are currently over 7500 Board-certified physiatrists in the United States, and the field is gaining popularity in other countries. It has become a popular residency choice for medical students. As the population ages and improved medical care allows more people to live longer with disabilities, the need for physiatrists continues to grow. Physiatry is one of the few specialties for which the supply is not likely to exceed the demand for the next decade.

Further reading www.aapmr.org

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The physiatric history and physical examination General description The physiatric history and physical (H&P) differs from a medical or surgical (med/surg) H&P because of its focus on functional status, social supports, disposition, and goals. Although all of the components of the med/surg H&P must be present, this section will focus on the elements of the H&P that differ from the typical med/surg H&P.

Reason for admission This should include the reason that the patient was admitted to an acute rehabilitation unit, not necessarily the medical diagnosis. For example, the patient may have had a hip fracture, but the reason for admission is impaired mobility.

Psychosocial and functional history It is important to obtain an assessment of the patient’s previous functional status and of barriers that the patient may encounter when he or she returns home. The following information should be obtained: • Home situation (With whom does the patient live? Are family members available to help at home? What is the family members’ health status?) • Home environment (Does the patient live in a ranch home on one level or in a four-story walk up?) • Stairs inside the home and number of stairs to enter the home • Previous functional status (Did the patient use a walker or a cane prior to this admission? Does he or she have a raised toilet seat in the bathroom? Are the washer and dryer down a flight of stairs in the basement?) • Work history (What was the patient’s employment? What was the job description? Does the patient plan to return to work? Does the work environment pose any obstacles to mobility?)

Review of systems Ask about the patient’s pain in detail, including pain score, quality, duration, characteristics, aggravating factors, and alleviating factors.

Diagnostic test results Since rehabilitation patients usually have been hospitalized prior to the rehabilitation admission, be sure to include any tests that have been done to date, as well as the results.

Physical examination Special attention should be paid to the patient’s skin, evaluating for possible skin breakdown. A thorough neurological examination should be performed, including cognition (comprehension, expression, social interaction, problem solving, and memory). The patient’s speech should be evaluated for fluency, comprehension and repetition. A thorough evaluation of the patient’s range of motion and strength in all four extremities should be performed.

THE PHYSIATRIC HISTORY AND PHYSICAL EXAMINATION

Use the following scale to assess muscle strength: • 0 – No movement in the extremity • 1 – Movement in the muscle that is nonfunctional (insufficient to move a joint) • 2 – Able to move the joint only when gravity is eliminated • 3 – Able to move the joint through the full range of motion against gravity, but not against resistance • 4 – Ability to move the joint against gravity and with some, but not full, resistance • 5 – Full strength against resistance Since many of your patients are at high risk for deep vein thrombosis (DVT), measure the thigh girth (15 cm above the superior aspect of the patella) as well as the leg girth (15 cm above the medical malleolus) bilaterally. A significant difference in girth measurements may lead the physician to suspect DVT on admission. In addition, if the patient develops symptoms of DVT later in the course of treatment, these measurements could prove helpful. If the patient has increased tone (spasticity) or decreased tone (flaccidity), it should be noted. The functional evaluation of the rehabilitation patient must be completed. This should include an assessment of the patient’s bed mobility, ability to move supine to sit, transfer sit to stand, maneuver a wheelchair, and ambulate (including the distance walked). Any assistive devices and amount of assistance required should be documented.

Assessment In the assessment, a statement should be made that the patient is an appropriate candidate for acute inpatient rehabilitation due to his or her current functional status (if this is an acute rehabilitation admission).

Goals The goals section of the H&P should include an assessment of the patient’s personal goals. This should be discussed with the patient in order to fully develop a treatment plan. In addition, short-term goals as well as long-term goals should be listed. This directs the treatment team to pursue a common goal within realistic time frames. Although these goals may need to be modified according to the patient’s progress, they should represent a reasonable estimate based on the previous functional status, the patient’s goals, and what the physiatrist feels is realistic given the patient’s prognosis. The estimated length of stay should also be addressed. Again, this gives the team a time frame to achieve certain goals.

Treatment plan It is important to develop a treatment plan that addresses the patient’s physical condition as well as prevent possible complications. Since most rehabilitation patients are at risk for DVT and decubiti, preventive measures should be part of the plan. Pain management issues must be addressed as well. Again, this gives the team a time frame to achieve certain goals.

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General principles

Rehabilitation: the team approach Rehabilitation is unique among the medical specialties in that a team of specialists treats the patient with the goal of improving the functional status of the patient. The physician (physiatrist) is the leader of the team and must have the appropriate management skills to coordinate all disciplines and treatments. It must always be remembered that the most important member of the team is the patient. The team usually consists of the physiatrist, physical therapist, occupational therapist, nurses, social worker or case manager, recreational therapist, dietitian, psychologist, speech pathologist, and member of any other discipline that treats the patient. The patient and his or her family and support system must be considered part of the team and included in discussions regarding care. It is usually extremely helpful to have a family meeting before discharge to review the discharge plan prior to the patient leaving the facility (as rehabilitation should continue after discharge). The patient and the family should be included in this meeting. At the beginning of an inpatient stay in an acute rehabilitation hospital, each member of the team evaluates the patient. Goals (both long term and short term) are set. It is important that the patient be asked what his or her goals are, as these may be surprisingly different from the team’s goals. Each member of the team also should set realistic goals for the patient. The team meets at least weekly to evaluate the goals that the patient has met, the impediments to meeting current goals, and modifications that may need to be made to future goals.

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General principles

The 75% rule Historical background Medicare implemented the “75% rule” in 1983. Under this rule, in order to be eligible for payment, an inpatient rehabilitation facility was required to have at least 75% of the admissions fall within a specific list of qualifying conditions1 (see Table 1.1). This rule was not strictly enforced, and in June of 2002, the Centers for Medicare and Medicaid Services (CMS) temporarily suspended enforcement of the rule. However, beginning July 1, 2004, the CMS Final Rule began to phase in the 75% rule as a cost-saving measure. There would be substantial financial penalties if the required number of patients did not have the appropriate diagnosis. As of January 2008, the 75% rule was reduced to 60% (i.e., 60% of all patients discharged from an inpatient rehabilitation facility were required to fall into the diagnostic groups listed in Table 1.1). The original intent of the 75% rule was to distinguish between facilities that should be reimbursed under the acute care hospital prospective payment system (IPPS) and those that should be reimbursed on a cost basis.2 Discussions are ongoing regarding the ultimate status of this legislation, which is sure to affect the field of rehabilitation medicine and the access of patients to care.

Impact Numerous advocacy groups feel that the conditions established over two decades ago do not adequately reflect the care or diagnosis provided by today’s rehabilitation facilities and that this regulation ignores advances in rehabilitative care. Many think that it will prolong patients’ recuperation and delay a return to an independent lifestyle. For example, most joint replacement patients are not included in the 75% rule. Cardiac, pulmonary, and transplant patients are also not included. Many clinicians feel that this regulation jeopardizes Medicare recipients’ access to needed care.2,3 Acute rehabilitation facilities have faced closure, and patients are being discharged to lower levels of care.

Future goals The future of the 75% rule will impact the quality and care of patients requiring rehabilitation services. Perhaps the best summation is provided by the American Academy of Physical Medicine and Rehabilitation (AAPM&R), which states the following in their position paper: “AAPM&R encourages CMS to rely upon exclusion criteria that reflect the needs of Medicare patients who require intensive rehabilitative services and who benefit from rehabilitation therapies and other services to improve their functional ability.”3 1 New Estimates of the Impact of Enforcement of the “75% Rule” on Inpatient Rehabilitation Services Volume. The Moran Company. September 2005. 2 Joint position statement regarding the 75 percent rule. Available at: http://www.rehabnurse.org/ docs/75rule.doc. 3 Position on the Medicare conditions of participation for rehabilitation hospitals: The “75% rule”. American Academy of Physical Medicine and Rehabilitation position paper. February 2003.

THE 75% RULE

Table 1.1 Medical conditions requiring intensive rehabilitation services (according to the 75% rule) 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Stroke Spinal cord injury Congenital deformity Amputation Major multiple trauma Fracture of femur (hip fracture) Brain injury Neurological disorders, including multiple sclerosis, motor neuron diseases, polyneuropathy, muscular dystrophy, and Parkinson’s disease Burns Active, polyarticular rheumatoid arthritis, psoriatic arthritis, and seronegative arthropathies resulting in significant functional impairment. Systemic vasculidities with joint inflammation, resulting in significant functional impairment Severe or advanced osteoarthritis involving two or more major weightbearing joints (a joint replaced by a prosthesis no longer is considered to have arthritis.) Knee or hip joint replacement, or both, during an acute hospitalization immediately preceding the inpatient rehabilitation stay and also meeting one or more of the following specific criteria: a. Bilateral knee or bilateral hip replacement during the acute hospital admission immediately preceding the admission to the acute rehabilitation facility b. Extreme obesity (body mass index of at least 50) c. Age 85 or older

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Impairment, disability, and handicap Searching for a definition of impairment, disability, or handicap is met with a fundamental dilemma because there remains a lack of universal standard definitions of any one of these terms. Furthermore, these terms are often used interchangeably when in fact the terms are by no means synonymous. The primary terms and definitions were born out of the International Classification of Impairments, Disabilities and Handicaps (ICIDH) published by the World Health Organization (WHO) in 1980. Presently, the primary organizations and agencies referenced for these definitions are the Social Security Administration (SSA), Americans with Disabilities Act (ADA), American Medical Association (AMA) (published in Guides to the Evaluation of Permanent Impairment) and the WHO (published in International Classification of Functioning, Disability and Health [ICF], 2001). There may also be definitions and criteria uniquely formulated by a particular state. Different government agencies and organizations develop variations of each definition to meet specific mandates or criteria for the population they serve. As a result, the definitions can differ from state to state and also can differ within each state. The different definitions and criteria also cannot be universally applied. Depending on the objective to be met, one agency’s definition and criteria is applicable where another’s may be ineffective. For example, in determining the degree of injury or determining work injury benefits one may refer to the AMA Guides (in states that use them). For application for Social Security disability insurance (SSDI) and supplemental security income (SSI) refer to the SSA. In protecting the individual from discrimination after an injury refer to the ADA. Given the variation in different agencies’ definitions, it is possible to have a person with a particular impairment deemed disabled by one agency or organization but considered not disabled by another. The objective of this chapter is to provide a focused reference to the various definitions of terms published by each of the above agencies and organizations and to highlight some distinguishing aspects of each. There will be particular emphasis on the ICF because (as a revision of the ICIDH, 1980) it attempts to create an international, universal standardized vocabulary and method of determining impairment, disability, and handicap by applying new terms and concepts. Note, however, that the conventional terms disability, impairment, and handicap and their respective definitions continue to remain the standard of reference to date. Therefore, a working knowledge and understanding of their use is required.

Impairment The different definitions of impairment follow. AMA guides A loss or loss of use or derangement of any body part, organ system, or organ function.

IMPAIRMENT, DISABILITY, AND HANDICAP

SSA An anatomical, physiological, or psychological abnormality which can be shown by medically acceptable clinical and laboratory diagnostic techniques. WHO A loss or abnormality in body structure or psychological function (including mental function). In this case, the definitions are fairly uniform and the concept fairly clear. Impairments can be traumatic loss of a limb, limited elbow joint range of motion secondary to an olecranon fracture, cardiomyopathy, multiple sclerosis, development of posttraumatic stress, etc. Some distinguishing points with regard to some of the organizations and agencies will be noted below. The AMA Guides focus on applying a rating to impairment where only impairments that interfere with activities of daily living (ADL) are ratable. The AMA also uses additional terms to characterize the impairment— functional loss and anatomic loss, defined as follows: Functional loss A reduction in the ability of a body part or system to perform a task in its normal or usual way, compared with either known populations or the individual’s prior known history. Anatomic loss Any measurable diminution of normal anatomic integrity, compared with either known populations or the individual’s prior known history. The ADA functions to protect an individual from a variety of defined forms of discrimination if an impairment “substantially interferes with major life activity.” The ICF views impairment as not being the same as the underlying pathology but as the manifestation of the pathology. The ICF recognizes impairment to be temporary or permanent, regressive or static, intermittent or continuous, slight or severe, and can fluctuate over time. The ICF holds the opinion that impairment is a deviation from certain generally accepted population standards in the biomedical status of the body and its functions, and definition of their constituents is undertaken primarily by those qualified to judge physical and mental functioning according to these standards. The ICF emphasizes reference to “body structure” and “body function” essentially to replace impairment as a term and has defined four categories: (1) lack or loss, (2) reduction, (3) addition or excess, and (4) deviation.

Disability The various agencies and organizations use their definition or concept of impairment or body structure or function deviation to validate or provide a basis of evidence to assist a person who can no longer compete in the workplace or who has a diminished capacity to function in his or her environment because of a medical condition. However, the degree of disability is influenced by multiple factors and is not directly proportional

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to the degree of impairment or body or structure deviation. Definitions used by the various agencies and organizations follow. AMA guides An alteration of an individual’s capacity to meet personal, social, or occupational demands or statutory or regulatory requirements because of an impairment. ADA • A physical or mental impairment that substantially limits one or more of the major life activities of such individual • A record of such an impairment • Being regarded as having such an impairment Any one of the three needs to be met. SSA The inability to engage in any substantial, gainful activity by reason of any medically determinable physical or mental impairment(s), which can be expected to result in death or which has lasted or can be expected to last for a continuous period of not less than 12 months. WHO An activity limitation (resulting from an impairment) that creates difficulty in the performance, accomplishment, or completion of an activity in the manner or within the range considered normal for a human being. There is a further distinction between true disability, defined as “the discrepancy between the current functional capacity and normal capacity,” and significant disability, defined as “a discrepancy between current functional capacity and what the person needs or wants to do.” These definitions suggest that a disability is based on the person’s capacity (physical or psychological) to meet functional requirements or achieve determined goals when having a medical condition. These terms are applicable only when there is a description of what it is the person is unable to do as the result of a medical condition. Example: A 40-year-old concert pianist loses the fifth digit of the nondominant hand. The impairment is the limb or digit amputation. The disability is the inability to properly form chords to adequately complete the task of piano playing.

Handicap This term is particularly misunderstood and often used interchangeably with disability. Of the agencies or organizations referenced above, the WHO offers the only definition: A disadvantage resulting from an impairment or disability that interferes with a person’s efforts to fulfill a role that is normal for that person. The word disadvantage in the definition implies an obstacle that can be increased or reduced to either prevent or allow an individual’s participation in his or her life situation. Example: A truck driver has an impairment (medical condition) as a result of a traumatic partial foot amputation in an accident. He is able to operate

IMPAIRMENT, DISABILITY, AND HANDICAP

his truck through application of a prosthetic foot (thus no disability), but he is handicapped because the state law prevents granting a driver’s license to an amputee. Example: A woman who has right hemiparesis secondary to a stroke is handicapped relative to her environment because she is unable to negotiate stairs to either enter or exit her home. Installing an elevator eliminates the handicap. The ICF suggests an assessment of the total person, considering their life experience, in the context of the person’s unique social and physical environment, because two people of the same age and gender with identical medical conditions can be affected in dramatically different ways. In an attempt to achieve this, the ICF has replaced handicap with the term participation restriction. The ICF proposes that one must consider the individual’s physical, psychological, social, and political environment as potential barriers restricting a person with a medical condition from participation in what he or she needs or wants to do—that is, “involvement in a life situation” or “the lived experience.” Disability (or activity limitation) differs, as it defines whether a person has a reduction or an alteration in the ability to perform a physical or mental task (activity limitation) when having a medical condition. The WHO essentially does not see handicap as entirely separate from disability. The ICF distinguishes disability as an umbrella term that denotes the negative aspects of the interaction between an individual (with a health condition) and that individual’s contextual (environmental) and personal factors. In fact, the objective of the ICF is to develop a formulation that defines disability uniquely using three domains: • Body structure and functions (impairment) • Person (activity) • Contextual factors (participation) as a secondary effect of injury and disease. The ICF states that it has moved away from disability being a “consequences of disease” classification to it becoming a “components of health” classification. Unfortunately, though widely recognized and referenced, there is no WHO international standard.

Conclusion Determining the degree to which a person’s life is impacted by a medical condition is complex and in part perplexing. Physicians, and particularly physiatrists, are often burdened with the task of being the key interpreter. Impairment, disability, and handicap continue to remain the primary terms used in both the medical and legal arenas, despite the inherent confusion of definitions. The WHO proposes new terms, definitions, and algorithms to function as a universal, international standard as published in the ICF. Although the WHO’s objective has not yet been achieved, clinicians should be familiar with the new terms and definitions and have a general knowledge and understanding of the existing terms and definitions and how to apply them.

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Further reading Braddom RL. (ed.) (2006). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders. Cocchiarella L, Andersson GBJ (eds.) (2001). Guides to the Evaluation of Permanent Impairment, 5th ed. Chicago: American Medical Association Press. Cocchiarella L, Lord SJ (eds.). (2001). Master the AMA Guides, 5th ed. Chicago: American Medical Association Press. Delisa JA, Gans BM, (eds.) (1998). Rehabilitation Medicine: Principles and Practices, 3rd ed. Philadephia: Lippincott-Raven. Rondinelli RD, Katz RT (eds.) (2001). Disability Evaluation. Physical Medicine and Rehabilitation Clinics of North America, Vol. 12, No. 3. World Health Organization (WHO) (1980). International Classification of Impairments, Disabilities and Handicaps: A Manual of Classification Relating to the Consequences of Disease. Geneva: World Health Organization. World Health Organization (WHO). (2008). International Classification of Functioning, Disability and Health (ICF). Geneva: World Health Organization.

Chapter 2

Head and neck Jay M. Weiss Rawa Araim Lyn Weiss Jose Mathew An overview of cervical pain 16 Cervical radiculopathy 18 Myelopathy 22 Cervical spondylosis 24 Cervical sprain and strain and whiplash 26 Cervical myofascial pain 28 Headache 30

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An overview of cervical pain Cervical pain is a symptom that may be the result of one or more diagnoses. Approximately 10% of the adult population has neck pain at any one time. Neck pain can be associated with arm or shoulder pain and can radiate from the neck to the trapezius area (unilateral or bilateral), the upper extremities, or the head (cervicogenic headaches). Few patients with neck pain lose time from work and less than 1% develop neurological deficits. Neck pain can arise from a variety of causes, such as: • Cervical disc disease • Cervical spondylosis • Cervical myofascial pain • Cervical strain and sprain including flexion extension injury (whiplash-associated disorders) The presence or absence of neurological signs determines the initial treatment of neck pain (see Fig. 2.1).

AN OVERVIEW OF CERVICAL PAIN

Neck pain

No neurological signs Conservative management

Neurological signs Myelopathic

Mild weakness or numbness

Referral to surgery

Moderate to severe weakness or numbness

Trial of conservative management

Trial of conservative management with close followup

If no improvement, consider interventional spine referral

If no improvement in 2 weeks, consider referral to interventional spine or surgery

Figure 2.1 Algorithm for treatment of neck pain.

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Cervical radiculopathy General description Cervical radiculopathy is most commonly due to compression of a cervical nerve root that causes pain or dysfunction. The compression is usually caused by cervical disc herniation or boney hypertrophy of the zygoapophyseal (or facet) joint, vertebral body, or uncovertebral joint, resulting in narrowing of the neural foramen. Noncompressive radiculopathies can be related to diabetes mellitus, neoplasm, or infection. In the cervical spine there are seven vertebrae. The nerve roots are numbered according to the vertebra below it (with C8 arising between C7 and T1). In contrast, in the thoracic spine and lumbar spine, the nerve roots are numbered on the basis of vertebra above (so the T1 nerve root exits below T1).

Clinical manifestations Cervical radiculopathy typically presents as neck pain radiating to the upper extremity. There may be associated sensory symptoms in a specific dermatomal distribution (see Fig. 2.2). Although weakness or sensory loss can occur, pain and paresthesia are usually the reasons for presentation. The spinal level involved determines the manifestation (see Table 2.1).

C2

C3 C4 C5 T2 T5 T4 T5 T6 T7 T8 T9 T10 T11

C6 C7 C8

T12 L1

C2 C3 C4 C5 T1 C6 C7 C8 T5 T7 T9 T1 L1 L3 L5

S1 S2 S3 S4 S5

T2 T4 T6 T8 T10 T12 L2 L4

C6 C7

L2

L3

L4

S1 S2

S1 L5 L4 S1 L5 L4

Figure 2.2 Dermatomal distribution of nerve roots. This figure was published in Weiss L, Silver JK, Weiss J (2004). Easy EMG: A Guide to Performing Nerve Conduction Studies and Electromyography. Philadelphia: Butterworth-Heinemann/Elsevier, p. 173. Copyright Elsevier (2004). Reprinted with permission.

CERVICAL RADICULOPATHY

Table 2.1 Cervical radiculopathy features by level (in order of frequency of occurrence) Level

Subjective

Exam

C7

Neck pain radiating to the affected arm, mostly to the third, or second and third digit (possibly with numbness in that distribution)

Motor: Weakness in elbow extension, wrist flexion and extension. Sensory: Decreased sensation digit 3, or 2 and 3. Reflex: Triceps may be decreased.

C6

Neck pain radiating to the shoulder, lateral arm and thumb, or thumb and second digit

Motor: Weakness in elbow flexion, wrist extension, and forearm pronation. Sensory: decreased in first 2 digits. Reflexes: Biceps, brachioradialis may be decreased.

C8

Neck pain radiating to the shoulder, medial side of arm, and ulnar side of hand

Motor: Weakness in hand intrinsics (finger abduction and adduction), thumb abduction and thumb and finger flexion. Sensory: Decreased in fourth and fifth digits. Reflexes: No abnormalities.

C5

Neck pain radiating to the shoulder

Motor: Weakness in shoulder abduction and external rotation, and elbow flexion. Sensory: Decreased lateral shoulder. Reflexes: Biceps and brachioradialis may be decreased.

Differential diagnosis The primary differential diagnosis includes spondylosis, cervical sprain, myofascial pain, and brachial plexopathy. Pain that radiates to bilateral upper extremities usually indicates a myofascial etiology.

History Most cases occur spontaneously without previous trauma. Patients complain primarily of pain in the neck and into an extremity (generally in a specific distribution). The C7 nerve root is the most commonly involved nerve root, followed by C6, C8, and C5.1 Patients may report pain and paresthesia or sensory loss in a specific (dermatomal) distribution. Less commonly, patients may report weakness in an involved extremity.

Physical The physical examination should adequately assess motor and sensory function in both upper extremities. The clinician should note which extremity is dominant so that a subtle weakness in the dominant extremity 1 Radhakrishnan K, Litchy WJ, O’Fallon WM, Kurland LT (1994). Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 117 (Pt 2):325–335.

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is appreciated. Frequently patients with cervical radiculopathies are not aware of subtle weaknesses, as patients are usually preoccupied with the pain or sensory complaints. Reflexes should be tested, and may be decreased (asymmetrical) if a radiculopathy is present. Gait and lower extremity reflexes should be assessed to look for signs of myelopathy (scissoring gait or increased reflexes). Cervical compression (Spurling’s sign) and manual traction may reproduce or alleviate symptoms, respectively.

Diagnostic testing Magnetic resonance imaging (MRI) is useful for evaluation of the spinal canal, intervertebral disc, nerve root, and foramen. If MRI is contraindicated, computed tomography (CT) is appropriate. Electrodiagnostic studies may be performed to establish the diagnosis, rule out peripheral neuropathy or peripheral nerve entrapment, and provide assessment as to the degree of nerve damage. Electromyography (EMG) is particularly helpful in distinguishing between C8 radiculopathies and ulnar neuropathies, but can also be helpful at higher levels.

Special considerations In elderly patients, MRI findings are usually present, even in asymptomatic patients. The high sensitivity of MRI may yield findings that are not of clinical significance. Therefore, MRI and neuroimaging results must be put into context based on the patient’s clinical picture. In addition, patients may have multiple etiologies for their pain.

Management (treatment) Depending on the level of pain and neurological involvement, treatments may include physical therapy (cervical traction), nonsteroidal anti-inflammatory drugs (NSAIDs), pain medications, oral steroids, or membrane-stabilizing medication (gabapentin or pregabalin). Epidural steroid injections may be performed for cases that do not respond to these treatments. Because most cases of cervical radiculopathy resolve over time, it is difficult to definitively determine the value of any interventions. Surgical discectomy is generally reserved for intractable pain or progressive or significant neurological dysfunction.

Complications and red flags Progressive or significant neurological deficits should lead to more aggressive treatment, including an evaluation for spine surgery. Always assess for myelopathic lesions (upper motor neuron signs in the lower extremities, such as increased reflexes or spasticity).

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Myelopathy General description Myelopathy refers to a neurological deficit related to damage to the spinal cord. Myelopathy can occur as a result of extradural, intradural, or intramedullary processes. In general, myelopathy is clinically divided into categories based on the presence or absence of significant trauma, presence or absence of pain, and the mode of onset (slowly progressive or insidious onset vs. a stepwise progression vs. a sudden onset).1 Among the most common causes of spinal cord compression are osteophytes or disc material. Other causes include extradural or intradural masses (carcinomatous metastasis) and trauma. Myelopathy may result from primary carcinomas, inflammatory, infectious, or vascular processes, radiation, HIV, transverse myelitis, or nutritional or neurodegenerative changes. Intradural causes include cysts or syrinx, progressive posttraumatic myelomalacic myelopathy, and benign neoplasms (meningiomas, arachnoid cysts, epidermoid cysts, and nerve sheath tumors).

Clinical manifestations The clinical manifestations will depend on the level of the lesion, the rapidity of progression, and the type of insult (see Table 2.2).

History When trying to determine the etiology of myelopathy, it is important to elicit whether there is a history of spinal trauma, the onset and progression of symptoms, and if pain, weakness, numbness, incontinence, or gait disturbance are present.

Physical The physical findings will depend on the location of the insult to the spinal cord. Usually, there are upper motor neuron findings below the level of the lesion (i.e., hyperactive reflexes, Babinski sign, spasticity). Depending on the lesion, there may be lower motor neuron findings at the level of the lesion (i.e., hypoactive reflexes, decreased tone, atrophy, fasciculations).

Diagnostic testing The appropriate tests for the diagnosis of myelopathy depend on whether the patient presents with trauma or pain, and the mode of onset.1 MRI has become the mainstay of testing for myelopathy. CT may be more useful if trauma or bony injury is suspected. Depending on the presentation, some of these studies may need to be done urgently or emergently.

1 Seidenwurm DJ, Brunberg JA, Davis PC, De La Paz RL, Dormont PD, Hackney DB, Jordan JE, Karis JP, Mukherji SK, Turski PA, Wippold FJ II, Zimmerman RD, McDermott MW, Sloan MA, Expert Panel on Neurologic Imaging (2006). Myelopathy [online publication]. Reston, VA: American College of Radiology (ACR).

MYELOPATHY

Management (treatment) Myelopathy frequently requires spinal surgery, especially when cauda equina syndrome or progressive neurological deficits are present. In these neurological emergencies, urgent spine surgery or another intervention (radiation therapy, or intrathecal, epidural, or systemic medications) is required. Table 2.2 Spinal cord lesions Spinal cord lesion Spinal cord transection

Symptoms Loss of sensation and motor below the lesion, loss of bowel and bladder

Causes Trauma, transverse myelitis, mass

Dorsal (posterior) cord syndrome

Loss of sensation, vibration, and proprioception below the lesion. Pain and temperature preserved. May have motor or bladder dysfunction

Syphilis, mass, Friedreich ataxia, multiple sclerosis (MS)

Ventral cord syndrome (anterior 2/3 of spinal cord preserving the posterior columns)

Loss of pain and temperature, weakness and bladder dysfunction. Preservation of proprioception and light touch

Spinal cord infarction, disc herniation, radiation myelopathy

Central cord syndrome (injury to center of the spinal cord)

Loss of pain and temperature, weakness—arms greater than legs, sacral sensory sparing

Syringomyelia, tumor (intramedullary), trauma

Brown–Sequard syndrome (spinal hemisection)

Ipsilateral loss of proprioception and weakness, contralateral loss of pain and temperature

MS, trauma

Motor syndrome

Weakness without sensory loss

Poliomyelitis, amyotrophic lateral sclerosis (ALS)

Conus medullaris syndrome (L1–L2 vertebral level injury to sacral cord S1–S5)

Saddle anesthesia, bowel and bladder dysfunction

Disc herniation, trauma, tumor, L1 fracture, vascular injury, spina bifida, tethering of cord

Cauda equina syndrome (L2 to sacrum vertebral level injury to nerve roots)

Asymmetrical pain, flaccid leg weakness, sensory loss, bladder dysfunction, areflexia

Disc herniation, tumor, stenosis in region of the cauda equina, sacral fracture

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Cervical spondylosis General description Cervical spondylosis is a chronic degenerative condition of the cervical spine. Spondylosis changes are ubiquitous with age and are frequently asymptomatic. Spondylosis can affect the vertebral bodies, the intervertebral disks (e.g., disk herniation, spur formation), or the contents of the spinal canal (nerve roots and/or spinal cord). Degenerative changes can also involve the facet joints, longitudinal ligaments, or ligamentum flavum. Chronic cervical degeneration is the most common cause of progressive spinal cord and nerve root compression. Spondylitic changes can result in spinal canal, lateral recess, and foraminal stenosis. Spinal canal stenosis can result in myelopathy.

Clinical manifestations Spondylosis, when symptomatic, will manifest primarily as cervical pain and/ or posterior headache. The pain may be perceived locally, or it may radiate to the occiput, shoulder, scapula, or arm. The pain can interfere with sleep. If the spinal canal or intervertebral foramen is sufficiently compromised, nerve involvement can be present (see Myelopathy and Radiculopathy sections, pp. 18, 22).

History Symptoms are usually of insidious onset, as this is a chronic degenerative process. Acute injury, strain, or abnormal positioning may precipitate the onset or realization of symptoms.

Physical On examination, cervical motion is frequently decreased. Crepitus, tenderness, spasm, or guarding may be present. The cervical examination should include a neurological assessment of the upper extremities for neurological compromise. Gait and lower extremity reflexes should be assessed to rule out myelopathy.

Differential diagnosis Adhesive capsulitis, cervical disc disease, cervical sprain and strain, myofascial pain, multiple sclerosis (MS), and rheumatoid arthritis are included in the differential diagnosis.

Diagnostic testing No specific lab testing is diagnostic of cervical spondylosis. Plain radiographs are most commonly used to assess spondylosis and will show degenerative changes. CT or MRI can be used to evaluate for spinal cord compression. CT myelography is commonly used prior to surgical decompression. EMG/nerve conduction velocity (NCV) can be used to evaluate nerve root dysfunction. Somatosensory evoked potential (SSEP) can provide a functional evaluation of the spinal cord (primarily used if myelopathy is suspected) but is not useful if radiculopathy or peripheral nerve entrapment is being considered.

CERVICAL SPONDYLOSIS

Management Physical therapy of the cervical spine and surrounding musculature is the mainstay of conservative treatment for patients with cervical spondylosis. Modalities including electric stimulation, ultrasound, and heat frequently provide symptomatic relief and restore motion, allowing normal movement and exercise. Mechanical or manual traction is a widely used technique. The use of cervical exercises has been advocated in patients with cervical spondylosis. Isometric exercises often are beneficial to maintain strength of the neck muscles. Manual therapy (e.g., massage, mobilization, manipulation) may provide further relief for patients with cervical spondylosis. If transcutaneous electrical nerve stimulation (TENS) provides relief in therapy, a home unit should be considered. When pharmacological therapies are used, the potential risk (especially of long-term use) must be weighed. Topical treatments (counterirritant gels and creams, lidocaine, or diclofenac patches) can be helpful and are generally safest. Acetaminophen and NSAIDs are frequently used. Other medications include tramadol and, less frequently, opioid analgesics. Trigger point injections can also provide symptomatic relief. Surgical intervention is generally reserved for cases with neurological involvement.

Complications Cervical myelopathy is the most serious consequence. Nerve root impingement may also occur. Chronic pain syndrome may result if the patient’s complaints of pain are not adequately addressed.

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Cervical sprain and strain and whiplash General Cervical and upper back pain can occur with injuries (straining with lifting, trauma, or falls) or rapid flexion and extension, as can occur with a motor vehicle accident (MVA). Because there may not be any specific radiographically detectable lesion, the specific diagnosis for the same condition can vary by practitioner. In whiplash-associated disorders (WAD), the mechanism of injury is a rapid extension of the neck followed by a rapid flexion. The muscles, tendons and/or ligaments of the neck can be injured (either grossly torn or disrupted on a microscopic level). Anterior neck muscles such as the sternocleidomastoid can also be disrupted. The initial evaluation of these disorders involves assessment of neurological involvement or spinal instability (especially in the case of whiplash or other trauma). Barring neurological involvement or spinal instability, conservative treatment can be initiated.

Clinical manifestations Cervical sprain or strain and WAD present primarily with pain in the cervical region and upper back, head, and upper extremities. If pain radiates, it is typically diffuse and not in a dermatomal distribution. A dermatomal distribution should lead to consideration of radiculopathy or other nerve entrapment.

Differential diagnosis While the etiology in WAD or a strain or fall may be obvious, the exact type and location of the injury and its mechanism may not be. Commonly implicated structures are paraspinal muscles, trapezius, sternocleidomastoid muscle, scalenes muscle, spinal ligaments, facet joints, vertebrae, and intervertebral discs. Fractures, nerve injury, or headache related pain syndromes should be included in the differential diagnosis.

History In cases of strain or sprain, there is usually a history of an event that caused the symptoms. In WAD, the etiology is obvious. In addition to establishing the mechanism of injury, the history should determine any evidence of “red flags” such as numbness or weakness (particularly with cervical motion), which could indicate nerve compromise or instability. Patients may complain of associated headaches.

Physical As with most cervical disorders, the neurological status of the extremities should be assessed to rule out other disorders. The primary findings are generally tenderness to palpation and decreased or abnormal cervical motion (due to pain or guarding). Muscle spasm may be present.

Diagnostic testing In the absence of nerve compromise or spinal instability, imaging is generally not helpful in the early stages. Radiological studies (X-ray) can be

CERVICAL SPRAIN AND STRAIN AND WHIPLASH

useful in trauma to rule out fracture, and flexion/extension views can evaluate instability. CT may show subtle fractures that plain X-rays can miss. MRI can evaluate the spinal cord and the intervertebral disc for herniations. In cases of possible nerve involvement, EMG/NCV studies can be valuable.

Special considerations There is a great deal of controversy about and variability in reported outcomes in soft tissue cervical injuries. In many cases, workers’ compensation, no-fault/motor vehicle insurance laws, or disability considerations introduce the possibility of secondary gain or may encourage the reporting of symptoms. A review of the literature gives wide variations in outcomes, some noting no increased neck pain 1 year after MVA (compared to controls without MVA), and other studies noting symptoms in 58% of patients 2.5 years after MVA.1

Management (treatment) While there is variability among different practitioners, physical therapy of the cervical spine is commonly employed. Modalities including electric stimulation, ultrasound, and heat frequently provide symptomatic relief and restore motion, allowing normal movement and exercise. Mechanical or manual traction are widely used techniques. The use of cervical exercises has been advocated in patients with cervical spondylosis. Isometric exercises are often beneficial to maintain strength of the neck muscles. Manual therapy (e.g., massage, mobilization, manipulation) may provide further relief. Cervical collars are generally not recommended as their use may delay recovery.2 Muscle relaxants, NSAIDs, and analgesics are commonly used as an adjunct to therapy. Trigger point injections may be used as an adjunct as well.

Complications and red flags Appropriate imaging should be performed if there is evidence of instability or progressive neurological involvement, as this may require surgical intervention. Muscular pain not responding to conservative treatment should be further evaluated. In general, treatments that are not beneficial should be discontinued.

Further reading Glass LS, Harris JS, Blais BR, et al. (2004). Neck and upper back complaints, In Occupational Medicine Practice Guidelines, 2nd ed. Beverly Farms, MA: OEM Press, pp. 165–194. 1 Rodriquez AA, Barr KP, Burns SP (2004). Whiplash: pathophysiology, diagnosis, treatment, and prognosis, Muscle Nerve 29:768–781. 2 Spitzer WO, Skovron ML, Salmi LR, et al. (1995). Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining “whiplash” and its management. Spine 20(8 Suppl): 267.

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Cervical myofascial pain General description Cervical myofascial pain is pain originating in the muscles and fascia around the neck. The primary muscle involved is the trapezius. The cause of this pain can be acute (an injury or strain) or chronic (tension, posture). The clinical picture can overlap with cervical sprain or whiplash; however, myofascial pain is characterized by diffuse tender areas in the muscle. These tender areas will refer pain on pressure and are termed trigger points. While this clinical phenomenon has been described by many, it cannot be objectively verified by pathological, laboratory, or radiological findings. This has led to some controversy. Fibromyalgia has a similar presentation and symptoms may overlap with those of myofascial pain. However, in fibromyalgia among other differences, the tender points are more diffuse (see Chapter 6, Fibromyalgia, p. 166).

Clinical manifestations Cervical myofascial pain involves primarily the trapezius in the cervical and upper thoracic region. Pressure on trigger points will typically radiate pain in a characteristic distribution that is not dermatomal. A dermatomal distribution should lead the clinician to consider radiculopathy or other nerve entrapment.

Differential diagnosis Cervical spondylosis, radiculopathy, and sprain may all present similarly. There may be myofascial components in these disorders. The presence of trigger points indicates a myofascial component.

History There may be a history of trauma, repetitive use, or overuse. Stress may precipitate and perpetuate myofascial pain. Some acute injuries may develop into myofascial pain.

Physical As with most cervical disorders, the neurological status of extremities should be assessed. There should be no neurological findings if the diagnosis is only myofascial (i.e., normal reflexes, strength and sensation). The primary findings are generally tenderness to palpation, and decreased or abnormal cervical motion (due to pain or guarding). Tight bands in the muscle may be palpated in addition to trigger and tender points.

Diagnostic testing There are no specific radiological, pathological, or blood findings in myofascial pain. Lab tests to rule out arthritides may be indicated. With persistent cervical pain, MRI can evaluate the spinal cord and the intervertebral discs for herniations. In cases of possible nerve involvement, EMG/NCV studies can be valuable.

CERVICAL MYOFASCIAL PAIN

Special considerations As with any diagnosis that cannot be objectively verified by testing, controversy exists regarding the diagnosis.

Management (treatment) Trigger point injections are commonly employed. Physical therapy of the cervical spine is usually beneficial. Stretch and spray technique with vapocoolant spray can be helpful.1 Modalities including electric stimulation, ultrasound, and heat frequently provide symptomatic relief and restore motion, allowing normal movement and exercise. Mechanical or manual traction are widely used techniques. The use of cervical exercises has been advocated for patients with cervical spondylosis. Isometric exercises are often beneficial to maintain strength of the neck muscles. Manual therapy (e.g., massage, mobilization, manipulation) may provide further relief. Cervical collars are generally not recommended. Muscle relaxants, NSAIDs, and analgesics are commonly used as an adjunct to therapy. Antidepressants are sometimes very helpful. If there is an abnormal sleep pattern, this should be addressed.

Complications and red flags Positive neurological findings should lead to consideration of another diagnosis. If the patient is not responding to treatment, testing should be performed to rule out other diagnoses.

Further reading Frontera WR, Silver JK, Rizzo TD (eds.) (2008). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier, pp. 37–40. 1 Travell JG, Simons DG (1983). Myofascial Pain and Dysfunction. Philadelphia: Williams and Wilkins, pp. 183–201.

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Headache General Headache, or cephalalgia, is defined as diffuse pain in various parts of the head. The pain is not confined to the distribution of a nerve. Headache is among the most common pain problems encountered in practice.

History To ascertain the cause of the headache, patients should be asked the following questions: • Is this your first or worst headache? • How bad is your pain on a scale of 1 to 10 (1 meaning not too bad, and 10 meaning very bad)? Do you have headaches on a regular basis? • Is this headache like the ones you usually have? • What symptoms do you have before the headache starts? What symptoms do you have during the headache? What symptoms do you have right now? • When did this headache begin? How did it start (gradually, suddenly, other)? What were you doing (or do you do) that triggered the headache? • Where is your pain? Does the pain seem to spread to any other area? If so, where? • What is the quality of your pain (throbbing, stabbing, dull, other)? • Do you have other medical problems? If so, what? • Do you take any medicines? If so, what? • Have you recently hurt your head or had a medical or dental procedure?

Physical The primary purpose of the physical examination is to identify causes of secondary headaches. The examination should target areas identified as abnormal during the headache history. The general physical examination should include vital signs, funduscopic and cardiovascular assessment, and palpation of the head and face. A complete neurological examination is essential, and the findings must be documented. The examination should include mental status testing, level of consciousness, cranial nerve testing, pupillary responses, motor and strength testing, deep tendon reflexes, sensation, pathological reflexes (e.g., Babinski’s sign), cerebellar function, gait testing, and signs of meningeal irritation (Kernig’s and Brudzinski’s signs). Particular attention should be given to detecting problems related to the optic, oculomotor, trochlear, and abducens nerves (cranial nerves II, III, IV, and VI, respectively).

Diagnostic testing The diagnosis is usually made on the basis of the patient’s history and physical, but the physician should consider further testing if indicated. • A CT scan should be done to rule out acute hemorrhage in instances of trauma. • MRI can help assess posterior fossa pathology and is more specific than CT scans for intracranial pathology.

HEADACHE

• CT scanning without contrast medium, followed by lumbar puncture if the scan is negative, is preferred to rule out subarachnoid hemorrhage within the first 48 hours. • Lumbar puncture is useful for evaluating the cerebrospinal fluid (CSF) for blood, infection, and cellular abnormalities. • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP): elevation can suggest temporal arteritis. Tests for Lyme disease, HIV, and infectious mononucleosis may be performed if clinically suspicious.

Differential diagnosis Tension (muscle spasm), cluster (histamine), and migraine headaches are the usual causes of headaches not associated with structural lesions (see Table 2.3). Headache with serious underlying causes includes brain tumor, intracranial hemorrhages, meningitis, temporal arteritis, and glaucoma.

Management (treatment) (see Table 2.3) Depending on the cause of the headache, treatment includes acetaminophen, NSAIDs, tryptans, and (rarely) opiates. Prophylactic treatments of migraine Table 2.3 Characteristics of migraine, tension, and cluster headaches Location

Migraine Tension Bilateral Hemicranial, often unilateral; bifrontal or global in 30%

Cluster Unilateral, usually begins around eye or temple

Signs and symptoms

Throbbing lasting 2–20 hours, nausea and/or vomiting. Aura is classic. No aura is common.

Tight band-like pain exacerbated by noise, bright lights, fatigue, or stress

Ipsilateral lacrimation and redness of the eye; stuffy nose; pallor; sweating; Horner’s syndrome, focal neurological symptoms, sensitivity to alcohol

Duration

4–72 hours

Variable

30 minutes to 3 hours

Appearance

Patient prefers to rest in quiet room

Patient may remain active or may rest

Patient remains active

Workup

CT scan with contrast or MRI on first presentation

Imaging not necessary, Diagnosis of exclusion unless used to rule out other causes

Treatment

Abortive: ASA, NSAIDS, tryptans, ergots, rarely opiates Prophylactic: propranolol, verapamil, amitryptaline, valproic acid

Relaxation, massage, NSAIDs, regular diet, exercise, Botox Prophylactic: TCAs, SSRIs, calcium channel blockers, betablockers

Abortive: 100% oxygen, tryptans, ergots, intranasal lidocaine, corticosteroids Prophylactic: Calcium channel blockers, ergots, valproic acid, prednisone

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headaches include the beta-blockers, anticonvulsant, tricyclic antidepressant (TCA), monoamine oxidase (MAO) inhibitors, and serotonoergic drugs. Botulinum toxin has been used fully success in tension headaches. The underlying cause of secondary headaches should be addressed.

Complications and red flags “Worst headache ever” and “first severe headache” are complaints that suggest a serious underlying disorder. Other symptoms that deserve serious attention include abnormal neurological findings, headaches worsening over days or weeks, fever, vomiting preceding the headache, and onset after age 55 (see Table 2.4). Table 2.4 Red flags in evaluation of acute headaches in adults Red flag

Differential diagnosis

Possible workup

Headache beginning after Temporal arteritis, mass 50 years of age lesion

ESR, neuroimaging

Sudden onset of headache

Subarachnoid hemorrhage, pituitary apoplexy, hemorrhage into a mass lesion or vascular malformation, mass lesion (especially posterior fossa mass)

Neuroimaging; lumbar puncture if neuroimaging is negative

Headaches increasing in frequency and severity

Mass lesion, subdural hematoma, medication overuse

Neuroimaging, drug screen

New-onset headache in a patient with risk factors for HIV infection or cancer

Meningitis (chronic or carcinomatous), brain abscess (including toxoplasmosis), metastasis

Neuroimaging; lumbar puncture if neuroimaging is negative

Headache with signs of systemic illness (fever, stiff neck, rash)

Meningitis, encephalitis, Lyme Neuroimaging, lumbar puncture, serology disease, systemic infection, collagen vascular disease

Focal neurological signs Mass lesion, vascular or symptoms of disease malformation, stroke, (other than typical aura) collagen vascular disease

Neuroimaging, collagen vascular evaluation (including antiphospholipid antibodies)

Papilledema

Neuroimaging, lumbar puncture

Mass lesion, pseudotumor cerebri, meningitis

Neuroimaging of brain, Headache subsequent to Intracranial hemorrhage, head trauma subdural hematoma, epidural skull, and possibly cervical spine hematoma, posttraumatic headache

Further reading Clinch CR (2001, Feb 15). Evaluation of acute headaches in adults. Available at: http://www.aafp.org

Chapter 3

Spine Lyn Weiss Rebecca Trangco-Evans Shilo Kramer Sina Menashehoff Jay M. Weiss Walter J. Gaudino Christopher Burrei Thomas A. Riolo Thomas Pobre Compression fractures 34 Osteoporosis 36 Scoliosis 42 Thoracic radiculopathy and thoracic intervertebral disc herniations 48 Lumbar sprain, strain 50 Lumbar radiculopathy 54 Lumbar spinal stenosis 58 Cauda equina and conus medullaris syndrome 60 Lumbar spondylosis 62 Spondylolisthesis 64 Spondylolysis 68

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Compression fractures General description Compression fractures are fractures of the vertebrae, most commonly due to osteoporosis, but they can also occur with trauma or tumors.

Clinical manifestations Severe pain in the area of the fracture (usually the lower thoracic or upper lumbar vertebrae) is the most common manifestation. The pain is usually sharp and relieved with rest. Activity often increases the pain. The pain is worse for the first 2–3 weeks after fracture, but generally remains severe until about 6–8 weeks. Pain may be due to the compression fracture itself or associated paraspinal muscle spasm. Chronic pain may develop. Although rare, compression fractures can be asymptomatic.

Differential diagnosis The differential diagnosis includes neoplasm (especially if pain is worse at night), abdominal visceral disorders (especially pancreatic), or abdominal aortic aneurysm.

History Pain in the area of compression is the most common symptom. Compression fractures are most commonly associated with osteoporosis, although they may be secondary to trauma. Risk factors for osteoporosis and subsequent compression fracture include smoking, alcohol use, low body mass, Caucasian, sedentary lifestyle, glucocorticoid use, rheumatoid arthritis, and decreased vitamin D and calcium intake. Patients may complain of gastrointestinal discomfort (due to abdominal protuberance). Decreased lung volume may lead to shortness of breath.

Physical Patients with compression fractures may demonstrate kyphosis (Dowager’s hump) and loss of height. The patient’s abdomen may protrude. Increased pain with lateral rotation and bending may indicate costal iliac impingement.1

Diagnostic testing X-rays usually show compression involving the anterior aspect of the vertebral body. Bone scanning may show increased activity at the site of the fracture.

Special considerations Patients with compression fractures suffer significant morbidity. They may have severe back pain for 2–3 months after the fracture, and 70% have

1 Cucurillo S (2004). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical Publishing, p. 686.

COMPRESSION FRACTURES

chronic pain that limits their activities. In addition, there is a 15% increase in mortality during the 5 years after the fracture.2,3

Management (treatment) Vertebroplasty (percutaneous injection with methylmethacrylate via fluoroscopic guidance) and kyphoplasty (restoring height of the vertebral body by inserting an inflatable balloon into the vertebral body and filling the space with methylmethacrylate) have both been used in the treatment of compression fractures. Kyphoplasty may help to restore vertebral height (reducing a 30* wedge deformity to as little as 5*), whereas vertebroplasty does not restore vertebral height. Both procedures help to increase structural stability and reduce pain. Opioid analgesics are frequently necessary for pain relief and occasionally bed rest may be required. Orthoses may be used (if tolerated) for pain relief and to prevent flexion; the orthoses generally promote extension. The aim is to load the posterior elements and unload the vertebral bodies. Prolonged use of an orthotic should be avoided as it can lead to weakened trunk muscles and decreased mobility. Spinal extension exercises should be initiated as soon as pain is manageable. Therapy may also include pectoral stretching, isometric abdominal strengthening, deep-breathing exercises, and weight-bearing exercises. Treatment should also be directed at the cause of compression fracture. Osteoporosis, if present, should be treated (see Management in Osteoporosis section, p. 38).

Complications and red flags Retropulsion of fragments may lead to spinal cord injury. Complications of vertebroplasty and kyphoplasty can also occur.

2 Bernstein J (ed.) (2003). Musculoskeletal Medicine. Rosemont, IL: American Academy of Orthopaedic Surgeons, p. 144. 3 Osteoporosis: review of the evidence for prevention, diagnosis, and treatment and cost-effectiveness analysis. Introduction. Osteoporosis Int 1998; 8(Suppl 4):S7–S80.

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Osteoporosis General description Osteoporosis is a skeletal disorder characterized by compromised bone strength that predisposes to an increased risk of fracture. Bone density is >2.5 standard deviation (SD) below the mean (T score ≤2.5) of young healthy adults. Osteoporosis is caused by an increase in bone resorption without an increase in bone formation, leading to decreased bone mass, disrupted trabecular connectivity, loss of architecture, and increased cortical porosity. There is a normal ratio of organic and mineral components.

Clinical manifestation Osteoporosis is a silent disease—fracture is commonly the first presentation. Thin, white females with advanced age are at highest risk. The most common sites of fractures are the vertebral spine (mid-thoracic and upper lumbar), hip, and wrist (in descending order). Compression fractures of the vertebra may present with acute back pain that is worse on weight bearing. Half of these fractures are subclinical and patients might not seek medical attention.1 Chronic pain can be due to microfractures that are visible only on bone scanning.

Differential diagnosis The differential diagnosis includes osteomalacia, Paget’s disease, metastatic bone disease causing fractures, immobilization, genetic disorders (e.g., osteogenesis imperfect), and endocrine- (e.g., hypogonadism) and drugrelated (glucocorticoids) disorders.

History Fractures can occur with a history of minimal or no trauma, such as after an affectionate hug1 or a fall from sitting or standing position. Risk factors include white female, advanced age, low body weight, smoking, excess alcohol use, certain medications (see Boxes 3.1 and 3.2), previous fracture as an adult, inadequate physical activity, and a family history of osteoporosis.

Physical Multilevel vertebral fractures can lead to kyphosis, abdominal protrusion, and loss of height. As a consequence of kyphosis, decreased pulmonary function and changes in the abdominal cavity can lead to shortness of breath and esophagitis, respectively. Kyphosis can also lead to iliocostal friction syndrome.

Diagnostic testing Dual energy X-ray absorptiometry (DEXA) is the gold standard for bone density measurement. Plain X-ray, bone scan, CT scan, or MRI may be used to assess for fractures. An X-ray of the thoracolumbar spine may show increased lucency of vertebral bodies, loss of horizontal trabecula, increased prominence of cortical end plates and anterior wedging, or loss in both anterior and posterior height of vertebral bodies (as in the case of complete compression fractures).1 1 Braddom R (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: WB Saunders, pp. 932–933.

OSTEOPOROSIS

Box 3.1 Medical conditions that may increase risk for fractures2,3 • Endocrine • Hyperthyroidism, hyperparathyroidism, hypogonadism, Cushing’s syndrome, diabetes mellitus type 2, hyperprolactinemia, hypercalciuria, hyperthyroidism • Renal • CRF, ESRD, RTA, renal osteodystrophy • Rheumatological/connective tissue • Ankylosing spondylitis, rheumatoid arthritis, Ehlers–Danlos, Marfan syndrome • Gastrointestinal/hepatic • Gastrectomy/bariatric surgery, celiac disease, malabsorption of calcium, cirrhosis • Infiltrative • Multiple myeloma, leukemia, mastocytosis, thalassemia • Nutritional/metabolic • Eating disorders, vitamin B12 deficiency, vitamin D deficiency, elevated homocysteine levels • Genetics • Osteogenesis imperfect, Ehlers–Danlos, homocystinuria • Immobilization

Box 3.2 Medications contributing to bone loss4 • • • • • • • • •

Glucocorticoids Long-acting progestins Aromatase inhibitors Gonadotropin-releasing hormone agonists Anticonvulsants Cytotoxic drugs Long-term heparin Lithium Proton pump inhibitors

2 Frontera WR, Silver JK (eds.) (2002). Essentials of Physical Medicine and Rehabilitation. St. Louis: Hanley & Belfus. 3 Hodgson SF, Watts NB, et al. (2003). American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocr Pract 9(6):544–564. 4 Yang YX, Lewis JD, Epstein S, Metz DC (2006). Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA 296(24):2947–2953.

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Laboratory studies to rule out secondary causes include complete blood count (CBC), chemistries, 25(OH)D, parathyroid hormone (PTH), thyroid-stimulating hormone (TSH), alkaline phosphatase, renal/liver function, gonadal function, and 24-hour urine for calcium and creatinine.

Special consideration The female: male ratio is 7:1 for vertebral fractures, 2:1 for hip fractures, and 5:1 for Colle’s fractures. There is a 15%–20% mortality rate (male >female) for hip fracture. Less than 50% of hip fracture patients recover prefracture functional level. Comparison DEXA scans must be done in the same laboratory when used to assess response to treatment.

Management Prevention (nonpharmacological) measures consist of adequate intake of calcium (1200–1500 mg/day) and vitamin D (sunlight/supplementation 800–1000 IU/day, to achieve >30 ng/mL 25(OH)D levels), good general nutrition, regular weight bearing exercises, avoidance of tobacco and excess alcohol, and fall prevention strategies. Treatment depends on the extent of osteoporosis (see Table 3.1). For pharmacological treatment see Table 3.2.

OSTEOPOROSIS

Table 3.1 Guidelines for therapy1 T score −1 SD (normal)

−1 to −2.5 SD (osteopenia)

−2.5 SD or more (osteoporosis)

No pharmacologic treatment Preventive measure, patient education, diet Calcium and vitamin D

Consultation for treatment, antiresorptive if (+) fracture Preventive measures Patient education, pain management

Pharmacological intervention Pain management, modalities if indicated Thoracic weighted kypho-orthosis ± lower back support

Lifting technique, weight training, jogging short distances

Limit load lifting 10–20 lbs Weight training 3x a week, walking 40 min/ day; back/abdominal strengthening

Back extensor strengthening when acute pain subsides; start strengthening program with 1–2 lb and increase as tolerated Walking 40 min/day as tolerated Limit load 5–10 lbs

Abdominal and back strengthening exercises

Fall prevention

Balance evaluation, assistive device Home evaluation for safety, fall prevention

Bone mineral density (BMD) testing every 3–5 years, no further testing if T score well above minimum

When on therapeutic program, BMD testing yearly for 2 years, follow-up every 2 years

Repeat BMD yearly every 2 years, then every 2 years once stabilized

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Class

Dose

Action

Adverse reaction

Alendronate (Fosamax)

Biphosphonate

10 mg/day, 70 mg once a week taken with a full glass of water before breakfast; remain in upright position 30–45 minutes after dose

Antiresorptive, acts on osteoclast, dvertebral (50%) and novertebral fracture (51%)

Esophageal irritation

Risedronate (Actonel)

Biphosphonate

Antiresorptive, dvertebral (45%) and nonvertebral fractures (36%)

Esophageal irritation

Ibandronate

Biphosphonate

5 mg/day, 35 mg once a week taken with a full glass of water before breakfast; remain in upright position for 30–45 minutes 2.5 mg/day, 150 mg monthly PO or 3 mg IV every 3 months

Antiresorptive, dvertebral fractures (52%)

Esophageal irritation Osteonecrosis of the jaw with IV preparation

Raloxifene (Evista)

60 mg/day PO Selective estrogen receptor Modulator

Antiresorptivedvertebral fractures (30%), no effect on nonvertebral fractures

Leg cramps, hot flashes, deep vein thrombosis

Cacitonin (Miacalcin)

Hormone

200 units nasal spray or 50–100 mg Antiresorptive, dvertebral fractures (33%), no effect on every other day SC/IM injection nonvertebral fractures

Teriparatide (Forteo)

PTH

20 microgram /day SC or IM for maximum of 2 years

Estrogen/ progesterone

Hormone

0.3 mg PO daily/2.5–5 mg (day 1–10 cycle)

Acts on osteoblasts, dvertebral fractures (65%) and nonvertebral fractures (53%) Antiresorptive

Spine

Medication

CHAPTER 3

Table 3.2 Pharmacological treatment of osteoporosis

Nasal irritation

Hypercalcemia, nausea, leg cramps, dizziness. Black box warning: osteosarcoma in rodent studies Risk of breast and endometrial cancer; not as commonly used after Women’s Health Initiative studies

OSTEOPOROSIS

Further reading Gregg EW, Cauley JA, Seeley DG, et al. (1998). Physical therapy and osteoporotic fracture risk in older women. Study of Osteoporotic Fractures Research Group. Ann Intern Med 129(2):81–88. NIH Consensus Development Panel on Osteoporosis, Prevention, Diagnosis, and Therapy (2001). Osteoporosis prevention, diagnosis and therapy. JAMA 285(6);785–795. Rossouw JE, Anderson GL, Prentice R, et al. (2002). Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. JAMA 17:288(3):321–333.

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Scoliosis General description The word scoliosis is taken from the Greek language, translated to mean “curvature.” By definition, scoliosis refers to the spine curving laterally, either to the right or left side, and can be seen in childhood or adulthood. A normal spine viewed from behind the patient (posteroanterior [PA] view on radiograph) appears straight from the neck down to the buttocks. A scoliotic spine viewed from behind will resemble the shape of an S or C curve. To study the biomechanics behind scoliosis, visualization of the spine in the three-dimensional (3-D) planes is required. To simplify the issue, one can imagine that as the spine curves to either the right or the left, the involved vertebrae must rotate to compensate for the curve to keep the body in balance. The spine can curve abnormally mainly in two areas: the thoracic and/ or lumbar spine. If scoliosis occurs in the thoracic spine, the thoracic vertebrae, which are attached to the thoracic ribs, will rotate and result in rib prominence on the opposite side of the curve. If the scoliosis in the thoracic spine is very severe, it can lead to abnormal function of visceral organs within the thoracic cage, such as the heart and lungs.

Clinical manifestations Most authors believe that most patients with scoliosis never present with pain. It is only in severe cases (Cobb angles ≥70*), where nerve impingement or severe pulmonary (restriction in inhalation) and cardiac (cor pulmonale) defects are involved, that scoliotic patients complain of pain. As the spine curves laterally, the affected vertebrae rotate, affecting bone, ligament, and muscle connections to the spine. Rib prominence on the opposite side of the curve as well as leg length discrepancies are commonly seen with scoliosis. Because structure and function are highly integrated, these dysfunctional areas will ultimately lead to abnormal posture and strain on muscles, leading to pain and stiffness.

Differential diagnosis The differential diagnosis in a patient with scoliosis includes tumors, embryological defects (failure of segmentation of vertebrae or ribs), trauma, spinal stenosis, ankylosing spondylitis, and spondylolysis.

Etiologies The etiologies of scoliosis can be divided into three major categories: idiopathic, congenital vertebral, and neuromuscular defects (see Fig. 3.1). Each of these categories has many other subgroups, but idiopathic and congenital vertebral defects comprise the majority of presentations.

SCOLIOSIS

Etiologic classifications of scoliosis

Idiopathic • Infantile • Juvenile • Late onset/ Adolescent

Congenital Vertebral defects • Hemivertabre • Wedge Vertebrae

Neuropathy • Cerebral Palsy • Myelomeningocele • Spinal cord injuries

Myopathy • Duchenne muscular dystrophy • Nemaline myopathy

Neuromuscular

Tumors • Osteoma • Osteoblastoma • Neurofibroma • Astrocytoma

• Leg length discrepancy • Neurofibromatosis

Figure 3.1 Classifications of scoliosis

Infantile idiopathic scoliosis (0–3 years of age) Most patients with infantile idiopathic scoliosis present before 6 months of age with a curved spine that usually develops within the upper lumbar/ lower thoracic region. Most of these infants’ deformities revert to a normal curvature within the next few years. Diagnosis is usually made based on the upright PA and lateral views on radiograph. The treatment differs based on the degree of curvature. The Cobb angle is used to measure the amount of scoliosis. A person who has a Cobb angle ≥10° as determined by the X-ray (not with a scoliometer) is diagnosed as having scoliosis. The Cobb angle is determined by drawing a perpendicular line (on the X-ray) from the top most deviated vertebrae and the bottom most deviated vertebra (see Fig. 3.2). The two perpendicular lines meet to form the Cobb angle.

Treatment On the first visit, treatment is usually not initiated. Most patients with an initial curve angle greater than 20˚ and an increase of 5˚ on the following office visit should be treated aggressively (office visits should be scheduled within 4 to 6 weeks). Treatment options include bracing or casting. If signs of scoliosis persist, an orthotic device must be worn 23 hours a day. Fusing the vertebra is usually not an option at this stage, although some physicians will insert a supporting rod if there is rapid progression.

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COBB ANGLE

Figure 3.2 Determining the Cobb angle.

Juvenile idiopathic scoliosis (3–10 years of age) History This group of patients manifests with signs beginning after age 3 but before age 10. Patients in this group are usually asymptomatic. Females make up most of these patients. Some authors believe that pain can be a symptom early on due to defects in walking habits. Unlike the infantile group, there seems to be a rapid progression of the deformity if not corrected early. Physical During the examination, the physician should assess the symmetry among different body limbs, including shoulders, leg lengths, anterior superior iliac spine, posterior superior iliac spine, ischial tuberosities, and pubic symphysis. Skin texture and discoloration should be examined as well to rule out any neuromuscular defects. Neurological exams should be conducted to assess for any deficits. The Adams test assesses the paravertebral region of the patient. The patient stands with feet together and is asked to flex forward until at a 90* angle. Extreme paravertebral rotation and other irritant anomalies can become apparent during examination.

SCOLIOSIS

The use of a scoliometer is not recommended for diagnosis due to the lack of experience of most physicians with the device. Diagnosis Diagnosis should be made with radiographs of the lateral and PA views. Patients with a Cobb angle ≥10* based on the film (not with a scoliometer) are diagnosed with scoliosis. Patients in this age group should also have radiographs of the brain to exclude other spinal pathologies. Treatment Initial curvatures of Cobb angle ≥20* should be treated aggressively if the patient presents on the following visit with an increase of ≥5* in curvature within the next 4–6 months (increase in curvature is about 1* a month). If the patient presents with a curvature >25* on the first visit, the physician might want to reexamine the patient earlier than the normal 4-month follow-up visit to prevent further increase in curvature. Treatment in this patient population involves bracing the individual. If the patient progresses rapidly, surgery can be considered (although not done in most cases). Surgery consists of fusing the vertebra together. Most physicians don’t consider this a viable option, as growth of the spine is prevented.

Adolescent idiopathic scoliosis (10 years of age to maturity) This age cohort accounts for most of the scoliosis seen by physicians (about 80%). The onset is usually manifested by puberty but before maturity. The majority of patients with adolescent onset are girls (92%). History Most of these individuals do not have any symptoms and their deformities are recognized by an examiner, be it a parent, a primary care physician, or a school nurse. Most of these patients have a convex curve to the right in the thoracic region. Neurological deficits should be considered, especially in left-sided convex curves. Further imaging studies should be performed on these patients to check for intraspinal pathologies (neurofibroma, astrocytoma). Physical and diagnosis The physician should conduct all of the tests used to assess juvenile idiopathic scoliosis for examination and diagnosis. Treatment Treatment for this cohort has to be based on the level of skeletal maturity and the expected progression of the curve. Most curves won’t have an angular increase if they have already hit menarche. In some instances, however, there will be a progression—mostly with curves >40*—even after menarche. Females have a much greater tendency to have curve progression than males (10:1). Most patients with adolescent idiopathic scoliosis do not require treatment. Individuals with Cobb angle ≥20* with a progression of 5* should be treated.

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Most physicians use the Milwaukee brace as the primary treatment. The brace has to be worn for most of the day (23 hours; it may be removed for bathing only). Electrical stimulation has been used as an adjuvant. Surgery is only indicated once bracing has failed and the curve has progressed to ≥50*.

Further reading Bulstrode C, Buckwalter J, Carr A, Marsh L, Fairbank J, Wilson-Macdonald J, Bowden G (2002). Oxford Textbook of Orthopedics and Trauma, Vol. 2. New York: Oxford University Press, pp. 615–621. Cassar-Pullicino VN, Eisenstein SM (2002). Imaging in scoliosis: what, why and how? Clin Radiol 57:543–562. Miller NH (1999). Cause and natural history of adolescent idiopathic scoliosis. Orthop Clin North Am 30:343–352. Newton, PO, Wenger, DR (2001). Idiopathic and congenital scoliosis. In Morrissy RT, Weinstein SL (eds.), Lovell and Winter’s Pediatric Orthopaedics, 5th ed. Philadelphia: Lippincott Williams & Wilkins, p. 677. Roach JW (1999). Adolescent idiopathic scoliosis. Orthop Clin North Am 30:353–365. Tunnessen, WW (1999). Scoliosis. In Signs and Symptoms in Pediatrics, 3rd ed. Philadelphia: Lippincott, Williams & Wilkins, p. 619. Weinstein S, Buckwalter J (2005). Turek’s Orthopaedics: Principles and Their Application, 6th ed. Philadelphia: Lippincott Williams & Wilkins, pp. 482–490.

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Thoracic radiculopathy and thoracic intervertebral disc herniations General description Thoracic radiculopathy is due to compression, irritation, or abnormality of a thoracic nerve root that causes pain or dysfunction. This compression is usually due to a thoracic disc herniation or bony hypertrophy of the zygoapophyseal (or facet) joint, the vertebral body, or the uncovertebral joint, which results in narrowing of the neural foramen. Noncompressive radiculopathies can be related to diabetes mellitus, neoplasm, or infectious causes. In the thoracic spine and lumbar spine, the nerve roots are numbered on the basis of vertebra above (so the T11 nerve root exits between T11 and T12). Due to the limited motion of the thoracic spine (compared to the lumbar or cervical spines), thoracic disc herniations are much rarer than cervical or lumbar herniations. When they do occur, they are usually in the lower thoracic spine (probably because of the greater mechanical forces there) with the majority occurring between T11 and T12.

Clinical manifestations The thoracic nerves supply the thoracic paraspinal muscles and the intercostal muscles. They do not supply limb muscles. Therefore, the primary symptoms are sensory (pain, paresthesia, dysesthesia). In a lateral disc herniation there will be unilateral and dermatomal symptoms, causing scapula area, chest, or abdominal pain or dysesthesia (depending on the level involved). Central or central lateral disc herniations can have a varying degree of spinal cord compression and can appear as an upper motor lesion with bowel or bladder involvement.

Differential diagnosis The primary differential diagnosis of unilateral dermatomal thoracic pain is postherpetic neuralgia (recurrent herpes zoster infection of a nerve root; also known as shingles). Thoracic sprain or myofascial pain, or referred pain from internal organs may also mimic the pain of a thoracic radiculopathy. Due to the rarity of thoracic disc herniations, imaging to rule out neoplasm should be considered (particularly in the presence of unexplained weight loss). Osteoporotic compression fractures can cause cord or root compromise and present similarly to thoracic herniations.

History There may or may not have been a precipitating event. An attempt should be made to determine if there are associated factors (particularly for referred visceral pain). A medical history should include an assessment for diabetes, weight loss, or bowel or bladder changes that may guide further workup.

THORACIC RADICULOPATHY

Physical The physical examination may be unremarkable except for sensory disturbance in a thoracic dermatomal distribution. Lower extremity coordination and reflexes and gait should be normal. If they are abnormal, consider myelopathy. Thoracic range of motion should be assessed for abnormalities or significant scoliosis as well as determining if positioning is provocative.

Diagnostic testing MRI is useful for evaluation of the spinal canal, intervertebral disc, nerve root, and foramen. If MRI is contraindicated, CT is appropriate. Electrodiagnostic studies may be helpful in determining whether herniations are clinically significant (primarily EMG of the paraspinals and somatosensory evoked potentials).

Management (treatment) Depending on the level of pain and neurological involvement, treatments may include physical therapy, NSAIDs, pain medications, oral steroids, or membrane-stabilizing medication (gabapentin or pregabalin). Fluoroscopically guided spinal nerve injections can be both therapeutic and diagnostic. Surgical discectomy can be helpful in refractory cases, especially with progressive or significant neurological dysfunction.

Complications and red flags Tumor should be high on the differential diagnosis for thoracic radiculopathies. Progressive or significant neurological deficits should lead to more aggressive treatment, including an evaluation for spine surgery. Always assess for myelopathic lesions (upper motor neuron signs in the lower extremities, such as increased reflexes or spasticity).

Further reading Kimura J (2001). Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice, 3rd ed. New York: Oxford University Press, p. 632. Rosenberg D (2008). Thoracic radiculopathy. In Frontera WR, Silver JK, Rizzo TD (eds.) Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier, pp. 219–221.

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Lumbar sprain, strain General description Low back pain (LBP) is one of the most common afflictions of humankind. It is estimated that approximately two-thirds of adults are affected by mechanical LBP at some point in their lives, making it the second most common complaint in ambulatory medicine and the third most expensive disorder in terms of health-care dollars spent (surpassed only by cancer and heart disease). Most cases of LBP are self-limiting and due to mechanical etiologies. Lumbar sprains and strains account for most of the transient cases of LBP. Sprains are injuries to the ligaments that support the spine. Ligaments are made of strong collagen fibers and connect bone to bone. The most commonly strained ligaments are the posterior longitudinal ligament, interspinous ligament, and iliolumbar ligaments. Sprains are more common in older persons who have weak supporting spinal muscles. Strains are injuries to the muscles and musculotendinous junctions. These injuries usually occur in younger persons who have well-developed supporting muscles. These injures spare the ligaments. All posterior spinal muscles and corresponding tendons can be involved, though the most susceptible muscles are those spanning several joints. The L4–5 and L5–S1 areas bear the highest loads and tend to undergo the most motion.1 Consequently, these areas are found to sustain most spinal strain or sprain injuries. Most load-bearing strain and sprain injuries occur during the strongest coupling patterns (i.e., lateral bending with flexion-extension, or axial rotation with lateral bending).1

Clinical manifestations The pain is usually of acute onset after movement stressing the spine, especially in a vulnerable position. The pain may also occur after holding a static position that stresses the ligaments for a period of time. Nachemson has shown that the positions increasing ligamentous stress and intradiscal pressures the most are sitting, lifting from a standing position with extended knees, and leaning forward while seated in a chair.2,3 Holding these positions for a prolonged period of time will stress the supporting ligaments and muscles of the spine, increasing the likelihood of LBP. Pain is usually noted across the low back and does not radiate into the leg beneath the buttocks. If the iliolumborum ligament is sprained, the patient may experience unilateral pain that radiates into the groin. Localized central back pain may be due to a sprain of the supraspinous or interspinous ligament. As there is no nerve involvement, patients will not have sensory deficits or bowel or bladder disorders.4 1 Radebold A (2005, Dec 6). Lumbosacral spine sprain/strain injuries, E Medicine. Updated Nov 21, 2007. 2 Nachemson AL (1981). Disc pressure measurements. Spine 6(1):93–97. 3 Nachemson AL (1995). Intradiscal presuure. J Neurosurg 82(6):1095. 4 Bigos SJ, Boyer OR, Braen GR (1994). Acute low back problems in adults. Clinical Practice Guideline, Quick Reference Guide Number 14. Public Health Agency, Agency for Health Care Policy and Research. Rockville, MD: Department of Health and Human Services.

LUMBAR SPRAIN, STRAIN

Differential diagnosis The differential diagnosis includes other causes of back pain, such as herniated disc, spinal stenosis, spondylosis, spondylolisthesis, lumbar facet and sacroiliac joint dysfunction, vertebral fracture, and referred pain from the hips (see Table 3.3). Other less likely but more serious causes of LBP include epidural and psoas abscess, discitis, tumor, and aortic aneurysm.

History It is important to obtain the following key information: the mechanism of injury, description of events leading to the pain, previous similar episodes and their treatment, localization, duration, quality of the pain, radiation, movements that aggravate or minimize the pain, any history of bowel or bladder incontinence or retention, and leg numbness or weakness.

Physical examination Typical symptoms include pain and spasm localized over the posterior lumbar spinal muscle bellies lateral to the spinous process or at the insertion of the muscle at the iliac crest. The patient should be assessed for muscular imbalances or weakness of abdominal and posterior spinal muscles, as this constitutes a risk factor of sprain and strain injuries. Table 3.3 Characteristics of facet syndrome, sacroiliac (SI) joint dysfunction, and lumbar strain Facet syndrome

SI joint dysfunction

Lumbar strain

Hyperextension with side flexion increases pain. Unilateral. May radiate into buttock. Does not peripheralize. No dural symptoms

Unilateral hard step down increases pain. Unilateral gluteal pain. Radiates into the posterior thigh and leg to S1, 2 levels. Buttock pain with valsalva. No radicular pain with valsalva

Flexion with forceful ipsilateral rotation increases pain. May radiate to the groin. No dural symptoms or peripheralization

Physical Lumbosacral examination ROM within normal limits. Pain is provoked with ipsilateral extension/ rotation. Improves with flexion and opposite rotation

+ Gaenslen, Yoeman’s, and Stork tests

Localized pain on palpation. Lumbosacral ROM within normal limits. Contralateral lateral flexion provokes pain

History

Test definitions Gaenslen test: Patient is supine. One knee is brought to the chest. The opposite leg is extended passively and hangs off the table. Yoeman’s test: Patient is prone. Stabilize the sacrum with one hand. The opposite hand extends the hip with the knee extended. Stork test: Patient stands on one leg and hops. Alternate to opposite leg.

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If the injury is confined to a sprain or strain injury, the following should be absent: structural deformities, a generalized mid-back pain indicating disk involvement, and neurological symptoms. Range of motion (ROM), particularly in flexion, is usually painful and decreased. Any neurological compromise, (e.g., numbness in the lower extremity, motor weakness, reflex changes) or any urinary or fecal incontinence indicates the possible presence of nerve route impingement or spinal canal stenosis.

Imaging studies Initially, no lumbar X-rays are needed unless there is a history of a fall, osteoporosis, or severe pain. Most patients do well with a 1- to 2-week period of conservative treatment prior to obtaining X-rays. If the patient is still symptomatic after 2 weeks, standard anteroposterior (AP) and lateral radiographs of the lumbar spine should be obtained to (1) exclude a fracture, rheumatic disease, or tumor and (2) evaluate degenerative joint disease and overall spinal alignment. If the individual with LBP does not respond to conservative treatment and/or develops neurological signs, a CT scan or an MRI may be considered to evaluate disk herniation and involvement of the nerve roots.

Special considerations Vascular and hip pathology may coexist and confuse the clinical picture.

Treatment After the initial injury, no more than 24–48 hours of relative rest is recommended. The patient should be treated with NSAIDs if there are no contraindications. Gastrointestinal protection with an H2 blocker or proton pump inhibitor (PPI) should be used if needed. Ice and electric stimulation to the affected area should be used for the initial 48 hours to control pain and muscle spasm. Protected mobility of the lumbar spine should be started after 24 hours. This will help restore the normal lumbosacral rhythm. Early mobility allows the muscles and ligaments to heal in an elongated pattern. This will prevent scar fibers that restrict the normal lumbar mobility. Muscle relaxants such as metaxalone, cyclobenzaprine, or methocarbamol and low-dose narcotics may be used for a short period of time to allow restoration of the normal lumbar movement. Once the pain is relieved, a program to improve abdominal strength and lumbar flexibility should be initiated.

Complications and red flags The onset of leg numbness, vascular insufficiency in the legs, objective limb weakness, reflex changes, urinary or bladder incontinence, fever, or abdominal pain should alert the physician to reevaluate the diagnosis and perform the appropriate investigations.5 The natural history of this condition is gradual improvement over 2–4 weeks. If the patient’s pain does not improve or progressively worsens, further evaluation and imaging of the lumbar spine are indicated. 5 Ombregt L (1995), A System of Orthopedic Medicine. Philadelphia: WB Saunders.

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Lumbar radiculopathy General description Lumbosacral radiculopathy results from nerve root impingement and/or inflammation causing neurological symptoms in the lower extremities and low back pain. Radiculopathy is primarily caused by direct neural compromise from a disc herniation, hypertrophy and spurring from the zygapophyseal joints, and hypermobility of vertebral segments (i.e., spondylolisthesis and spondylolysis). In the lumbar spine there are five vertebral bodies with each nerve root exiting inferior to the vertebrae (L4 nerve root exits below the L4 vertebral body). Lumbar nerve root compressions usually take place as the root exits its foramen, but compression may take place anywhere along the cauda equina within the spinal cord.

Clinical manifestations The onset of lumbosacral radiculopathy is generally sudden with low back pain radiating to one or both lower extremities. Occasionally, the patient’s presenting symptom may include only lower extremity involvement. Clinical localization is often difficult and sensory impairment is a more reliable localizing sign than motor impairment (see Table 3.4; see Fig. 2.2 in Chapter 2). Single root involvement does not necessarily cause prominent weakness; however, certain muscle groups may be correlated with certain lumbar root levels (see Table 3.5). Given the multiplicity of lumbar root supply, the patient may present only with complaints of pain and paresthesias without neurological deficit. Table 3.4 Sensory complaints by level of lumbar involvement Root level

Sensory or pain complaints

L1, L2, L3

Anterior aspect of thigh

L4

Knee to medial malleollus

L5

Buttock, posterior lateral thigh, lateral leg dorsum of foot, first four toes

S1

Posterior thigh, posterior leg, lateral foot

S2–S5

Posterior thigh, perianal region, genital region

Table 3.5 Root level and corresponding muscle groups Root level

Corresponding leg muscle and reflexes

L2

Hip flexion

L3

Knee extension, thigh adduction

L4

Inversion of foot, patella reflex

L5

Great toe extension

S1

Foot eversion, Achilles reflex

LUMBAR RADICULOPATHY

Differential diagnosis The differential diagnosis includes myofascial pain, peripheral neuropathy, polyneuropathy, sacroiliac dysfunction, meralgia paresthetica, spinal stenosis, and cervical or thoracic spinal cord compression.

History Lumbar radiculopathy typically presents as low back pain radiating to the lower extremity that is generally sudden in onset. It is commonly related to work and sports trauma, but the patient may not report any specific traumatic or inciting event. L5 and S1 radiculopathy is by far the most common lumbar radiculopathy. L1, L2, and L3 root involvement is rare. In addition to pain, presenting symptoms may include numbness, tingling, paresthesias, dysesthesias, and weakness, frequently in a specific myotomal or dermatomal pattern.

Physical Physical examination should include a complete evaluation of both the neurological and musculoskeletal systems. Patients may be unaware of mild sensory and motor abnormalities; as such, they may not be offered in the history. Gait should be evaluated for foot drop, Trendelenberg sign, and other findings that may signal neural compromise. Posture should be assessed for scoliosis and pelvic asymmetry. Reflexes should be assessed and may be decreased or absent if radiculopathy is present. A myotomal exam should be performed to determine if focal weakness is present and a dermatomal sensory exam should be performed in an attempt to localize any sensory impairment. Provocative maneuvers such as straight-leg raise may provide evidence of dural tension indicating radiculopathy. Finally, a palpatory and musculoskelal exam should be performed to evaluate for joint pathology that may mimic radiculopathy.

Diagnostic testing Imaging studies Radiographs are the most common type of imaging modality used in patients with low back pain. X-rays can detect serious structural pathology such as fracture, spondylolisthesis, and spondylolysis, but are of limited value in evaluating patients with herniated discs. MRI is superior to CT scanning for evaluating the lumbar spine and is considered the study of choice for nerve root impingement. Myelograms are rarely used in evaluation of patients with acute low back pain. Discography is rarely necessary in the evaluation of low back pain. Electrodiagnostic studies NCV/EMG studies may be helpful when the diagnosis remains unclear (e.g., peripheral nerve entrapment, peripheral polyneuropathy vs. radiculopathy), in evaluation of patients who have limb pain or when attempting to localize a specific nerve root level. SSEP studies are of essentially no value in the assessment of radiculopathy.

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Special considerations MRI should be reserved for selected patients, in particular those with progressive neurological decline, significant neurological deficit, and possible malignancy or infection. In the absence of red flags, many patients can and should be managed without MRI, and MRI is not necessary in patients with radiculopathy unless results are likely to guide treatment.

Management (treatment) Most patients with lumbar radiculopathy enjoy resolution of their symptoms within 6 weeks. Based on the severity of symptoms and neurological involvement, treatment may include exercise, physical therapy, osteopathic manual medicine, and/or medication including but not limited to NSAIDs, muscle relaxants, oral steroids, narcotic pain relievers, selective serotonin reuptake inhibitors (SSRIs), and membrane-stabilizing medications (gabapentin, pregabalin, lamotrigine). If conservative treatment is not successful, occasionally fluoroscopically guided epidural, facet, and selective nerve root injections may be used to control symptoms. Surgical intervention is typically reserved for acute paralysis, progressive neurological dysfunction, and intractable pain.

Complications and red flags Progressive neurological decline or significant neurological deficit merits more aggressive intervention. Patients with conus lesions, cauda equina lesions, arachnoiditis, and tumors and/or malignancies may present with symptoms such as paralysis, upper motor neuron signs, genital and perianal sensory changes, and bowel or bladder incontinence. These signs and symptoms require urgent or emergent evaluation.

Further reading Braddom RL (1996). Physical Medicine and Rehabilitation. Philadelphia: W.B. Saunders. Dumitru D (1995). Electrodiagnostic Medicine. Philadelphia: Hanley and Belfus. Kimura J (1989). Electrodiagnosis in Diseases of Nerve and Muscle. Philadelphia: F.A. Davis.

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Lumbar spinal stenosis General description Lumbar spinal stenosis is compression of the spinal canal, nerve roots, or cauda equina due to decreased space in these structures. Stenosis can be either congenital (9% of cases) or acquired. Acquired stenosis can be caused by soft tissue structures (discs, ligamentous hypertrophy, tumors, cysts, infection) or bony structures (degenerative changes in the vertebrae, osteophytes, facet joints, Paget’s disease, scoliosis, or spondylolisthesis). Stenosis is usually classified as central (narrowing of the spinal canal) or lateral (within the nerve root canal or intervertebral foramina). A lumbar canal AP diameter of ≤10 mm is considered diagnostic for lumbar stenosis.

Clinical manifestations Back or buttock pain is the primary symptom, with leg pain (unilateral or bilateral) noted in 90% of cases. The pain radiates below the knee only about half the time. Patients usually demonstrate neurogenic claudication (pain with ambulation that is relieved by sitting or flexing the spine, in contrast to vascular claudication, relieved by rest) (see Table 3.6).

Differential diagnosis The primary differential diagnosis includes other sources of back pain (sciatica, osteoarthritis, cauda equina syndrome, tumor, spondylolisthesis, infectious process, lumbar facet syndrome, and vertebral fracture), peripheral vascular disease, and peripheral neuropathy.

Table 3.6 Neurogenic claudication vs. vascular claudication Neurogenic claudication

Vascular claudication

Pathology

Spinal stenosis

Peripheral arterial disease

Symptoms

Back or buttock pain. Usually Pain usually in lower leg does not radiate past knees

Worse with:

Spinal extension (going down Exertion stairs)

Better with:

Spinal flexion (going up stairs), sitting

Rest

Pulses

Usually normal

Usually decreased

Treatment

Physical therapy, NSAID, pregabalin, epidural steroids injections, spinal surgery

Antiplatelet agents, progressive exercise, arterial vasodilators, vascular bypass grafting operation, stenting procedures

Positive tests

CT or MRI of the LS spine demonstrating stenosis

Vascular studies demonstrating decreased arterial blood flow in the extremity

LUMBAR SPINAL STENOSIS

History Patients are usually over the age of 50. Flexion of the spine usually helps alleviate the pain (i.e., walking up steps). Extension usually exacerbates the pain. Patients often state they feel better when pushing a grocery cart, as this position tends to bring the lumbar spine into flexion.

Physical Frequently the exam is unremarkable as the symptoms occur with prolonged extension. Depending on the structures involved, the patient may exhibit weakness, atrophy, decreased sensation, or diminished reflexes. If the S1 nerve root is affected, straight-leg raising may be positive. Symptoms may be exacerbated with lumbar extension.

Diagnostic testing A CT scan or an MRI is useful for evaluation of the spinal canal and related structures. Electrodiagnostic studies may be performed to evaluate neurological involvement and rule out other conditions. EMGs are positive in about 90% of patients1. Findings include electrodiagnostic evidence of single or multiple root involvement, often bilaterally. If tests are negative, consider arterial Doppler studies to rule out vascular disease.

Special considerations Vascular or hip pathology may coexist and complicate the diagnosis.

Management (treatment) Depending on the level of pain and neurological involvement, treatments may include physical therapy (directed at spinal flexion exercises), NSAIDs, pain medications, membrane-stabilizing medication (gabapentin, pregabalin, or lamotrigine), or epidural steroid injections. Laminectomy and/or spinal fusion may be indicated in extreme cases when pain or neurological involvement is severe.

Complications and red flags Cauda equina syndrome (bowel or bladder incontinence and perianal numbness) may occur in severe lumbar stenosis as a result of sacral nerve root impingement and requires immediate intervention.

1 Lumbar spinal stenosis. Clinical features, diagnostic procedures, and results of surgical treatment in 68 patients. Hall S - Ann Intern Med - 01-AUG-1985; 103(2): 271–5.

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Cauda equina and conus medullaris syndrome General description The spinal cord terminates between the first and the second lumbar vertebrae in a bulbous enlargement called the conus medullaris (CM). Distal to the conus is a collection of nerve roots, which innervates the lower extremities. This collection of nerves is called the cauda equina (CE). The conus medullaris is considered part of the spinal cord, whereas the CE is considered peripheral nerves. Therefore, injury to the CM will result in upper motor neuron signs and symptoms, whereas injury to the CE will result in a lower motor neuron lesion. Cauda equina syndrome (CES) may result from any lesion that compresses CE nerve roots. The most common causes of CES are lumbar stenosis, spinal trauma (including vertebral fractures), disc herniation, severe spondylolisthesis, tumors, spinal infection, complications of epidural injections, mass effect from a spinal hemorrhage, and tethered cord. Tumors of the spinal cord are a rare cause of CES or conus medullaris syndrome (CMS). The incidence of spinal cord tumors is 0.5–2.5 cases per 100,000. Extradural spinal cord tumors comprise 55% of spinal cord tumors, intradural–extramedullary tumors account for 45%, and intramedullary tumors account for only 5%. Most of the extradural tumors come from tumor metastasis; most intradural–extramedullary tumors are schwannomas, neurofibromas, or menigiomas. The intramedullary (within the cord) tumors are usually ependymomas (60%) or astrocytomas (33%).

Clinical manifestations Patients with CES may complain of low back pain that usually radiates into the legs. Weakness and sensory loss of the lower extremities is usually asymmetric. The patient may complain of urinary and bowel incontinence or retention. Since CES is a lower motor neuron lesion, deep tendon reflexes will be depressed.

Differential diagnosis Acute inflammatory demyelinating polyneuropathy (AIDP), neuropathy, spinal cord infarction, syringomyelia, sciatica, multiple sclerosis, and lumbosacral plexopathy are included in the differential diagnosis.

History and physical examination The onset may be either rapid or insidious, depending on the mechanism of injury. Patients can present with symptoms of isolated CES, isolated CMS, or a combination of both. Table 3.7 describes the salient findings in both conditions.

Radiography Plain X-rays are easy to obtain and are useful in screening for spinal fractures, spondylolisthesis, or destructive changes. MRI with gadolinium contrast is the gold standard for diagnosis of CES. MRI delineates the soft tissues and can help define the pathologic process.

CAUDA EQUINA AND CONUS MEDULLARIS SYNDROME

Electrodiagnositic testing may define the lesion or rule out other causes of pain or weakness. CT scanning provides details of any bony involvement and is especially helpful in cases of traumatic CES or CMS. CT can help define bone architecture and spinal stability. SPECT bone scanning can help determine if there are areas of remote metastasis or inflammatory conditions.

Treatment Surgical intervention is the mainstay of treatment. Once the diagnosis is confirmed, consultation with a neurosurgeon or spinal orthopedist is mandatory on an emergent basis. In acute compression of the conus medullaris or cauda equina, decompression should be done as soon as possible. In chronic cases, decompression of the impingement may be delayed. Surgical treatment is aimed at relieving the pressure on the neural structures by laminectomy, discectomy, and/or spinal stabilization. Medical therapy should address any infectious process that may be contributing to the compression. Methylprednisolone and GM1 ganglioside treatment may help to decrease the neurological deficit by decreasing inflammation on the compressed neural tissue.

Complications Complications of CMS and CES are permanent bowel and bladder incontinence or retention, lower extremity paralysis, deep venous thrombosis, pulmonary embolism, and impotence. Prompt and appropriate intervention is needed to minimize these complications.

Table 3.7 Conus medullaris syndrome vs. cauda equina syndrome Conus medullaris syndrome Cauda equina syndrome Presentation

Sudden and bilateral

Gradual, may be unilateral

Vertebral level

L1–L2

L2–sacrum

Motor and reflexes Symmetric lower extremity Severe asymmetric, weakness with hyperreflexia areflexic paraplegia Sensory

Symmetric saddle distribution. Sensory loss to pinprick and loss of temperature sensation. Sensory dissociation may be present.

Asymmetric saddle numbness. Loss of sensation in specific dermatomes in the legs. No sensory dissociation

Sphincter and sexual dysfunction

Impotence is frequent. Early and severe bowel, bladder, and sexual dysfunction

Less prominent than in CMS. Flaccid bladder (if sacral levels are affected)

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Lumbar spondylosis General description Lumbar spondylosis refers to the degenerative changes found on the lumbar spine. It describes the overgrowth (osteophytes) found mostly on the anterior and lateral edges of the superior and inferior end of the vertebral body. It is inevitable with aging. Over 80% of the population over the age of 40 years shows findings of lumbar spondylosis.

Clinical manifestations Most patients with lumbar spondylosis are asymptomatic. Low back pain and stiffness are the usual complaints when spondylosis is symptomatic. With involvement of the facet joints, pain is exacerbated with lumbar extension. Neurological symptoms can develop with impingement of the neural structures (spinal stenosis). Patients complain of radicular symptoms with nerve root impingement. Neurogenic claudication develops with lumbar spinal stenosis.

Differential diagnosis Causes of low back pain such as sprain or strain, vertebral fracture, osteoporosis, spondyloarthropathies, or primary and metastatic tumors should be ruled out. Neurological complaints and deficits, when present, are usually due to other conditions such as herniated nucleus pulposus, peripheral neuropathy, and lumbar spinal stenosis.

History Patients are usually over 40 years old and present with complaint of low back pain with no known precipitating event. Other causes of back pain have been ruled out, and X-ray of the lumbar spine shows overgrowth of osteophytes.

Physical Examination should include assessment of flexibility of the spine and extremities, inspection for deformities, atrophy, and vascular insufficiency, and a complete neurological examination. The examination should direct attention to further evaluation of the common causes of low back pain: discogenic, facet, radicular, myofascial, and psychogenic. Assessment for nonorganic signs (Waddell) of low back pain will assist the clinician in recognizing if psychological factors contribute to the pain.

Diagnostic testing Routine standard anteroposterior and lateral radiographs of the lumbar spine usually confirm diagnosis of lumbar spondylosis. Diagnostic testing that includes MRI, CT scan, and electrodiagnosis is used to assess other causes of back pain as directed by the history and physical examination.

LUMBAR SPONDYLOSIS

Special considerations Some authors believe that lumbar spondylosis is usually not a source of morbidity. The presence of spondylosis alone does not definitively establish it as the cause of pain.

Management (treatment) Management is directed to symptomatic treatment of low back pain as the presenting symptom. This includes NSAIDs, muscle relaxants, physical therapy, and patient education. Specific management of the complications is addressed in the appropriate chapter.

Complications and red flags Neurological deficits can result from osteophyte impingement of the nerve roots or spinal canal. Look for an aortic aneurysm if an osteophyte disappears on follow-up X-ray.

Further reading Alvarez JA, Hardy RH Jr (1998). Lumbar spine stenosis: a common cause of back and leg pain. Am Fam Physician 57(8):1825–1834, 1839–1840. Borenstein D (2004). Does osteoarthritis of the lumbar spine cause chronic low back pain? Curr Rheumatol Rep 6(1):14–19. Gibson JN, Grant IC, Waddell G (1999). The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine 24(17):1820–1832. Rothschild BM (2008, Oct). Lumbar spondylosis. eMedicine. Schaufele MK, Walsh AM (2008). Lumbar degenerative disease. In Frontera WR, Silver JK, Rizzo TD (eds.), Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders Elsevier, pp. 229–236. Schneck CD (1985). The anatomy of lumbar spondylosis. Clin Orthop Rel Res 193:20–37.

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Spondylolisthesis General description Spondylolisthesis is a forward translation of a vertebral body with respect to the vertebra below. Spondylolisthesis occurs most commonly in the lower lumbar spine. There are several different types of spondylolisthesis (Table 3.8). The most common type is spondylolytic (isthmic) spondylolisthesis. The slippage usually occurs at the L5/S1 level in most types (except at the L4/5 level in the degenerative type). Risk factors for the development of spondylolisthesis include lumbar hyperextension, periods of growth acceleration, spina bifida occulta, and scoliosis. Spondylolisthesis is graded by the amount of slippage (see Box 3.3 and Fig. 3.3).

Clinical manifestations The patient may complain of achy low back pain (LBP). The onset of pain is usually insidious but may be related to a specific traumatic episode. The pain is usually worse with spinal extension and relieved by rest. Spondylolisthesis may be present, yet asymptomatic. Table 3.8 Types of spondylolisthesis Type1 congenital

Inherited, due to abnormal facet development. Associated with spina bifida. Occurs at L5/S1 mainly. Pars is intact. There is a high occurrence of nerve root pressure due to intact lamina of L5 being pulled against dural sac. Significant slippage seldom develops because the neural ring is intact.

Type 2 isthmic (spondylolytic)

Most common Most common at ages 5–8 years. Results from shear stress at pars interarticularis. Incidence in males > females. The younger the child, the greater the risk of further listhesis. Once growth stops, further slippage is unlikely. Pars is disrupted on both sides of the neural ring. Most common at the L5/S1 level. Usually there is no nerve damage unless there is a high grade of listhesis.

Type 3 degenerative

Due to long-standing intersegmental instability. This may be caused by multiple small compression fractures of the inferior articular processes of the vertebra, allowing it to slip forward. Occurs 6 times more often in females than in males. Usually occurs at the L4 interspace. This type seldom exceeds 33% slip unless there has been prior surgical intervention.

Type 4 posttraumatic

Traumatic spondylolisthesis is secondary to a severe, acute injury that fractures parts of the supporting bones other than the pars and allows forward slip of the upper vertebra on the one below.

Type 5 pathological

Spondylolisthesis is due to local or generalized bone disease affecting the pedicle, the pars, or the superior and inferior articular processes, resulting in forward slips of the vertebra on the one below. It is relatively rare.

SPONDYLOLISTHESIS

Differential diagnosis The differential diagnosis includes other causes of back pain such as herniated disc disease, spinal stenosis, spondylosis, spondylolysis, lumbar facet, sacroiliac joint dysfunction, vertebral fracture, and referred pain from the hips. Other less likely causes of low back pain include epidural and psoas abscess, discitis, and aortic aneurysm and neoplasm.

History Lumbar spondylolisthesis usually occurs in children and older adults. It is not a common cause of LBP in young adults. It may occur in patients older than 60 years of age as a sequela of degenerative disc disease. Radiation of pain into the buttocks is not uncommon.

Physical examination Physical examination may reveal an exaggerated lumbar lordosis. With high-grade vertebral slippage, a palpable step-off may be felt over the spinous process at the level above the slipped vertebra. Tenderness to deep palpation of the spinous process above the slip may be present.

Box 3.3 Grading of spondylolisthesis The Meyerding technique involves dividing the superior aspect of the vertebra below the slip into four equal divisions. Assess where the posterior arch of the slipped vertebral body lies with respect to these four quadrants. • Grade 1: Less than 25% slippage (see Fig. 3.3) • Grade 2: Between 25% and 50% slippage • Grade 3: Between 50% and 75% slippage • Grade 4: Between 75% and 100% slippage • Grade 5: Greater than 100% slippage (also called spondyloptosis)

Figure 3.3 Grade 1 spondylolisthesis (L5 on S1).

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Special considerations Vascular and hip pathology may coexist and confuse the clinical picture.

Treatment Most patients experience pain relief and functional recovery with conservative treatment, which consists of physical therapy and pain management with NSAIDs, narcotics, and muscle relaxants for acute pain. Physical therapy consists of physical modalities, William’s flexion exercises, and increasing flexibility of the hamstrings and heel cords. As a general rule, physical therapy should not be started until after an adequate rest period and once pain with daily activities has subsided. Bracing with a thoracolumbosacral orthosis (e.g., Boston antilordotic brace) may offer relief for those who do not respond to activity restrictions or whose daily activities are producing symptoms. This type of bracing is usually effective in most patients with less than 50% slippage. The brace is generally worn for 3–6 months and may be worn during activity. Avoidance of spine hyperextension and rotation is important. Surgical treatment is reserved for those who fail conservative treatment or have neurological deficits. Indications for surgery include progressive slip, intractable pain, neurological deficits, and segmental instability with severe pain. The natural history of this condition is gradual improvement over 2–4 weeks.

Complications and red flags The onset of leg numbness, vascular insufficiency in the legs, objective limb weakness, urinary or bladder incontinence, fever, or abdominal pain should alert the practitioner to undertake further evaluation and imaging of the lumbar spine. Younger patients require more careful observation, even if the initial symptoms resolve, because of their greater risk for progression. Complications include slip progression, loss-of-motion segments, neurological deficit (cauda equina syndrome, radiculopathy), and residual deformity (following fusion of a high-grade spondylolisthesis).

Further reading Debnath UK, Freeman BJ, Grevitt MP, Sithoe J, Scammell BE, Webb JK (2007). Clinical outcome of symptomatic unilateral stress injuries of the lumbar pars interarticularis. Spine 32(9):995–1000. Micheli LJ, Curtis C (2006). Stress fractures in the spine and sacrum. Clin Sports Med 25(1)75–88.

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Spondylolysis General description Spondylolysis refers to a bone defect of the pars interarticularis. It gives the classic “Scotty dog” appearance on X-ray (see Fig. 3.4). Spondylolysis occurs most commonly at the L5 vertebra (about 90% of cases). It may be congenital (malformation of the facet joints), but is usually acquired due to repeated microtrauma to the vertebral body (usually with hyperextension activities). It is seen with higher frequency in adolescents and young adults who participate in sports that require extreme flexion and extension (gymnastics, wrestling, rowing, pole vaulting, and diving). Spondylolysis may lead to forward slipping of the vertebra (see Spondylolisthesis, p. 64).

Clinical manifestations Patients usually complain of a dull, aching low back pain, usually exacerbated by hyperextension. The pain may also be noted in the buttocks and/ or posterior thigh. Spondylolysis may be present, yet asymptomatic.

Differential diagnosis The differential diagnosis includes other causes of back pain such as herniated disc disease, spinal stenosis, spondylosis, spondylolisthesis, lumbar facet, sacroiliac joint dysfunction, vertebral fracture, and referred pain from the hips. Other less likely causes of low back pain include epidural and psoas abscess, discitis, and aortic aneurysm and neoplasm.

Spondylolysis

Figure 3.4 Oblique X-ray of the lumbar spine. Note the “collar” on the “Scotty dog”. The fracture of the pars interarticularis appears as “lucency”.

SPONDYLOLYSIS

History Patients are often young adults or adolescents (frequently athletes) who complain of low back pain.

Physical Patients may have limited range of motion of the spine, with increased pain on trunk extension. Palpation of the spine may reveal tenderness at the site of the spondylolysis or spasm of the surrounding paravertebral muscles. Tight hamstrings are seen in 80% of patients. Symptoms may be increased by the one-legged hyperextension maneuver (the patient stands on one leg and leans backward).

Diagnostic testing (see Table 3.9) X-rays are usually performed first (obtain lateral and oblique views). Bone scanning may be performed to assess the age of the injury.

Management (treatment) In children or adolescents with an acute spondylolysis, rigid antilordotic bracing is employed (usually for 23 hours a day). This will reduce the stress on the pars interarticularis. Once the symptoms subside, physical therapy to improve trunk strength can be started.

Table 3.9 Radiological studies for diagnosis of spondylolysis Plain film The best initial diagnostic test. AP view not as diagnostic as the radiography lateral and oblique lateral. The classic finding on plain X-ray is lucency in the region of the pars interarticularis. The lesion looks like a collar on a Scotty dog. (Fig. 3.4) The Scotty dog appears best on lateral oblique radiographs. Standing flexion/extension films should be obtained to assess the degree of instability of the involved vertebra. They are also useful in detecting an occult spondylolisthesis. Bone scan

Bone scanning, especially SPECT scanning, is very sensitive in diagnosis of spondylolysis. Bone scanning has been shown to reveal a pars defect despite negative plain X-rays. SPECT scans may identify preclinical fractures that do not show up on CT scanning. This may be due to bony stress that is not significant enough to produce a fracture. Use of a bone scan is to determine acuteness of the spondylolytic lesion. Positive bone scan results and negative radiographic findings suggest recent injury (may benefit from immobilization). Negative bone scan results and positive radiographic findings suggest an old injury that is not healed.

CT

CT scans are the best diagnostic tool for characterization of the defect. CT can also identify herniated nucleus pulposis and facet joint degeneration and stage the extent of the pars deficit. Thin-cut (1–1.5 mm) CT imaging is most effective.

MRI

MRI may visualize edema in the marrow around the site of an acute spondylolytic defect. It is also helpful in identifying the presence of nerve root compression as a result of foraminal or central canal stenosis.

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Treatment for adults usually consists of symptomatic treatment (NSAIDs, analgesics, avoidance of inactivity, education, spine stabilization exercises, and hamstring stretching). Operative treatment is rarely indicated.

Complications and red flags If a patient does not respond to conservative measures, other causes of back pain, such as infection, tumor, or herniated disc, should be ruled out.

Chapter 4

Upper extremity Libi Rind Thomas Pobre Frederick Weiss Yasha Magyar Charles Ruotolo Tamir Aldad Shahab Mahboubian Alexander Knijnikov Wilbur J. Asheld John J.W. Asheld, III Shoulder bursitis 72 Shoulder tendonitis 74 Shoulder impingement syndrome 76 Management (treatment) 80 Rehabilitation after rotator cuff surgery 82 Adhesive capsulitis 86 Rehabilitation of superior labral tears 88 Epicondylitis 90 Bicipital tendonitis 92 Ulnar neuropathy at the elbow and cubital tunnel syndrome 94 Radial tunnel syndrome and supinator syndrome 96 Olecranon bursitis 98 Carpal tunnel syndrome 100 Wrist pain 104 De Quervain’s tenosynovitis 106 Ganglion cyst 108 The hand: hand basics 110 Mallet finger 112 Phalanx dislocations 114 Thumb ligament injuries 116 Trigger finger 118

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Shoulder bursitis General description A bursa is a bag-like structure containing a small amount of fluid whose function is to minimize friction between two moving structures. Inflammation of the bursa is called bursitis. Clinically significant bursitis in the shoulder includes that of the subdeltoid (subacromial), subcoracoid, and the subscapularis bursa. The subacromial bursa is most commonly affected; it is part of the subdeltoid that is underneath the acromion. Subacromial bursitis is commonly associated with tendonitis of the underlying supraspinatus tendon, rotator cuff tears, and shoulder impingement syndrome.

Clinical manifestations Bursitis may present with moderate to severe shoulder pain that is referred to the deltoid insertion or down the lateral aspect of the arm. It is typically present with shoulder movement but may be noted at rest (especially if there is pressure over the bursa). Pain may be so severe that it limits active shoulder movement and interrupts sleep. Passive movement is usually most restricted by pain in abduction.

Differential diagnosis The differential diagnosis includes rotator cuff tendonitis, rotator cuff tear, shoulder impingement syndrome, septic arthritis, gouty arthritis, fracture or dislocation around the shoulder, cervical radiculopathy, and referred pain from visceral organs.

History The history should include inquiry about the presence or absence of acute trauma and repetitive activity to the shoulder joint. Information about the patient’s job and avocational activities is important in establishing the diagnosis.

Physical In the acute stage, pain will limit the extent of physical examination performed. The superficial subdeltoid bursa may be swollen and is tender to palpation. Active range of motion is severely limited by pain. Passive range of motion may be limited by pain in a noncapsular pattern.

Diagnostic testing Diagnosis is normally made with clinical examination. X-ray is useful to rule out fracture and dislocation of the shoulder. Anesthetic infiltration of the bursa should relieve the pain and restore active range of motion in bursitis and tendonitis. Muscle strength should be normal in the absence of rotator cuff tear. Bursa fluid aspiration and analysis should be done when palpable effusion is present, and infection or gout is suspected.

SHOULDER BURSITIS

Special considerations Poorly localized or vaguely described shoulder pain is usually extrinsic in origin. Causes such as cervical root impingement and visceral pathology should be considered.

Management (treatment) Immobilization in a sling, ice massage, and NSAIDs are useful in the initial treatment of shoulder bursitis. Local injection of the bursa with triamcinolone plus local anesthesia has proven effective and should be considered if pain continues to be disabling after 72 hours. Always avoid injection directly into the tendon, as this may increase the likelihood of tendon rupture.

Complications and red flags Rotator cuff tear should be ruled out in the presence of weakness and in cases where pain persists after treatment.

Further reading Cyriax J (1983). Cyriax’s Illustrated Manual of Orthopaedic Medicine. Oxford: Butterworth Heinemann, pp. 33–48. Magee D (1992). Orthopedic Physical Assessment. Alberta: WB Saunders, pp. 117–129. Mercier L (1987). Practical Orthopedics. Chicago: Year Book Medical Publishers, pp. 44–52, 236–237.

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Shoulder tendonitis General description While any tendon surrounding the shoulder can develop tendonitis, the biceps tendon as it passes through the bicipital groove and the rotator cuff tendons (usually the supraspinatus) are most commonly affected. The mechanism of injury includes cumulative trauma due to compression or impingement under the acromion and coracoacromial ligament (usually from overhead activities) as well as blunt trauma to the shoulder region. Cumulative trauma can result from tensile overload causing microtears.

Clinical manifestations Shoulder pain, especially with activity, is the chief complaint. Other complaints include weakness and decreased functional use, especially with overhead activities. For rotator cuff pathology, symptoms include pain at the site of the greater tuberosity, night pain, exacerbation of the pain when lying on the shoulder, and pain along the lateral insertion of the deltoid on the humerus.

Differential diagnosis Supraspinatus tendonitis, biceps (long head) tendonitis, subacromial bursitis, rotator cuff tear (partial or full thickness), shoulder impingement, capsular laxity, labral tear, adhesive capsulitis, suprascapular neuropathy, and cervical radiculopathy should be included in the differential diagnosis (see Table 4.1).

History Patients will complain of pain of varying intensity. Pain can occur after exercise, subsiding within 24 hours (grade 1), during exercise without activity limitation (grade 2), interfering with exercise (grade 3), interfering with activities of daily living (ADLs) (grade 4), or pain at rest, which can also interfere with sleep (grade 5). Patients might have found some relief with rest and/or NSAIDs or acetaminophen.

Physical Muscle strength and range of motion of the shoulder should be assessed. Special tests to determine if tendonitis is present are described in Table 4.1. Neurological and vascular assessment of the upper extremity should be normal. If abnormalities are found, consider neurovascular diagnoses.

Diagnostic testing In patients with bicipital tendonitis, the bicipital groove X-ray view may reveal medial wall angle, spurs, and degenerative changes. Caudal tilt may show spurring. X-rays may reveal a hooked acromion contributing to cumulative trauma. MRI should be considered in patients resistant to treatment to rule out other disorders or to identify a tendonitis.

SHOULDER TENDONITIS

Management (treatment) Conservative management includes relative rest, NSAIDs and physical therapy including friction massage (biceps tendon only), exercise therapy, functional activities, modification of ADLs, cryotherapy, and postural strengthening. If there is no improvement or if symptoms worsen, consider a steroid/anesthetic injection into and around the tendon sheath. Do not inject into the tendon itself, as this can weaken the tendon. Surgery may be needed in recalcitrant cases.

Complications and red flags Many internal organs can mimic shoulder pain: breast cancer, pericarditis, cardiac ischemia, pulmonary pathology, gallstones, peptic ulcer, irritation of the diaphragm, liver abscess or tumor, pancreas, and ruptured spleen. A complete review of systems is indicated for every patient.

Table 4.1 Shoulder tendonitis Maneuver

Description

Implication

Jobe’s (empty can)

Shoulder at 90* abduction, 30* forward flexion and internally rotated resists adduction by examiner

Supraspinatus tendonitis

Yergason’s

Elbow is flexed and forearm supinated against resistance

Bicipital tendonitis

Speed’s

Shoulder flexion is resisted with the elbow extended and supinated

Bicipital tendonitis

Hawkin’s

Stabilize the shoulder with one hand, and with the shoulder forward flexed to 90* and the patient’s elbow flexed to 90*, internally rotate the shoulder

Impingement of the supraspinatus tendon

Neer’s

Stabilize the scapula and slowly forward flex the shoulder with the elbow straight

Impingement

Painful arc

Pain noted when patient actively abducts shoulder from 60* to 120*

Impingement

Drop arm

When patient slowly lowers arm from full abduction, the arm drops from midabduction

Full-thickness rotator cuff tear

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Shoulder impingement syndrome General description Shoulder impingement syndrome was once described as a syndrome of shoulder pain attributed to impingement of the rotator cuff tendon against the inferior surface of the anterior third of the acromion, the coracoacromial ligament, and the acromioclavicular joint,1 particularly in the forward flexed and internally rotated position. This syndrome has evolved to refer to a constellation of signs, symptoms, and imaging studies that occurs secondary to mechanical and/or degenerative forces occurring within the shoulder. Neer described three stages of shoulder impingement: Stage I denotes a reversible condition marked by edema and hemorrhage, seen in the second or third decade. Stage II is a condition of fibrosis and tendinopathy due to chronic inflammation and repeated episodes of impingement. Bursa and tendon are thickened. The condition is seen in patients aged 25–40 years and is usually present for years. Stage III describes rotator cuff tears, bony changes, and significant tendon degeneration secondary to prolonged tendonitis.2 The pathophysiology of impingement syndrome has been attributed to compressive and/or degenerative forces affecting the long head of the biceps tendon, subacromial bursa, and the rotator cuff tendons (see Fig. 4.1). The space becomes diminished in overhead motion corresponding to the “painful arc.” Encroachment occurs in overhead internal rotation as the greater tuberosity abuts the acromion. Attritional loss of rotator cuff tendon may occur from friction force.3 Overuse, instability, cuff weakness, acromial morphology, calcific changes, and acute trauma have been implicated. Insult to the subacromial structures may occur via multiple compressive or degenerative mechanisms. Thickening of bursa and tendon may occur secondary to overuse and inflammation. Cephalad humeral migration secondary to weak cuff musculature or scapular dyskinesia may further minimize the subacromial space. Another type of impingement occurs in athletes involved in sports such as tennis and baseball. The humeral head impinges the rotator cuff against the superior posterior labrum, in abduction and external rotation4 (midpoint of pitch, serve, or throw).

Risk factors Risk factors include repetitive overhead motion, glenohumeral instability, scapular dyskinesia or instability, osteophytic changes, and acromial angle, thickness, and morphology (association with acromial variations type II curved and especially type III hooked).

Clinical manifestations Patients present with the gradual onset of insidious pain, or pain precipitated acutely by traumatic bursitis. The pain is worsened during or after overhead activities and at night, particularly in the internally rotated and

SHOULDER IMPINGEMENT SYNDROME

N

OMIO

ACR A RS

S SUPRASPINATU

BICEP long head

TOID DEL

BU

Figure 4.1 Anatomy of the shoulder. forward flexed position. Symptoms are localized to the lateral, superior, anterior shoulder, which may refer to the deltoid region. A painful arc may be present between 60* and 120* of abduction. Weakness and stiffness may occur secondary to pain initially or develop secondary to disuse with chronicity. Bony pain over the anterior acromion may be suggestive of os acromiale. Subacromial bursitis, tendonitis, arthritis, or glenohumeral instability may coexist.

Differential diagnosis The differential diagnosis includes acromioclavicular arthritis, glenohumeral arthritis, rotator cuff tear, glenohumeral instability, adhesive capsulitis, labral tear, myofascial pain, subacromial bursitis, infraspinatus syndrome, swimmer’s shoulder, cervical radiculopathy, brachial plexopathy, elbow pathology, bicipital tendonitis, supraspinatus tendonitis, thoracic outlet syndrome, calcific tendonitis, phrenic nerve irritation, and myocardial infarction.

History Patients will complain of pain during range of motion, especially in overhead activities. They may hear a clicking or crepitus. The pain may be worse at night and the patient may not be able to sleep on the affected side. It may be referred to the deltoid region. It is important to get a history of any trauma. The patient should be asked about the onset, duration, and location of symptoms, as well as any exacerbating or remitting factors.

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Physical Patients may have decreased range of motion of the shoulder and pain on certain maneuvers (see later). There may be weakness in flexion, abduction, and/or internal rotation. On palpation of the shoulder, there may be tenderness over the acromion or over the greater tuberosity. Atrophy of the shoulder muscles may indicate a tear in the rotator cuff muscles. Neer’s sign, Neer impingement sign, passive painful arc maneuver Stabilize the scapula with one hand (to prevent scapular motion) while the other hand raises the ipsilateral arm in forced forward elevation. This causes the greater tuberosity to impinge against the acromion and will result in pain.2 Hawkins–Kennedy test, Hawkins impingement sign Flex the shoulder to 90* and then forcibly internally rotate the arm. The greater tuberosity is forced into the leading edge of the coracoacromial ligament and will result in pain.5 Yocum’s test The ipsilateral hand is placed on the contralateral shoulder and the patient elevates the elbow without raising the shoulder.6 If pain is reproduced, the test is positive. Diagnostic testing X-rays On the AP view, spurring of the anterior edge of the acromion may be seen with related sclerosis and subchondral cysts at the greater tuberosity,7 acromioclavicular joint arthritis, tendon calcification, Bankart or Hill-Sachs lesion, or glenohumeral joint osteoarthrosis. On the axillary view, an unfused acromial epiphysis, glenoid avulsion, or Hill-Sachs lesion may be noted. To view the outlet, obtain supraspinatus outlet views. There is an increased risk for impingement if the space is <7 mm. This view can also be used to assess the acromial morphology. Risk for impingement is increased with a curved or hooked acromion. When the clinical scenario correlates with roentgenograms and the cuff is believed to be intact, additional imaging may not be required.8 Additional imaging is used primarily to determine the presence and severity of a cuff tear.9 MRI MRI is useful in evaluation of partial and small full-thickness tears, the acromioclavicular joint, os acromiale, and lateral acromial morphology. Ultrasound This may be useful in identifying moderate or large full-thickness tears.10

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Management (treatment) • Most patients will succeed with conservative treatment. Better outcomes are associated with younger age, shorter duration of symptoms, and type I flat acromion.11 Initial precautions and activity restriction include avoidance of a painful arc and restriction of overhead movement. Long-term goals include restoration of satisfactory function. • Week 1–2: Decrease inflammation. Treat with relative rest, compression, cryotherapy, a short course of NSAIDs followed by prn use, and ultrasound. Aim for gentle, pain-free range of motion, minimize pain at rest before progressing. • Week 2–4: Increase range of motion. Stretch posterior shoulder girdle and use pendulum exercises, joint mobilization, postural training, and isometric strengthening. Establish full pain-free range of motion before progressing further. • Week 4–8: Increase strength with progressive resistance exercises of the shoulder musculature, with focus on shoulder depressors, scapular stabilizers, cuff muscles, muscle balancing, and correction of dysfunctional biomechanics. • Week 8: Return to play or activity. Do proprioceptive neurofacilitation activities, and continue progressive strength and flexibility exercises of the cuff and girdle, with graded return to functional activity. Maintenance (prevent recurrence of symptoms): Start a home exercise program, continue strengthening the cuff and scapular stabilizers, maintain range of motion, and use proper biomechanics. A subacromial injection may be diagnostic as well as therapeutic. Usually a mixture of corticosteroid and anesthetic is used. Direct injection into tendons should be avoided. No more than three injections should be done in a year. Surgical referral may be indicated if recovery fails after appropriate treatment for more than 6–18 months. Some clinicians refer sooner according to the specific clinical scenario, such as patient age, activity needs, or severity of symptoms. Patients with associated instability or larger acute rotator cuff tears may need earlier surgical consultation. Resection of the coracoacromial ligament or a more definitive anterior acromioplasty may be indicated for subacromial decompression.5

Complications and red flags Visceral pain from phrenic nerve irritation or myocardial infarction, as well as elbow and cervical pathology, may refer to the shoulder. Chronic impingement may lead to inflammation, degeneration of the cuff, bony change, and progression to partial and full tears in the rotator cuff. Impingement has been associated with bicipital tendonitis.2,5 Progression from rotator cuff tendonitis to tendinopathy to tear may occur. Pain and disuse may lead to muscle atrophy, loss of range of motion, adhesive capsulitis, or reflex sympathetic dystrophy.

MANAGEMENT (TREATMENT)

References 1. Neer CS II (1972). Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am 54(1):41–50. 2. Neer CS II (1983). Impingement lesions. Clin Orthop 173:70–77. 3. Meyer AW (1931). The minute anatomy of attrition lesions. J Bone Joint Surg 13:341–360. 4. Davidson PA, Elattrache NS, Jobe CM, Jobe FW (1995). Rotator cuff and posterior–superior glenoid labrum injury associated with increased glenohumeral motion: a new site of impingement. J Shoulder Elbow Surg 4:384–390. 5. Hawkins RJ, Kennedy JC (1980). Impingement syndrome in athletes. Am J Sports Med 8(3):151–158. 6. Malanga G, Nadler S (2006). Musculoskeletal Physical Examination. Philadelphia: Elsevier. 7. Cone RO III, Resnick D, Danzig L (1984). Shoulder impingement syndrome: radiographic evaluation. Radiology 150:29–33. 8. Bigliani LU, Levine WN (1997). Subacromial impingement syndrome. J Bone Joint Surg Am 79-A:1854–1868. 9. Ostlere G (2003). Imaging the shoulder. Imaging 15:162–173. 10. Paavolainen P, Ahovuo J (1994). Ultrasonography and arthrography in the diagnosis of tears of the rotator cuff. J Bone Joint Surg 76-A:335–340. 11. Morrison DS, Frogameni AD, Woodworth P (1997). Non-operative treatment of subacromial impingement syndrome. J Bone Joint Surg 79-A:732–737.

Further reading Flatow EL, Soslowsky LJ, Ticker JB, Pawluk RJ, Helper M, Ark J, Mow VC, Bigliani LU (1994). Excursion of the rotator cuff under the acromion. Patterns of subacromial contact. Am J Sports Med 22:779–788. Neer CS II (1990). Shoulder Reconstruction, Philadelphia: WB Saunders, pp. 141–142.

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Rehabilitation after rotator cuff surgery Background Rotator cuff disorders comprise a spectrum of pathology including rotator cuff tendonosis and impingement syndrome, partial-thickness rotator cuff tears, full-thickness rotator cuff tears, and massive irreparable rotator cuff tears. To understand a comprehensive rehabilitation program one needs to understand the principles of rotator cuff repair, the principles of tendon healing, and potential postoperative complications. The goal of any postoperative rehabilitation program should be to maximize function and patient satisfaction while minimizing any postoperative complications. Principles of repair The principles of rotator cuff repair as first described by Neer include reshaping of the acromion without damaging the deltoid origin, restoring motion, releasing and repairing torn tendons, and starting an individualized surgeon-specific rehabilitation program. Two of the most common postoperative complications after rotator cuff repair surgery are re-tear and stiffness.

Rehabilitation To minimize re-tears, active motion is limited in the early postoperative period. During this period, passive motion and pendulum exercises are started while immobilizing the shoulder in a sling. Variations on this theme may be individualized according to the size of tear, quality of tendon tissue, strength of tendon repair, and preoperative shoulder stiffness. Larger rotator cuff tears are more likely to re-tear than smaller tears. Large tears may also be less likely to have stiffness because the capsule is torn with the tendon tear and may also be released at the time of the repair. In this scenario, more restrictions may be placed on early motion to prevent re-tear. For smaller tears, the risk of re-tear is reduced. In small tears the capsule is intact and attached to the tendon during the repair, which may cause a higher rate of stiffness after repair. The re-tear rate of rotator cuff repair varies from 11% to 94% for arthroscopic repair and 20% to 65% for open repairs. Preoperative stiffness increases postoperative motion deficits. To limit postoperative motion loss, a preoperative program to maximize motion should be instituted. Other options for patients who are unable to gain preoperative motion include a staged procedure to manipulate the shoulder, or performing a capsular release prior to performing the rotator cuff repair. Simultaneous capsular release at the time of rotator cuff repair has also been advocated. Preoperative fatty infiltration and muscle atrophy is irreversible and, as such, will limit strength gains postoperatively.1 Even though fatty infiltration and muscle atrophy are irreversible, functional outcomes can be greatly improved by surgical repair.2 Rotator cuff repair surgery for massive rotator cuff repairs is indicated for relief of pain.

REHABILITATION AFTER ROTATOR CUFF SURGERY

Patients should be counseled that strength return is inconsistent and unreliable because of the high rate of re-tear and the irreversible nature of muscle atrophy. Other options for massive rotator cuff tears are tendon transfers (lattismus or teres major) or reverse shoulder replacement. A rotator cuff rehabilitation program should be broken down into four phases: • Tendon healing phase • Motion restoration phase • Initial strengthening • Strength restoration Phase 1 In phase 1, the shoulder should be protected in a sling to limit contraction of the rotator cuff muscles and stress on the rotator cuff repair. Failure to protect the repair greatly increases the re-tear rate even when using optimal repair techniques.3 Depending on the original size of the tear, shoulder stiffness, and strength of the repair, passive motion may be started during phase 1. Pendulum exercises may be done by the patient, as well as passive motion at formal therapy. The balance between motion and stressing the tendon repair must be determined by the surgeon. This is balanced by the fact that postoperative stiffness is usually regained by rehabilitation, whereas re-tears are only fixed by revision surgery. Phase 2 In phase 2, tendon healing has progressed. Stretching exercises with the goal of motion restoration are now emphasized. This usually occurs 4–8 weeks after surgery. Aggressiveness of this program is balanced by the size of tear and shoulder stiffness. Patients with large anterior tears involving the subscapularis tendon should limit external rotation as well as abduction with external rotation. Patients with large posterior tears involving the infraspinatus may limit internal rotation stretching. Phase 3 Phase 3 focuses on initiating strength training. This should begin after attaining significant motion. For patients with significant limitation of glenohumeral motion, rotator cuff strengthening should be delayed but scapular stabilization strengthening may be started. For patients who have regained most of their motion, strengthening of internal rotation and external rotation of the glenohumeral joint is first started.

1 Gerber C, Schneeberger AG, Hoppeler H, Meyer DC. (2007) Correlation of atrophy and fatty infiltration on strength and integrity of rotator cuff repairs: a study in thirteen patients. J Shoulder Elbow Surg 16(6):691–696. 2 Burkhart SS, Barth JR, Richards DP, Zlatkin MB, Larsen M (2007). Arthroscopic repair of massive rotator cuff tears with stage 3 and 4 fatty degeneration. Arthroscopy 23(4):347–354. 3 Gerber C, Schneeberger AG, Perren SM, Nyffeler RW (1999). Experimental rotator cuff repair: a preliminary study. J Bone Joint Surg Am 81(9):1281–1290.

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Phase 4 Phase 4 focuses on maximizing strength gains. This phase starts when scapular stabilizer strength and internal and external rotator cuff strength have progressed. In phase 4, supraspinatus and deltoid strengthening is begun. Supraspinatus and deltoid strengthening should only be started after regaining normal scapulohumeral motion. Multiple studies have shown that strength progression occurs over 12 months.4,5 Phase 1, days 1–28 Use an abduction sling and start pendulum exercises. For patients with passive external rotation (ER) <10* at 1 week, start passive range of motion (ROM) with a therapist. For patients with passive ER <30* at 2 weeks, start passive ROM with a therapist. Phase 2, weeks 4–8 Discontinue using the sling, start active assistive motion, provide formal therapy for patients with <170* of forward elevation and/or ER <30*. Phase 3 (strength restoration), weeks 8–12 Start scapular stabilizer strengthening and internal (IR) and external rotation strengthening. Limit IR/ER strengthening if the patient has marked stiffness until motion returns. Phase 4, week 12+ (only started when normal scapulohumeral rhythm has returned) Supraspinatus and deltoid strengthening is practiced. (For patients with large to massive rotator cuff tears and marked abnormal scapulohumeral rhythm, supraspinatus and deltoid strengthening may never be started.)

4 Rokito AS, Zuckerman JD, Gallagher MA, Cuomo F (1996). Strength after surgical repair of the rotator cuff. J Shoulder Elbow Surg 5(1):12–17. 5 Kirschenbaum D, Coyle MP Jr, Leddy JP, Katsaros P, Tan F Jr, Cody RP (1993). Shoulder strength with rotator cuff tears. Pre- and postoperative analysis. Clin Orthop Relat Res 288:174–178.

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Adhesive capsulitis General description Codman originally coined the term “frozen shoulder” in 1934 to describe a condition of a painful loss of shoulder motion with normal X-rays.“Adhesive capsulitis” was coined by Nevaiser in 1946 to describe the apparent “adhesions” of the glenohumeral capsule of patients with frozen shoulders at the time of arthrography that limit overall joint space volume. Adhesive capsulitis can result from a primary or idiopathic cause as well as by a secondary or known cause. Secondary causes include intrinsic, extrinsic, and systemic causes. Primary idiopathic adhesive capsulitis is poorly understood but a very frequent cause of shoulder pain and motion loss. The cumulative risk of at least one episode of frozen shoulder is 2%. Frozen shoulder or adhesive capsulitis is more common in women than in men, usually occurs in the fourth to sixth decade of life, and more often affects the nondominant extremity. Systemic causes of adhesive capsulitis include diabetes mellitus, hyperthyroidism, ischemic heart disease, inflammatory arthritis, and cervical spondylosis. Bilaterality occurs in 6%–50% of cases of adhesive capsulitis but usually not at the same time. The highest rate of bilaterality occurs with insulin-dependent diabetes mellitus.

Clinical manifestations Frozen shoulder or adhesive capsulitis is a condition in which shoulder motion is limited in active and passive motion. Adhesive capsulitis commonly occurs in four phases: • Phase 1 marks the start of the disease with increased shoulder pain. This may occur after minor trauma. Phase 1 is short, lasting days to weeks. • Phase 2 marks the beginning of stiffness and continued pain at rest. This stage lasts 3–6 months. • Phase 3 is the progressive stiffness or frozen phase. This phase is marked by the resolution of pain at rest but continued pain at the extremes of motion. This stage can last from 3 to 18 months. • Phase 4 is the thawing or resolution phase when shoulder motion is regained. Many patients regain only partial motion after suffering through these four stages.

Differential diagnosis Loss of shoulder external rotation with the arm at the side and with the shoulder abducted helps distinguish adhesive capsulitis from shoulder bursitis, tendonitis, or rotator cuff tears. Other disorders in the differential diagnosis include fractures, cervical radiculopathy, complex regional pain syndrome, neoplastic disorders, labral disorders, and osteoarthritis.

ADHESIVE CAPSULITIS

History Patients will complain of decreased range of motion of the shoulder, which may interfere with activities of daily living. Pain (more commonly at night) is more common with overhead activities and in the early stages of adhesive capsulitis.

Physical Both passive and active range of motion of the shoulder will be limited. Shoulder external rotation and abduction may be particularly limited and painful. There may be tenderness to palpation of the shoulder.

Diagnostic testing X-rays can be helpful to rule out other pathology. Joint space narrowing may be noted. MRI and arthroscopy may be required to confirm the diagnosis if conservative management fails or to evaluate other etiologies of shoulder disorders.

Management (treatment) Management of adhesive capsulitis should include therapy and may include NSAIDs (or a short course of oral steroids), analgesics, injections into the subacromial space, or suprascapular nerve blocks. Capsular distension or manipulation under anesthesia is rarely required. Patients with adhesive capsulitis should begin an aggressive treatment program as soon as possible. Treatment of adhesive capsulitis varies with the stage of condition. Initial treatment of adhesive capsulitis begins with a daily stretching program. Stretching for external rotation at the side, abduction external rotation, forward elevation, and internal rotation should be done 3–5 times/day and for short periods of time. Patients should expect an increase in pain after initiation of stretching, and they should be reassured that this is only temporary. An initial intra-articular injection of a corticosteroid and an oral steroid taper may help decrease pain in phases 1 and 2. Surgical intervention during the first two stages has a high failure rate and should be avoided. For patients in phase 3 who have 3 progressive months with no gains in motion, a shoulder manipulation under anesthesia or an arthroscopic capsular release may be used to improve shoulder motion. Postoperative stretching should begin immediately to maintain motion gains. Formal physical therapy may be used as an adjunct to a home stretching program. Modalities may also be employed to help diminish pain. Strengthening exercises should be avoided, as these tend to generate pain (pain control is necessary to be able to aggressively stretch). An exception, however, is the use of scapular stabilizer strengthening, which may improve periscapular pain.

Complications and red flags Permanent loss of range of motion may develop if the condition is not treated appropriately and aggressively.

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Rehabilitation of superior labral tears Background Superior labral tears (SLAP tears) can be caused by a traumatic injury or be the end result of an overuse injury in overhand throwers. Traumatic SLAP tears can occur from traction and/or compression. A common mechanism is a fall on an outstretched arm. Patients with a SLAP tear may complain of subtle instability, locking, catching, or anterior shoulder pain. Physical examination tests for a SLAP tear include the Speeds, Yergason, and relocation tests and the active compression test. In the overhand thrower, a superior labral tear is usually associated with a significant loss of glenohumeral internal rotation and scapular dyskinesis. Often the thrower will have a prior history of shoulder pain with a specific instance of sudden increase in pain and drop-off in performance.

Types of SLAP tears There are four types of SLAP tears: • Type 1 has degenerative fraying of the labrum but is attached to the glenoid. • Type 2 is detached from the glenoid. • Type 3 is a bucket-handle tear of the superior labrum but is attached to the glenoid. • Type 4 extends from the superior labrum into the biceps tendon.

Treatment Treatment of SLAP tears depends on the type of tear, the patient’s age, and the patient’s complaints and findings. In patients undergoing arthroscopy a type 1 tear is debrided, a type 2 tear is repaired back to the glenoid, a type 3 tear is excised, and a type 4 tear is debrided. In type 3 tears, a repair is performed when the remaining portion of the labrum is detached after resection of the bucket-handle tear. The biceps tendon in a type 4 tear is debrided. For bicep tendon tears involving <50% of the tendon, the tendon is left intact. For tears involving >50% of the tendon, the tendon is either tenodesed or released. Tenodesis should be performed in patients under the age of 50 and in patients with a prominent biceps muscle where a Popeye deformity would be unacceptable. In patients over the age of 50 and those without a prominent biceps muscle a tenotomy may be performed.

Rehabilitation For type 1 and 3 tears after debridement, a sling is used for comfort. Active assisted motion is begun immediately and strengthening exercises are begun as motion is restored. For type 2 tears and repaired type 3 and 4 tears: • Weeks 1–4: Use a sling for the first 3–4 weeks. Pendulum exercises are begun for forward elevation to 90*, with no external rotation >30*. No biceps contraction should be done.

REHABILITATION OF SUPERIOR LABRAL TEARS

• Weeks 4–8: Active assisted range of motion for full forward elevation. No abduction external rotation. No biceps strengthening. The patient may start internal and external rotation strengthening and scapular stabilizer strengthening. • Weeks 8–12: The patient may start supraspinatus strengthening if the scapulohumeral rhythm is normal. The patient may initiate biceps strengthening, and may start posterior capsular stretching. • Weeks 12–16: The patient may perform abduction and external rotation stretching if this is not fully restored. Strengthening of the rotator cuff and scapular stabilizers should be continued. • Weeks 16+ The patient may start throwing rehabilitation (for overhand athletes).

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Epicondylitis General description Epicondylitis is subacute or chronic inflammation of the myotendinous junction of the wrist flexor and extensor muscle groups as they originate from the elbow’s medial and lateral epicondyles, respectively. Lateral epicondylitis is commonly referred to as “tennis elbow,” primarily affects the extensor carpi radialis brevis (ECRB), and occasionally the extensor digitorum communis muscles. Medial epicondylitis, or “golfer’s elbow,” affects the flexor carpi radialis and pronator teres muscle origin.

Clinical manifestations Elbow pain is invariably the presenting complaint of all patients with epicondylitis. Pain can be mild and present only with the use of the hands, or severe enough to affect sleep and basic activities of daily living. Pain is typically worse with activities that involve contraction of the forearm muscles.

Differential diagnosis Arthritis of the radiocapitellar joint and posterior interosseous nerve entrapment commonly present as lateral elbow pain and may be incorrectly diagnosed as lateral epicondylitis. Other causes of elbow pain that should be considered in the differential diagnosis are olecranon bursitis, ulnar nerve entrapment in the elbow, ligamentous injury, and radial head fracture.

History A repetitive activity that involves contraction of the forearm muscles prior to the onset of the pain is usually elicited. This may be in the form of repetitive wrist turning, hand gripping, or use of tools. Although tennis and golf playing, especially by the novice, may cause the injury, they are the minority of the patients with epicondylitis.

Physical Local tenderness of the epicondyle and the myotendinous junctions of the muscles originating from the epicondyles, together with exacerbation of pain with resisted extension (lateral epicondylitis) and resisted flexion (medial epicondylitis) of the wrist are the main positive examination findings. Resisted extension of the middle finger with elbow in extension reproduces the pain in lateral epicondylitis. The elbow range of motion is normally full, and swelling is not a usual finding.

Diagnostic testing Diagnostic tests are not necessary in most cases. X-ray of the elbow may be requested to rule out fracture and arthritis. Electrodiagnostic evaluation should be done if nerve entrapment is entertained.

Special considerations The benefit from most forms of treatment will usually be only temporary unless the offending activity that caused the problem is avoided or modified and faulty mechanics corrected.

EPICONDYLITIS

Management (treatment) The mainstay of management is activity modification. Ice, massage, NSAIDs, physical therapy, and counterforce bracing are helpful during the painful phase. Local infiltration of the myotendinous origin with corticosteroid and local anesthesia is successful in controlling pain most of the time. Surgery is reserved for cases that fail conservative treatment.

Further reading Anderson BC (1999). Orthopedics for Primary Care: Diagnosis and Treatment, 2nd ed. Philadelphia: WB Saunders. Frontera WR, Silver JK (2002). Essentials of Physical Medicine and Rehabilitation. Philadelphia: Hanley and Belfus. Galloway, M, Demaio, M, Mangine, R (1992). Rehabilitative techniques in the treatment of medial and lateral epicondylitis. Orthopedics 15:1089.

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Bicipital tendonitis General description Bicipital tendonitis is inflammation of the long head of the biceps tendon as it passes through the bicipital groove on the anterior proximal humerus. It is one of the cumulative trauma disorders that affect the shoulder. Repetitive lifting and reaching results in inflammation and microtear of the tendon.

Clinical manifestations Anterior shoulder pain aggravated by lifting and overhead activity is the usual complaint of patients with bicipital tendonitis.

Differential diagnosis Conditions that present as anterior shoulder pain should all be considered in the differential diagnosis. The more common conditions include rotator cuff tendonitis, impingement syndrome, subacromial bursitis, acromioclavicular joint arthritis, and labral tear. Poorly localized shoulder pains are usually extrinsic in origin. Cervical radiculopathy can present as shoulder pain radiating from the neck. Elbow pathology can produce pain radiating to the shoulder.

History A repetitive activity that involves contraction of the biceps muscle and overhead reaching prior to onset of the pain may be elicited. This can be in the form of repetitive lifting and reaching. Pain is well localized; patient can almost always pinpoint the area of pain. Patients also complain of pain aggravated by lifting heavy objects and shoulder movement.

Physical Local tenderness is elicited with palpation of the bicipital groove. This area of tenderness is about 2.5 cm distal to the anterior edge of the acromion, and can be identified by internally and externally rotating the humerus (see Fig. 4.1). Pain may be aggravated by resisted flexion of the elbow and supination of the forearm. The patient may also have a painful arc. Provocative tests such as Yergason’s test and Speed’s test the empty can test (see Shoulder tendonitis, Table 4.1) can be positive. Muscle strength is limited only by the pain.

Diagnostic testing Special testing is usually not necessary. X-ray of the shoulder is usually normal, or may reveal calcification in the bicipital groove. MRI is indicated in patients suspected of having rotator cuff tear. Diagnostic injection with local anesthetic to the bicipital groove can help differentiate bicipital tendonitis from rotator cuff tendonitis and subacromial bursitis.

Special considerations Concomitant shoulder pathology is common in the setting of bicipital tendonitis, and it is the major reason for failure of treatment.

BICIPITAL TENDONITIS

Management (treatment) Management in the acute phase is directed toward control of pain by reducing inflammation. This is done by activity modification with restriction of lifting and reaching, ice massage to the anterior shoulder, NSAIDs, and physical modalities such as phonophoresis and iontophoresis. Local infiltration of the surrounding tendon sheath with corticosteroid and local anesthesia is reserved for patients whose condition has failed to respond to the above measures.

Complications and red flags Rupture of the biceps long head tendon can occur in the setting of chronically inflamed tendon with minor muscle contraction. The rupture presents as a visible bulge of recent onset on the anterior arm proximal to the cubital fossa and concomitant ecchymosis on the inner arm. Elbow flexion strength is not significantly affected. Surgery is rarely indicated.

Further reading Frontera WR, Silver JK (2002). Essentials of Physical Medicine and Rehabilitation. Philadelphia: Hanley and Belfus. Hoppenfeld S (1976). Physical examination of the shoulder. In Physical Examination of the Spine and Extremities. Upper Saddle River, NJ: Prentice Hall.

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Ulnar neuropathy at the elbow and cubital tunnel syndrome General description In order to understand ulnar neuropathy at the elbow (UNE), it is important to review the anatomy of the ulnar nerve. The ulnar nerve arises from the medial cord of the brachial plexus and travels inferiorly down the medial and posterior aspects of the arm behind the medial epicondyle (in the ulnar groove) and through the cubital tunnel. The cubital tunnel is made up of the ulnar collateral ligament and the aponeurosis between the two heads of the flexor carpi ulnaris. This superficial region is often referred to as the “funny bone.” The nerve then continues along the ulna and enters the hand through Guyon’s canal. It ultimately supplies sensation to the fifth digit and half of the fourth digit. The ulnar nerve can be entrapped or traumatized throughout its course. Cubital tunnel syndrome is the entrapment of the ulnar nerve as it passes through the cubital tunnel. Entrapments elsewhere in this region are more accurately termed UNE. UNE often occurs after trauma to the region and/ or dislocation of the elbow.

Clinical manifestations Patients suffering from UNE may present with paresthesia and numbness in the fourth and fifth digits (dorsal and palmar aspects of the hand), pain at the elbow radiating toward the hand, and hand intrinsic muscle weakness and atrophy.

Differential diagnosis This includes cervical radiculopathy, medial cord brachial plexopathy, thoracic outlet syndrome, and ulnar nerve compression at Guyon’s canal.

History History of a traumatic event involving the elbow may be described. Chronic pressure at the ulnar groove and repetitive elbow flexion and extension can also predispose to the entrapment. Less commonly, a head injury may lead to an ulnar neuropathy in patients with heterotopic ossification or a spastic extremity.

Physical • Upon initially examining the patient, note the elbow carrying angle and any exaggeration of that angle. • Palpate the ulnar nerve in the ulnar groove behind the medial epicondyle and note its mobility. Ulnar nerve subluxation may be present and should be ruled out upon palpation. • Examine motor function including finger abduction and thumb adduction, particularly the pinching of the thumb and fingers. Patients often have difficulty buttoning a shirt.

ULNAR NEUROPATHY

• Froment’s sign tests for adductor pollicis weakness. Ask the patient to hold a piece of cardboard between the first and second digits against resistance. A positive test is marked by flexion of the interphalangeal joint of the thumb and a grip strength 2/3 of the normal side. • Tinel’s sign: Lightly percuss over the ulnar nerve at the elbow. A positive test is marked by a reproduction of the tingling sensation. Because the nerve is superficial at this location (and patients without UNE may have a positive test), testing should be compared bilaterally for hypersensitivity to percussion.

Diagnostic tests Radiography Osteophytes and associated degenerative joint disease of the elbow may be seen. EMG Conduction velocity of the ulnar nerve across the elbow may be decreased compared to its distal and proximal segments. Decreased amplitudes may be noted in both the ulnar sensory nerve action potential (SNAP) and the dorsal ulnar cutaneous nerve SNAP. This helps differentiate an ulnar nerve lesion at the elbow (where both the ulnar sensory nerve and the dorsal ulnar cutaneous nerve would be affected) from an ulnar nerve lesion at the wrist (where the dorsal ulnar cutaneous nerve would be spared). In severe axonal lesions, ulnar motor amplitudes may be decreased, and abnormal spontaneous potentials (denervation) may be noted in ulnarly innervated muscles.

Treatment • Extension splint preventing >70* of flexion may be used at night and/or a sheepskin elbow pad (to protect the ulnar nerve at the elbow). • NSAIDs may be used if there is inflammation at the cubital tunnel. • Avoid repetitive elbow flexion and pronation. • Surgical release of the nerve at the cubital tunnel and or transposition of the nerve may be necessary in recurrent or refractory cases.

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Radial tunnel syndrome and supinator syndrome Radial tunnel syndrome and the supinator syndrome both refer to entrapment of the radial nerve in the forearm. Radial tunnel syndrome is the result of compression of the posterior interosseous nerve (a branch of the radial nerve) as it passes through the lateral muscular septum. Supinator syndrome is entrapment of the posterior interosseous nerve in the fibrous opening of the supinator muscle known as the arcade of Frohse. The syndromes often occur in patients who perform repetitive tasks that involve wrist extension and forearm rotation such as piano playing, keyboarding, and/or driving. The conditions are often misdiagnosed as lateral epicondylitis (tennis elbow).

Clinical manifestations Patients suffering from radial tunnel syndrome or supinator syndrome present with deep aching lateral elbow and forearm pain. Pain may radiate up the shoulder and neck. Pain is aggravated by use of the hand.

Differential diagnosis The diagnosis is often entertained only after failure of treatment of lateral epicondylitis.

History Patients may have a history of congenital anomalous structures, trauma, or repetitive tasks involving wrist and finger extension and forearm rotation.

Physical • Locate the exact point of pain, as it will help differentiate between radial tunnel syndrome and lateral epicondylitis. • Pain in epicondylitis is near the muscle attachment on the lateral epicondyle whereas radial tunnel syndrome or supinator syndrome presents with pain lower down the forearm where the radial nerve courses about the radial head. • Resisted extension of the middle finger with elbow in extension reproduces the pain in lateral epicondylitis. • Sensation should be intact with entrapment of the radial nerve in the forearm, as the superficial radial sensory nerve branches off before this area of impingement. Strength in supination should be normal. However, there may be a decrease in strength in the distally innervated muscles (finger extensors and ulnar wrist extensor).

Diagnostic tests The steroid test will help differentiate between a radial tunnel syndrome and lateral epicondylitis. A glucocorticoid/lidocaine injection into the area of the lateral epicondyle should resolve epicondylitis symptoms whereas the same injection into the radial tunnel will yield little relief. Electrodiagnostic testing will reveal normal radial sensory studies. Radial motor studies may be normal or reveal decreased amplitude. Abnormal

RADIAL TUNNEL SYNDROME AND SUPINATOR SYNDROME

spontaneous potentials (denervation) may be noted in radially innervated muscles distal to the supinator (in supinator syndrome). It is not unusual for EMG findings to be absent in some cases. This does not rule out the diagnosis.

Treatment • Immediately avoid tasks that aggravate the condition and require frequent wrist extension. • A lightweight arm splint should be worn at night if symptoms are worse during sleep. • Physical therapy should be used to strengthen forearm muscles. • Surgical release has been used rarely for patients who do not respond to conservative management.

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Olecranon bursitis The olecranon bursa is a small sac lined with synovial membrane and filled with synovial fluid. The purpose of the sac is to cushion the olecranon and allow the skin to move freely over the bone beneath it. Olecranon bursitis is the inflammation and/or irritation of the bursa and can be easily identified when inflamed, as the bursa is superficial.

Clinical manifestations Patients suffering from olecranon bursitis present with profound edema and pain. The bursa stretches and ultimately may limit range of motion of the elbow. A comorbid infection of the bursa may present with additional edema and erythema.

History Patients often have a history of gout, rheumatoid arthritis, sepsis, hemorrhage, or trauma involving pressure on the elbow. Traumatic bursitis is often seen in professions involving regular elbow use, such as carpentry.

Physical • Tenderness over bursa • Elbow pain with motion and at rest • Apparent swelling of bursa

Diagnostic tests • Radiograph: Bone spurs are often seen at the tip of the elbow. • If infection or a crystal disease is suspected, aspirate bursal fluid and examine it to identify an infection and/or crystals under polarized microscopy.

Treatment • If infection is identified, prescribe an antibiotic regimen. • Noninfectious bursitis should be treated with elbow elevation and ice. • If there is no resolution, repeated aspiration and glucocorticoid steroid injections should be considered. • NSAIDs have repeatedly been found to be less successful than steroids.

Further reading American Academy of Orthopaedic Surgeons (AAOS). Olecranon bursitis. www.aaos.org Anderson BC (1999). Orthopedics for Primary Care: Diagnosis and Treatment, 2nd ed. Philadelphia: WB Saunders. Frontera WR, Silver JK (2002). Essentials of Physical Medicine and Rehabilitation. Philadelphia: Hanley and Belfus. Galloway M, Demaio M, Mangine R (1992). Rehabilitative techniques in the treatment of medial and lateral epicondylitis. Orthopedics15:1089. Jobe FW, Ciccotti MG (1994). Lateral and medial epicondylitis of the elbow. J Am Acad Orthop Surg 2:1. Loh YC, Lam WL, Stanley JK, Soames RW (2004). A new clinical test for radial tunnel syndrome— the Rule-of-Nine test: A cadaveric study. J Orthop Surg 12:83–86. Wheeless CR III (2009). Wheeless’ Textbook of Orthopaedics. Available at: www.wheelessonline.com

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Carpal tunnel syndrome Compression of the median nerve in the carpal tunnel is the pathology that results in the signs and symptoms of carpal tunnel syndrome (CTS). The floor (or bottom) and sides of the carpal tunnel are made up of the carpal bones; the top of the tunnel is the transverse carpal ligament (see Fig. 4.2). Besides the median nerve, the tunnel also contains the flexor tendons of the fingers (flexor digitorum superficialis and profundus, and the flexor pollicis longus). Half of all cases of CTS occur in patients 40–60 years old, predominantly in females (70%). An increase of pressure of 30 mmHg has been shown to cause venous congestion in the nerve and compromise axonal transport.

Clinical manifestations • CTS is the most common nerve entrapment in the body. • Nerve compression may result in ischemia, leading to numbness and tingling in the radial 3 fingers (see Fig. 4.3) • Prolonged nerve compression may lead to atrophy of the thenar eminence. Risk factors include the following: • Repetitive hand work (prolonged wrist flexion or extension, frequent gripping and/or squeezing) • Endocrine imbalance (especially diabetes and thyroid disease) • History of neuropathy • Rheumatoid arthritis • Pregnancy

History • Patients usually complain of pain in the wrist and fingers with the presence of paresthesia in the radial 3 fingers. • Nighttime pain or numbness may be especially predictive of CTS. • Weakness or clumsiness in the hand. The patient may complain of dropping items or an inability to grip items.

Physical examination • Start off with examination of the cervical spine and elbow to rule out nerve compression in more proximal regions. • Perform a thorough vascular exam. • Assess for any thenar muscle atrophy. • Two-point discrimination should be checked at the tips of the fingers on the radial and ulnar borders (should be <5–6 mm). • Tinel test may be positive (tapping over the median nerve at the volar wrist reproduces the numbness or paresthesias in a median distribution). • Phalen test may be positive (maximally flexing both wrist for 1–2 minutes reproduces the numbness or paresthesias in a median distribution). Reverse Phalen test may also be positive (forced extension of both wrists for 1–2 minutes reproduces the symptoms). • The Semmes–Weinstein monofilament test, using various sizes of nylon filaments, is the most predictable sensory test.

CARPAL TUNNEL SYNDROME

Flexor tendons Median Ulnar artery nerve

Radial artery Flexor retinaculum

Tra pez iu

m

Ulnar nerve

Ha

ma

te

Capitate

ezoid Trap

Exte

nso r

tend

ons

Figure 4.2 Anatomy of the carpal tunnel. This figure was published in Weiss L, Silver JK, Weiss J (2004). Easy EMG: A Guide to Performing Nerve Conduction Studies and Electromyography. Philadelphia: Butterworth-Heinemann/Elsevier, p. 122. Copyright Elsevier (2004). Reprinted with permission.

A

B

Figure 4.3 Median nerve sensory distribution dorsal (A), palmar (B). This figure

was published in Weiss L, Silver JK, Weiss J (2004). Easy EMG: A Guide to Performing Nerve Conduction Studies and Electromyography. Philadelphia: ButterworthHeinemann/Elsevier, p. 121. Copyright Elsevier (2004). Reprinted with permission.

Diagnosis Electromyography (EMG) studies should be performed to diagnose a median neuropathy at the wrist, to rule out other pathology (peripheral neuropathy, more proximal median neuropathy, ulnar neuropathy, or cervical radiculopathy), to determine the severity of nerve compression, and to prognosticate.

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Differential diagnosis • • • • • • • • • •

Cervical root impingement (C6–7) Thoracic outlet syndrome Cubital tunnel syndrome Ulnar neuropathy Pronator syndrome Peripheral neuropathy Median neuropathy in the forearm Brachial plexopathy Anterior interosseous nerve syndrome Raynaud’s phenomenon

Treatment • Patients should avoid aggravating activities. • Workplace modifications • Wrist splinting (in neutral). The wrist splint should be worn during sleep. • NSAIDs • Cortisone injections into the carpal tunnel Occupational or physical therapy should be consulted for teaching activity modification, especially work-related activities, or for nerve gliding exercises that might decrease symptoms of nerve compression. Surgical release of the transverse carpal ligament is performed when nonoperative measures have failed, in patients with constant numbness, or in patients with motor weakness. The goal of surgical intervention is to prevent progression of the condition and allow for the nerve to heal and recover. The carpal tunnel release may be done as an open procedure or as an endoscopic procedure. The surgeon will make an incision in the wrist and cut the ligamental roof on the tunnel; this will increase the size of the tunnel and thus decrease the pressure within the tunnel. Most patients will experience improvements in their symptoms after surgery. A complete recovery may take up to 1 year.

Special considerations Elderly patients with pain, paresthesias, and numbness may not respond well to surgical treatment because of the high rate of fibrosis and axonal loss.

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Wrist pain General description The wrist joint is formed by the articulation of the carpal bones and the distal end of the radius. The carpal bones are arranged into distal and proximal rows. The scaphoid, also called the carpal navicular, provides the stabilizing link between the proximal and distal rows. The wrist joint is supported by a complex system of ligaments, the triangular fibrocartilage complex (TFCC), and the dorsal and ventral retinaculum. The wrist joint is prone to injury because of its location and mobility. Injury to the wrist joint can be due to acute trauma or repetitive stress.

Clinical manifestations Patients with a wrist problem typically complain of pain with motion, swelling (either localized or diffuse), or numbness and paresthesia in cases of nerve entrapment.

Differential diagnosis Distal radius fracture, scaphoid fracture, ligamentous sprain, TFCC tear, and perilunate dislocation are conditions commonly seen after a fall onto an outstretched arm. Repetitive stress can also produce injuries producing wrist pain. This includes de Quervain’s tenosynovitis, carpal tunnel syndrome, arthritis of the thumb carpometacarpal joint, and ganglion cysts.

History The history should include the standard inquiry about pain: onset, duration, palliation or provocation, quality, location, and radiation. In cases of acute trauma, the mechanism of injury will provide valuable information regarding the force of impact and the structure likely to be injured. Questions about the patient’s occupation and avocational activities and prior injuries and surgery will provide insight in cases of chronic pain and those due to cumulative trauma disorders.

Physical Examination starts with inspection and measurement of wrist range of motion (see Table 4.2). Knowledge of wrist anatomy is essential in proper examination. Tenderness is generally elicited over the area of pathology, whether it is a sprain, fracture, or tenosynovitis.

Diagnostic testing Anteroposterior X-ray of the wrist in neutral position, radial and ulnar deviation, and lateral view in neutral position, flexion, and extension (carpal series) should be done in the initial evaluation of a patient with wrist trauma. This is sufficient in most instances for the diagnosis of obvious fractures and dislocations. Major ligamentous injuries can be diagnosed by the relative positions of the carpal bones to each other. MRI may be necessary in cases where X-ray is negative and pain persists after treatment. Electrodiagnostic examination should be done in cases of suspected nerve entrapment.

WRIST PAIN

Table 4.2 Tests for wrist pain Test

Maneuver and positive findings

Significance

Phalen

Flexing and holding the wrist in full flexion for 30–60 seconds reproduces the symptoms of tingling of the fingers.

Carpal tunnel syndrome

Tinel sign

Tapping over the volar carpal ligament produces tingling of the fingers.

Carpal tunnel syndrome

Scaphoid compression test

Holding the thumb and pushing it along the metacarpal axis toward the scaphoid reproduces pain.

Scaphoid fracture, osteoarthritis

Finkelstein test

The wrist is ulnarly deviated with the patient’s fingers over the thumb in a fist. This reproduces pain over the radial side of the wrist.

De Quervain’s tenosynovitis

Special considerations Scaphoid fracture may not be apparent on X-rays taken immediately after trauma. Immobilization must be provided with a thumb spica cast and repeat X-ray taken after 1–2 weeks.

Management (treatment) Management is specific to the condition causing pain.

Further reading Hoppenfeld S (1976). Physical Examination of the Spine and Extremities. East Norwalk, CT: AppletonCentury-Crofts.

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De Quervain’s tenosynovitis General description De Quervain’s tenosynovitis refers to the inflammation and stenosis of the abductor pollicis longus and extensor pollicis brevis tendon sheath under the first extensor compartment of the wrist. Repetitive use of the thumb, as in pinching, leads to inflammation and thickening of the tendon sheath. It is one of the most common cumulative disorders of the wrist and hand.

Clinical manifestations A patient with this condition typically presents with a complaint of pain of the thumb and the radial side of the wrist. Patients will splint the involved extremity, as thumb and wrist movement aggravates the pain.

Differential diagnosis Osteoarthritis of the thumb carpometacarpal joint, ganglion cyst, tendonitis of the extensor tendons, and radial sensory nerve entrapment can present similarly.

History In most cases the patient is unable to attribute the pain symptoms to specific events. The onset of pain is usually acute. Repetitive movement or unaccustomed use of the thumb, as in pinching, and shaking of the wrist, may be elicited in the history.

Physical Tenderness of the first extensor compartment over the radial styloid and aggravation of pain with movement of the thumb are the classic findings on examination. Pain may be produced by resisted abduction and extension of the thumb. The Finkelstein test, done by ulnar deviating the wrist with the thumb in the palm, reproduces the pain (see Figure 4.4).

Diagnostic testing Diagnosis is arrived at clinically and no diagnostic test is necessary. X-ray of the wrist will be normal.

Management (treatment) Pain relief is the primary goal of treatment in the acute stage. This is accomplished by immobilization in a thumb spica splint, ice massage, physical modalities such as phonophoresis and iontophoresis, and NSAIDs. Local injection of the tendon sheath with corticosteroid and anesthetic is usually effective in cases that fail the above treatment. Surgery involving decompression of the compartment is reserved for cases that failed injection treatment.

DE QUERVAIN’S TENOSYNOVITIS

Figure 4.4 Finkelstein test.

Further reading Hoppenfeld S (1976). Physical Examination of the Spine and Extremities. East Norwalk, CT: AppletonCentury-Crofts.

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Ganglion cyst General description A ganglion is a cystic swelling over joints and tendon sheaths. The cyst contains a collection of fluid that is clear and similar to synovial fluid. The exact etiology is unknown. There may be a history of trauma, such as a fall, or a direct blow. There is an increased incidence of these cysts in women and in people who perform repetitive or strenuous activity with their wrist.

Physical findings Patients will present with a well-defined lump or mass. The cyst is usually painless and does not affect joint function. Occasionally, the patient may complain of pain and loss of motion. Transillumination differentiates it from a solid tumor.

Differential diagnosis Other causes of swelling include benign or malignant tumors, or a ruptured tendon. Aspirating the cyst is usually diagnostic.

Treatment Ganglion cysts may come and go over time. If the cyst is small and the patient is pain free, no treatment is indicated. If the cyst is large and painful, consider aspirating the cyst and injecting corticosteroid. Surgery should be reserved for symptomatic ganglion cysts that failed conservative treatment.

Further reading (wrist chapters) American Academy of Orthopaedic Surgeons (2002, April 28) Wrist sprains. http://orthoinfo.aaos. org/topic.cfm?topic=A00023 4/1/2008 Braddom RL (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Elsevier. Brotzman BS, Wilk KE (2003). Clinical Orthopaedic Rehabilitation, 2nd ed. Philadelphia: Mosby. Doherty GM (2006). Lange Current Surgical Diagnosis and Treatment, 12th ed. New York: McGraw-Hill. Elstrom JA. Virkus WW, Pankovich AM (2006). Handbook of Fractures, 3rd ed. New York: McGraw-Hill. Hoppenfeld S (1976). Physical Examination of the Spine and Extremities. East Norwalk, CT: AppletonCentury-Crofts. Koval KJ, Zuckerman JD (2006). Handbook of Fractures, 3rd ed. Philadelphia: Lippincott Williams & Wilkins. Medline plus. A service of the U.S. National Library of Medicine and the National Institutes of Health. Wrist injuries and disorders. Retrieved April 2, 2008, at: http://www.nlm.nih.gov/medlineplus/wristinjuriesanddisorders.html Skinner HB (2006). Lange Current Diagnosis and Treatment in Orthopedics, 4th ed. New York: McGraw-Hill. Thompson JC (2002). Netter’s Concise Atlas of Orthopaedic Anatomy. Philadelphia: Saunders Elsevier.

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The hand: hand basics The hand is a very complex and unique part of the human body that allows us to perform the most delicate tasks with precision. • The anatomy of the hand may be simply divided into the palmar (volar) and dorsal aspects. • The volar portion of the hand contains the major blood vessels, digital nerves, the flexor tendons, and the muscles that control finger movement. • The dorsal portion of the hand is less complex and contains only the extensor tendons and interossei muscles. • The bony architecture is complex and consists of the distal aspect of the ulna and radius, 8 carpal bones, 5 metacarpals, and 3 phalanges for each finger, with the exception of the thumb, which has only a proximal and distal phalanx.

Physical examination Asymmetry • Upon initial examination of the hand, one must always compare its appearance to the contralateral side. • Look for swelling, erythema, edema, skin color and markings, flexion creases, and nail beds, and compare each individual finger. • Note any gross deformities. Joint range of motion (passive and active) • Interphalangeal (IP) thumb joint: normal ROM, 0–80* • Metacarpophalangeal (MCP) thumb joint: normal ROM, 0–50* • Distal interphalangeal (DIP) and MCP finger joints: normal ROM, 0–90* • Proximal interphalangeal (PIP) finger joints: normal ROM, 0–100* • Wrist: normal values, 80* of flexion and 70* of extension Vascular assessment • Palpate the radial and ulnar arteries (use a Doppler as needed). • Check the capillary refill in each finger (should be <2 seconds). • A pulse oximeter may be used to measure the oxygen saturation of each individual finger. • Perform the Allen test (see Special tests, next page). Neurological assessment Median nerve • Examine the sensation on the volar tip of the index finger. • Perform a two-point examination (normal: <5 mm). • Apposing the thumb to the little finger will test the motor function of the median nerve. Ulnar nerve • Examine the sensation on the volar tip of the little finger. • Ask the patient to cross the fingers (the motor branches of the ulnar nerve innervate the intrinsic muscles of the hand) to test the motor function of the ulnar nerve.

THE HAND: HAND BASICS

Radial nerve • The radial nerve has no motor branch in the hand. • The sensation of the radial nerve is tested on the dorsal aspect of the hand in the first web space. Assessment of bones, tendons, and ligaments • Each bone is palpated to rule out a fracture. • Swelling can be variable.

Special tests Allen test • Press firmly on radial and ulnar arteries and have the patient open and close the fingers actively several times. • Take pressure off one artery and observe for vascular refill in the digits within 15 seconds. (A slow or absent refill suggests vascular obstruction or an incomplete arch.) Tinel sign • Percussion over the median nerve at the wrist produces numbness, tingling, and pain in the thumb and index and middle fingers. • Test for carpal tunnel syndrome (CTS). Phalen test • Flexion of the wrist completely for 1 minute produces numbness, tingling, and pain in the hand. • Test for CTS. Finkelstein test (see Fig. 4.4) • Passive hyperflexion of thumb MCP and IP joints (thumb in fist) with ulnar deviation of the wrist causes pain over the abductor pollicis longus and extensor pollicis brevis. • Test for de Quervain’s tenosynovitis. Compression/grind test • Hold the proximal phalanx and the MCP joint of the thumb and forcefully push against the trapeziometacarpal joint. • Pain during this maneuver is consistent with arthritis in the carpometacarpal (CMC) joint of the thumb.

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Mallet finger Mallet finger (baseball finger) describes a flexion deformity of the distal phalanx of the fingers (see Fig. 4.5). It is due to a loss of continuity of the terminal extensor tendons that create the lateral bands at the distal interphalangeal joint (DIP), and is usually caused by a forced flexion of the joint. Following this injury, there is an unopposed flexion from the flexor digitorum profundus (FDP) tendons resulting in the flexion deformity. Mallet finger may occur at any age. However, the highest incidence occurs in males during adolescence and young adulthood (range, 11–40 years). Females with mallet finger are usually middle aged (range, 41–60 years). The incidence of this injury increases progressively from the radial to ulnar side of the hand. A classification system is used to establish an appropriate treatment plan, as shown in Table 4.3.

Clinical manifestation • The mechanism of injury is usually from a sports-related activity with a sudden, acute, forceful flexion of the extended DIP.

Figure 4.5 Mallet finger. Table 4.3 Mallet finger classification Type I (most common)

Closed or blunt trauma with loss of tendon continuity with or without a small avulsion fracture

Type II

Laceration at or proximal to the DIP joint with loss of tendon continuity

Type III

Deep abrasion with loss of skin, subcutaneous cover, and tendon substance

Type IV

A: Transepiphyseal plate fracture in children B: Hyperflexion injury with fracture of the articular surface of 20%–50% C: Hyperextension injury with fracture of the articular surface usually >50% and with early or late volar subluxation of the distal phalanx

MALLET FINGER

• The result is a rupture of the extensor tendon or avulsion of the tendon with or without a small fragment of bone from its dorsal insertion. • Forced hyperextension of the distal joint may result in a fracture at the dorsal base of the distal phalanx involving 1/3 or more of the phalanx.

History • The DIP joint of the involved finger is held in flexion and active extension is lost; full passive extension usually is present. • Hyperextension of the PIP joint also may be observed.

Physical examination • Note any laceration, swelling, or abrasions to the distal aspect of the involved finger. • Isolate DIP and ask the patient to flex and extend the distal phalanx. • Monitor sensation and capillary refill (must be <2 seconds). • Obtain radiographs to rule out any fractures.

Differential diagnosis • Flexion contracture/osteoarthritis of the DIP • Fracture of the dorsal base of the distal phalanx with secondary mallet finger deformity • Transepiphyseal plate fracture of the distal phalanx

Treatment • Continuous maintenance of the DIP in extension with a splint for 6–8 weeks is the preferred initial treatment. The splint must be worn at all times for the treatment to be effective. • If an extensor lag persists, a second course of full-time splinting for an additional 8 weeks may be required. • Chronic mallet deformities (seen 2–3 months post-injury) may improve with prolonged splinting of the distal joint. • If the patient has severe symptoms, surgical options should be considered. • Type I injuries have much better results with nonoperative treatment. • Type II–IV injuries must be repaired or reconstructed surgically. • Occupational or physical therapy is beneficial for patients to regain range of motion of their finger after the treatment (surgical or nonsurgical) is completed.

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Phalanx dislocations Dislocations of the fingers are considered to be a discontinuation of the articulation at one of three locations: metacarpophalangeal joint (MCP), proximal interphalangeal joint (PIP), or the distal interphalangeal joint (DIP). Since the thumb has only two phalanges, any dislocation would occur at the MCP or interphalangeal joint (IP). Dislocations of the finger joints may be associated with capsular, ligamentous, or tendon injuries and with fractures. Classification of dislocations is based on direction of the displacement of the distal fragment, as shown in Table 4.4.

Clinical manifestation Finger dislocations usually occur in the skeletally mature population. Pediatric patients usually sustain Salter-Harris type fracture displacements because the physes (growth plate) is weaker than the ligaments and capsular structures. Such injuries often occur from some kind of trauma: • Hyperextension-type injuries lead to dorsal dislocation. • Hyperflexion injuries result in volar dislocation of the phalanges.

History • Type of trauma associated with the injury (sports, motor vehicle accident, etc.) • Mechanism of injury (hyperextension vs. hyperflexion or closed fist) • Time and events since injury

Physical examination • • • •

Pain and tenderness occur at the involved joint. Swelling and ecchymosis are usually present in acute injuries. Assess the neurovascular status of the hand and fingers. Assessment for ligamentous instability should be performed after the joint has been reduced and the swelling has subsided. • Radiographs determine the type and severity of dislocation.

Table 4.4 Phalanx dislocations MCP dislocation

PIP dislocation

DIP dislocation

Dorsal: volar plate injury; may be irreducible

Dorsal: most common; associated with volar plate injury

Volar or dorsal

Volar: central slip disruption

Volar: rare; associated with central slip disruption

Simple: reducible

Lateral: collateral ligament injury

Rotatory: rare; head of proximal phalanx “buttonholes” through lateral band

Complex: irreducible, secondary to volar plate blocking reduction

PHALANX DISLOCATIONS

Differential diagnosis • • • • •

Chronic dislocation Fracture dislocation Collateral ligament injury Septic tenosynovitis Rheumatoid arthritis

Treatment • After an attempted closed reduction, the finger should be ranged to assess for any mechanical block within the joint. • If there is adequate motion, the injured finger should be immobilized with a splint for 3–4 weeks, followed by night splinting for 3 additional weeks. • Rest, ice, compression, and elevation (PRICE) protocol should be followed to minimize swelling and pain. • Dislocations that are not reducible require surgical intervention. • “Buddy taping” is an effective way to protect ligamentous injuries. • Physical or occupational therapy includes active and passive ROM exercise once the ligamentous injuries have healed. Therapy is extremely important after surgical repair in order to reduce swelling and prevent stiffness.

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Thumb ligament injuries Two major ligaments stabilize the MCP joint of the thumb: the ulnar collateral ligament (UCL) and the radial collateral ligament (RCL) (see Fig. 4.6). Of the two, the UCL is more commonly injured, usually from a forced radial deviation (abduction) of the thumb. The RCL may also be injured, but its occurrence is much less common. In severe types of injuries, both ligaments may be ruptured. Thumb ligament injuries occur equally in males and females, and in all age groups. The classification for the ligamentous injuries includes partial or complete tears of the ligaments. Bony avulsion fractures at the base of the proximal phalanx may accompany the injury. Thumb ligament injuries are also known as Gamekeeper’s thumb or Skier’s thumb.

Clinical manifestation Thumb ligament injuries usually occur from a forced radial deviation (abduction) of the thumb during a high-velocity activity. Skiers and those who play ball-handling sports, such as baseball, football, and basketball, have a greater risk of sustaining such an injury. • Skiers can injure the thumb ligament in accidents involving the ski poles or from a fall. • Ball-handling players often sustain thumb injuries when the ball forcefully abducts the digit, resulting in a UCL tear. When the thumb is hyperextended by the ball, the RCL may be torn instead. Capsular injuries or Stener lesions A Stener lesion is a radiographic finding indicating a complete rupture of the UCL with the adductor aponeurosis interposed between the distally avulsed ligament and its insertion into the base of the proximal phalanx.

Ulnar collateral ligament

Radial collateral ligament

Figure 4.6 Ligaments of the thumb.

THUMB LIGAMENT INJURIES

This is important to recognize because the capsule may prevent proper healing from occurring.

History • Mechanism of injury (hyperextension, flexion, vs. abduction) • Timing of injury • Presence of pain and swelling localized to the base of the thumb

Physical exam • Neurovascular exam must determine motor function, perfusion, and sensation. • Weakness with pinch function usually exists in ligament ruptures. • Examine the base of the thumb for ligamentous laxity and compare it to the uninjured hand: • Examine the thumb with 20–30* of flexion. • Carefully abduct the thumb passively and compare the angle of deviation to the uninjured thumb. • An angulation of >30* on the injured thumb or >15* compared to the uninjured thumb is diagnostic for a ligamentous injury. • Radiographs should be obtained to assess for the presence of a Stener lesion or a fracture fragment. • A digital block may be necessary to complete a full examination because of pain and swelling in the acute setting.

Differential diagnosis • First metacarpal or proximal phalanx fractures • First CMC joint arthritis • Volar plate injury

Treatment A thumb spica splint or cast immobilization is indicated for 4 weeks for a partial rupture, or up to 6 weeks if an associated avulsion fracture is present. For acute injury • Rest, elevation, ice • Immobilization in a thumb spica splint • Analgesics • Orthopedic follow-up For chronic injury • Thumb spica brace • Activity modification • Orthopedic surgery consultation for elective ligament repair or reconstruction may be necessary with a complete rupture. Physical or occupational therapy is helpful postoperatively to increase range of motion and strength, and to assist in resuming activities.

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Trigger finger “Trigger finger” results from localized stenosing tenosynovitis of the deep and superficial tendons of the fingers. As the affected digit is flexed, a painful catching sensation occurs from the inflamed tendon at the A1 pulley. Once the digit snaps, or “triggers,” into a flexed position, extension becomes difficult and painful and often must be performed manually. Trigger finger most often occurs in the middle or ring finger and occasionally in the thumb. Females are affected more than males. Patients with rheumatoid arthritis may have trigger finger in several fingers.

Clinical manifestation As the inflamed tendon passes through the constricted sheath at the A1 pulley with flexion and extension, a painful clicking is produced. This is a self-perpetuating problem because the irritation from triggering continues to increase the swelling in the tendon. With severe or chronic cases, the affected digit may lock in flexion or extension. If the digit is locked in flexion, a PIP joint flexion contracture may develop. The etiology of trigger finger is unknown. Risk factors include the following: • Rheumatoid arthritis • Increased age • Diabetes mellitus

History Patients often complain of having their finger “stuck” after certain activities that require gripping or flexing of their fingers. This can be painful. Assess the duration of the problem as well as whether symptoms are increasing.

Physical examination Palpate the flexor tendon sheath at the distal palmar crease and have the patient flex and extend the affected digit. A nodule should be felt as the tendon triggers under the examiner’s finger. Tenderness will usually accompany the triggering. Determine if there is normal passive ROM in each joint of the finger (MCP, PIP, and DIP). There is true triggering if the finger locks as the digit is taken through a passive ROM. Determine whether the patient is able to actively flex and extend the digit past the triggering point.

Differential diagnosis • • • • • • •

Chronic dislocation of MCP joint Flexor tendon rupture Extensor tendon rupture Saggital band rupture Contracted joints Posterior interosseous nerve syndrome Tumor of tendon sheath

TRIGGER FINGER

Treatment • Noninvasive treatment includes warm soaks and gentle massage. • Corticosteroid injection into the tendon sheath (not the tendon itself) may resolve the triggering (see Fig. 4.7). • If nonoperative measures fail, surgical incision of the A1 pulley is indicated. • Physical or occupational therapy is important to maintain range of motion and prevent the tendons from developing adhesions and contractures.

Figure 4.7 Corticosteroid injection into the tendon sheath. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/Elsevier, p. 59. Copyright Elsevier (2007). Reprinted with permission.

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Further reading (hand chapters) Chinchalkar SJ, Gan BS (2003). Management of proximal interphalangeal joint fractures and dislocations. J Hand Ther 16:117–128. Deibert MC, Aronsson DD, Johnson RJ, et al. (1998). Skiing injuries in children, adolescents, and adults. J Bone Joint Surg 80A:25–32. Freiberg A, Mulholland RS, Levine R (1989) Nonoperative treatment of trigger fingers and thumbs. J Hand Surg 14A:553–558. Glickel SZ, Barron OA, Catalano LW III (2005). Dislocations and ligament injuries in the digits. In Green D, Hotchkiss R, Pederson WC (eds.). Green’s Operative Hand Surgery, 5th ed. Philadelphia: Elsevier Churchill Livingstone. Green DP, Butler TE Jr. (1996). Fractures and dislocations in the hand. In Rockwood CA, Green DP, Bucholz RW, Heckman JD (eds.). Rockwood and Green’s Fractures in Adults, 4th ed. Philadelphia: Lippincott-Raven, 1996. Griggs SM, Weiss APC, Lane LB, et al. (1995). Treatment of trigger finger in patients with diabetes mellitus. J Hand Surg 20A:787–789. Hoppenfeld S (1976). Physical Examination of the Spine and Extremities. Norwalk, CT: Appleton & Lange. Packer GJ, Shaheen MA (1993). Patterns of hand fractures and dislocations in a district general hospital. J Hand Surg 18B:511–514. Trumble TE (2000). Anatomy and examination of the hand. In Principles of Hand Surgery and Therapy. Philadelphia: WB Saunders.

Chapter 5

Lower extremity Albert Villafuerte Jay M. Weiss Maryam Rafael Aghalar Divyajot Sohal Derek Higgins Adaku Nwachuku Francine G. Moshkovski Osteoarthritis of the hip 122 Trochanteric bursitis or greater trochanter pain syndrome 126 The knee 128 Knee osteoarthritis 132 Knee bursitis 136 Patellar and quadriceps tendonitis, Osgood Schlatter 140 Medial and lateral collateral ligament injuries 142 Anterior cruciate ligament injury 144 Meniscal injuries 146 Patellofemoral pain 150 The ankle 152 The foot 160

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Osteoarthritis of the hip General characteristics The hip joint, a ball-and-socket joint, consists of the acetabulum and proximal femur (greater and lesser trochanter, proximal femoral shaft, femoral head and neck). Stability of the hip joint depends on the integrity of the synovial capsule and iliofemoral, pubofemoral, and ischiofemoral ligaments. The iliofemoral ligament (Y ligament of Bigelow), which arises from the anterior inferior iliac spine and runs to the intertrochanteric line, resists hyperextension. The pubofemoral ligament, which runs from superior pubic ramus to blend into the iliofemoral ligament, resists excessive extension and abduction. The ischiofemoral ligament, which runs from the ischium to the femoral neck, resists excessive extension.

Clinical manifestations Osteoarthritis (OA) of the hip is usually of insidious onset. The main symptom of OA of the hip is pain with weight bearing. Range of motion generally decreases over time. This condition presents with degenerative changes, loss of cartilage, and osseous hypertrophic changes. It may affect the capsule, synovium, and/or cartilage. Bursitis or tendonitis can coexist with OA.

Differential diagnosis OA can be present with other disorders and frequently coexists with lumbar osteoarthritis and spinal stenosis. A high lumbar radiculopathy can present with pain in the groin. Hip flexor tendonitis or iliopectineal bursitis may present similarly. Due to the nature of OA and frequency of coexisting disorders, the primary pain generator is not always obvious. Iliopectineal bursitis or iliopsoas/hip flexor tendonitis usually presents with anterior hip pain that is often related to snapping of the iliopsoas tendon over the iliopectineal eminence, or inflammation or irritation of tendons of the hip flexors.

History Patients are usually over the age of 50. Risk factors for osteoarthritis include congenital dislocation of the hip, slipped capital epiphysis, Legg Calve-Perthes disease, advancing age, and a positive family history. Patients generally report improvement of pain and function with over-the-counter analgesics, and they should be questioned about their use. The pain may have been present for years at the time of presentation. Frequently, use of a cane in the opposite hand gives dramatic relief of pain. Pain in osteoarthritis is typically aggravated by activity and relieved by rest. It also tends to be worse at the end of the day. The pain, typically in the anterior groin region, is usually aggravated by a movement of the hip joint. Morning stiffness, which is usually less than 30 minutes, generally improves with activity, but may recur after a period of inactivity.

OSTEOARTHRITIS OF THE HIP

Physical An antalgic gait is frequently seen. Patrick’s or FABERs test (flexion, abduction, external rotation) can radiate pain to the groin. Frequently, internal rotation is more limited than external rotation. Resisted hip flexion and local palpation can help determine whether hip flexor tendonitis is present. Passive extension may aggravate tendonitis or bursitis.

Diagnostic testing Routine lab work (CBC, ESR, rheumatoid titer) is characteristically normal in OA, as this is a noninfectious, noninflammatory process. However, these tests may be helpful in ruling out other disorders. X-rays are frequently helpful and can show joint space narrowing, osteophytes, and sclerosis. MRI and CT of the hip may be helpful in diagnosing certain cases of unexplained hip pain and in evaluating the spine.

Management The goal of treatment is to minimize pain and restore function. Treatment options include medications, physical therapy, and instruction in proper use of a cane. Hip replacement surgery is a commonly performed procedure with very successful outcomes in most cases. Intra-articular injections are used much less frequently in the hip than in the knee. Frequently, several treatments are used simultaneously. Weight loss in obese patients should be encouraged.

Medications Analgesics, including acetaminophen and NSAIDs, are often used. NSAIDs are less commonly used because of greater awareness of complications (especially GI and cardiac) in older patients with long-term use. Opioid analgesics should be avoided in treating OA. Tramadol can be helpful in some patients with OA. Glucosamine and chondroitin are often used, although evidence of their effectiveness is primarily anecdotal.

Physical therapy Physical therapy (PT) may help restore range of motion, decrease pain, and increase strength. The hip joint is under forces several times the weight of the body. The abductors must contract with a force sufficient to maintain the trunk level while the weight of the body is medial to the joint. Use of a cane in the opposite hand can allow the abductors to rest and dramatically decrease forces on the hip (and pain). The use of a cane is thus very important for many patients and can help maintain mobility.

Surgery In severe cases where pain limits function and PT and medication are not successful, surgery may be indicated. Total hip replacement involves the insertion of prosthetic femoral and acetabular components (arthroplasty); in partial hip replacement (hemiarthroplasty) only the femoral component is replaced. Total hip replacement is a very commonly performed operation that can lead to markedly decreased pain as well as restoration and preservation of function in patients with severe hip OA.

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Complications and red flags Pain at night and not relieved with non-weight bearing should be investigated more thoroughly and may require MRI, CT, or bone scan.

Further reading Frontera WR, Silver JK, Rizzo TD (eds.) (2008). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: WB Saunders Elsevier,

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Trochanteric bursitis or greater trochanter pain syndrome General description Bursae around the greater trochanter can potentially become inflamed and painful. The largest is the subgluteus maximus bursa, which is located between the insertion of the gluteus medius muscle into the lateral greater trochanter and the converging fibers of the tensor fasciae latae and the gluteus maximus muscle as they all form the iliotibial tract. Bursal irritation is usually due to repetitive movements such as running, or to acute direct trauma of the hip, such as from falling, contact sports, or lateral hip surgery. Bursitis can also occur with conditions associated with gait disturbances, such as lumbosacral spine disease, leg-length discrepancy, sacroiliac joint disorders, knee arthritis, or ankle sprain. Since these bursae are deep under the muscles, the typical signs of “bursitis,” such as local heat, redness, and swelling, may not be appreciated. Thus the term greater trochanter pain syndrome is alternately used by some practitioners.

Clinical manifestations Patients usually report pain located over the lateral hip that can extend down the thigh but never distal to the knee. Pain is usually exacerbated by lying down on the affected side and may awaken the patient from sleep. Patients also complain of more pain when they walk, run, perform strenuous activities, or climb stairs. The quality of the pain can be achy but sometimes may be described as sharp and intense. Occasionally, a patient may describe a paresthesia in the upper thigh that does not follow any specific dermatomal segment.

Differential diagnosis The differential diagnosis includes sciatica/radiculopathy, occult fracture, stress fracture, metastatic disease to the femur or soft tissue, avascular necrosis of the femoral head, iliotibial band tendonitis, gluteus medius tendonitis, osteoarthritis of the hip, and meralgia paresthetica.

History Patients should be questioned regarding onset, provocation, quality, radiation, severity, and timing of pain to evaluate for bursitis. However, a thorough history needs to be taken to rule other etiologies of hip pain (trauma, recent surgery, cancer history, history of osteoarthritis).

Physical The most important physical finding is local tenderness over the greater trochanter with palpation. The hips should be flexed 90* to best palpate the greater trochanter. Pain can be elicited with other movements such as internal and external rotation, especially with resisted hip abduction. Physical findings such as pain with hip flexion and extension only, significant limited range of motion, and referred knee pain or groin pain can indicate hip joint pathology such as osteoarthritis or synovitis. Swelling,

TROCHANTERIC BURSITIS

local heat, and redness are difficult to appreciate compared to bursitis of the olecranon or prepatella. A detailed neurological examination of both lower extremities, including tests of strength, reflexes, and sensation, must be performed to rule out sciatica or lumbosacral pathology. Measuring leg length or assessing a patient’s gait is important to uncover a possible leg-length discrepancy.

Diagnostic testing Trochanteric bursitis is generally diagnosed clinically, but certain testing may be done to rule out other causes of hip pain. Blood work can rule out infection or other connective tissue disease. A CT scan, MRI, or plain radiograph of the hip and femur can rule out fracture, degenerative changes, or pelvic metastasis and can also evaluate leg-length discrepancy, sacroiliac joint diseases, and other structural back diseases. A plain radiograph may show calcifications in the bursa and MRI might show increased intensity signal in the bursa. However, these tests are not diagnostic since some asymptomatic patients may have these findings as well. Diagnostic anesthetic injection of the bursa resulting in pain reduction can also confirm the diagnosis when it is hard to differentiate similar presentations.

Management (treatment) The goals of treatment are to reduce inflammation, correct any gait disturbance, and prevent recurrence through proper stretching exercises. Inflammation can be reduced by use of heat, ice, NSAIDs, and local injection of the bursa with corticosteroids and analgesics. Gait disturbances such as leg-length discrepancy can be corrected with shoe lifts. Other aides can be used to help with gait such as a knee brace, high-top shoes for ankle support, canes, walkers, and custom-made foot orthotics. Proper stretching exercises include cross-leg pulls, glutealstrengthening stretches, and iliotibial band stretches. Other suggestions are to limit weight bearing, avoid pressure on the bursa, and restrict activities that make the pain worse. Modalities such as transcutaneous electrical nerve stimulation (TENS) and ultrasound can be used in resistant cases.

Complications and red flags There are no serious complications of trochanteric bursitis. Surgery (iliotibial band release or bursectomy) is rarely performed but can be considered for refractory cases. If a patient does not respond to conservative treatment, other causes of hip pain must be further investigated and ruled out (i.e., metastasis, fracture, etc).

Further reading Shbeeb M, Matteson EL (1996). Trochanteric bursitis (greater trochanter pain syndrome). Mayo Clin Proc 71:565–569. Rouzier P, Whte T, Gilfilan T, Johnson J, Rouzier PA (1999). The Sports Medicine Patient Advisor. Amherst MA: SportsMed Press.

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The knee General description The knee is primarily a hinge joint with a small degree of internal and external rotation. The distal end of the femur terminates in the medial and lateral femoral condyles. These articulate with the tibia and the patella (see Fig. 5.1). The patella primarily provides mechanical advantage to the quadriceps muscles (aiding extension). The normal range of motion of the knee is from 0* (full extension) to 135* of flexion. The stability of the knee comes from the simple nature of the joint (modified hinge) and the ligaments and muscles surrounding it.

Menisci The menisci are fibrocartilage tissues on the medial and lateral tibia. They articulate with the medial and lateral femoral condyles and provide stability to the knee joint.

Ligaments The primary ligaments of the knee are the cruciate ligaments and the collateral ligaments. The anterior cruciate ligament arises lateral and anterior to the tibial spine and attaches to the femur between the condyles. It primarily resists anterior translation of the tibia on the femur, but also supplies rotatory stability. The posterior cruciate ligament travels from the anterior intercondylar region of the femur and attaches to the lateral posterior tibia. This prevents posterior translation of the tibia on the femur and helps to resist rotation (see Fig. 5.2). The medial and lateral collateral ligaments cross the knee joints on their respective sides of the knee. The medial collateral ligament provides medial joint stability and prevents displacement of the knee by valgus (medial) stress. Its counterpart, the lateral collateral ligament, prevents bony displacement secondary to varus (lateral) stress (see Fig. 5.3)

Figure 5.1 Knee, anterior view.

THE KNEE

Figure 5.2 Knee, posterior view.

Figure 5.3 Knee, lateral view.

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Muscles The two main groups of muscles around the knee are the quadriceps and the hamstrings. The quadriceps muscles originate on the femur (or pelvis) and insert on the patella. The patella attaches to the anterior tibia through the patella tendon. These muscles are among the strongest muscles in the body and can (and do) support the full weight of the body during movement. The hamstring group primarily flexes the knee and extends the hip. The medial hamstring muscles (semimembranosus and semitendinosus) cross the posteromedial knee and insert in the medial tibia. The semi-tendinosus inserts near the insertion of the sartorius and gracilis (near the pes anserine bursa). The biceps femoris are the lateral hamstring muscles. Besides providing movement, these muscles add stability to the knee and can compensate for some ligamentous deficiencies.

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Knee osteoarthritis General description Osteoarthritis (OA) is a noninflammatory progressive degenerative disorder characterized in the knee by pain and decreased function. OA is commonly referred to as “wear-and-tear” arthritis and is more common in patients with obesity or a history of repetitive trauma. It is characterized by a loss of joint space (cartilage destruction) and osteophytes. Its primary manifestation is pain that can lead to loss of function.

Clinical manifestations OA of the knee is usually of insidious onset. The main symptom of OA of the knee is pain. Range of motion will generally decrease over time. As the cartilage degenerates, there is frequently associated ligamentous laxity (especially medial and lateral). There tends to be a greater loss of the medial joint space and a varus deviation of the knee.

Differential diagnosis OA can be present with other disorders and frequently coexists with OA of the hip and spinal stenosis. Lumbar radiculopathy (at the L3 level) can present with pain in the knee region. OA is generally not confused with rheumatoid arthritis (RA) as OA has a more limited distribution, generally later onset, and different X-ray picture. Patellofemoral pain can coexist with OA and present similarly. Due to the nature of OA and the frequency of coexisting disorders, it is not always obvious what the primary pain generator is.

History Patients are usually over the age of 50. The pain is generally difficult to precisely locate. Pain occurs generally with weight bearing, but also with movement (getting up from a chair, ascending or descending stairs). Patients usually report improvement of pain and function with over-thecounter analgesics, and they should be questioned about their use. The pain may have been present for years at the time of presentation.

Physical Crepitus on range of motion is frequently present. A valgus deformity may be visible on gait examination. Knee range of motion may be decreased. Medial and lateral laxity is common. Anterior cruciate ligament (ACL) laxity is not a feature of OA. A joint effusion may be present. Some of examination findings may be masked by obesity.

Diagnostic testing Routine lab work (CBC, ESR, rheumatoid titer) is characteristically normal in OA, as this is a noninfectious, noninflammatory process. However, these tests may be helpful in ruling out other disorders. X-rays are frequently helpful and can show joint-space narrowing (especially medially), osteophytes at the lateral joint margins, and sclerosis. MRI and CT of the knee generally contribute little to the diagnosis (but may be helpful in evaluating the spine).

KNEE OSTEOARTHRITIS

Management The goal of treatment is to minimize pain and restore function. Treatment options include medications, physical therapy, orthoses, physical modalities, injections (see Fig. 5.4), and surgery. Frequently, several treatments are used simultaneously. Weight loss in obese patients should be encouraged.

Medications Analgesics, including acetaminophen and NSAIDs, are frequently used. NSAIDs are less commonly used than years ago because of increased awareness of complications (especially gastrointestinal and cardiac) in older patients with long-term use. Opioid analgesics are generally to be avoided in treating OA. Tramadol can be helpful in some patients with OA. Glucosamine and chondroitin are commonly used, although the evidence of their effectiveness is primarily anecdotal.

Physical therapy Physical therapy (PT) may help restore range of motion, decrease pain, and increase strength. Therapists can give a trial of TENS, which may be helpful for pain control. Patients can be taught to self-administer TENS at home. Topical analgesics and counterirritants may also be helpful, and knee sleeves are reported by some patients to be useful.

Lateral approach

Prepatellar bursa Patella

Femur

Joint capsule (articular capsule)

Tibia Fibula

Figure 5.4 Knee joint injection—lateral approach. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections. Philadelphia: ButterworthHeinemann/Elsevier, p 45. Copyright Elsevier (2007). Reprinted with permission.

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Injections Corticosteroid injections can be helpful, especially in cases of knee effusion. The effusion is aspirated before injection of the corticosteroid. In the past decade, hyaluronic acid injections have become common and widely accepted as treatment for OA of the knee. Several different (but similar) preparations are available. All are prefilled syringes injected intraarticularly in the knee in a series of 3 to 5 injections. Relief of symptoms for months is common. The injections can be periodically repeated.

Surgery In severe cases where pain limits function, knee replacement (arthroplasty) may be indicated. This is a very commonly performed operation that can lead to markedly decreased pain as well as restoration and preservation of function.

Complications and red flags Pain at night and not relieved with nonweight bearing should be investigated more thoroughly and may require MRI, CT, or bone scan.

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Knee bursitis Bursae are soft tissue sacs containing synovial fluid. They can be found between muscle groups, at the sites of tendinous insertion to bones, or in localized subcutaneous sacs. Their anatomical location reduces friction within the joint. More than 100 bursae exist within the human body; the 12 bursae within the knee joint are listed below.

Anterior bursa • Between the skin and the patella; known as the prepatellar bursa (irritation or inflammation of this bursa is known as “housemaid’s knee”) • Between the distal femur and deep to quadriceps femoris muscle; known as the suprapatellar bursa • Between the patella ligament and the medial tibia • Between the skin and the tibial tuberosity

Medial bursa • Between the knee capsule and the medial head of the gastrocnemius muscle • Between the tendons of the semimembranosus and semitendinosus muscles • Between the tibial head and the tendon of the semimembranosus muscle • Between the tendon of semimembranosus muscle and deep to medial collateral ligament • Between the tendons of the gracilis and the semitendinosus muscles and superficial to the medial collateral ligament known as the pes anserine bursa (irritation or inflammation of this bursa is known as pes anserine bursitis)

Lateral bursa • Between the lateral collateral ligament and the tendon of biceps femoris muscle • Between the tendon of the popliteus muscle and the lateral femoral condyle • Between the lateral collateral ligament and the tendon of popliteus muscle • Between the lateral head of gastrocnemius muscle and knee capsule

General description Irritation or injury of the bursa leads to a condition known as bursitis. Synovial bursae are susceptible to injury through a variety of modalities. Direct trauma, as seen in athletes, can lead to bleeding within the bursa space. The presence of the “foreign” fluid within the sac causes an inflammatory response leading to acute bursitis. Custodians, house cleaners, or carpenters often present with bursitis secondary to repetitive microtrauma. Anatomical malalignment of the lower extremity is a suggested etiology for knee bursitis. A valgus deform-

KNEE BURSITIS

ity predisposes a patient to anserine bursitis, whereas a varus strain may lead to infrapatellar bursitis.

Clinical manifestation The commonly inflamed bursae around the knees are the prepatellar and the pes anserine bursa. Patients with prepatellar bursitis complain of pain and swelling on the anterior knee, whereas patients with pes anserine bursitis complain of pain medially. Pain is generally well localized over the inflamed bursae and is present with knee movement and at rest. Range of motion of the knee may be limited by pain.

Differential diagnosis The differential diagnosis of knee pain and swelling include fracture, ligamentous injury, meniscal injury, tendonitis, arthritis, tumor, patellar dislocation, and muscle tear. Bursitis can be secondarily infected or secondary to infection or systemic disease. Staphylococcus aureus is commonly implicated in septic bursitis. Rheumatological patients prone to bursitis include those with rheumatoid arthritis and gout sufferers. Bursitis may develop when monosodium urate crystals deposit within the bursa.

History Patients should be asked about recent trauma, the onset, duration, and location of pain and swelling, and exacerbating and remitting factors. Repetitive activities that cause pressure or friction on the anterior knee may elicit prepatellar bursitis. Other causes of pain in the lower extremity that result in abnormal gait pattern may precede the development of pes anserine bursitis. Medial compartment knee OA is often associated with pes anserine bursitis.

Physical Patients with prepatellar bursitis (housemaid’s knee) will have a palpable, tender cystic swelling over the anterior aspect of the knee just below the patella and at midpoint on the patellar tendon. Erythema and warmth may be present in acute cases. Knee range of motion may be limited by pain. Bursal thickening or cobblestone-like roughness may be palpable in chronic cases. The pes anserine bursa is not palpable because of its deeper location. Patient with pes anserine bursitis will have localized tenderness over the pes anserine insertion on the medial proximal tibia. This should be differentiated from medial collateral ligament injury by the absence of pain and laxity with valgus stress of the knee joint.

Diagnostic testing Diagnosis is made clinically. Blood and radiographic examinations are used to exclude other diagnoses. Ultrasonography can help identify deeply localized nonpalpable bursa. Bursal aspiration may be used therapeutically and aspirate examination may help differentiate bursitis from trauma, gout, or infection.

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Management The initial treatment of acute bursitis is “PRICE”: protection of the skin overlying the bursa; rest of the affected area; ice 20 minutes on, 20 minutes off for the first 24 to 48 hours to relieve pain; compression of the joint; and elevation (more commonly, the protocol is referred to as PRICE and the protection is implied, though not stated). NSAIDs and selective cyclooxygenase 2 (COX-2) inhibitors have been shown to alleviate symptoms. Physical therapy may be indicated to increase muscle flexibility, thereby reducing stress on the bursa. Some authors consider aspiration and drainage, followed by compression and protection, as the treatment of choice for prepatellar bursitis. Corticosteroid injection is indicated for bursitis resistant to physical therapy and other medical treatment and for chronic recurrent nonseptic bursitis. Surgical excision (bursectomy) is rarely required in symptomatic chronic cases.

Complications Patients who are not treated appropriately may develop chronic bursitis.

Further reading Cuccurullo S (2004). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical Publishing. Klippel J, Dieppe P (1994). Rheumatology. St. Louis: Mosby. Pecina M, Bojanic I (1993). Overuse Injuries of the Musculoskeletal System. Boca Raton, FL: CRC Press.

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Patellar and quadriceps tendonitis, Osgood Schlatter General description Patellar tendonitis, sometimes called “jumpers knee,” is an overuse syndrome that can occur in athletes or “weekend warriors,” especially those with inadequate training regimens. Large forces on the patellar tendon insertion (especially in eccentric contractions) can cause microtears, which can overload the tissue’s regenerative capacity. Less commonly, this can occur at the quadriceps insertion on the patella. Osgood Schlatter is a variant in which the microtears (or avulsion) occur at the epiphysis of the tibial tubercle. Osgood Schlatter generally occurs in adolescence and is due to the relatively greater strength of the patellar tendon compared to the tibial epiphysis at its insertion. It occurs in about 20% of adolescents who are active in sports (usually after a growth spurt).

Clinical manifestations Pain is generally noted after activity and is localized most often to the inferior pole of the patella (tendon attachment). Less commonly, pain is seen at the quadriceps attachment to the superior pole of the patella. In Osgood Schlatter, the pain is most pronounced at the tibial tubercle. In all cases, the pain should be localized. Pain is generally not present at rest or with normal walking. If training is not altered and symptoms progress, pain can be present during the workout or even during rest periods. It can progress to the point where even walking is painful. If ignored, in extreme cases, tendon rupture can occur.

Differential diagnosis Other causes of anterior knee pain, including patellofemoral pain, stress fractures, quadriceps tendon avulsion, bursitis, osteoarthritis, or a plica, should be considered. The history, age, and physical examination should help to differentiate between these.

History Patients are usually participating in a sport that involves jumping (basketball, volleyball, track and field, or, less commonly, running). They may not recall an inciting episode, but will note the presence of pain after athletic activity. The pain may be associated with a period of increased training (i.e., early in a season), or starting a new sport. Patients will report a local tenderness.

Physical There is frequently localized tenderness over the involved area of the patella. The knee examination is usually unremarkable. Generally, walking will not re-create the symptoms. Very prominent tibial tubercles may be noted in Osgood Schlatter.

PATELLAR AND QUADRICEPS TENDONITIS, OSGOOD SCHLATTER

Maneuvers that stress the quadriceps muscle (extending the knee against resistance or squatting with the knee in flexion) may reproduce the pain. The patient may have tight hamstring muscles. There is no laxity of the knee joint, and range of motion is normal.

Diagnostic testing Laboratory values are usually normal. X-rays are usually normal, but should be done if erythema or warmth is noted in order to rule out osteomyelitis. MRI and CT are generally not indicated, but may show avulsion of a portion of the developing ossification center and overlying hyaline cartilage of the tibial tubercle or patellar tendonitis.

Management The PRICE (rest, ice, compression, elevation) protocol and NSAIDs are adequate in most cases. It is important to evaluate the training errors that may have caused this disorder and to avoid them. After a pain-free period, stretching should begin followed by a gradual return to activity. In Osgood Schlatter, it is not uncommon for an adolescent to miss an entire athletic season in order for symptoms to resolve.

Complications and red flags Pain occurring at rest or waking the patient from sleep may indicate a more serious diagnosis and may require MRI, CT, or a bone scan.

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Medial and lateral collateral ligament injuries General description The medial and lateral collateral ligaments (MCL and LCL) cross the knee joints on their respective sides of the knee and resist valgus and varus movement of the knee, respectively. The MCL is more commonly injured. It can be injured acutely or chronically; injuries can range from a stretch of some fibers to a complete tear or avulsion of all fibers. Because of the mechanism of injury in MCL tears and the attachment near the meniscus, medial meniscal injuries are frequently associated with MCL tears.

Clinical manifestations Medial knee pain and a feeling of instability are common symptoms of an MCL injury. Effusion is less common than in meniscal or anterior cruciate ligament (ACL) injuries, although these may coexist.

Differential diagnosis The primary differential diagnosis includes medial meniscal tears, osteoarthritis, pes anserine bursitis, and ACL tear. Frequently these (especially meniscal and ACL tears) can coexist. Radiculopathy can present with medial knee pain.

History There can be a history of a valgus blow to the knee, or the symptoms can be more insidious in onset. No specific injury may be recalled. Effusion is frequently not present. The patient may recall feeling a “pop,” but this is not as common as in ACL tear.

Physical The main finding is medial knee laxity with a valgus force. There is also frequently medial joint line tenderness. Generally there is not a significant effusion. It is important to test for ACL integrity and for meniscal injury.

Diagnostic testing X-rays are important in ruling out a fracture. MRI is the best method of visualizing the MCL.

Management The PRICE protocol, bracing, or nonweight bearing may be necessary in the acute stage. Strains and partial tears have a good prognosis. Most complete tears can be treated nonsurgically with physical therapy, including strengthening and bracing.

Complications and red flags Pain at night or with immobilization that is not explained by the injury should be appropriately worked up. Any traumatic injury can predispose to complex regional pain syndrome.

MEDIAL AND LATERAL COLLATERAL LIGAMENT INJURIES

Further reading DeLisa J (2005). Physical Medicine and Rehabilitation, Principals and Practice, 4th ed. Philadelphia: Lippincott Williams and Wilkins, pp. 571–572.

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Anterior cruciate ligament injury General description The knee has two cruciate ligaments. By far, the most clinically important is the anterior cruciate ligament (ACL), as it is the primary stabilizer of the knee. The cruciate ligaments are named according to their tibial attachments. Therefore, the ACL arises on the posterolateral intercondylar area of the femur and attaches anteriorly on the tibia. The posterior collateral ligament (PCL) originates on the femur and attaches posteriorly on the tibia. The ACL prevents anterior translation of the tibia on the femur. The PCL prevents posterior translation of the tibia on the femur. The ACL also limits external rotation of the tibia on the femur and hyperextension. The PCL is rarely injured with the exception of dashboard injuries in a motor vehicle accident when the tibia hits the dashboard and momentum carries the femur forward. The ACL is commonly injured in athletic activity, particularly with sudden changes of direction (cutting) and hyperextension. The ACL may also be injured through contact injuries, especially with valgus stress as in a tackle in football. When injured in this manner, frequently other structures are involved (medial collateral ligament and medial meniscus).

Clinical manifestations With an ACL tear, a “pop” is frequently reported. The patient is usually unable to walk and an effusion commonly occurs within hours. A partial tear may occur where some of the ACL fibers are intact or a complete tear may result. In younger athletes an avulsion of the attachment of the ligament may occur.

Differential diagnosis The primary differential diagnosis is a meniscal tear and medial collateral ligament injury. Generally, swelling will occur quickly (within hours) with an ACL tear and slowly (within 24 hours) with a meniscal tear.

History In noncontact cases, the patient may experience a cut or rapid movement with a “pop” and immediate pain. Patients are generally unable to continue activity after an injury. Contact cases may include a tackle or block, especially with valgus stress to the knee. In both cases, symptoms are of immediate onset.

Physical An effusion is usually present in acute injuries. The knee is generally maintained at approximately 20* of flexion as that gives the greatest capsular laxity (largest volume for the effusion). Flexion or extension beyond this position yields increased intra-articular pressure and pain. The patient should be assessed for other knee injuries besides assessing for ACL injuries. This includes valgus and varus testing to evaluate the

ANTERIOR CRUCIATE LIGAMENT INJURY

collateral ligaments, McMurray test for meniscus, assessment of range of motion, and apprehension test to rule out patellar instability. The main tests for ACL integrity are the Lachman test, lateral pivot shift test, and anterior drawer test. In the acute period these may not be tolerated, or they may be negative due to lack of relaxation of other muscle groups (primarily hamstring). In the Lachman test, the knee is flexed to about 20–30*. The examiner attempts to slide the tibia anteriorly while fixing the femur. Excessive movement without a hard end point is positive. The opposite side should be evaluated for comparison. In the lateral pivot shift test, the knee is initially fully extended. The leg is then internally rotated while a valgus stress is applied as the knee is flexed. The clinician feels for anterior migration of the tibia on the femur. A positive test indicates rupture of the ACL. The anterior drawer test is similar to the Lachman test but performed at 90* of flexion and with the foot on the floor or table. The examiner may (or may not) sit on the patient’s foot and apply an anterior force to the proximal tibia. The knee is then assessed for anterior laxity. This test tends to be less sensitive (but easier to perform, especially in large patients) than the Lachman test. As with most tests, the nonaffected side should be tested for comparison. The posterior drawer test should also be performed to assess the PCL.

Diagnostic testing X-ray is useful (especially in contact injuries) to rule out fractures. MRI has become the best method of visualizing the ACL. It is also excellent for evaluating meniscal injuries.

Management In the acute phase, the patient should be non-weight bearing or partial weight bearing. The PRICE protocol and analgesics (NSAIDs and/or opioid analgesics) should be used to reduce pain and swelling. X-rays should be considered to rule \out a fracture, which would be treated differently than a ligament tear. In some cases, arthrocentesis may be necessary to relieve swelling and pain in the acute phase. Weight bearing and range of motion can be started as soon as tolerated. Physical therapy to maintain range of motion and strength of the knee muscles should be started early. Depending on the degree of injury, the patient’s goals, and athletic level, surgical reconstruction of the ACL may be appropriate. Individual surgeons generally have their own postreconstruction rehabilitation protocols.

Complications and red flags Pain at night or with immobilization that is not explained by the injury should be appropriately worked up. Any traumatic injury can predispose the patient to complex regional pain syndrome.

Further reading Miller MD, Cooper DE, Warner JJP (1995). Review of Sports Medicine and Arthroscopy. Philadelphia: WB Saunders, pp. 3–43. Reid DC (1992). Sports Injury Assessment and Rehabilitation. Churchill Livingstone, pp. 437–549.

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Meniscal injuries General description The knee menisci distribute the load of the body weight across the tibial plateau; they are the “shock absorbers” of the knee. They play a role in joint lubrication and guide normal knee motion. Injuries to the menisci create an environment for accelerated degenerative changes of the articular cartilage, often resulting in early degenerative joint disease. Meniscal tear can be isolated or in association with a medial collateral or anterior cruciate ligament tear. Older individuals may develop degenerative tears without any history of trauma.

Presentation Patients with an isolated meniscus tear can present several weeks after the injury with complaints of knee locking and catching and the knee “giving out.” Knee effusion may be present. Severe tears with concomitant ligament injuries are usually seen acutely, as they are associated with more pain and limitation of knee motion and function.

Differential diagnosis Intra-articular loose bodies, osteochondral fracture, cruciate and collateral ligament injury, and osteochondritis dessicans can present similarly or coexist.

History Twisting of the knee with the foot planted is the usual mechanism of injury if a history of trauma is present. Onset of knee swelling may be slow (likely effusion) or rapid (likely hemarthrosis). Effusion develops hours after injury and is associated with tear of the inner avascular portion of the meniscus. Hemarthrosis develops within minutes of injury and is associated with tear of the outer vascular region of the meniscus and with cruciate ligament tear. History of intermittent catching or locking of the knee often leads to a tentative diagnosis of meniscal tear.

Physical The physical findings of knees with meniscal tear are nonspecific. Physical examination may be completely normal in some cases. Effusion with limitation of knee range of motion may be present in acute cases. Joint line tenderness may be elicited. Special tests (see Table 5.1) are described by various authors, but the sensitivity and specificity of the special tests are highly variable.

Diagnostic testing Plain X-ray of the knee is often sufficient in the initial evaluation to rule-out fracture after acute trauma. Diagnosis is confirmed by MRI or arthroscopy. MRI should be done in cases where surgery is considered.

Management Initially, treatment consists of ice, elevation, NSAIDs, and bracing.

MENISCAL INJURIES

Table 5.1 Specific knee tests Test

Setup

Maneuver

Interpretation

McMurray

Patient supine with hip and knee fully flexed (Note: snap in extreme flexion indicates posterior horn tear; click at 90* flexion indicates lesion of midmeniscus)

Apply a valgus force and externally rotate the tibia while extending the knee. Apply a varus force and internally rotate the tibia while extending the knee.

Audible or palpable “pop” or “snap” indicates a medial meniscal tear. The snap is produced as the torn fragment rides over the femoral condyle during extension. Audible or palpable “pop” or “snap” indicates a lateral meniscus tear.

Apley

Patient in a prone position, with the knee flexed 90*, and the leg stabilized by the examiner’s knee

Distract the knee while rotating the tibia internally and externally. Next, compress the knee while internally and externally rotating the tibia again.

Pain during this maneuver indicates ligamentous involvement. Pain during this maneuver indicates a meniscal tear.

Bragard sign

Patient in a seated position (use if + medial anterior joint line pain)

Examiner externally rotates the tibia, which displaces meniscal lesion forward, if one exists.

Palpable tenderness along the anterior medial joint line indicates anterior medial lesion.

Bounce home

Patient is supine with his or her heel cupped in the examiner’s hand

Examiner fully flexes the knee and then passively extends the knee.

If knee does not reach complete extension or has a rubbery or springy end feel, knee movement may be blocked by a torn meniscus.

Childress

Patient standing

Instruct the patient to squat with the knee fully flexed and attempt to “duck walk.”

If motion is blocked, a meniscal lesion is indicated; however, pain in this position may indicate a meniscal tear or patellofemoral joint involvement.

O’Donoghue Patient in a prone Examiner rotates the position with the tibia internally and knee flexed 90* externally twice, then fully extends knee and repeats rotations.

Increased pain during rotation in either or both knee positions indicates a meniscal tear or joint capsule irritation.

Payr sign

Medial knee pain indicates a posterior horn lesion of the medial meniscus.

Patient sitting cross-legged

Examiner exerts downward pressure along the medial aspect of the knee.

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Conservative treatment for older athletes and individuals with no mechanical symptoms includes 3–6 weeks of reduction in weight-bearing activities and strengthening through rehabilitation. After this period, refer patient for arthroscopy if function remains limited, mechanical symptoms develop, or there are recurrent episodes of pain and swelling. For elite athletes, patients with mechanical symptoms, those experiencing swelling with sports activity, or refractory cases, refer patients for arthroscopic evaluation. Considerations include the following: • Tears in the “red zone” (vascular, thick, lateral portion of meniscus) have the greatest healing potential. These are the only tears that are repairable (repair is usually performed in young or elite athletes). • Tears in the “white zone” (avascular, thin, medial portion of meniscus) are debrided with a partial meniscectomy. This is removed to prevent future arthritic changes. For rehabilitation following meniscectomy, start with range-of-motion and stretching exercises, then isometric, followed by isotonic exercises. A stationary bicycle may be used. When the patient regains full range of motion, isokinetic exercises and endurance training are introduced, followed by jogging on a trampoline. Finally, track jogging is implemented followed by agility and sport-specific training. Rehabilitation following meniscal repair is similar but with more limitations on weight bearing and longer intervals between stages.

Further reading Braddom RL (ed.) (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: WB Saunders Elsevier. Hoppenfeld S (1976). Physical Examination of the Spine and Extremities. East Norwalk, CT: AppletonCentury-Crofts. Mink JH, Levy T, Crues JV 3rd (1988). Tears of the anterior cruciate ligament and menisci of the knee: MR imaging evaluation. Radiology 167:769–774.

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Patellofemoral pain General description Patellofemoral pain (pfp) is among the most common causes of knee pain. It is an anterior knee pain caused by the patella’s articulation with the femoral condyles. It is more common in women than in men, probably because of the increased Q angle (angle between the axis of the tibia and femur). Muscle imbalance, especially the lateral quadriceps overpowering the medial quadriceps (primarily the vastus medialis), is felt to play a role in this pain. The term chondromalacia patella is frequently used interchangeably with pfp, but more accurately should be reserved for instances of pathological changes in the patellar cartilage (primarily seen on arthroscopy).

Clinical manifestations The pain is generally felt in the front of the knee, usually relieved with rest and generally not severe with weight bearing. There is usually minimal radiation of the pain, which is usually localized to the anterior part of the knee. Pfp should be considered in all females with anterior knee pain. In the last few degrees of extension, the quadriceps pulls the patella upwards, but in 90* of knee flexion the quadriceps contraction drives the patella into the femoral condyles. This can be worsened by patellar misalignment or tight lateral ligaments, driving the lateral facet of the patella into the lateral femoral condyle.

Differential diagnosis Osteoarthritis of the knee can present with a similar insidious onset and with anterior or nonfocal knee pain. Pfp is more commonly aggravated with rising up or stair climbing and less likely to hurt with weight bearing (standing and walking) than osteoarthritis. Lumbar radiculopathy or plexopathy and pes anserine bursitis can cause anterior knee pain. Chondromalacia patella can be a sequela of pfp and can coexist. A plica (a redundant fold of synovial tissue) can also be a cause of anterior knee pain. Other disorders to consider include patella tendonitis, peripatellar bursitis, Osgood-Schlatter disease, ligamentous disorders, and meniscal lesions.

History Patients are more often female, but pfp does occur in males. Most patients report an insidious onset. Bilateral complaints are common. Pain is typically reported with ascending or descending stairs. There may be a history of recently increased activity that precipitated the pain.

Physical The examination may be normal, including evaluation of the ligaments. Provocative maneuvers such as getting up from squatting or sitting may re-create the pain. Resisted extension from a fully flexed position may also be helpful. Patella compression may re-create the anterior knee pain. Quadriceps atrophy is not common.

PATELLOFEMORAL PAIN

Attention should be paid to how the patella tracks (with sitting and standing), and whether patella alta (high riding patella) is present.

Diagnostic testing Plain X-rays (including patella or sunrise views) may be helpful. The Q angle is frequently increased in women and may be measured on radiographs. MRI, CT, and bone scans are generally not necessary for the diagnoses, but may be helpful in excluding other disorders.

Management In the acute phase, PRICE (rest, ice, compression, and elevation) along with NSAIDs may be indicated. The aim of longer-term treatment is to maintain patellar tracking by preferentially strengthening the medial quadriceps (vastus medialis). Terminal knee-extension exercises (the last 20–30*) and quad setting exercises (isometric quad contractions in extension) are felt to preferentially strengthen the vastus medialis. These have the added advantage of not loading the patellofemoral articulation. Patellar taping and patellar tracking braces or patellar tendon straps (Cho-Pat is the type most frequently mentioned) are helpful in some cases. If these do not help or if they aggravate symptoms, a tight lateral retinaculum may be present. Surgical release of a tight lateral retinaculum is occasionally necessary.

Complications and red flags Pain at night or pain that is not relieved with non-weight bearing should be investigated more thoroughly and may require MRI, CT, or bone scan.

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The ankle Retrocalcaneal and achilles bursitis Between the posterior superior portion of calcaneus and distal Achilles tendon lies a bursa. Another exists between the skin and Achilles tendon. Thickening, inflammation, and increased fluid collection may result from repetitive pressure and shearing. Retrocalcaneal or Achilles bursitis and Achilles tendonitis may coexist. The pain of retrocalcaneal bursitis is felt about an inch or two lower than the pain of Achilles tendonitis. Bursitis is often caused by exercising (running, walking, jumping), especially on uneven ground. Other causes include wearing of poorly fitted shoes, direct trauma, infection, rheumatoid arthritis, gout, and idiopathic causes. Signs and symptoms • Patients may present with posterior ankle or heel pain, swelling, and tenderness. Pain may be noted in the morning and with increased activity after prolonged sedentary states. Pain may be worse upon push-off, at the beginning of exercise, or when running uphill. • Limping and limited range of motion, and difficulty wearing shoes are also common complaints. • If the bursa is infected, the skin over the heel may be warm and erythematous. Fever may be present. Associations • Haglund’s deformity is prominence of the posterior superior calcaneal tuberosity. This bony enlargement contributes to inflammation of the overlying tissues and the Achilles tendon. Most often it occurs in women and is known as “pump bump” because of the rigid backs of pump-style shoes that create pressure when ambulating. • Severs’ disease or calcaneal apophysitis is most common in active children ages 8–15 years old. It is associated with a rapid growth spurt. The pull of the muscles and tendons causes irritation, usually where the Achilles tendon inserts into the calcaneus. Diagnosis: clinical Obtain plain films if there is trauma, to rule out a fracture or bone spur. Use CT or MRI to evaluate the extent of degeneration of tissues and/or tendon. Treatment Conservative • Rest, ice, elevation, compression (PRICE) • Heel pads or lift/wedge for shoes, arch support, orthotics, change footwear • NSAIDs and steroid injections may be used if bursitis is diagnosed. Consider aspiration of fluid and antibiotics if infection is suspected. Flare-ups of gout attacks and arthritic episodes can be prevented by eating a proper diet, exercising, and taking anti-gout medications. Use antirheumatological medications if warranted.

THE ANKLE

Physical therapy This includes stretching, strengthening of tissues and the Achilles tendon, range-of-motion exercises, and modalities such as ultrasound to increase blood flow. • Counsel patients to gradually increase activity over a period of time and then modify activity. • If retrocalcaneal bursitis is associated with Achilles tendonitis, casting is required for several weeks to allow better healing and prevent further inflammation and pain. Surgical excision of bursa or parts of bone from the heel can be done if conservative measures fail. Always avoid injection directly into the tendon, as this may increase the likelihood of tendon rupture.

Tendonitis Chronic overuse of tendons leads to microscopic tears within the collagen matrix, which gradually leads to weakness of the tissue. Other factors such as inadequate vascularization, age, and mechanical factors like sudden, forceful range of motion can facilitate further degeneration and may result in rupture. Tendon disorders can involve the tendinous insertion to the bone, the sheath, or the main tissues of the tendon. Signs and symptoms • Patients may complain of pain, inflammation, swelling, and/or tenderness over the affected site. • A popping or snapping sensation is described if rupture, subluxation, or dislocation occurs. There may be accompanying ecchymosis. A defect or gap may be palpated. • Weakness, with inability to actively range ankle and foot (Table 5.2) Table 5.2 Muscles involved in ankle and foot pain Anterior ankle pain • Dorsiflexors • Deep peroneal nerve entrapment Inversion Tibialis anterior (L4, 5) Extensor hallucis longus (L5, S1)

Eversion Extensor digitorum longus (L5, S1) Peroneus tertius (L5, S1)

Posterior ankle pain Lateral ankle pain • Plantar flexors • Plantar flexors • Tibial nerve • Superficial entrapment peroneal nerve entrapment Eversion Inversion Peroneus longus (L5, Gastrocnemius S1, S2) (S1, 2) Peroneus brevis (L5, Soleus (S1, 2) S1, S2) Tibialis posterior (L4, 5) Flexor digitorum longus (S1, 2) Flexor hallucis longus (S2, 3) Plantaris (S1, 2)

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Provocative test Pain is aggravated with resisted range of motion. See Table 5.2. Imaging Plain films are used to evaluate bony architecture and avulsion fracture. MRI may show microtears and degeneration of soft tissue and/or tendon. Treatment Conservative • PRICE • NSAIDs, steroid injections around the tendon. Always avoid injection directly into the tendon. • Rehabilitation involves physical therapy for stretching, and strengthening of tissues and affected tendon. Modify activity. Heel pads or lift/wedge for shoes, arch support, and orthotics can be used. • For rupture, subluxation, or dislocation: If the injury is acute, treatment may involve placing the ankle in a short-leg cast for 4–6 weeks. Surgery is indicated if conservative measures fail. Achilles tendon The lateral and medial heads of the gastrocnemius unite into an aponeurosis, which joins the deep tendon of the soleus to form the Achilles tendon. The tendon inserts onto the middle one-third of the posterior calcaneal surface. Achilles tendon pathology is a common cause of posterior ankle pain (see Table 5.3).

Ankle sprains Sprains comprise about 15% of all athletic injuries secondary to repetitive lower extremity activity. In athletes, it is a common cause of disability and loss of participation. Most patients with benign injuries have full recovery. However, recurrent trauma can result in functional instability, chronic pain and inability to return to previous level of performance. Ankle sprains often occur in basketball, martial arts, ballet, and soccer. Special ankle tests (see Fig. 5.5) Anterior draw The patient is seated. The examiner stabilizes the patient’s distal tibia anteriorly with one hand, and with other hand applies an anterior pull on the heel with the foot held in gentle plantar flexion. Translation >5 mm or a difference in the anterior translation from the asymptomatic ankle suggests tear of the anterior talofibular ligament (ATFL). Talar tilt The patient is seated, the ankle and foot should be placed in ~10–20* of plantar flexion. The examiner stabilizes the distal tibia just proximal to the medial malleolus with one hand. With other hand, apply inversion force to the talus and calcaneus, as a unit. Tilting at the ankle joint, a side-to-side difference >5 mm with a soft end point indicates injury to the ATFL and calcaneofibular ligament (CFL).

THE ANKLE

Table 5.3 Achilles tendon Mechanism of injury

Tendonitis Rupture Inflammation secondary to • Structural weakening from microtears ongoing tendonitis • Poor vascularization • Sudden unexpected force in a healthy tendon

Causes

Same as tendonitis Running, jumping, toe raises, or activities requiring any type of significant push-off with toes. Age, increased mileage or intensity, change in footwear, hyperpronation, pes planus, and tight hamstrings and heel cords also play a role.

Signs and symptoms

Swelling, tenderness, posterior ankle pain, pain with push-off, decreased range of motion (ROM)

Special tests Pain is aggravated by restricted plantar flexion, inversion

An audible pop or snap, sudden sharp posterior ankle pain, swelling, tenderness, ecchymosis, decreased ROM, palpable defect in tendon, antalgic gait. Feeling of getting “kicked” in back of leg Positive Thompson’s test: Separation or rupture of tendon causes inability of foot plantar flexion with squeezing of the calf

Imaging

• Plain films may show avulsion • Plain films may show fracture of calcaneus, soft tissue soft tissue changes, bony changes pathology • MRI shows disruption of fibers • MRI may show microtears, degeneration of tissue, tendon

Treatment

Conservative • PRICE • NSAIDS, steroid injection (avoid injection directly into tendon) • Rehabilitation: splinting, bracing, heel lifts, stretching, strengthening • Change footwear • Increase activity gradually

Conservative • Bracing in a plantar-flexed position for ~8–12 weeks. Dorsiflexion is increased gradually to neutral position at the end of 12 weeks. • Has high rate of re-rupture Surgical (preferred for active individuals): Tendon is repaired and casted for about 2 weeks. It is then placed in a plantar flexion dial lock brace for ~4–6 weeks and gradually brought to neutral. Extensive rehabilitation with gradual increase in activity is recommended.

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Lateral Ankle Sprain • Inversion on plantar flexed foot • “Rolling over ankle” • Lateral pain, swelling, ecchymosis, unable to weight bear

Anterior Talofibular ligament (ATFL): Most commonly injured Calcaneofibular ligament (CFL): 2nd most commonly injured Posterior Talofibular ligament (PTFL): Last injured

* Anterior Draw – Tests ATFL ** Talar Tilt – Tests ATFL and CFL

Medial Ankle Sprain • Eversion, pronation of foot with internal rotation of upper body • Medial pain, swelling, ecchymosis, unable to weight bear

Syndesmotic Injury/ Anterior, High Ankle Sprain • Hyperdorsiflexion of ankle • Forceful eversion, external rotation of ankle • Anterior aspect, high ankle pain, swelling, unable to weight bear

Deltoid ligament/Medial collateral ligament injury (4 parts) • Anterior and Posterior tibiotalar ligaments • Tibionavicular ligament • Tibiocalcaneal ligament

Ankle Syndesmosis (4 parts) • Anterior, posterior, and transverse tibiofibular ligaments • Interosseous ligament

***Kleiger’s Test – Tests deltoid ligament

****Squeeze Test (Pott’s Compression Test) ***** Cotton Test (Tibiotalar Shuck Test) ******External Rotation Stress Test

Figure 5.5 Mechanism of ankle sprain. Kleiger’s test The patient’s knee is flexed over the end of the table, with foot relaxed. The examiner grasps the foot and rotates laterally in the mortise of the ankle. Increased instability compared contraterally with or without pain is indicative of a positive test and indicates deltoid ligament injury. Talar displacement may also be palpated. Squeeze test The examiner grasps then squeezes the patient’s distal tibia and fibula proximally, compressing the interosseous ligaments. Pain at the ankle joint distally indicates a syndesmotic injury. Cotton test The examiner holds the patient’s lower leg with one hand while alternately applying medial and lateral force to the talus with the other hand. Pain in the syndesmosis indicates injury.

THE ANKLE

Anterior talofibular ligament

Posterior talofibular ligament

Calcaneo fibular ligament

Figure 5.6 Ankle, lateral view. Table 5.4 Grades of lateral ankle sprains Grade 1 (mild)

Grade 2 (moderate)

Grade 3 (severe)

Grade 4 (dislocation)

• Partial ATFL tear, no instability • Negative anterior draw stress test • Negative talar tilt stress test

• Complete ATFL tear • Partial CFL tear • Positive anterior draw stress test • Negative talar tilt stress test

• Complete ATFL tear • Complete CFL tear • Positive anterior draw stress test • Positive talar tilt stress test

• Complete ATFL tear • Complete CFL tear • Complete PTFL tear

ATFL, anterior talofibular ligament; CFL, calcaneofibular ligament; PTFL posterior talofibular ligament.

External rotation stress test The patient’s knee is flexed to 90*. The examiner stabilizes the tibia and fibula with one hand and externally rotates the ankle with the other hand. Pain in syndesmosis indicates injury. Note: Always compare the symptomatic ankle with the contralateral side. Some patients have generalized ligamentous laxity that may yield falsepositive results. Lateral ankle sprain (see Fig. 5.6) • Most common ankle sprain, approximately 85% of all injuries • Mechanism of injury is inversion (see Fig. 5.5) • Special tests (see Fig. 5.5) • Grades 1–4 (see Table 5.4)

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Imaging • Plain films: anteroposterior (AP), lateral, oblique • Stress views Anterior draw may show a >5 mm displacement Talar tilt may show 5–10* difference when compared to the contralateral ankle CT, MRI Treatment • Grades 1 and 2 Acute phase: PRICE, NSAIDs, analgesics, early mobilization Conservative: rehabilitation—range of motion, strengthening, stretching, proprioceptive exercises, taping, bracing, modalities • Grade 3: conservative vs. surgery Trial of rehabilitation and bracing for about 6 months If active individual, failed conservative treatment, and/or instability, consider repair or reconstruction of ligaments as early as 3 months post-injury • Grade 4: surgery Medial ankle sprain (Fig. 5.7) • Approximately 5% of all ankle sprains • Mechanism of injury (see Fig. 5.5) • Special test (see Fig. 5.5) • Grades 1–3 Grade 1: stretch Grade 2: stretch partial tear Grade 3: full tear • Complications include syndesmosis ankle injuries Deltoid ligament complex

C5.S11.3.4

Anterior tibiotalar ligament

Tibionavicular ligament

Figure 5.7 Medial ankle.

Posterior tibiotalar ligament

Tibiocalcaneal ligament

THE ANKLE

• Imaging: AP, lateral, and oblique plain films, CT, MRI • Treatment is the same as for lateral ankle sprains. Syndesmosis/anterior ankle sprain A syndesmosis is an articulation in which adjacent bones are bound together by a ligament. The syndesmosis of the ankle maintains the integrity of the ankle mortise by resisting forces that attempt to separate the tibia and fibula. It consists of the following: • Anterior, posterior, and transverse tibiofibular ligaments • Interosseous ligament Mechanism of injury (see Fig. 5.5) Special tests (see Fig. 5.5) Imaging • AP, lateral, oblique, mortise views, proximal fibula view plain films Rupture of the anterior tibiofibular ligament can extend through the interosseous membrane. This may result in a proximal fibula fracture or a Maisonneve fracture. Therefore, it is important to obtain a proximal fibula view plain film. • MRI, CT Treatment is conservative vs. surgical stabilization of the ankle mortise.

Further reading American Academy of Orthopaedic Surgeons (AAOS) (2003). Orthopaedic Knowledge Update: Foot and Ankle, 3rd ed. Rosemont, IL: AAOS. Braddom RL, (ed.) (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: WB Saunders Elsevier. Brotzman BS, Wilk KE. (2003). Clinical Orthopaedic Rehabilitation, 2nd ed. Philadelphia: Mosby. Flynn JM, Widmann RF (2001). The limping child: evaluation and diagnosis. J Am Acad Orthop Surg 9:89–98. Hoppenfeld S (1976). Physical Examination of the Spine and Extremities. East Norwalk, CT: AppletonCentury-Crofts. Saltzman CL, Tearse DS (1998). Achilles tendon injuries. J Am Acad Orthop Surg 6:316–325.

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The foot General description The foot, an appendage that absorbs from two to six times our body weight, is often a source of musculoskeletal pain complaints. Subtle imbalances or abnormalities such as leg-length discrepancy or pes planus are common and can predispose the foot to injury and overuse. The foot functions as a lever arm to propel the body forward. It is a stable base of support for standing, and absorbs shock for running, jumping, and landing. It also acts as a proprioceptive organ to adapt to surface changes. It is helpful to consider the foot as three separate regions: • The hindfoot is composed of the talus and calcaneus (large bones), and is prone to impact injuries. • The midfoot is composed of the tarsal bones, navicular, cuboid, and cuneiforms (rounded bones), and is prone to rotational injuries. • The forefoot is composed of the metatarsals and phalanges (thin bones like levers), and is prone to overuse and stress.

Plantar fasciitis Clinical manifestations The plantar fascia is a fibrous aponeurosis on the plantar aspect of the foot. It originates from the medial calcaneal tuberosity and inserts into the transverse tarsal ligament, flexor sheath, volar plate, and periosteum of the proximal phalanges. One of the most common orthopedic pain syndromes, plantar fasciitis usually presents as heel pain, predominantly in the early morning upon stepping out from bed. The pain then eases after a few minutes of walking, but recurs later in the day. Walking on hard surfaces, running, and prolonged standing exacerbate the pain. The pain is usually unilateral. Differential diagnosis The primary differential diagnoses include calcaneal fracture, plantar fascia rupture, tarsal tunnel syndrome, seronegative spondyloarthropathies, gout, or rheumatoid arthritis (see Table 5.5). History The onset is usually gradual and not associated with trauma. Plantar fasciitis may occur after sudden weight gain, onset of an exercise program, or a rapid increase in activity. It is common during pregnancy and in middle age. In athletes, the condition is usually related to improper training, such as rapidly increasing mileage, intensity, or duration of workouts. Other factors may be running on steep hills, changing training surfaces, or wearing worn-out or new shoes. Physical The most common finding is localized tenderness over the medial calcaneus in the area of plantar fascia insertion. Passive dorsiflexion of the toes may increase the pain. Patients often have restricted or painful dorsiflexion

THE FOOT

Table 5.5 Common causes of foot pain Pathology

History

Physical

Diagnostic Treatment testing

Metatarsalgia

Pain on ball of foot with ambulation

None Localized tenderness to metatarsal head

Hallux valgus

Pain first MTP Bunion joint deformity

Hallux rigidis

Pain, stiffness first MTP joint

Stress fractures Low-risk sites: Second through fourth metacarpal shafts High-risk sites: Talus, tarsal navicular, proximal fifth metatarsal shaft, great toe sesamoids, base of the second metatarsal bone1 Posterior tibial tendonitis2

Tarsal tunnel syndrome (posterior tibial nerve entrapment)4

Metatarsal pad in shoe or orthotic

None

“Bunion last,” or wide, soft shoes,surgery

None

Orthotics, surgery

Tender to Repetitive impact leading palpation over affected area to insidious onset of localized pain Sudden increase in athletic training

X-rays (frequently negative) Bone scan, MRI, or CT

Ice, rest, analgesics. Taping, casting, CAM walker. Orthopedic consult for sites at high risk of non-union

Aching pain over the medial ankle and longitudinal arch; pronated, flat foot

Swelling of the tendon sheath, tenderness, pain on passive stretching of the tendon, pain on active ankle movement

X-rays (frequently negative), MRI, ultrasound

Rest, ice, stretching, NSAIDs, injection, casting, orthotics

Aching, paresthesias, bottom of foot and toes Worse at night

+ Tinel’s sign over flexor retinaculum + Dorsiflexioneversion test3

Nerve conduction studies, MRI

Orthotics, arch supports, proper footwear with 1” heel, injection, surgical decompression

Decreased ROM first MTP joint

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Table 5.5 (Contd.) Pathology

History

Physical

Diagnostic Treatment testing

Morton’s neuroma5

Aching, paresthesias of forefoot and toes

MRI Plantar tenderness between third and fourth metatarsal heads + squeeze test of forefoot

Metatarsal pad or bar, orthotics, ice, injection, surgical excision

MTP, metatarsophalangeal; ROM, range of motion.

of the ankle because of a tight Achilles tendon, or tight gastrocnemius/ soleus muscles. Localized swelling is uncommon, but the plantar fascia may feel thickened, nodular, or tight. Diagnostic testing Most cases of plantar heel pain or plantar fasciitis can be diagnosed by the history and physical exam alone. X-rays, bone scans, and blood tests are used when patients have atypical presentations or fail to respond to treatment within 6 months. Special considerations Asymptomatic adults commonly have heel spurs on X-ray, and this is not considered to be the cause of the pain. It is now thought to be more likely the result of the inflammation or trauma.6 Management (treatment) Plantar fasciitis is best treated conservatively. Treatment requires the use of multiple modalities, patient education, and time. Improvement is slow and gradual and may take up to a year. Initial treatment should address the local inflammation, underlying mechanical abnormalities, and training errors. Because plantar fasciitis is viewed as an overuse syndrome, relative rest should be the first-line treatment in both athletes and non-athletes. Patients with plantar fasciitis should be told never to walk barefoot. Old worn-out shoes should be discarded. Common treatment techniques are ice massage, shoe orthotics (especially to correct pronation), splinting the foot overnight in dorsiflexion, physical therapy modalities, and Achilles stretching. Corticosteroid and anesthetic injection can be considered at the site of fascial attachment using a medial approach to avoid the fat pad. Extracorporeal shockwave therapy (ECSWT), a high acoustic force, is a newer FDA-approved modality. For recalcitrant cases, referral for limited surgical release of the fascia with decompression of local nerves with or without heel spur excision can be an option. The effectiveness of this treatment remains unproven.7

THE FOOT

Complications and red flags Associated paresthesias may indicate concomitant entrapment of the lateral plantar nerve, the medial calcaneal nerve, or the nerve to the adductor digiti minimi.

References 1. Boden BP, Osbahr DC, Jimenez C (2001). Low-risk stress fractures. Am J Sports Med 29:100. 2. Mosier SM, Pomeroy G, Manoli A 2nd (1999). Pathoanatomy and etiology of posterior tibial tendon dysfunction. Clin Orthop Relat Res 365:12–22. 3. Kinoshita M, Okuda R, Morikawa J, et al. (2001). The dorsiflexion-eversion test for diagnosis of tarsal tunnel syndrome. J Bone Joint Surg Am 83-A:1835. 4. Wilemon WK (1979). Tarsal tunnel syndrome. Orthop Rev 8:111. 5. Wu KK (1996). Morton’s interdigital neuroma: a clinical review of its etiology, treatment, and results. J Foot Ankle Surg 35:112. 6. DeMaio M (1993). Plantar fasciitis Orthopedics16(10):1153–1163. 7. Crawford F, Thomson C (2003). Interventions for treating plantar heel pain. Cochrane Database Syst Rev 2003(3):CD000416.

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Chapter 6

Pain syndromes Rafael Abramov Fibromyalgia 166 Myofascial pain syndrome 172 Complex regional pain syndrome 176 Postherpetic neuralgia 180

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Fibromyalgia Background The most common reason for patients to visit a physician is pain. The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”1 Chronic pain differs from acute pain in several aspects: it is more diffuse, the relationship between tissue pathology and perceived severity is poor or absent, and successful therapeutic modalities of acute pain often fail in treating chronic pain. The chronic pain and fatigue syndromes are recently recognized entities which constitute a public health burden that modern medicine has not approached effectively. Research advances of the past several decades shed light on chronic pain states, identifying them as central pain syndromes influenced by a variety of biochemical, environmental, and genetic factors. One of these syndromes is a common disorder called fibromyalgia.

Definition Fibromyalgia, or fibromyalgia syndrome (FMS), is a complex disorder recognized as earlier as the 17th century. However, it was not until 1987 that the American Medical Association recognized it as a legitimate clinical entity and a potential cause of disability. In 1990, The American College of Rheumatology set forth criteria for classification of fibromyalgia: 1. History of widespread pain for at least 3 months 2. Pain in at least 11 of 18 tender point sites on digital palpation with a force of ~4 kg (see Fig. 6.1)

Pathophysiology The pathophysiology of fibromyalgia is not well understood. It integrates the musculoskeletal, neuroendocrine, and central nervous systems. The most widely accepted hypothesis, substantiated by research, suggests that fibromyalgia is a state of whole-body hypersensitivity to pain due to a decrease in a patient’s threshold to various stimuli including pain, heat, noise, and strong odors. This phenomenon is known as central sensitization and is secondary to biochemical changes causing an abnormality in central processing of nociceptive pain input. The well-researched biochemical changes are described next. Decreased serotonin Serotonin is a neurotransmitter linked to sleep, pain perception, headaches, and mood disorders. Decreased levels of serotonin have been detected in patients with fibromyalgia. Serotonin regulates stimulation of the hypothalamic–pituitary–adrenal (HPA) axis. Low levels of serotonin may further worsen HPA axis dysfunction, and HPA axis dysfunction can be the cause of low serotonin levels.

1 International Association for the Study of Pain. Pain termi-nology. www.iasp-pain.org

FIBROMYALGIA

Locations of tender point sites in fibromyalgia: • Occiput: bilaterally at the suboccipital muscle insertions • Low cervical: bilaterally at the anterior aspect of the intertransverse spaces at C5–C7 • Trapezius: bilaterally at midpoint of upper border • Supraspinatus: bilaterally at origins above spine of scapula near the medial border • Second rib: bilaterally at the second costrochondral junction • Lateral epicondyle: bilaterally 2 cm distal to the epicondyles • Gluteal: bilaterally in upper outer quadrant of buttocks in the anterior fold of the muscle • Greater trochanter: bilaterally posterior to trochanteric prominence • Knee: bilaterally at the medial fat pad proximal to joint line

Figure 6.1 Tender-point sites for the classification criteria of FMS.

Increased substance P Substance P is a neurotransmitter released into cerebrospinal fluid (CSF) when axons are stimulated. High levels increase the sensitivity of nerves to pain or heighten awareness of pain, so that even normal stimuli can result in exaggerated nociception. Decreased growth hormone Growth hormone is produced during delta sleep and is involved in tissue repair. Therefore, disrupted stage 4 (delta) sleep associated with fibromyalgia may account for low levels of growth hormone. Growth hormone stimulates the production of insulin-like growth factor I (IGF-I) in the liver. Most patients with fibromyalgia have low levels of IGF-I. These low levels are both specific and sensitive for fibromyalgia.

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Increased nerve growth factor Nerve growth factor is 4 times higher in the spinal fluid of patients with fibromyalgia than in others. This chemical is important to the pathophysiology of fibromyalgia because it enhances the production of substance P in afferent neurons, increasing the person’s sensitivity or awareness to pain. Nerve growth factor may also play a role in spreading or redistributing perceived pain signals. Changes in cortisol, ACTH, CRH Normally, adrenocorticotropic hormone (ACTH) is released from the anterior pituitary after stimulation by corticotropin-releasing hormone (CRH). This stimulates the adrenal cortex to produce glucocorticoids, which are powerful mediators of the stress-adaptation response. The general consensus is that chronic pain is stressful, and the amount of stress depends in part on a person’s intrinsic coping mechanisms. Persistent stress often alters neuroendocrine rhythms, causing a paradoxical pattern of HPA axis dysfunction, characterized by an exaggerated ACTH response to CRH but blunted adrenal secretion of cortisol. The five main neuroendocrine abnormalities associated with dysfunction of the HPA axis are as follows: • Decrease in free cortisol levels in 24-hour urine samples • Loss of normal circadian rhythm with elevated evening cortisol level (normally, it should be at the lowest level in the evening) • Insulin-induced hypoglycemia associated with overproduction of ACTH • Decrease in growth hormone levels • Cortrosyn (ACTH) stimulation test with reduced adrenal corticosteroid release

Epidemiology Fibromyalgia is the second most common disorder encountered by rheumatologists (after osteoarthritis). It is found in 2%–4% of the population, with no racial preference. The female-to-male ratio is 5–10 to 1. The symptoms are usually first seen at ages 20–55 years, but the disease can strike in childhood and in the geriatric population.

Etiology The true cause of FMS is unknown.

Clinical presentation The most obvious feature is widespread pain above and below the waist, on the left and on the right side of the body, for at least 3 months with at least 11 tender point sites (see Fig. 6.1). The tender points are the most powerful classifiers of fibromyalgia. However, patients can present with various nonspecific symptoms including sleep disturbances, fatigue, stiffness, tension headaches, irritable bowel syndrome, depression, mood disturbances, and paresthesias. The most important part of the physical examination is reporting pertinent negatives such as the absence of bursitis, tendinitis, myofascial pain, excessive joint mobility, adenopathy, true synovitis, thyromegaly, and abnormal deep-tendon reflexes.

FIBROMYALGIA

Differential diagnosis • • • • • • • • • •

Myofascial pain syndrome Mood disorders Rheumatoid arthritis Systemic lupus erythematosus (SLE) Complex regional pain syndrome Osteoarthritis Cervical and lumbar degenerative disc disease Meralgia paresthetica Post-polio syndrome Hypothyroid myopathy

Laboratory analysis The laboratory analysis should be normal; it is used to rule out other disorders. • Complete blood count (CBC) • Comprehensive metabolic panel • Liver function tests (LFTs) • Thyroid function tests (TFTs) • Certain rheumatologic serologies • Creatinine (Cr) • Creatine kinase • C-reactive protein (CRP) • Erythrocyte sedimentation rate (ESR) • Calcium and phosphorus levels

Diagnosis Diagnosis is clinical, based on definition and associated symptoms discussed previously.

Management The condition is chronic with occasional exacerbations. Thus, the most important aspect is patient education and provision of means to manage the pain disorder. It is important to get the patient active and try to regulate sleep. The common treatment regimen is a balance between pharmacological treatments and activity modifications. Medications Three medications are FDA approved for the treatment of fibromyalgia: • Lyrica (pregabalin): start 75 mg twice daily and taper up to 450 mg/day • Cymbalta (duloxetine): start 30 mg daily for a week and taper up to 120 mg/day • Savella (milnacipran): start 12.5 mg for a week and taper up to 100 mg/day within a week Other medications to consider are as follows: • Amitriptyline 10–25 mg at bedtime for short-term relief of sleep disturbances • Fluoxetine 20 mg daily; works best in combination with amitriptyline • Cyclobenzaprine (can be used in combination with amitriptyline and fluoxetine)

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• Simple acetaminophens or NSAIDs. Tramadol; avoid other antiinflammatory agents including steroids • Other selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine dual-reuptake inhibitors (SNRIs) Rehabilitation The patient must understand the possibility of short-term increase in pain and fatigue after initiating a rehabilitation program. • Osteopathic manipulative medicine • Muscle energy treatments • Facilitated positional release • Muscle inhibition • Physical therapy • Passive stretching and strengthening of affected muscle groups • Modalities Electrotherapy Cryotherapy Therapeutic heat Pool therapy • Low-intensity aerobic exercise regimen: Always initiate below the patient’s capacity and gradually increase the regimen. • Cognitive and recreational therapy Procedures • Trigger point injections: 1 or 2 mL of local anesthetic, usually 1% lidocaine, injected, into the tender point • Acupuncture

Further reading Bennett RM (1999). Emerging concepts in the neurobiology of chronic pain: evidence of abnormal sensory processing in fibromyalgia. Mayo Clin Proc 74:385–398. Braddom RL (2006). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders. Geenen R, Jacobs JW, Bijlsma JW (2002). Evaluation and management of endocrine dysfunction in fibromyalgia. Rheum Dis Clin North Am 28(2):389–404. Goldenberg DL (2004). Management of fibromyalgia syndrome. JAMA 292(19):2388–2395. International Association for the Study of Pain. Pain terminology. http://www.iasp-pain.org Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, et al. (1990). The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia: report of the Multicenter Criteria Committee. Arthritis Rheum 33:160–172.

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Myofascial pain syndrome General description Myofascial pain syndrome (MPS) is a regional skeletal muscle condition presenting with vague complaints of poorly localized muscle pain and stiffness. It is characterized by hyperirritable and tender spots within taut bands of skeletal muscle called “trigger points.” The pathophysiology is unknown. Trigger points do not have any abnormal histological findings, and electromyograms of muscle affected by myofascial pain are normal.

Differential diagnosis • • • • • • • • • • • •

Fibromyalgia Polymyositis Polymyalgia rheumatica Somatization disorder Poor sleep Psychogenic rheumatism Migraine and tension headaches Shoulder impingements Muscular sprains and strains Bursitis and tendinitis Radiculopathy Complex regional pain syndrome

History Patients can be of any age or either sex. They generally describe poorly localized pain in muscles and joints with sensory disturbances that are usually worse with exercise and stretching. The onset can be acute (after a specific event) or chronic from overuse or poor posture.

Physical examination Posture should be evaluated, including stance, scoliosis, and any right-toleft asymmetries. The range of motion of all affected limbs and spine, with observation of barriers during passive motion, should be recorded. Assess for pain with movement or joint subluxations. Strength testing may reveal subtle weakness or muscular imbalances. Soft tissue palpation (including superficial and deep tissue texture with about 3 lbs of force) should be performed, observing for taut bands, twitch response, jump sign, or reproducibility of the patient’s symptoms. The neurological examination is usually normal, but patients may report non-dermatomal sensory disturbances. A taut and tender muscle band, which reproduces a patient’s typical pattern of referred pain when an appropriate amount of pressure is applied, can be palpated locally. A local twitch response is elicited by snapping the trigger point manually. The involved region may exhibit decreased range of motion and some pain-related local muscle weakness.

MYOFASCIAL PAIN SYNDROME

Diagnostic imaging and laboratory studies No specific imaging or lab work is diagnostic. They can be used to rule out other causes of pain.

Management Spray-and-stretch technique This involves passive stretching of the affected muscle. • Position the patient for maximum decrease in muscle tension. • Clearly identify the trigger points and mark them. • Apply vapocoolant (ethyl chloride) over the entire length of the affected muscle. • Passively stretch the muscle by applying gentle pressure. • Repeat “spray and stretch” until full range of motion is attained. • Use caution with vapocoolant—do not spray for >6–10 seconds with each stretch. Osteopathic manipulative treatment • Strain–counterstrain technique • Facilitated positional release (FPR) technique • Progressive inhibition of neuromuscular structures (PINS) technique Physical therapy • Improve etiologic and predisposing factors: poor posture, body mechanics, etc. • Modalities • TENS • Ultrasound • Massage Other treatments • Aerobic exercises • Acupuncture • Medication • Short-term use of muscle relaxants and NSAIDs (can be used in combination) Invasive techniques Trigger point injection • Use of 22–27 gauge 1.5–2 inch needle is recommended • Local anesthetic: • <1 mL of 1% lidocaine is used most often. • Procaine is preferred because it is selective for small unmyelinated fibers that control pain perception. • Steroids: use if there is an adjacent area of inflammation, e.g., frozen shoulder • Botulinum toxin: emerging therapy • Dry needling: multiple advances of a needle into the trigger point Technique for trigger point injection (see Fig. 7.1) • Position the patient for maximum decrease in muscle tension. • Clearly identify the trigger points and mark them.

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• Use aseptic techniques with appropriate skin preparation. • Grasp the skin overlying the trigger point with the thumb and second finger to isolate the taut band. • Apply vapocoolant (ethyl chloride). • Advance the needle at an ~30–45* angle 1–1.5 cm away from the trigger point. • Aspirate to prevent intravascular injection. • Inject medication or use dry needling technique. Complications of Trigger Point injections • Pneumothorax • Hematoma • Bleeding • Transient nerve block • Soft tissue infection • Postinjection soreness • Vasovagal reaction • Allergic reaction

Complications • • • • • • •

Chronic pain syndrome Physical deconditioning syndrome Insomnia Depression Obesity Medication dependence Anxiety

Further reading Frontera WR, Silver JK (2002). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Henley and Belfus.

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Complex regional pain syndrome General description Complex regional pain syndrome (CRPS) is a multi-symptom syndrome presumed to be the result of abnormal activity of the autonomic nervous system. Type 1, or reflex sympathetic dystrophy (RSD) is without nerve injury. Type 2, or causalgia, has obvious nerve injury.

Clinical manifestations • Pain: burning, constant, deep • Edema: pitting, brawny • Skin changes: thin hair, brittle nails, rash, ulcers, hyperhidrosis, color changes • Motor function abnormalities: weakness, tremors, spasms, dystonia, bizarre movements • Sensory function abnormalities: allodynia, hyperpathia, dysesthesia CRPS can consist of 3 stages. Stage 1 (acute) • 2–3 months: warm stage • Pain limited to the site • Localized edema • Limited mobility • Stiffness • Hyperhidrosis Stage 2 (dystrophic) • 3–6 months • Pain is increased • Edema is widespread • Spotty osteoporosis • Muscle wasting • Scant and coarse hair Stage 3 (atrophic) • >6 months: cold stage • Atrophy (irreversible) • Intractable pain • Severe edema • The entire limb may be affected. • CRPS may spread to other body parts in 3 ways: • Continuity type: proximally from a site of injury, e.g., hand to shoulder • Mirror-image type: opposite site or limb • Independent type: separated distant region of the body

Differential diagnosis • Tendon and ligament pathology • Plexopathy of various etiology

COMPLEX REGIONAL PAIN SYNDROME

• • • • • • • • • •

Neuropathy of various etiology Vertebral disc pathology Cellulitis Lymphedema Post-polio syndrome Chronic pain syndrome Spasticity Thoracic outlet syndrome Scleroderma Peripheral neuropathy

History There is usually a history of an insult to affected site with a disproportionate presentation of symptoms. The insults include, but are not limited to the following: • Trauma: sprain, dislocation, fractures, surgery, burn, crash injury • Ischemic heart and brain diseases • Infections, e.g., herpes zoster • Musculoskeletal disorders • Malignancy • Idiopathic

Pathophysiology The autonomic nervous system appears to assume abnormal function. The exact mechanism for this is unknown.

Diagnostic testing No single test is sensitive or specific. Diagnosis is usually made clinically. • X-rays: patchy osteoporosis after 3 weeks, diffuse bony demineralization after 2 months, fibrous ankylosis seen in stage 3 • Triple-phase bone scan: diffuse abnormal activity, stage 3 is more sensitive and specific • Thermogram: compares side-to-side skin temperature (usually low in affected limb) • Sweat test: measures resting sweat output, stimulated sweat output, and resting skin temperature • EMG/NCS: usually normal, but can help rule out other causes • Diagnostic sympathetic ganglion block: if therapeutic, it helps to identify the cause as likely CRPS • Laser Doppler imaging: tests autonomic reflexes bilaterally

Management Rehabilitation Physical and occupational therapy • Gentle weight bearing progressing to active weight bearing • Desensitization techniques and distraction exercises • Contrast baths • Home exercise program • Hydrotherapy and pool therapy • Massage, moist heat, TENS, ultrasound

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• Compression garments to decrease edema and desensitize the limb Interventional rehabilitation • Sympathetic blockade: series of 3–6 blocks • Stellate ganglia block for upper extremity • Lumbar sympathetic block for lower extremity • Sympathectomy • Chemical destruction with phenol injection • Surgical destruction • Cryoprobe or radiofrequency lesioning Psychological support Medications • NSAIDs and acetaminophens • Gabapentin 3600 mg in divided doses daily • Amitriptyline 50–150 mg daily • Clonidine 0.1–0.3 mg patch every 72 hours • Beta-blockers, calcium channel blockers, calcitonin, mexiletine (“membrane stabilizers”) • Opioids Surgical • Surgery is rarely used and may exacerbate symptoms. • Amputation Spinal cord stimulation • Used in disease refractory to all other modals of treatment

Prognosis and special considerations Prognosis varies. Early recognition and treatment of disease lead to the best results, but this is difficult given the lack of awareness and variability of symptoms. Patients with CRPS are often targeted as malingerers or as having psychogenic instability.

Further reading Bailey A, Audette J (2008). Complex regional pain syndrome. In Frontera WR, Silver JK, Rizzo, TD (2008). Essentials of Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders Elsevier, pp. 511–517.

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Postherpetic neuralgia General description Varicella-zoster virus (VZV, also known as human herpes virus 3 [HHV-3]) is the virus responsible for herpes zoster. Primary infection (usually in childhood) results in chicken pox. The virus enters the sensory nervous system (dorsal root, geniculate or trigeminal ganglia), where it remains dormant. The virus can reactivate with advanced age or immunocompromised states, causing shingles—skin rash with pain in a dermatomal distribution with predilection for the mid to lower thoracic (T3–T12), upper lumbar (L1–L2), and ophthalmic dermatomes. Persistent pain can be a cause of postherpetic neuralgia. Postherpetic neuralgia is pain that persists more than 30 days after the onset of the cutaneous eruption. It is the most common complication of VZV infection. The incidence and the duration of postherpetic neuralgia is directly associated with increased age.

Clinical manifestations Patients present with a history of resolved or resolving skin eruptions and persistent pain. Pain can be facial, ophthalmic, and/or truncal and is usually located in a dermatomal distribution.

Differential diagnosis • • • • • •

Trigeminal neuralgia Cavernous sinus syndromes Hemifacial spasm Migraine and cluster headaches Traumatic peripheral nerve lesions Idiopathic facial pain

History Patients are frequently older, with painful vesicular eruption in a dermatomal distribution. Pain is usually nonremitting, although the eruptions are resolved. Patients with postherpetic neuralgia can have associated decreased appetite, impaired sleep, and diminished libido.

Physical Patients usually exhibit a hypopigmented rash or evidence of cutaneous scarring in a dermatomal distribution, with enduring pain. The pain is frequently described as burning and/or stabbing. The patient may complain of allodynia (painful hypersensitivity to otherwise nonpainful stimuli) or sensory deficit with anesthesia at the affected site, while the uninvolved side is normal.

Diagnostic testing The diagnosis of postherpetic neuropathy is clinical.

Management Treatment is complex and requires a comprehensive approach (see Table 6.1).

POSTHERPETIC NEURALGIA

Table 6.1 Treatment of postherpetic neuralgia Agent

Initial dose

Comments

Adverse effects

Pregabalin

150 mg orally daily (FDA approved)

Titrate to a total daily dose of 600 mg divided bid or tid

Dizziness, somnolence, dry mouth, blurred vision, edema

Gabapentin

300 mg orally daily (FDA approved)

Titrate to a total daily dose of 1800 mg divided tid

Somnolence, dizziness, ataxia, nystagmus

Opioids

Oxycodone 5 mg orally every 6 hours (other agents can be used as well)

Total daily dose of 80 mg or more may be necessary

Sedation, nausea, dizziness, tolerance, abuse, constipation

Tricyclic antidepressants

Nortriptyline or desipramine 10–25 mg orally at bedtime

Total daily dose of 75–150 mg may be necessary

Sedation, confusion, anticholinergic effects

Lidocaine 5% patch

Up to 3 patches can be used at a time for a maximum of 12 hours (FDA approved)

Apply to intact/ healed skin. Rapid onset

Localized skin irritation

Capsaicin (0.025%–0.075% cream)

Topically 3 to 4 times daily

Apply to intact or healed skin. Maximal benefit in days to weeks

Localized skin irritation and burning sensation

Other treatment options, such as intrathecal corticosteroids, cryotherapy, sympathetic nerve blocks or surgical intervention, may be considered to achieve adequate pain relief in postherpetic neuralgia of long duration and resistant to other treatments.

Special considerations Zostavax is a shingles prevention vaccine approved by the FDA for individuals age 60 years and older. It does not prevent nor treat postherpetic neuralgia or primary varicella. It is injected subcutaneously in a single dose of 0.65 mL and is a live attenuated virus vaccine.

Further reading Gnann JW Jr, Whitley RJ (2002). Clinical practice. Herpes zoster. N Engl J Med 347(5):340–346.

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Procedures and medications Lyn Weiss Jay M. Weiss Waqaas A. Quraishi Nicholas Renaldo Albert Villafuerte Thomas Pobre Divyajot Sohal Ajendra Sohal Electrodiagnosis 184 Trigger point injection 192 Musculoskeletal injection and aspiration 194 Interventional spinal procedures 202 Physical modalities 212 Pain pharmacology 216

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Electrodiagnosis Overview Electrodiagnostic testing most commonly refers to electromyography (EMG) and nerve conduction studies (NCS). Together, they are usually referred to as EMG or EMG/NCS. Less commonly used electrodiagnostic testing includes somatosensory evoked potentials (SSEP), single fiber EMG (SFEMG), and repetitive stimulation studies. These advanced procedures are beyond the scope of our discussion. Electrodiagnostic testing is used to evaluate the peripheral nervous system, the neuromuscular junction, and the muscles. The physician must be knowledgeable in anatomy, neurophysiology, and the response of nerves and muscles to pathology. Since one cannot learn how to perform and interpret EMGs in the span of a few pages, the goal here will be to describe the test, clarify when and why EMG testing is performed, understand what conditions can be evaluated by the test, explain the limitations of the test, and briefly describe what should be included in a report.

General description of EMG testing Electrodiagnostic testing can be divided into two basic parts: the nerve conduction study and the needle examination. The nerve conduction study involves stimulating the nerve (usually at multiple sites) and picking up the electrical recording of the action potential. Both sensory and motor responses can be recorded by picking up activity over the muscle (for a motor nerve) or directly over the nerve (for a sensory nerve or a mixed motor and sensory nerve). Usually, the latency, amplitude, and conduction velocity of the resulting wave form is analyzed and compared to normal values, as well as to other nerves in the patient’s body. The electromyographer can then determine whether there is a generalized or localized injury to a nerve, determine whether the lesion affects primarily the axon or the myelin surrounding the nerve fiber, and evaluate the severity of the disorder. The needle portion of the examination involves inserting a thin needle into the muscle to evaluate the electrical activity of the muscle. Different muscles are tested, depending on the suspected problem. Muscles are usually tested at rest and with minimal voluntary muscle contraction. Since muscles respond in distinct ways to injury or disease, the electromyographer can assess the integrity of the nerve and muscle through needle EMG. By carefully planning the exam and based on the pattern of abnormalities, the physician can localize the nerve or nerves involved and make inferences about different disorders affecting the nerves and/ or muscles. The test is mildly painful, and the patient should be told what to expect. At no time should the test proceed if the patient is uncomfortable and requests that the testing be terminated.

ELECTRODIAGNOSIS

Why EMG testing is performed Electrodiagnostic testing is a physiological test of nerves and muscles. Many clinicians prefer an anatomical test (such as MRI or CT) to obtain information about disease or injury. In many cases, EMG and MRI can be complimentary. For many diagnoses, electrodiagnostic testing, when done correctly, is a much more specific test than MRI. MRI may show diseased anatomy, but whether or not those findings are of clinical significance may not be apparent. For example, over 57% of patients asymptomatic for low back pain over the age of 60 will have a positive MRI scan.1 Eighty percent of MRIs were abnormal in a group of 98 asymptomatic subjects in a study published in the New England Journal of Medicine.2 The literature supports use of electrodiagnostic testing instead of (or in conjunction with) MRI in the evaluation of low back pain. Electrodiagnostic testing can be used to assess the following: • Confirm or rule out a suspected diagnosis • Assess for nerve and or muscle injury • Localize a lesion (frequently determining location of surgical release) • Assess severity of injury • Prognosticate • Assess age of injury In the event of nerve injury, the electrodiagnostic test can help determine severity and prognosis by establishing if the injury is neurapraxic (damage to the myelin causing conduction block, but with the axons still intact), axonotmetic (damage or loss of some axon fibers) or neurotmetic (complete disruption of the axon, myelin, and the connective tissue structures, as in a nerve transection).

Conditions that can be evaluated by the test Electrodiagnostic testing can be used to evaluate many conditions, including the following: • Peripheral neuropathy • Entrapment neuropathy (including carpal tunnel syndrome, ulnar neuropathy at the elbow, peroneal (aka fibular) neuropathy at the fibular head, tarsal tunnel syndrome) • Brachial plexopathy (see figure on inside cover) • Lumbosacral plexopathy • Cervical or lumbosacral radiculopathy • Spinal stenosis • Neuromuscular junction disorders (myasthenia gravis, Lambert–Eaton syndrome) • Myopathies • Disorders of the anterior horn cell

1 Boden SD, Davis DO, Dina TS, et al. (1990). Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation, J Bone Joint Surg 72(3):403–408. 2 Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. (1994). Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 331(2):69–73.

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Nerve conduction studies Motor nerve studies Motor nerve conduction studies involve electrical stimulation of a motor nerve and recording the electrical activity from the muscle supplied by that nerve. An active electrode is placed over the muscle body. A reference electrode is placed distally (ideally over nonmuscle). The ground electrode is usually placed between the active electrode and the stimulator. The nerve is stimulated near the active electrode and then at a more proximal site. This procedure requires knowledge of the anatomical path of the nerve. An electrical recording is made of this evoked potential or compound muscle action potential (CMAP). The most important parameters assessed from this CMAP are the amplitude, distal latency, and the appearance (morphology) of the waveform. The machine is set to optimize the appearance of the nerve. Gain refers to amplification of the waveform and is expressed in microvolts or millivolts/vertical division. The horizontal coordinate is time expressed in milliseconds/horizontal division. The amplitude is a reflection of the number of muscle fibers firing that contribute to the action potential. This is based on the number of functioning axons. Amplitude in CMAPs is usually measured in millivolts. The distal latency represents the time in milliseconds for the nerve impulse to travel from the site of stimulation to the end of the nerve, cross the neuromuscular junction, and depolarize the muscle (measured in milliseconds). By stimulating the nerve at different sites and obtaining CMAPs at each of those sites, a conduction velocity can be calculated (in meters/ second) once the distance between stimulations is measured. The velocity can be measured for different segments of the nerve (V = D/T). CMAP amplitude is also assessed at each of these stimulation sites. Nerve compression frequently manifests as localized areas of nerve slowing or as loss of amplitude from the proximal to distal segment. This loss of amplitude across a section of a nerve is referred to as conduction block (neurapraxia). Slowing of conduction velocity, conduction block, or prolonged distal latency represents damage to the myelin sheath. Damage to the axon itself manifests as a reduced-amplitude CMAP both proximally and distally. Abnormalities of the amplitudes and velocities may become more apparent using side-to-side comparison. Since motor studies involve measuring the conduction of a nerve in the physiologic direction of conduction (proximal to distal for motor studies), these studies are said to be orthodromic. All motor studies are orthodromic, whereas sensory studies can be orthodromic or antidromic (see Sensory nerve studies). Sensory nerves studies Sensory nerve studies are performed by electrically stimulating a sensory nerve and then picking up the electrical response of that nerve at a different location. If a nerve is electrically depolarized, the action potential (wave of depolarization) travels both proximally and distally. If a sensory nerve is stimulated distally and recorded proximally (the physiologic direction of conduction) it is referred to as orthodromic stimulation.

ELECTRODIAGNOSIS

Proximal stimulation with distal recording from a sensory nerve is antidromic conduction (opposite the physiologic direction of conduction). These potentials are referred to as sensory nerve action potentials (SNAP). Amplitude, latency and conduction velocities are obtained as above, when stimulating the sensory nerves. However, since there is no neuromuscular junction in a sensory nerve, the latency is directly proportional to the conduction velocity. Late responses (H reflexes and F waves) As noted above, when a nerve is electrically depolarized the impulse is propagated both proximally and distally. The CMAP is a measure of the distal (orthodromic) propagation of that impulse. The antidromic impulse travels proximally to the anterior horn cell, and a small percentage of those fibers generate an impulse back along the same axons. This response (occurring later than the CMAP) is called an F wave and reflects the time it takes for the impulse to travel antidromically along the motor fiber to the spinal canal and back along the motor nerve (now orthodromically) to the muscle. Given their variability and because most muscles are supplied by multiple root levels, F waves have limited clinical usefulness in cases of radiculopathy or peripheral nerve entrapments. F waves are primarily used to assess proximal conduction in disorders such as Guillain–Barre syndrome. H reflexes are analogous to a true reflex. The sensory fiber is electrically stimulated and this impulse synapses at the spinal level (mono- or oligosynaptic), activating a motor fiber. An H reflex measures the time it takes for the impulse to travel proximally into the spinal canal and then distally to the muscle (the impulse is traveling orthodromically in both directions— proximally on sensory fibers and distally on motor fibers). H reflexes are usually obtained in the gastrocnemius/soleus muscle from tibial nerve stimulation in the popliteal fossa. They can also be obtained from the flexor carpi radialis (FCR) muscle from median nerve stimulation at the elbow. While the H reflex to the gastrocnemius/soleus muscle can be affected by S1 radiculopathy (or C6/7 radiculopathy in the case of the FCR muscle), anything that affects the fibers in the pathway either orthoor antidromically can affect the H reflex.

Needle EMG examination The EMG part of the testing involves insertion of a sterile needle into various muscles. Because dozens of muscles can be examined by needle exam, the test must be individualized to provide the greatest diagnostic yield in any clinical situation. In contrast to many medical tests, this test must be performed (not merely interpreted) by a physician, as the choice of muscles examined may change on the basis of results obtained. The position of the American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) (as well as the American Academy of Neurology, American Academy of Physical Medicine and Rehabilitation, and Department of Veterans Affairs) is that the needle EMG examination must be performed by a physician with special training in electrodiagnostic medicine (generally neurologists or physiatrists).3 3 AANEM Position Statement. Who Is Qualified to Practice Electrodiagnostic Medicine? Approved AANEM May 1999. aanem.org.

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The needle examination of each muscle has four distinct components: insertional activity, activity at rest, motor unit morphology, and recruitment. The first two components are performed with the muscle at rest, and with the gain set at 100–200 microvolts per division and a sweep speed of 10 msec/division (100 msec or .1 second/screen). The last two components of the test are performed with a gain of 500–1000 microvolts/ division and the same sweep.

Insertional activity and activity at rest It is important for the muscle to be at rest during this part of the exam. This may require repositioning or special maneuvers such as contraction of antagonist muscles to achieve relaxation in a muscle. With the muscle at rest, the needle is inserted. The needle is moved a few millimeters at a time through the muscle. The activity triggered by needle movement or probing is termed insertional activity and should cease almost immediately after needle movement stops. If it persists abnormally long it is termed increased insertional activity. When the muscle is at rest, it should be electrically silent. Muscle that has been damaged or denervated will discharge spontaneously (abnormal spontaneous potentials). These potentials can be picked up by the needle electrode and have an initial downward (positive) deflection. They take the form of positive sharp waves (PSWs), which are monophasic or fibrillation potentials (fibs) that are biphasic. They fire at a regular rate of about 0.5–15 Hz and have a distinctive sound. PSWs sound like dull thuds and fibs sound like raindrops hitting a roof. If these potentials are present after needle movement ceases, they are graded on a scale of 0–4, based on their quantity. If the potentials are present in more than one area, but relatively rare and generally not more than one per screen, this is graded as +1. If they are in more areas of the muscle they are +2. In +3 PSWs or fibrillation potentials it would be difficult to find muscle without abnormal potentials. If PSWs and/or fibrillation potentials fill the screen everywhere in the muscle they are +4. While there is some subjectivity to this scale it is the most commonly used one and generally works well. Motor unit morphology and recruitment Motor unit morphology must be evaluated with minimal muscle contraction (so as to be able to visualize individual motor units). To visualize the motor units, the gain is usually set at 500–1000 microvolts per division. The motor units are assessed for duration, amplitude, and appearance, including number of phases (number of baseline crossings +1). Pathology will alter the morphology of the motor units, so it is important to distinguish normal from abnormal units. Muscle contractions get stronger in two ways: each individual motor unit fires more rapidly and/or other motor units contribute to the contraction. The pattern of increasing the firing rate of a motor unit and adding (recruiting) additional motor units is the recruitment pattern. This will be altered in disorders of the nerve or muscle.

ELECTRODIAGNOSIS

Specific disorders and their electrodiagnostic findings Carpal tunnel syndrome • Prolonged median motor and/or sensory latency (this may be either absolute latency or compared to the ulnar latency of the opposite hand) • Slowing of the sensory nerve across the carpal tunnel (generally requires a midpalm and a wrist stimulation to localize the slowing) • Abnormal spontaneous potentials may be noted in the abductor pollicis brevis muscle in severe cases. Radiculopathy • Normal sensory responses • Usually normal motor responses • Abnormal spontaneous potentials should be noted in the corresponding paraspinal muscles as well as two limb muscles supplied by the same nerve root but different peripheral nerves. Ulnar neuropathy at the elbow • Normal median studies • Slowing (or conduction block) of the ulnar motor nerve (or sensory slowing) across the elbow segment • Needle EMG abnormalities if present are in an ulnar distribution only (although forearm findings may not be present). Plexopathies • Abnormal sensory studies of the corresponding nerve (decreased amplitude) • There may be abnormal motor studies of the corresponding nerve (decreased amplitude). • Abnormal spontaneous potentials in muscles innervated by the corresponding nerve, but not other muscles or paraspinal muscles Motor neuron disease • Abnormal spontaneous potentials in muscles throughout the body (abnormalities may be focal in the early stage) • Normal sensory studies • Motor studies may demonstrate decreased amplitudes. Myopathy • Normal sensory studies • There may be decreased amplitude of the motor studies (depending on the amount of atrophy). • Needle study may reveal abnormal spontaneous potentials and shortduration, polyphasic, low-amplitude motor units. • Early recruitment (a minimal contraction may cause many motor units to fire) Neuropathy • Can be motor, sensory, or both and axonal, demyelinating, or mixed • Increased distal latencies, slowed conduction velocities, conduction block, or decreased amplitudes (depending on the type of neuropathy) • Acquired and congenital neuropathies can have different appearances.

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Depending on the type of neuropathy: • The motor fibers may be affected (motor neuropathy) • The sensory fibers may be affected (sensory neuropathy) • Both (mixed sensory motor neuropathy) It is also important to assess if the neuropathy is demyelinating (slowing of conduction velocity, conduction block, and/or prolonged distal latency), axonal (decreased amplitude), or both.

Limitations of the test The biggest limitation of the test is the electromyographer’s ability to accurately design and interpret the test. Technical factors, as well as patient tolerance, may also limit the ability to obtain an adequate test. Contraindications to the test include putting a needle into a cellulitic area, and an external pacemaker, or a demand pacemaker if there is stimulation across the area (i.e., Erb’s point). It is important to always do a thorough history and physical before proceeding with the test to guide the electromyographer on what nerves and muscles to test. Anticoagulation is not an absolute contraindication, but the risks and benefits (as well as whether the test can be delayed until anticoagulation will be discontinued) must be considered. It is important to know the physiology of the peripheral nerve and the fibers being tested so the limitations of EMG/NCS can be realized. Large myelinated fibers are primarily tested, so small fiber disorders can be missed. It can take weeks for certain abnormalities to show on EMG. A test done too early (generally the first few weeks after an injury) can be falsely negative or misleading. Radiculopathies without significant axonotmesis may be missed. A negative study may not completely rule out a diagnosis!

What to include in a report The report should include enough information to convey your findings to the referring physician. This should include a brief history and physical, description of the electrodiagnostic findings, table of the data and/or waveforms, conclusion, and possible recommendations. The conclusion should attempt to answer any specific questions that are asked in the referral.

Further reading Weiss L, Silver J, Weiss J (2004). Easy EMG. Philadelphia: Butterworth Heinemann.

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Trigger point injection Janet Travell’s The Trigger Point Manual appeared as a first edition in 1983, but the idea of the trigger point started much earlier. Described as “muscular rheumatism” or “fibrositis,” Travell used the term “trigger point” to describe taut bands of skeletal muscle that when provoked or palpated elicited a pattern of referred pain either locally or to other trigger points. Such areas are called active or primary trigger points and latent or secondary trigger points, respectively. Travell introduced myofascial pain syndrome, the hallmark of which is a pain response arising from these local areas of muscle tenderness. Theories abound as to the exact nature of a trigger point. The most recent theory postulates that small, involuntary muscle fibers are implicated. These intrafusal muscle fibers are activated by adrenaline and enter a state of sympathetic muscle spasm. The local muscle changes can in turn cause the release of mediators that augment the pain response. Once first-line treatments (i.e., manual massage along muscle lines, spray and stretch techniques, dry needling) prove ineffective, the trigger point injection (TPI) is a useful modality. Using one of myriad solutions (usually lidocaine or marcaine, although botulinum toxin is now also being used) and proper technique (including proper positioning, see Fig. 7.1), the medication is introduced into the trigger point. The needle is then withdrawn to the subcutaneous level and reinserted in several different plains, eliciting a latent twitch response (LTR) and medication is again introduced, until the LTRs cease. The muscle is then ranged fully to open the fibers back up and restore proper blood flow.

Contraindications for TPI • • • •

Anticoagulation or bleeding disorders Presence of local or systemic infection Allergy to anesthetic agents Acute muscle trauma

Figure 7.1 Trigger point injection.

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Musculoskeletal injection and aspiration This is an extensive introduction of a common procedure performed in the offices of orthopedists, physiatrists, rheumatologists, and other qualified providers. Musculoskeletal injections are performed throughout the body. Ultrasound guidance can be used in some injections for both accurately targeting the injection site and avoiding potential complications (i.e., injection into vascular, neural, or peritoneal structures). Certain injections and aspirations require special imaging (fluoroscopy) and anesthesia. These procedures are usually performed in the operating room or in fluoroscopy suites under controlled settings. These procedures usually involve the spine, hip, or pediatric patients. Other injections and aspirations may be performed more locally. Following is a brief outline of such procedures around the shoulder, knee, and hip.

Knee joint The knee joint is the largest and most accessible joint for a physician to aspirate and inject in the office setting. Arthrocentesis allows for the drainage of painful effusions, infected synovial fluid, and hemarthroses. Gross and microscopic evaluation of the aspirate is frequently necessary in differentiating the possible etiologies of fluid collections, including the crystalline arthropathies, osteoarthritis, rheumatoid arthritis, septic arthritis, occult fracture, and hemarthrosis (when an etiology is unclear). Knee effusions produce suprapatellar or peripatellar effusions and balottment of the patella on physical exam. Needle insertion is most reliably done through a superiolateral approach with the patient supine and the knee extended. A combination of corticosteroids and local anesthetics or a hyaluronate derivative is injected. Corticosteroids modulate the inflammatory response to acute injury and chronic arthritic processes. Hyaluronate derivatives affect the synovial cells and viscosity. Correct needle placement limits the amount of systemic corticosteroid absorption. Intra-articular steroid or hyaluronate derivative injections should be used in combination with other modalities including rest, NSAIDs, and disease-modifying antirheumatic drugs. Needle placement into the knee joint is contraindicated with associated osteomyelitis, bacteremia, hemarthrosis in the setting of systemic coagulation/coagulopathy, underlying prosthesis, and overlying cellulitis. Technique (see Fig. 5.4) 1. The patient is supine, with knee extended, joint palpated, and absorbent chuck placed under the knee. The knee is examined to determine the nature and extent of the effusion, identify any overlying cellulitis, and palpate bony and soft tissue landmarks. 2. Palpate the superolateral edge of the patella. Evert the patella and feel for the soft spot below the superolateral edge. With a pen, mark the site of injection and aspiration approximately 1 cm lateral and 1 cm superior to the superolateral edge.

MUSCULOSKELETAL INJECTION AND ASPIRATION

3. Prepare the skin with betadine. Setup includes the following: 20 cc syringes x2, 18 gauge 1.5' needle x1, sterile gloves, Band-Aid, ace bandage, and laboratory collection bottles (culture containers, hematology and chemistry tubes). 4. Assemble equipment and don sterile gloves. Insert the needle at the predetermined spot while everting the patella. Guide the needle into the knee joint at approximately 45* distally and medially. Pull back the plunger when 1 inch of the needle has advanced. The syringe should fill with synovial fluid. When the syringe has reached capacity, unscrew the hub (a needle holder may be necessary) and exchange the syringe for further aspiration. 5. Cleanse the area with alcohol, place a Band-Aid or sterile gauze on it, and wrap the knee with an ace bandage to prevent reaccumulation. 6. Inject aspirated material into the laboratory bottles. 7. Intra-articular hyaluronate derivatives may be injected once weekly for 3–5 weeks depending on the specific brand. If arthrocentesis is used for purely diagnostic purposes, e.g., to rule out a septic joint, empiric antibiotic treatment can safely commence while cultures are testing. Complications for intra-articular injection include local fat necrosis and skin depigmentation, accelerated joint destruction/avascular necrosis, systemic absorption, transient hyperglycemia in diabetics, and iatrogenic introduction of bacteria. Greater trochanteric bursa (see Fig. 7.2) • Located laterally over the greater trochanter of the proximal femur • Injections indicated for trochanteric bursitis related to trauma, pressure, obesity, osteoarthritis (OA), or illiotibial (IT) band irritation • The patient is positioned in the lateral decubitus position with hip and knee flexed. The injection site is the point of maximal tenderness. The area is sterilized and the needle inserted directly down to the bone and withdrawn several millimeters before injecting. Pes anserine bursa (see Fig. 7.3) • Located below the joint line of the knee between the medial collateral ligament and the sartorius, gracilis and semitendinosus tendons. • Indicated in bursitis from direct trauma or repeated friction and inflammation. Also commonly seen in elderly females with OA. • The patient is positioned supine with knee flexed. The needle is inserted perpendicular to the tibia at the point of maximal tenderness down to the tibia and withdrawn several millimeters prior to instillation of medication. Iliotibial band (see Fig. 7.4) • Extends from the lateral iliac crest to the lateral proximal tibia (Gerdy’s tubercle) • Indicated for IT band syndrome, a disorder of pain and degenerative changes as the IT band rubs over the lateral femoral condyle. This is common in runners. • The patient is positioned laterally with the knee slightly flexed. The course of the IT band is followed down to the femoral condyle. The needle is inserted at the point of maximal tenderness.

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Greater trochanteric bursa

Iliotibial band

Figure 7.2 Trochanteric bursa injection. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: ButterworthHeinemann/Elsevier, p. 91. Copyright Elsevier (2007). Reprinted with permission. Semitendinosus Gracilis Sartorius

Pes anserine bursa

Medial knee

Figure 7.3 Pes anserine bursa injection. This figure was published in Weiss LD,

Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: ButterworthHeinemann/Elsevier, p. 96. Copyright Elsevier (2007). Reprinted with permission.

MUSCULOSKELETAL INJECTION AND ASPIRATION

Vastus lateralis Biceps femoris short head Biceps femoris long head

Iliotibial band

Patella

Figure 7.4 Iliotibial band injection. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/ Elsevier, p. 81. Copyright Elsevier (2007). Reprinted with permission.

Prepatellar bursa (see Fig. 7.5) • Located between the anterior patella and subcutaneous tissue. • Indicated in cases of bursitis usually related to direct trauma, repeated microtrauma, or infection. The patella is not balottable. • The patient is positioned supine. The needle is placed directly into the fluid-filled bursa angled from the side. Glenohumeral joint (see Fig. 7.6) • The most mobile joint in the body, the glenohumeral joint consists of the proximal humeral head and the glenoid fossa of the scapula. It is stabilized by soft tissues surrounding the joint, including the rotator cuff, glenohumeral ligaments, capsule, and glenoid labrum. • Injection is indicated for osteoarthritis, adhesive capsulitis, and rheumatoid arthritis. • Injections sites include anterior, posterior, and superior. The patient is positioned sitting up with arms relaxed at the side. Bony landmarks include the humeral head, acromion, and coracoid process. The most common approach is posterior. A soft spot can be palpated 1 cm inferior and medial to the posterolateral acromion. The needle is inserted in the direction of the anterior coracoid process. Aspirate as the needle is inserted to ensure that it hasn’t penetrated a blood vessel.

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Prepatellar bursa

Figure 7.5 Prepatella bursa injection. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections. Philadelphia: ButterworthHeinemann/Elsevier, p. 98. Copyright Elsevier (2007). Reprinted with permission.

Clavicle Acromion Glenoid labrum

Glenoid cavity

Tendon of long head of biceps brachii

Coracoid process

Figure 7.6 Glenohumeral joint injection—posterior approach. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections. Philadelphia: Butterworth-Heinemann/Elsevier, p. 17. Copyright Elsevier (2007). Reprinted with permission.

MUSCULOSKELETAL INJECTION AND ASPIRATION

Acromioclavicular joint (see Fig. 7.7) • Diarthroidal joint connecting the acromion to the distal clavicle • Injection is indicated for osteoarthritis and osteolysis of the distal clavicle. • The patient is positioned supine with the arm resting at their side. • The insertion site is found by following the clavicle to its end and palpating the AC joint’s depression. The needle is inserted either superiorly or anteriorly and directed inferiorly. Subacromial space (see Fig. 7.8) • This space is composed of the supraspinatus tendon, acromion, subdeltoid bursa, and coracoacromial ligament. • Injection is indicated for impingement syndrome, subdeltoid bursitis, adhesive capsulitis, and rotator cuff tendinosis. • The patient is positioned sitting up with arms at their side. The posterior edge of the acromion is palpated. The needle is inserted posteriorly, under the inferior edge of the posterior acromion. In some cases, the needle may be walked down the bone into the space.

Scapula

Acromion Acromioclavicular joint

Coracoid process Clavicle

Figure 7.7 Acromioclavicular joint injection. This figure was published in Weiss LD,

Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: ButterworthHeinemann/Elsevier, p. 20. Copyright Elsevier (2007). Reprinted with permission.

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Acromion

Coracoid process

Subacromial bursa

Humeral head

Figure 7.8 Subacromial bursa injection. This figure was published in Weiss LD,

Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: ButterworthHeinemann/Elsevier, p. 86. Copyright Elsevier (2007). Reprinted with permission.

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Interventional spinal procedures Cervical and lumbar epidural nerve blocks These injections, involving the introduction of local anesthetics, opioids, or steroids into the cervical or lumbar spine, have utility in the management of pain of various etiologies. Injection is mainly performed in an intralaminar, paramidline approach with a loss-of-resistance technique. This technique involves traversing the supraspinous ligament, interspinous ligament, and then the ligamentum flavum, after which a “sudden loss of resistance” equates entry of the epidural space (see Figs. 7.9, 7.10, and 7.11). Indications • Cervical/lumbar radiculopathy • Postoperative pain • Pain from cervical/lumbar spondylosis1 • Post-laminectomy syndrome • Pain from vertebral compression fractures2 • Diabetic polyneuropathy • Phantom-limb pain • Chemotherapy-related neuropathy or plexopathy • Cancer pain • Low-back syndrome • Complex regional pain syndrome (CRPS) • Diagnostic neural blockade to aid in the differential workup of pain source (i.e., pelvic, back, groin, genital, lower extremity pain) • Spinal stenosis Contraindications Contraindications include local infection, anticoagulation, coagulopathy, and sepsis.3 Complications • Dural puncture is reported to have a 0.5% incidence.4 It may result in CSF loss or introduction of air (pneumocephalus), which is responsible for significant post-procedure headaches. • Unintentional intravenous needle placement via epidural veins or arteries • Epidural hematoma is usually self-limiting. In settings of anticoagulation or coagulopathy, it may cause cord compression, cauda equina syndrome, paralysis, apnea, or death. • Infection—high incidence of spread given epidural vascularity • Urinary retention, incontinence5 • Direct trauma to spinal cord and nerve roots (more common in cervical injections) 1 Pages E. Anestesia metamerica. Rev Sanid Mil Madr 11:351–385. 2 Bromage PR (1978). Identification of the epidural space. In Bromage PR (ed.). Epidural Analgesia. Philadelphia: WB Saunders, p. 178. 3 Cousins MJ, Bromage PR (1988). Epidural neural blockade. In Cousins MJ, Bridenbaugh DO (eds.). Neural Blockade. Philadelphia: JB Lippincott, pp. 340–341. 4 Bromage PR (1978). Complications and contraindications. In Bromage PR (ed.). Epidural Analgesia. Philadelphia: WB Saunders, pp. 654–711. 5 Armitage EN (1987). Lumbar and thoracic epidural. In Wildsmith JAW, Armitage EN (eds.). Principles and Practice of Regional Anesthesia. New York: Churchill Livingstone, p. 109.

INTERVENTIONAL SPINAL PROCEDURES

Figure 7.9 Epidural injection. The needle tip is placed initially through the skin and fat and advanced into the spinous ligament. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: ButterworthHeinemann/Elsevier, p. 189. Copyright Elsevier (2007). Reprinted with permission.

Dura

Ligamentum flavum

Lamina

Epidural space

Figure 7.10 Epidural injection. The needle tip is advanced to the ligamentum flavum. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/Elsevier, p. 189. Copyright Elsevier (2007). Reprinted with permission.

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Figure 7.11 Epidural injection. The needle tip penetrates the ligamentum flavum

and enters the epidural space. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/ Elsevier, p. 190. Copyright Elsevier (2007). Reprinted with permission.

Caudal epidural nerve block Although used relatively infrequently, this injection preceded its lumbar counterpart by nearly 20 years (1901) (see Fig. 7.12). Proper technique includes the patient being positioned in a lateral or prone position. The caudal space is approached through the tough sacrococcygeal ligament that covers the sacral hiatus. The needle is placed over the sacrococcygeal membrane at an angle of about 60* to the coronal plane and perpendicular to the other planes. There is usually a loss of resistance as the membrane is pierced. General indications and contraindications mimic those of the lumbar and cervical approaches where anatomically relevant. There are, however, several key indications where the caudal injection may be preferred, such as prior lumbar surgery, which can distort anatomy, making a lumbar approach difficult (i.e., fusion, hardware in place), and patients on anticoagulation or who are coagulopathic (since the epidural venous plexus usually ends at S4.) Contraindications These include infection, sepsis, pilonidal cysts, and congenital anomalies of the dural sac or its contents. Complications Dural puncture, needle misplacement, hematoma or ecchymosis, infection, and urinary retention or incontinence can be complications.

Sacroiliac joint injection (see Fig. 7.13) The sacrum supports the axial spine and in turn articulates with the iliac wings to form the left and right sacroiliac (SI) joints. Numerous ligamentous and muscle attachments contribute to the stability of this joint. Imbalance

INTERVENTIONAL SPINAL PROCEDURES

1

Sacral canal

Sacral hiatus 2

Figure 7.12 Caudal epidural injection. Note the angle of the needles. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/Elsevier, p 194. Copyright Elsevier (2007). Reprinted with permission.

Figure 7.13 Diagram of the pelvis, demonstrating needle placement in the

sacroiliac joint. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/Elsevier, p. 199. Copyright Elsevier (2007). Reprinted with permission.

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in the joint can result from repeated lifting and bending, causing shift on the anteroposterior axis. Repeated forces can cause stress on the myofascial attachments and irritation of the joint lines. The SI joint lines are innervated by L3–S1 root levels and therefore may cause radicular-type symptoms when irritated. Common areas of pain in SI joint pathologies include the ipsilateral hip and greater trochanter regions.6 When evaluating the SI joint as a pain source, one must obtain appropriate history, radiography, and tests for pathological causes of sacroiliitis (e.g., ankylosing spondylosis). A variety of provocation maneuvers exist (e.g., Faber’s, Gaenslen’s tests) to evaluate for SI joint dysfunction. Injections can be used to curtail the inflammatory process and concomitant pain. The injections are placed in the synovial portion of the joint (lower 1/3) and are usually a mixture of a fast-acting anesthetic and a longer-acting corticosteroid. Injections in this portion of the joint are usually done with fluoroscopic guidance. Injections to the upper 2/3 of the joint may help with ligamentous irritation. When done correctly, the injected medication meets little resistance once the needle has passed through the overlying ligaments. In the setting of a hypermobile joint, proliferative injections consisting of dextrose have been hypothesized to strengthen the ligamentous and muscle attachments.7

Facet joint injection (see Fig. 7.14) The cervical and lumbar facet (zygapophyseal) joints are considered significant sources of chronic neck and low back pain.8 Facet joints are diarthrodial, made up of the inferior articular process and the superior articular process of the vertebra one level below. Facet blocks are performed by first properly identifying the anatomic landmark. This involves oblique images at 10–40* from midline for best needle visualization with rotation another 5–10* for joint visualization. Using proper imaging and feel, a mixture of dye, local anesthetic, and steroid are injected. Indications When making the decision to inject the facet joint, identify those with facet syndrome and which levels are symptomatic. Classically, this has been defined by dull, aching pain with tenderness on palpation over the facet joints with occasional overlying muscle spasm and aggravation of pain with loading the facet joint (rotation and extension). Pain may be unilateral or bilateral with occasional radiation. A definitive diagnosis is made by noting pain relief after injection of local anesthetic into the facet joint. Contraindications Like other injections, these injections should be avoided in patients with medication allergies, systemic or local infection, or coagulopathies. Severe foraminal stenosis is a relative contraindication to intra-articular facet joint injections. 6 Fortin JD, Dwyer AP, West S, Pier J. (1994). Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: asymptomatic volunteers. Spine 19:1475–1482. 7 Reeves KD (1995). Technique of prolotherapy. In Lennard TA (ed.). Physiatric Procedures in Clinical Practice. Philadelphia: Hanley and Belfus, pp. 57–70. 8 Bogduk N, Aprill C (1993). On the nature of neck pain, discography, and cervical zygapophyseal joint blocks. Pain 54:213–217.

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Figure 7.14 Diagram of the lumbar spine demonstrating needle placement for intrarticular lumbar facet injections. This figure was published in Weiss LD, Silver JK, Lennard TA, Weiss JM (2007). Easy Injections, Philadelphia: Butterworth-Heinemann/ Elsevier, p. 196. Copyright Elsevier (2007). Reprinted with permission. Complications The most common complication is a transient increase in pain. Other complications include dural penetration, spinal anesthesia, capsule rupture, infection, or vertebral artery puncture (cervical facets).

Selective nerve root blocks (SNRB) Nerve root blocks are a useful tool in the workup for back pain, but they are used in a different patient subset than are facet joint blocks. The aim of nerve root blocks is to anesthetize the desired nerve root for diagnostic and therapeutic purposes. Steroids are used in an attempt to produce long-term relief, primarily in patients with radiculopathy. SNRBs can be used when physical examination and radiological/EMG findings pinpoint a specific nerve root as the cause for pain. Pressure on the nerve may result in pain. Because the venous drainage lies on the outside of the nerve, pressure on the nerve increases the venous pressure. Extrinsic forces on the nerve can lead to resultant ischemia and pain within the nerve root, and pain referred to the respective dermatome. Similar to the other injections, the SNRB involves placing a mixture of local anesthetic and steroid in the superior region of the neural foramen, where the postganglionic nerve root exits. Indications • In patients who have recurrent radiculopathic symptoms after diskectomy, but no recurrent disk herniation, symptoms may be due to scar tissue tethering the nerve. Many patients can be treated successfully with SNRB.

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• Patients with disk herniations can be helped with nerve root blocks. Since 90% of disk herniations resolve naturally over time, early pain relief may help to avoid surgery. The pain is believed to result from inflammation of the nerve root rather than direct compression of the nerve root. As a result, potent anti-inflammatories (steroid) work well in quelling the process. • The injections may be efficacious when facet joint hypertrophy or cysts cause irritation of the nerve root. Contraindications These include a history of allergy to local anesthetics or steroids, systemic or overlying infection, or coagulopathy, or, in the case of facet joint injections, severe foraminal stenosis. Injections into the facet joints can cause joint swelling, worsening a preexisting foraminal stenosis. Complications These are rare but can include bleeding, infection, and allergic reactions. Intravascular injection may result in a suboptimal or false-negative result. Furthermore, intravascular injection can be dangerous if the agents are injected into the vertebral artery or radicular branches that enter the neural foramina at various levels. Spinal cord infarcts have occurred from cervical and lumbar SNRB. Direct trauma to the nerve root can occur via the spinal needle, causing increased pain and occasional root avulsion. Spinal anesthesia may occur if local anesthetic is inadvertently injected into the nerve root sleeve. During cervical procedures, doing so can lead to respiratory arrest. Some patients experience adverse effects from the steroids. Although usually transient, these effects can include insomnia, nightmares, and nervousness. Consider the total steroid dose when performing injections at multiple levels.

Other procedures Radiofrequency ablation (RFA) RFA involves using a needle (electrode) to deliver a current in either a constant (hot) or pulsatile (cold) fashion to cause neurolysis of the nerves. RFA can be used for medial branch blocks, SI joint blocks, dorsal root ganglia bocks, cervical sympathectomy, or lumbar sympathectomy. Indications These include failed conservative treatments, transient relief from repeated injections, or contraindications for surgical intervention. Contraindications These include coagulopathy, platelet dysfunction, or severe cardiopulmonary disease for procedures involving cervical and thoracic regions.9 Complications Complications are numerous: local post-procedure soreness, sensorimotor deficits from improper needle placement, vascular trauma (cervical region), 9 Falco FJE, Kim D, Zhu J, et al. (2006). Interventional pain management procedures. In Braddom R (ed.). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: WB Saunders.

INTERVENTIONAL SPINAL PROCEDURES

pneumothorax (thoracic), entry into the subarachnoid space via neural foramen (dorsal root ganglion RF), diaphragmatic paralysis and hoarseness (from cervical sympathectomy RF), puncture of abdominal viscera (lumbar sympathectomy RF), or direct disk, cord, or nerve root trauma. Nucleoplasty Nucleoplasty is a non-heat-driven process in which coblation and RF technology are used in a conductive medium to achieve tissue removal, such as in HNP with small disk protrusions that cause pain. This procedure uses a Crawford needle and coblation/coagulation wand to create multiple channels to remove disk material, thus reducing intradiscal pressure and reducing pain. This modality has been shown to be more effective in contained disk herniations with or without radiculopathy. Studies have shown statistically significant reductions in pain.10 Complications These include infection, bleeding, nerve injury, and discitis. Vertebroplasty/kyphoplasty This minimally invasive procedure is aimed at treating the pain and spinal instability surrounding acute vertebral compression fractures from 2 weeks to 1 year old. Anecdotally, many practitioners use a 6-month age limit for compression fractures. Further indications for vertebroplasty include refractory pain from the fracture. Recent studies have questioned the efficacy of vertebroplasty.11 Absolute contraindications are discitis, sepsis, and osteomyelitis. Relative contraindications include significant spinal canal compromise secondary to bone fragments, fractures older than 2 years, >75% collapse of vertebral body, fractures above T5, traumatic compression fractures, or disruption of the posterior vertebral body wall. The focus of vertebroplasty is on treating pain, whereas that of kyphoplasty is on restoring stability and vertebral height. Vertebroplasty involves tunneling a large-gauge needle into the vertebral body and injecting 3–5 mL of methylmethacrylate cement into the vertebral body. Similarly, in kyphoplasty two balloons are introduced via catheter into the vertebral body. The inflated balloon restores height and then allows for filling with the cement. Spinal cord stimulators (SCS) Stimulation of the dorsal column of the spinal cord is used to treat patients with chronic intractable pain. Although the exact mechanism is unknown, several theories exist, including the “gate” theory and direct inhibition of pain pathways in the spinothalamic tract. The SCS can either be totally implantable or have an external transmitter. SCS placement involves an initial trial stage when the lead is placed and managed externally. This is internalized, pending satisfactory results. 10 Singh V, Piryani C, Liao K, et al. (2002). Percuatneous disc decompression, using coblation, in the treatment of discogenic pain. Pain Physician 5:250–259. 11 Buchbinder R, et al. (2009). Randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med 361(6):557–568.

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Indications These include failed neck or back surgery, peripheral neuropathy, postherpetic neuralgia, CRPS I/II, epidural fibrosis or arachnoiditis causing chronic pain, radiculopathy, and phantom limb pain.12 Most patients have had chronic pain for >12 months that is refractive to other conservative therapies. Contraindications Coagulopathy, platelet dysfunction, local or systemic infection, and patients with psychological issues (i.e., drug seeking) are contraindications. Complications These include scar formation, lead migration, and infection with hematoma, cord compression, and paraplegia occurring infrequently. Intrathecal pumps These are used in the management of chronic pain as well as spasticity. A catheter is inserted intrathecally and connected to a pump. Initially, during the trial, the pump is external. If a satisfactory result is achieved, the lead is attached permanently and the catheter is tunneled through the subcutaneous tissue to an internal pump (which usually sits in a pocket in the anterior abdomen). The pump can then be adjusted to deliver the appropriate amount of medication. Intrathecal infusion bypasses the blood–brain barrier and hence allows a more directed effect on brain and spinal neuroreceptors with less medication. Several medications are used in these pumps. The two most common ones are preservative-free morphine (for pain management) and baclofen (for spasticity management). Complications These include spinal fluid leak or collection, infection, hematoma or bleeding, seroma formation at the pocket site, catheter occlusion, catheter migration, and pump dysfunction.13

Further reading Cathelin MF (1901). Une nouvelle voie d’injection rachidenne. Methode des injection epidurales par le procede du canal sacre. C R Soc Biol Paris 53:452. Gray D, Zahid B, Warfield C (2001). Facet block and neurolysis. In Waldman S (ed.). Interventional Pain Management. Philadelphia: WB Saunders, pp. 446–479. Katz J (1994). Caudal approach—single injection technique. In Katz J (ed.). Atlas of Regional Anesthesia. Norwalk, CT: Appleton & Lange, p. 129. Simon S (2001). Sacroiliac joint injection and low back pain. In Waldman S (ed.). Interventional Pain Management. Philadelphia: WB Saunders, pp. 535–539. Solonen KA (1957). The sacroiliac joint in the light of anatomical, roentological, and clinical studies. Acta Orthop Scand 27 (Suppl):27. Waldman S (ed.) (2001). Lumbar epidural nerve block. In Waldman S (ed.). Interventional Pain Management. Philadelphia: WB Saunders, pp. 415–422. Easy injections by Weiss, Silver, Lennard and Weiss (2007) Philadelphia: Butterworth-Heinemann/ Elsevier. 12 Carter ML (2004). Spinal cord stimulation in chronic pain: a review of the evidence. Anaesth Intensive Care 32:11–21. 13 Coffey RJ, Burchiel K (2002). Inflammatory mass lesions associated with intrathecal drug infusion catheters: report and observations on 41 patients. Neurosurgery 50:78–86.

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Physical modalities Physical modalities are treatment agents used in therapy to decrease pain, decrease inflammation or swelling, increase range of motion, and improve overall function (in the form of heat, cold, water, or electric currents).

Cold Uses for cryotherapy include pain control, spasticity management, and treatment of acute trauma to decrease edema and inflammation. Precautions and contraindications are cold hypersensitivity (Raynaud’s phenomenon/disease), cold intolerance, cryopathies (such as cryoglobulinemia and paroxysmal cold hemoglobinuria), sensory impairment, open wounds, cognitive impairment, and arterial insufficiency. Application • Cold packs are usually filled with silica gel. Before applying to the body part, wrap the cold pack in several layers of towel. The cold pack is applied for about 20–30 minutes depending on the indication. • In ice massage a frozen ice cup is applied to the body part using gentle, overlapping strokes. • Vapocoolant spray, such as Fluori-Methane spray, is sprayed in parallel strokes along the direction of muscle fibers immediately before stretching the muscle. It is generally used in the treatment of trigger points in the spray and stretch technique. • Cryotherapy compression units are used for acute musculoskeletal trauma and for control of edema in some postsurgical procedures. The unit alternately pumps circulating cold water and air into a sleeve, which is applied on the extremity.

Heat Uses of heat are to decrease joint stiffness and increase soft tissue extensibility, for pain control, and for muscle relaxation. Precautions and contraindications include impaired sensation, cognitive impairment, malignancy, acute trauma or inflammation, arterial insufficiency, an open wound, bleeding disorders, and edema. Application Hot packs These are usually made of silicate gel, covered in canvas. Before applying to the body part, the hot pack is wrapped in several layers of towel. Paraffin bath This constitutes a mixture of paraffin and mineral oil at a 6:1 or 7:1 ratio. It has low thermal conductivity and can be applied as follows: • Dipping: The body part is dipped in the paraffin bath about 6–10 times, followed by wrapping of the body part in plastic or wax paper, then in a towel or mitt. • Immersion involves several dips into the paraffin, followed by immersion of the body part for about 20–30 minutes.

PHYSICAL MODALITIES

• Brushing: Several layers of paraffin are brushed on the body part, followed by wrapping of the part in plastic, then in towels. This may be applied to more proximal body parts, such as knees and elbows. Fluidotherapy The unit contains finely ground cellulose particles, which are moved by circulating heated air. The patient places the body part into the cabinet through a portal and performs active range of motion (AROM). Hydrotherapy Uses of hydrotherapy include pain control, wound care, edema control, and water exercise. Precautions and contraindications (full body immersion) include bladder and bowel incontinence, uncontrolled seizure, multiple sclerosis, skin infections, cardiac instability, and disorientation. Contrast bath consists of alternating immersion of the body part in warm and cold water. Indications are rheumatological conditions, reflex sympathetic dystrophy (CRPS I), and musculoskeletal conditions such as sprain, strain, or tendonitis. Diathermy Ultrasound Ultrasound is acoustic vibration at a frequency >20,000 cycles/second. It can be continuous ultrasound (for thermal effects to increase soft tissue temperature) or pulsed ultrasound (for nonthermal effects). Indications include musculoskeletal conditions such as contracture, sprain, strain, and bursitis, and degenerative arthritis. Precautions and contraindications are malignancy, pregnancy, thrombophlebitis, skeletal immaturity, reproductive organs, brain, heart, spine laminectomy sites, pacemaker, and eyes. Avoid in areas with methylmethacrylate cement or plastic materials. Methods of application are as follows: • Direct application: Using a coupling medium, the sound head is applied directly to the body part. • Underwater application is used for irregular surfaces such as hands. Degassed water is used. Phonophoresis This is the application of ultrasound to facilitate delivery of medication molecules (such as corticosteroid) into the tissues. Indications include bursitis, epicondylitis, fasciitis, strains, tendonitis, and tenosynovitis. Short-wave diathermy An inductive coil in the form of either a cable or drum is used. When using a capacitive applicator the body part is placed between two plates, and the current passes from one plate to the other through the patient. Precautions and contraindications include skeletal immaturity, general heat contraindications, contact lenses, metal surgical implants, pacemakers, jewelry, and metallic intrauterine devices.

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Microwave diathermy Uses include heating of superficial muscles and hastening hematoma resolution. Precautions and contraindications are skeletal immaturity, pacemaker, pregnancy, reproductive organs, brain, fluid-filled cavities, and metal implants.

Electrotherapy Uses of electrotherapy are for relief of neuropathic and musculoskeletal pain, wound healing, edema control, and muscle reeducation. Precautions and contraindications are pregnancy, malignancy, sensory impairment, arterial or venous thrombosis, cardiac pacemaker, stimulation over the carotid sinus, and thrombophlebitis. Applications • Transcutaneous electrical nerve stimulation (TENS) • Conventional: low intensity, high frequency • Acupuncture-like: high intensity, low frequency • Burst mode: high-frequency stimulation is delivered in bursts at lowfrequency intervals. • Functional electrical stimulation (FES) is used to stimulate contraction of a weak muscle during functional activity. • Iontophoresis uses direct current to facilitate transdermal delivery of ionizable medications. • Interferential stimulation uses current produced by the interference of two medium-frequency currents. This is thought to be more comfortable than other waveforms.

Spinal traction Uses of spinal traction include herniated disc, degenerative disk disease and joint stiffness or hypomobility. Contraindications are spine malignancy, infection, osteoporosis, vascular compromise, cervical instability (Marfan syndrome, rheumatoid arthritis, Down’s syndrome), cauda equina compression, hiatal hernia, and aortic aneurysm. Applications • Sustained mechanical traction • Intermittent mechanical traction • Manual traction

Further reading Cameron MH (2008). Physical Agents in Rehabilitation—From Research to Practice. Philadelphia: WB Saunders. Cuccurullo SJ (ed.) (2004). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical, pp. 553–984. Mysiw WJ, Jackson RD (2007). Electrical stimulation. In Braddom RL, (ed.). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders Elsevier, pp. 479–506. Weber DC, Hoppe KM (2007). Physical agent modalities. In Braddom RL, (ed.). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders Elsevier, pp. 459–477.

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Pain pharmacology Introduction In addition to physiatric interventions, pharmacological interventions are usually essential to manage pain in a variety of pain syndromes, including both acute and chronic pain. It is incumbent on the physiatrist to understand the mechanism of pain generation, the available medications, their mechanism of action, as well as the side effects and risks of both under- and over-prescribing.

Types of pain There are several ways to classify pain—according to its duration, location, trigger, or source. Acute pain is usually defined as lasting <3–6 months. It is protective in nature and does not leave any residual pain. Acute pain could be thought of as having a beneficial outcome to the organism, in that it helps the organism avoid the insulting agent. Chronic pain is defined as pain lasting >3–6 months. Unlike acute pain, it does not serve any useful purpose, is not helpful to the body, and is associated with numerous psychobehavorial issues. Pain can also be described by the source of pain, such as nociceptive, neuropathic, or withdrawal pain. Many pain syndromes have a combination of sources. It is important to define the source of a pain syndrome, as pharmacological interventions differ in each category and overlap in some categories. In addition to analgesic agents, adjuvants remain a mainstay of pain management. Adjuvants are not typical analgesics but have the ability to potentiate the analgesic action of other medications. The World Health Organization (WHO) recommends a ladder approach to pain management. Initially mild analgesics (e.g., acetaminophen, nonopioids, or nonopioids with adjuvants) are used, with gradually progression to opioids (see Fig. 7.15).

Preemptive analgesia Preemptive analgesia is the concept of treating a potentially painful condition before it becomes chronic. Preemptive analgesia may prevent a chronic pain syndrome. This may be accomplished by pharmacological and interventional pain management techniques. For example, studies indicate that treating a patient with preemptive analgesia will prevent or reduce the intensity of phantom pain in a patient undergoing elective amputation.1

Categories of analgesics Acetaminophen Acetaminophen is usually the drug of choice for mild pain because of its effectiveness and low side-effect profile. However, it is not a totally benign

1 Gottschalk A, Smith D (2001). New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician 63:1979–1984.

PAIN PHARMACOLOGY

Opio to se id for mod ± Novnere pain erate ± Adju-opioid vant or Pinacin persis reasin ing g Opio modeid for mil ± No rate paind to ± Ad n-opioid juvan t P a or in in per crea sisin sing g No ± An-opioid djuv ant Pai

n

Figure 7.15 World Health Organization ladder of pain. drug. Many patients don’t realize how much acetaminophen they take. Acetaminophen is commonly found in combination with prescription pain medications. In reasonable doses it remains the drug of choice for treating mild pain, especially in pregnant women. More than 4 grams of acetaminophen a day could be toxic to the liver and should be avoided. Depending on the stage of acetaminophen toxicity, symptoms may vary from gastrointestinal (GI) upset to hepatic and renal failure that progresses to multisystem damage. Anti-inflammatory drugs Anti-inflammatory drugs include a spectrum of medications from nonsteroidal anti-inflammatory drugs (NSAIDs) to steroids. They are typically prescribed in acute and chronic pain conditions. Anti-inflammatory drugs act on the peripheral and central nervous systems and have a dual mechanism of action. Their therapeutic actions are thought to stem from their ability to block the formation of certain prostaglandins through inhibition of the cyclooxygenase (COX) enzymes. In general, COX-1 catalyzes the production of several cytoprotective prostaglandins that coat the stomach lining with mucus and aid platelet aggregation, among other functions. COX-2 catalyzes the conversion of arachidonic acid into the inflammatory prostaglandins involved in three key biological functions: sensitizing skin pain receptors, elevating body

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temperature through the hypothalamus, and recruiting inflammatory cells toward injured body parts.1 Aspirin, the oldest anti-inflammatory drug, is used for mild to moderate pain. It has equal preference for both COX enzymes. At low doses, it causes irreversible platelet damage for approximately a week. Its antiplatelet properties make it a useful drug for patients with a history of cerebrovascular events, myocardial infarctions (MI), or transient ischemic attacks (TIA). However, high doses of aspirin may increase risk of bleeding, which is important to keep in mind for patients who may undergo surgical intervention. The newest generation of anti-inflammatory drugs, COX-2 inhibitors, inhibits COX-2 isoenzymes, without significant COX-1 inhibition. Formation of inflammatory prostaglandins and thromboxane is reduced, both of which play a role in the inflammatory process. By inhibiting the COX-2 enzyme cytoprotective prostaglandin production is not disturbed and the GI tract is able to retain its COX-2 enzyme activity is typically expressed during inflammation, thus COX-2 inhibitors reduce inflammation. Because of selective COX-2 inhibition and continuation of COX-1 activity, the COX-2 inhibitors may promote thrombosis. This may lead to platelet aggregation and potential cardiovascular ischemia causing MI and/or stroke. Cardiovascular toxicity with these medications includes hypertension and congestive heart failure with fluid retention. Renal dysfunction may also occur with use of COX-2 inhibitors. Anti-inflammatory-induced gastropathy can be reduced by using histamine type 2 receptor (H2) blockers. Combining these drugs with proton pump inhibitors (PPIs) is beneficial in that PPIs given with anti-inflammatory drugs help prevent and reduce gastric ulcers.2 H2 blockers do not help in healing anti-inflammatory drug–induced gastric ulcers if the patient is still on the medication. They may, however, help when the anti-inflammatory drugs have been stopped. Combining anti-inflammatory drugs with GI prophylactic agents, such as misoprostol, helps in reducing GI toxicity. However, the side effects of misoprostol should be considered. Diarrhea occurs in almost 25% of patients taking this medication. Keep in mind that misoprostol is category X in pregnancy because of its abortive effects. Renal toxicity is another potential side effect from this line of medications. Renal toxicity is limited mostly to patients who have impaired renal function, but anti-inflammatory drugs can cause renal failure, edema, and hypertension. Without the production of prostaglandins, vasodilation of the afferent arterioles of the glomeruli does not occur. The glomerular perfusion and glomerular filtration rate (GFR) are decreased, thereby causing renal dysfunction. Altered renal function manifests as fluid retention, hypertension, and, in rare cases, interstitial nephritis and acute tubular necrosis. Sulindac is an

1 Gottschalk A, Smith D (2001). New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician 63:1979–1984. 2 El-Serag, HB, Graham DY, Richardson P, Inadomi, JM (2002). Prevention of complicated ulcer disease among chronic users of non-steroidal anti-inflammatory drugs. Arch Intern Med 162:2105–2110.

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anti-inflammatory that appears to have a better renal profile than that of its counterparts. Because of reported hepatic toxicity and hematological disorders with use of many of the anti-inflammatory drugs, they are approved for only short-term use. Anti-inflammatory drugs and probably even COX-2 inhibitors have a deleterious effect on osteogenesis and may be contraindicated in patients with spinal fusion. They have been known to cause delayed healing and are usually contraindicated in the postoperative phase. It is necessary to appreciate the side effects of these medications and ensure proper patient selection. An anti-inflammatory drug should not be given to a patient who has shown sensitivity to that drug. Tramadol Tramadol is available either alone, in combination with acetaminophen, or as a long-acting formula. Its mechanism of action is on mu receptors and on the noradrenergic and serotonergic systems. It has been found to be effective against neuropathic pain because of this mechanism of action. However, it is believed that tramadol may be potentially addictive and can reduce seizure threshold. It has no anti-inflammatory components, so there is no anti-inflammatory drug–induced gastropathy (although some patients may have mild GI discomfort). Caution must be used when prescribing tramadol with SSRIs because of the potential for causing serotonin syndrome, a triad of cognitive, autonomic, and somatic dysfunction that can be life threatening.

Opioid therapy Opioid therapy is the mainstay of treating chronic malignant and nonmalignant pain. Patient selection and dosing is of utmost importance, however. For every treatment plan created on the basis of opioid medication, goals for achieving pain control should be established. It is both the patient and physician’s responsibility to pursue these goals. If opioid therapy does not help in improving the quality of life, the medications are not worthwhile and their use is invalid. Pain management also involves the use of adjuvants with opioid medications. Physicians should bear in mind that adjuvants reduce the doses of opioids necessary to achieve analgesia and can also help in reducing the possibility and severity of side effects. At one time, the pendulum swung in favor of liberal use of opioids in treating chronic nonmalignant pain. Slowly, the pendulum is swinging back to very careful and selective use of opioids for nonmalignant pain. There are many issues involved in management of these patients. Many practitioners are not well informed about the indications and contraindications of opioid use. Some of the definitions related to the use of these medications are described next. Abuse The abuse of opioids relates to use of the medication for nontherapeutic purposes or use other than the prescribed purposes. This includes using opioids to get high or diverting the medication to others. Opioid partial agonists such as buprenorphine have been found to be a mu-receptor

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agonist (without opioid effects) and are used for outpatient treatment or office-based treatment of opioid abuse. Addiction Addiction is defined here as behavioral use or misuse of the drug, which includes compulsive use, continued use in spite of harm, craving, or similar misuse. Tolerance Tolerance is defined as a physiological state caused by regular use of opioids in which the medication effects decrease over time. Tolerance is a normal phenomenon. Withdrawal A physical withdrawal syndrome occurs upon discontinuation of opioids; this by itself does not indicate addiction or misuse. The withdrawal syndrome is generally characterized by sweating, tremors, vomiting, anxiety, insomnia, and muscle pain. This syndrome can occur with opioid withdrawal even in a patient whose use of the medication was reasonable and appropriate, and may be induced by the use of an antagonist or even mixed agonist–antagonists. It has also been suggested that an N-methyl-D -aspartic acid (NMDA) receptor antagonist may be helpful in reducing tolerance to the opioids. Further research is needed in this area. Aberrant behavior The physician prescribing opioids should be very attentive to the development of aberrant behaviors. Such behavior includes use and misuse of other drugs (including prescription drugs), illicit drug use, drug diversion, selling prescriptions, doctor shopping, and forgery of prescriptions. It is the treating physician’s responsibility to watch carefully for diversion or any possible illicit drug use. In such cases, appropriate action should be taken. It is estimated that up to one-third of patients may be misusing opioids or show aberrant behavior.3 Opioid risk tool There are several means of evaluating patients at risk for opioid misuse. The Opioid Risk Tool3 is used to assess and evaluate patients who may be at high risk for opioid misuse. The patient takes a five-question survey, which helps the physician determine if the patient is at risk for developing an addiction or misuse of the medications. Personal and family history of prescription, alcohol, and illegal drug abuse is assessed. Other screening tools are also available, such as the Screening and Opioid Assessment for Patients with Pain (SOAPP). A tool for opioid misuse measurement is the Current Opioid Misuse Measure (COMM), which may also help in evaluating patients during opioid therapy. These tools can be downloaded for free from Web sites such as painedu.org.

3 Webster LR, Dave B (2007). Avoiding Opioid Abuse While Managing Pain, North Branch, MN: Sunrise River Press.

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Practice guidelines For clinical and medicolegal purposes it is important to properly document the medical rationale for using opioids. Documentation should include an appropriate history and physical, diagnostic tests, and other treatment modalities. The rationale for opioid use, as well as failure of other treatment modalities because of either unsuccessful results or presence of significant side effects should also be documented. At each follow-up visit, it is reasonable to document analgesia, activities of daily living (ADLs), adverse effects, and aberrant behavior. Such documentation will prove beneficial in avoiding any medicolegal problems related to opioid treatment. A pain contract may help a patient adhere to opioid therapy and help the physician discharge the patient if treatment guidelines are not followed or goals are not met. Every opioid treatment should have related goals. It is the patient’s and physician’s responsibility to quantify and pursue those goals. Opioid therapy should help improve quality of life. Physicians should also be very careful about treating comorbidities and consider the liberal use of adjuvants. Adjuvants and other medications can help reduce the dose of opioids and thus help reduce side effects. Random urine and blood screening during opioid therapy is useful for confirming that the patient is not diverting the medication and is not using any illicit drugs. Quantification of the medication in the urine is also suggested but is currently not the standard of care. Opioid-induced hyperalgesia In certain patients increasing the dose of opioids does not help to reduce the pain. Rather, the patient feels more pain. This sensation can progress to development of an increased sensitivity to previously innocuous stimuli. Therefore, after prolonged use, the opioids will not reduce the pain. Also known as opioid-induced abnormal pain sensitivity, it is a phenomenon associated with the long-term use of opioids. In such patients it is reasonable to reduce rather than increase the dose of opioids. It is important to keep this concept in mind for patients who have been on long-term therapy without alleviation of their pain. Analgesic rotation Although it is natural for a patient to become tolerant to medications, there is no absolute cross-tolerance between the various opioids. It is customary and reasonable to rotate different opioids in order to decrease tolerance and improve pain control. Opioid rotation should be performed by calculating the dose and reducing the drug by about 40%. Such rotation will help patients prevent rapid escalation of doses and potential side effects. Side effects Opioids have numerous side effects, and these should be considered when formulating an appropriate treatment plan. The central nervous system response to opioid use manifests as drowsiness and cognitive dysfunction. Patients experiencing cognitive dysfunction should not be allowed to operate machinery. Once they reach a

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plateau and develop tolerance to the new dose, patients with fatigue and somnolence may use stimulants such as modafinil. Opioids in a certain patient population (i.e., the elderly) may cause delirium, mostly because of an increase in the metabolic byproducts. Use of anticholinesterase drugs, particularly those used for Alzheimer disease, may help in reducing these cognitive side effects. Gastrointestinal complications include nausea, vomiting, diarrhea, constipation, and other gastropathies. Opioid antagonists have been advised for treatment of constipation that does not respond to other typical therapeutic modalities. A preemptive use of laxatives and other modalities for treating opioid-induced constipation, particularly in the older population, is reasonable. In addition to the common side effects, individual opioids may have their own side effects. For example, morphine should not be used in a patient with renal insufficiency, as it may cause pleuritis secondary to histamine release. Methadone does not cause pleuritis, as it is an NMDA receptor antagonist. However, it can cause prolongation of the QT interval and can cause sleep apnea. Methadone has a long half-life but a short analgesic life. It has been responsible for deaths because a patient may take it excessively and quickly to relieve pain. This potential situation has led to a black-label warning for methadone. In patients with adrenal insufficiency, fentanyl or methadone remains a drug of choice. Opioids have been known to reduce immunity and affect hormones in both males and females. Low testosterone levels have been noted in adult males. When considering selection and dosing of opioids, long-acting, stronger analgesics such as methadone and fentanyl should not be used in opioidnaïve patients. It is better to start with a smaller dose of a short-acting medication and then reassess the patient’s pain. When the patient has reached a stable dose on short-acting opioids, a longer-acting opioid may be used. In addition, short-acting opioids give patients a “kick” because of the rapid increase in the blood level. This does not happen with long-acting opioids, which have a more steady blood level and may provide improved analgesia with fewer side effects. Opioids do not have a ceiling effect and can be slowly titrated as need before analgesic effect. Use of an opioid antagonist or even opioid agonist–antagonist in a patient who is on opioids may result in withdrawal syndrome. Opioids are Schedule 2 drugs. However, some opioids can be Schedule 3 drugs if combined with other medications. Codeine with acetaminophen may be a Schedule 3 drug, but it can be a Schedule 5 drug when combined with cough syrups.

Antidepressants Antidepressants remain an important analgesic adjuvant. A large percentage of patients with pain also suffer from depression. Other comorbidities noted in this patient population include anxiety and panic attacks. Antidepressants can help relieve these symptoms as well.

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The tricyclic antidepressants (TCAs) TCAs were the mainstay of antidepressants and neuropathic pain management for quite some time. Doses used in pain management are usually lower than doses used for depression. TCAs have anticholinergic, antialpha-adrenergic, and antihistamine side effects. They also have a propensity toward reducing seizure thresholds. Tertiary amines include amitriptyline, imipramine, and doxepin. They produce more sedation, anticholinergic effects, and orthostatic hypotension than with the secondary amines. The anticholinergic effects, such as cognitive dysfunction, glaucoma, and urinary retention, may become a concern when treating elderly patients for ailments such as diabetes or herpes zoster. Secondary amines such as nortriptyline and desipramine do not have significant side effects. TCAs typically have antimuscarinic side effects. Patients can suffer from dry mouth, blurry vision, and urinary retention. TCA toxicity can affect the central nervous system and the cardiovascular system. Symptoms include dry mouth, nausea, vomiting, hypotension, hallucinations, and seizures. Selective serotonin reuptake inhibitors (SSRIs) SSRIs are useful drugs in pain management. These drugs are similar to TCAs but without the side effects. They have been approved by the FDA for various pain conditions. Certain SSRIs (such as paroxetine) that have nonadrenergic properties may be more useful in treating pain and anxiety than others. SSRIs have been shown to be immunomodulatory and antiinflammatory against proinflammatory cytokine processes. Other antidepressants Bupropion is a norepinephrine and dopamine reuptake inhibitor that has been used for smoking cessation. Mirtazapine is a serotonin and norepinephrine antagonist. Trazodone and nefazodone belong to a group of serotonin 2 antagonist/ reuptake inhibitors. These drugs may cause sedation. Trazodone is used for its antidepressant and hypnotic properties. Care should be taken when prescribing it in males, as it can cause priapism. If an antidepressant can be used for treatment of comorbidities, in the setting of pain, it is preferred over the use benzodiazepines.

Antiseizure medications Antiepileptics have been used for neuropathic pain for quite some time. Phenytoin and carbamazepine have been used to treat trigeminal neuralgia. Although effective, these drugs have a significant side-effect profile and require blood-level monitoring. These two facets have encouraged the replacement of the antiepileptics with other medications such a gabapentin and other next-generation antiepileptics. Gabapentin is also used for neuropathic pain and migraine headaches. It can be prescribed in large doses without a significant potential for side effects. Common side effects include peripheral edema, dizziness, and drowsiness.

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Pregabalin has been approved for treating fibromyalgia, postherpetic pain, and diabetic neuropathy. It has a similar mechanism of action to that of gabapentin. Dizziness and drowsiness are common side effects associated with pregabalin. Other relatively common side effects include diplopia, memory disturbance, dysarthria, and ataxia. Other anticonvulsants can be useful when administered appropriately. Oxcarbazepine is an analog of carbamazepine, but can cause severe hyponatremia. Valproic acid has been used for management of headaches and neuropathic pain. However, it has a significant side-effect profile: nausea, sedation, alopecia, fatigue, edema, and dizziness. It is relatively contraindicated in pregnancy because of its teratogenicity. Lamotrigine has been used off-label for treatment of peripheral neuropathy, trigeminal neuralgia, cluster headaches, migraines, and reducing neuropathic pain. It has a black-box warning because of the potential for causing Stevens–Johnson syndrome and toxic epidermal necrolysis. Topiramate, another antiepileptic, is also prescribed for neuropathic pain. It is a carbonic anhydrase inhibitor, a mechanism of action that may account for the development of renal stones with use of the medication. Zonisamide has been approved as adjunctive therapy for partial-onset seizures, as well as migraines. It has been known to cause weight loss and cause renal calculi because it also is a carbonic anhydrase inhibitor.

Membrane stabilizers Lidocaine remains the membrane stabilizer of choice. It has been used orally, as a viscous substance, in conditions like mucositis. It has also been used transdermally as a patch for various neuropathic conditions. Intravenous lidocaine followed by mexiletine has been recommended for treating neuropathic pain and pain due to complex regional pain syndrome (CRPS). If the patient responds to an IV lidocaine challenge, an equivalent dose of mexiletine can be prescribed.

Muscle relaxants Antispasticity medications have been used as adjuvants to help reduce pain. • Baclofen, which acts on GABA B receptors, remains a mainstay of this treatment. Patients should be tapered off this medication slowly; they should not stop use suddenly, to avoid withdrawal symptoms similar to those with alcohol or benzodiazepine use. • Tizanidine and dantrolene are antispasmodic drugs indicated for spasticity due to traumatic brain injury, spinal cord injury, and various neurological disorders. • Dantrolene has a potential hepatotoxic side effect. Therefore, hepatic function tests should be performed every 3 months. • Diazepam, also a good antispasticity medication, should not be used for spasm only. The patient may become dependent on the medication and depression may occur in patients with chronic pain.

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• Other muscle relaxants include cyclobenzaprine, chlorzoxazone, carisoprodol, and methocarbamol. Carisoprodol can be converted to meprobamate and has addictive potential so it should be used carefully. • Dopamine agonists such as ropinirole and pramipexole have been used for treatment of restless leg syndrome and fibromyalgia. • NMDA receptor antagonists such as memantine are helpful in reducing opioid use. They also work in the dorsal column of the spinal cord for pain modulation. While other neuromedin B (NMB) receptor antagonists are available, such as intravenous ketamine or oral dextromethorphan and amantadine, memantine is much easier to use in physiatric practice.

Headache medications Ergotamines and triptans remain the drug of choice for treating migraine headaches. They can also be used in tension headaches and cervicogenic headaches. Beta-blockers can be used as migraine prophylaxis.

Corticosteroids Corticosteroids have a wide range of use in physiatric practice. Synthetic corticosteroids can be given to the patient in various modalities—topical, oral, intravenous, or injection. They are used in the treatment of acute CRPS, joint pain and inflammation, neuropathic conditions, acute radiculopathy, epidural cord compression, acute spinal cord injury, and pain conditions such as cluster headaches. The risks and benefits associated with steroid use must be explained to all patients. Significant side effects are associated with these medications and can mimic Cushing’s disease, a dysfunctional adrenal gland resulting in the production of excess cortisol. Weight gain, deposition of fat on the abdomen and upper back, appearance of black or blue striae, diabetes, and hypertension are just a few of the potential side effects of chronic corticosteroid use. Other possible complications with use of medication include osteoporosis, muscle weakness, water and salt retention, gastrointestinal upset when taken with NSAIDs, hair thinning, and mood swings. Corticosteroids should be prescribed diligently. Cases of avascular necrosis after just one course of Medrol have significant medicolegal implications. If used for a short term, prednisone is prescribed at a moderate dose and tapered off over the course of a week. The physician’s main goal is to achieve pain control and reduce inflammation quickly. Chronic use of steroids is designated for patients with chronic inflammatory diseases such as rheumatoid arthritis. Corticosteroids should be tapered gradually. Immediate discontinuation of the medications can cause steroid withdrawal syndrome. Patients can suffer from a relapse of the pathology they were being treated for or from adrenal deficiency, since there is a removal of glucocorticoids from their system.

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Uricosuric agents and gout Acute gouty attacks are initially managed with NSAIDs and corticosteroids. Colchicine, used for acute gouty attacks, has side effects including nausea and diarrhea. Colchicine has also been used to treat acute radiculopathy and similar conditions (because of its anti-inflammatory properties). It is often used along with probenecid, which promotes uric acid excretion into the urine. Allopurinol, a xanthine oxidase inhibitor, is used to prevent, but not treat, acute gout attacks.

Other drugs Other drugs that can be used in a physiatric practice include calcitonin and bisphosphonates for the treatment of osteoporosis, osteoporosis-induced compression fractures, bone metastasis, or CRPS. Use the medications when appropriately indicated, maintain proper documentation, and carefully monitor side effects.

Summary All medications should be used for the appropriate indication, and complete documentation of the patient’s use and reaction is essential. It is vital to be aware of and monitor all patients for possible side effects, as well as interactions with other medications. For example, the use of SSRIs with tramadol can cause serotonin syndrome, which could be potentially life threatening. Neuroleptics can cause neuroleptic malignant syndrome. Drugs such as Lamictal have been known to cause Steven–Johnson syndrome with significant morbidity and mortality. Always explain the risks and benefits to the patient, and document that you did so. Encourage patients to discuss any adverse or unusual reactions they are experiencing.

Further reading Ballantyne JC, Mao J (2003). Opioid therapy for chronic pain, N Eng J Med 349;1943–1953. Fishman SM, Benzon H, Raja SN, Molloy R, Liu S (2005). Essentials of Pain Medicine and Regional Anesthesia. New York: Elsevier Churchill Livingstone. Ong CK, Lirk P, Seymour RA, Jenkins BJ (2005). The efficacy of preemptive analgesia for acute postoperative pain management: a meta analysis, Anesth Analg 100:757–773. Stovitz, MD, Johnson RJ (2003). NSAIDs and musculoskeletal injuries: what is the clinical evidence? Physician Sports Med 31:35–40.

Chapter 8

Neurological disorders Thomas Pobre Jose Mathew Lyn Weiss Jay M. Weiss Rawa Araim Kenny Chantasi Parkinson’s disease 228 Multiple sclerosis 230 Disorders of the motor unit 236 Guillain–Barré syndrome (acute inflammatory demyelinating polyneuropathy) 240 Neuropathy 242 Myopathy 248

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Parkinson’s disease General description Parkinson’s disease is a progressive neurodegenerative disorder caused by nerve cell loss in the substantia nigra pars compacta and the locus ceruleus in the midbrain. The cell loss leads to striatal dopamine depletion and ultimately to reduced thalamic excitation of the motor cortex. The cause of Parkinson’s disease is unknown. The disease generally affects the middleaged and elderly.

Clinical manifestations The cardinal features of Parkinson’s disease are tremor, bradykinesia, and rigidity. Tremor is the presenting symptom in approximately 70% of patients and usually starts unilaterally. Tremor occurs at rest and has a frequency of 3–7 Hz. Bradykinesia is a generalized slowness of voluntary movement and typically starts distally, presenting as decreased manual dexterity and shuffling gait. Gait freezing and festination develop as the disease progresses. Rigidity is an increase in resistance to passive movement and occurs in 90% of patients with Parkinson’s disease. Postural instability is commonly mentioned as a fourth feature, but is not included in any published diagnostic criteria. Other motor features of Parkinson’s disease include masked facies, hypophonia, eyelid apraxia, impaired upward gaze and convergence, micrographia, stooped posture, and short-stepped shuffling gait. Non-motor symptoms include cognitive dysfunction, psychosis, mood disorders, sleep disturbance, fatigue, autonomic dysfunction, olfactory dysfunction, pain and sensory disturbance, and dermatological findings.

Differential diagnosis Signs and symptoms of Parkinson’s disease can be prominent in other neurodegenerative disorders and in secondary Parkinsonism. Essential tremor may be confused with Parkinson’s disease. The most common neurodegenerative disorder with features of Parkinson’s is dementia with Lewy bodies. Less common are corticobasal degeneration, multiple-system atrophy, progressive supranuclear palsy, and Huntington’s disease. Secondary Parkinsonism can be due to drugs, toxins, head trauma, structural brain lesions, infections, small vessel disease, and metabolic disorders.

History Patients with early Parkinson’s disease may complain of tremor of one arm or one leg at rest. Patients often complain of clumsiness or poor coordination, particularly of fine motor activities. Difficulty in initiating voluntary movements and complaints of weakness are manifestations of bradykinesia. Falls are late findings in Parkinson’s disease.

Physical Observe for tremor of the limbs when the patient is relaxed. Distracting a patient often accentuates a mild tremor and may uncover a latent one.

PARKINSON’S DISEASE

Evaluate bradykinesia by observing the speed, amplitude, and rhythm of finger tapping, hand gripping, and hand or heel tapping. Slowing and decrease in amplitude will be observed after a few seconds in mild cases. Movement becomes uncoordinated and hesitant with disease progression. Rigidity is evaluated by performing passive range of motion. Cogwheel rigidity can be seen in Parkinson’s disease; many will have leadpipe rigidity. Rigidity and tremor begin unilaterally and involve the same side. The contralateral side is eventually involved, but the initially affected side will be more severely affected throughout the course of the disease.

Diagnostic testing The diagnosis of Parkinson’s disease is based on clinical findings of signs and symptoms associated with the disease and the exclusion of similar diagnoses. Two out of the three cardinal manifestations must be present to make the diagnosis of idiopathic Parkinson’s disease. Excellent response to dopaminergic therapy is an important feature in support of the diagnosis. Neurodiagnostic testing is not helpful most of the time. MRI of the brain is performed to rule out structural lesions.

Special considerations Features found in patients with Parkinsonism without Parkinson’s disease include fall at presentation and early in the disease, poor response to levodopa, symmetry at onset, rapid progression, lack of tremor, and dysautonomia.

Management (treatment) The treatment of Parkinson’s disease can be divided into pharmacological, nonpharmacological and surgical. Most available pharmacological treatments are symptomatic in nature. Levodopa is the most effective drug for the treatment of the akinetic symptoms of Parkinson’s disease. Levodopa is combined with carbidopa, a peripheral decarboxylase inhibitor, to block its conversion to dopamine before it crosses the blood–brain barrier, and to prevent nausea, vomiting, and orthostatic hypotension. Other drugs available for the symptomatic treatment of Parkinson’s disease include MAO B inhibitor, dopamine agonist, COMT inhibitors, anticholinergic agents, and amantadine. Neuroprotective therapy is still in the theoretical stages. Nonpharmacological therapy includes patient and family education, support group services, exercise, nutrition, and physical, occupational, and speech therapy. Surgical management such as deep brain stimulation (DBS), thalamotomy, and pallidotomy are reserved for patients with advanced Parkinson’s disease who experience motor fluctuations while on pharmacological treatment.

Further reading Albin RL (2006), Parkinson’s disease: background, diagnosis and initial management. Clin Geriatr Med 22:735–751. Aminoff MJ (2004). Parkinson’s disease and other extrapyramidal disorders. In Kasper DL, Braunweld E, Fauci AS, et al. (eds.). Harrison’s Principle of Internal Medicine. New York: McGraw-Hill, pp. 2399–2406. Tolosa E, Wenning G, Poewe W (2006). The diagnosis of Parkinson’s disease. Lancet Neurol 5:75–86.

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Multiple sclerosis General description Multiple sclerosis (MS) is the most common autoimmune inflammatory demyelinating disease of the central nervous system (CNS). Although the cause is unknown, the most widely held theory is an inflammatory autoimmune disorder of myelin that is mediated by T cells. The disease affects primarily women of northern European descent who are of childbearing age. There is an increased risk of developing MS as the latitude increases from the equator. MS is characterized pathologically by multifocal areas of demyelination with loss of oligodendrocytes and astroglial scarring. Axonal injury is increasingly recognized as a prominent pathological feature of MS.

Clinical manifestations MS can cause a variety of symptoms, including changes in sensation (hypoesthesia), muscle weakness, abnormal muscle spasms, difficulty in moving, difficulties with coordination and balance (ataxia), problems with speech (dysarthria) or swallowing (dysphagia), visual problems (nystagmus, optic neuritis, or diplopia), fatigue, acute or chronic pain syndromes, bladder and bowel difficulties, sexual dysfunction, heat sensitivity, cognitive impairment, or emotional symptomatology (mainly depression). Lhermitte’s phenomenon (feeling of electrical sensation down the spine or limbs when the neck is flexed) is considered a classic MS finding, but it can be seen in several other conditions as well. The most common initial symptoms reported are changes in sensation in the arms, legs, or face (33%); complete or partial vision loss (optic neuritis) (16%); weakness (13%); double vision (7%); unsteadiness when walking (5%); and balance problems (3%). However, many rare initial symptoms have been reported, such as aphasia or psychosis. Fifteen percent of individuals have multiple symptoms when they first seek medical attention. For some people the initial MS attack is preceded by infection, trauma, or strenuous physical effort. MS is usually categorized as follows: 1. Relapsing remitting: The patient has episodes of relapses (characterized by either full recovery or residual deficits after the episodes) but no progression between relapses; 85%–90% of cases present in this manner at the onset of the disease. However, the patient usually eventually enters a progressive phase. 2. Secondary progressive: The patient develops progressive neurological deficits. This may occur with or without relapses, remissions, and plateaus. 3. Primary progressive: The patient has progressive deficits but with occasional plateaus and minor improvements (about 10% of cases at onset). The patient does not have acute attacks and has a steady decline in function. 4. Progressive relapsing: The patient has progression of disease from the onset with acute relapses. Between the periods of disease relapses, the neurological progression continues.

MULTIPLE SCLEROSIS

Differential diagnosis The differential diagnosis of MS includes encephalomyelitis, CNS vasculitis, Lyme disease, systemic lupus erythematosus (SLE), spastic paraparesis, Behçet syndrome, sarcoidosis, Sjogren’s syndrome, vitamin B12 deficiency, Guillain–Barré syndrome, transverse myelitis, syphilis, leukodystrophies, hereditary degenerative disorders, multifocal leukoencephalopathy, radiculopathy, myelopathy, and cerebrovascular accident (CVA).

History The classic clinical picture of MS is one of multiple neurological symptoms “disseminated in space and time.” More specifically, patients manifest episodic neurological dysfunction due to inflammation in different regions of the CNS over time. Common neuro-ophthalmological symptoms include unilateral visual loss and oscillopsia due to nystagmus and diplopia. Other common neurological symptoms include sensory disturbances, motor weakness, and trigeminal neuralgia. For this reason, patients with ophthalmic symptoms consistent with a possible MS attack should be questioned about historical features that may be suggestive of MS (e.g., prior neurological deficit, prior diplopia or loss of vision, prior neuroimaging studies).

Physical examination Classic MS findings on neurological examination include the following: • Optic neuritis—acutely, 50% of patients present with retrobulbar involvement; hence, fundoscopy results are normal. “The patient sees nothing and the doctor sees nothing.” After several weeks, optic atrophy may be seen. An afferent pupillary defect may be seen in the affected eye or visual acuity may be impaired (i.e., subtle to total blindness). • The classic finding is bilateral (unilateral is much less common) internuclear ophthalmoplegia (INO), a lesion in the median longitudinal fasciculus (MLF) resulting in a weakness in adduction of the ipsilateral eye with nystagmus on abduction of the contralateral eye, an incomplete or slow abduction of the ipsilateral eye upon lateral gaze, and preservation of convergence. Regardless of the stage or classification, most authorities question the diagnosis of MS in a patient without at least one of these findings: • Spinal cord involvement • Paralysis, spasticity, and hyperreflexia are indicative of upper motor neuron dysfunction (i.e., lateral corticospinal tracts). Decreased joint position and vibration sense (i.e., dorsal columns) are common findings. • Decreased pain and temperature (i.e., lateral spinothalamic tracts) are less common. The sparing of these symptoms may be diagnostically helpful. • Corticospinal tract findings tend to correlate with bladder, bowel, and sexual dysautonomias. • Cerebellar findings include disequilibrium, truncal or limb ataxia, scanning (i.e., monotonous) speech, intention tremor, and saccadic dysmetria; all are common findings.

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• Lhermitte’s sign: Neck flexion results in an electric shock–like feeling in the torso or extremities. • Cerebral: Most commonly, altered mental status and/or personality changes, focal findings (e.g., cranial nerve defects, hemiparesis, focal seizures, autonomic dysfunction), ataxia, or dysphasia are found. Unusual findings in MS include the absence of eye findings and isolated motor, sensory, cerebellar, and cranial nerve lesions.

Diagnostic testing Clinical data alone may be sufficient for a diagnosis of MS. If an individual has suffered two separate episodes of neurological symptoms characteristic of MS, and the individual also has consistent abnormalities on physical examination, a diagnosis of MS can be made with no further testing. MRI of the brain and spine is often used to evaluate individuals with suspected MS. MRI shows areas of demyelination as bright lesions on T2-weighted images or FLAIR (fluid-attenuated inversion recovery) sequences. Gadolinium contrast is used to demonstrate active plaques on T1-weighted images. Testing of cerebrospinal fluid (CSF) can provide evidence of chronic inflammation to the CNS. The CSF is tested for oligoclonal bands, which are immunoglobulins, found in 85%–95% of people with definite MS (but also found in people with other diseases). The brain of a person with MS often responds less actively to stimulation of the optic nerve and sensory nerves. These brain responses can be examined using visual evoked potentials (VEPs) and somatosensory evoked potentials (SSEPs). Decreased activity on either test can reveal demyelination that may be otherwise asymptomatic.

Treatment Relapsing-remitting symptomatic attacks should be treated. Patients are typically given high doses of intravenous corticosteroids, such as methylprednisolone, or plasma exchange to end the attack sooner and leave fewer lasting deficits. Medications for prevention of new attacks • Interferons are medications derived from human cytokines that help regulate the immune system. • Glatiramer acetate (trade name Copaxone): A synthetic medication made of four amino acids found in myelin. This drug stimulates T cells in the body’s immune system to change from harmful, proinflammatory agents to beneficial, anti-inflammatory agents that work to reduce inflammation at lesion sites. • Mitoxantrone (trade name Novantrone) is effective but limited by cardiotoxicity. Novantrone has been approved by the FDA for secondary progressive, progressive-relapsing, and worsening relapsingremitting MS. • Natalizumab (trade name Tysabri) is effective and safe alone, but in combination with other immunotherapies can lead to progressive multifocal leukoencephalopathy.

MULTIPLE SCLEROSIS

There are no approved treatments for primary progressive MS, though several medications are being studied. Rehabilitation The goal of a rehabilitation program for MS is to restore and maintain functions essential to health and daily living in individuals who have lost these capacities through injury or illness. Most rehabilitation programs are comprehensive in nature and have several different aspects: • Physical therapy (PT) is designed to help restore, improve, and maintain useful movement or function. • Occupational therapy (OT) focuses on specific activities of daily living (ADLs) that involve primarily the arms and hands. • Frenkel’s Exercises for Ataxic Conditions: This program consists of a planned series of exercises designed to help patients compensate for the inability to tell where arms and legs are in space without looking. • Speech therapy, provided by a speech/language pathologist, is designed to help improve communication skills in people who have difficulty speaking because of weakness or incoordination of face and tongue muscles. • Cognitive retraining is designed to help people compensate for loss of memory or slowed learning ability. • Bracing may be employed to assist in ambulation. • Spasticity management may involve medications, injections, positioning and/or bracing. The clinician should remember that sometimes the patient uses the spasticity to assist in ambulation (especially to compensate for weakness). Therefore, no permanent procedures should be employed before a trial of seeing how the patient responds to the decrease in spasticity. Other medications In addition to those noted above to prevent attacks, this may include medications for spasticity, pain, and bowel or bladder management.

Special considerations • Exercise improves general conditioning. Light resistive exercises can help prevent disuse atrophy. It is important not to exercise to the point of fatigue. • Fatigue worsens with increased temperatures, stress, and activity. • Heat causes delayed impulse conduction and may lead to conduction block. Therefore, heat modalities should be avoided in patients with MS.

Complications Many complications are also signs or symptoms and physical examination findings seen in MS. Complications include muscle weakness, sensorineural hearing loss, fasciculation, pruritus, syndrome of inappropriate antidiuretic hormone secretion (SIADH), urinary incontinence, seizures, pseudobulbar palsy, Raynaud’s phenomenon, cerebellar syndrome, neurogenic bladder, paresthesias, constipation, erectile dysfunction, optic atrophy, optic neuritis, neuromyelitis optica, Horner’s syndrome, internuclear ophthalmoplegia, nystagmus, fifth cranial nerve disorder, uveitis, spastic ataxia, and speech and swallowing disorders, including increased risk for aspiration.

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Red flags Certain clinical or laboratory red flags should alert physicians to a possible diagnostic error. These include symptoms that could be explained by localized disease, the presence of steadily progressive disease, the absence of clinical remission, the absence of oculomotor, optic nerve, sensory, or bladder involvement, and normal CSF findings. However, none of these findings excludes the diagnosis of MS.

Further reading Calabresi PA (2004, Nov 14). Diagnosis and management of multiple sclerosis. www.aafp.org.

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Disorders of the motor unit General description Motor neuron diseases are a diverse group of diseases that affect the motor neurons in the brain and/or spinal cord. They may have a predominantly lower motor neuron picture as in progressive muscular atrophy (weakness and decreased muscle tone or flaccidity), or a predominantly upper motor neuron picture as in primary lateral sclerosis. Unfortunately the most common form of motor neuron disease is amyotrophic lateral sclerosis (ALS). ALS is characterized by a mixed picture with both upper and lower motor neuron findings. Most cases of ALS occur spontaneously. However it is estimated that 5%–10% of ALS cases are familial in origin. In some of these familial cases an abnormality of the superoxide dismutase protein (SOD1) has been found. In the majority of ALS cases, a specific gene has not been identified. ALS is a progressive disease of the upper and lower motor neurons that is almost always fatal, with an average survival after diagnosis of 2 years.1 Poliomyelitis is an infectious disease of the lower motor neurons disease caused by a virus. This disease has been almost eradicated in the developed world because of widely used vaccines.

History ALS typically presents as asymmetric weakness. In the early stages the diagnosis may not be apparent. Some cases present with a lower motor neuron picture, whereas others present with an upper motor neuron picture. Unfortunately, most patients with an initial presentation suggesting primary lateral sclerosis (only upper motor neuron involvement), progressive muscle atrophy (lower motor neuron involvement), or primary bulbar involvement go on to develop ALS. Those with primary lateral sclerosis or progressive muscular atrophy who do not go on to develop ALS have a longer survival and slower progression. As this is a pure motor disorder, sensory loss is not present; sensory loss suggests another disorder.

Physical examination In the early stages, weakness may be localized and it may be difficult to establish a diagnosis. As the disease progresses, the weakness is usually more generalized and includes bulbar and respiratory muscles. Atrophy and fasciculations are usually present. Hyperreflexia, coordination abnormalities, abnormal gait, and pathological reflexes may also be present. Some upper motor neuron findings may not be apparent due to muscle wasting and flaccidity; this mixed picture can vary with time. The examination usually shows clear signs of upper and lower motor neuron involvement. Sensory abnormalities are not part of the disease, but may be a result of nerve entrapment. Sialorrhea (drooling) may be due to swallowing dysfunction and facial weakness. Decreased pulmonary 1 Miller RG, Mitchell J, Lyon M, Moore D (2002). Riluzole for amyotrophic lateral sclerosis (ALS)/ motor neuron disease (MND). Cochrane Database Syst Rev 2002(2):CD001447.

DISORDERS OF THE MOTOR UNIT

function eventually leads to respiratory failure and the need for ventilatory assistance. Weight loss and fatigue are also common.

Differential diagnosis The differential diagnosis depends on whether there is an upper motor neuron, lower motor neuron, or primarily bulbar presentation. Early on in the course of the disease, ALS can present similarly to multifocal motor neuropathy, myasthenia gravis, myelopathy, paraneoplastic syndrome, multiple sclerosis, and other disorders. In addition, the upper and lower motor neuron and bulbar forms of motor neuron disease (progressive muscular atrophy, primary lateral sclerosis, and progressive bulbar atrophy) may be indistinguishable from ALS and in many cases progress to ALS. The most widely accepted diagnostic criteria for ALS are the El Escorial criteria.2 These categorize the diagnosis as suspected, possible, probable, probable with laboratory support, and definite, on the basis of the number of regions of the body affected and whether upper and/or lower motor neuron signs are present. The four regions are the bulbar (cranial nerves), cervical, thoracic, and lumbosacral regions. A definite ALS diagnosis requires upper and lower motor neuron findings in three regions. The El Escorial criteria also allow electrodiagnostic findings to be used to support the diagnosis.

Diagnostic testing Electrodiagnostic studies (EMG/NCS), spinal imaging, and laboratory tests are commonly used. These tests are used to eliminate other diagnoses and to confirm the diagnosis. On EMG testing, lower motor neuron dysfunction is seen in a diffuse distribution with normal sensory studies. In familial ALS, genetic testing is frequently helpful.

Treatment Riluzole has been approved by the FDA for use in ALS. A meta-analysis has shown an increase in survival of several months. Other more recent reports (uncontrolled trials) suggest longer increases in survival. Most treatment is symptomatic and supportive. Other medication trials are ongoing. Medications for depression are commonly used but have no effect on the disease. Medications for spasticity may enable the patient to remain ambulatory longer or assist with activities of daily living. When pulmonary function decreases sufficiently, ventilatory assistance is needed. Most patients require assistance with mobility and are frequently confined to a wheelchair. Feeding tubes may be necessary. Strengthening, flexibility, and aerobic exercise should be used to maintain mobility and prevent or delay complications. Assistive devices and braces should be used to maximize mobility and function. The team approach should include a physiatrist, neurologist, and physical, occupational, respiratory, and speech therapists as well as a psychiatrist or

2 Brooks BR, Miller RG, Swash M, Munsat TL (2001). El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord.1(5):293–299.

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psychologist and social worker. Hospice referral is frequently appropriate and helpful for both the patient and family.

Complications ALS is almost invariably fatal within several years of diagnosis. Pulmonary complications including aspiration are common. Every attempt should be made to maintain function and provide supportive care to the patient and the family.

Further reading DeLisa J, Gans BM, Walsh NE, Bockenek WL (2004). Physical Medicine and Rehabilitation, Principals and Practice, 4th ed. Philadelphia: Lippincott Williams and Wilkins, pp. 931–956. Frontera WR, Silver JK, Rizzo TD (2008). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier, pp. 705–712. Kuwabara S, Sonoo M, Komori T, et al. (2008). Dissociated small hand muscle atrophy in amyotrophic lateral sclerosis: frequency, extent, and specificity. Muscle Nerve 37:426–430. Miller R, Mitchell J, Lyon M, Moore D (2002). Riluzole for amyotrophic lateral sclerosis (ALS)/motor neuron disease (MND). Cochrane Database Syst Rev 2002;(2):CD001447 Rowland L, Brown R, Sorenson E, Shefner J, Krivickas L, Miller R (2008). Motor neuron disease. 2008 Plenary AANEM 5th Annual Meeting, V. American Association of Neuromuscular and Electrodiagnostic Medicine.

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Guillain–Barré syndrome (acute inflammatory demyelinating polyneuropathy) General description Guillain–Barré syndrome (GBS) (also known as acute inflammatory demyelinating polyneuropathy, or AIDP) is considered an immune-mediated polyneuropathy of acute onset. The proposed mechanism for GBS is an antecedent infection that evokes an immune response. This, in turn, cross-reacts with peripheral nerve components.1 This immune response can be directed toward the myelin or the axon of the peripheral nerve. The subtypes depend on the neurological structures involved (see Diagnostic testing). The diagnostic criteria for GBS are listed in Table 8.1.

Clinical manifestations The patient usually presents with acute onset of rapidly progressive symmetrical muscular weakness. Symptoms progress over a period of 2 weeks and reach their nadir at 1 month. A variant of GBS, Miller–Fisher syndrome (MFS), presents with ophthalmoplegia, ataxia, and areflexia.

Differential diagnosis Other peripheral polyneuropathies, disorders of the neuromuscular junction, spinal cord disorders, and myopathies should be considered in the differential diagnosis.

History Patients will usually complain of progressive weakness and mild sensory symptoms. The patient may also complain of low back pain. It is important Table 8.1 Diagnostic criteria for Guillain–Barré syndrome (AIDP) Required features Supportive features

• • • • • • • •

• • Nonsupportive features (question • • the diagnosis of GBS) •

Progressive weakness of more than one limb Areflexia Progression of symptoms Relative symmetry Cranial nerve involvement Mild sensory symptoms Confirmatory NCS/EMG Lumbar puncture with elevated protein and normal WBC Autonomic dysfunction Return of function within weeks Sensory level Marked asymmetry Increased WBC in CSF

1 Hahn AF (1998). The Guillain-Barré syndrome. Lancet 352(9128):635–641.

GUILLAIN–BARRÉ SYNDROME

to ask about antecedent viral infections or immunizations, as these are sometimes noted in patients with GBS. Campylobacter jejuni infection is the most commonly identified precipitant of GBS.

Physical examination The patient will usually present with a fairly symmetrical weakness with depressed deep tendon reflexes. The weakness usually starts in the legs and progresses proximally. All muscles, including facial, respiratory, and bulbar muscles, can be affected. In approximately 30% of patients, the respiratory weakness will necessitate ventilatory support. Mild sensory abnormalities are noted in about 80% of patients. Dysautonomia can occur in 70% of patients and is manifest as tachycardia, bradycardia, arrhythmia, urinary retention, hypotension, hypertension, and ileus.

Diagnostic testing Elevated protein with a normal white cell count is usually noted on lumbar puncture. Electrodiagnostic testing is useful in making the diagnosis and can help distinguish the subtypes of GBS. Testing may reveal a demyelinating peripheral polyneuropathy in AIDP. Studies will show prolonged distal latencies, slowed conduction velocity, and delayed or absent F waves and H reflexes. Generally, abnormal spontaneous potentials (denervation) are not present on needle testing. Less common variants include a motor axonal peripheral polyneuropathy (AMAN, or acute motor axonal neuropathy) which results in decreased amplitude of compound motor action potentials (CMAPs) and abnormal spontaneous potentials (denervation) on needle study. A sensory motor axonal peripheral polyneuropathy is noted in acute sensory motor axonal neuropathy (ASMAN), manifesting as decreased amplitude in sensory nerve action potentials (SNAPs) and CMAPs and abnormal spontaneous potentials (denervation) on needle study. Testing for IgG antibodies to GQ1b may be useful in diagnosis of MFS.

Special considerations Since 30% of patients develop ventilatory failure requiring mechanical ventilation, supportive care is required. Dysautonomia may also lead to severe complications, and ICU monitoring is advisable. AMAN has a poorer prognosis than AIDP, since the axons take longer to regenerate and reinnervation is not always complete.

Management (treatment) Plasmapheresis or intravenous immune globulin (IVIG) are the mainstays of treatment. Rehabilitation should be initiated as soon as possible.2

Complications and red flags The patient must be monitored for respiratory dysfunction and dysautonomia.

2 Braddo`m R (1996). Physical Medicine and Rehabilitation. Philadelphia: WB Sanders, p. 985.

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Neuropathy General description Peripheral neuropathy is a generalized dysfunction of nerves in the peripheral nervous system. There are many conditions and disorders that can cause peripheral neuropathy. Therefore, neuropathy should be considered a symptom of a disease rather than a disease itself. Different disorders can affect different types of nerve fibers and parts of the nerve.

Clinical manifestations Patients with peripheral neuropathy usually complain of numbness, pain, burning, or paresthesias in a stocking-and-glove distribution. This is because the longer the nerve, the more it is affected. The feet are usually affected before the hands. Patients may complain of tripping, weakness, or difficulty with activities that involve dexterity. Activities of daily living may be compromised.

Differential diagnosis Vascular disorders can mimic some of the symptoms of peripheral neuropathy. Spinal disorders (myelopathy, spinal stenosis) should also be ruled out. Central nervous system disorders, such as multiple sclerosis, also need to be considered. Since peripheral neuropathy is predominantly symmetrical, any asymmetrical findings should lead the clinician to consider entrapment neuropathy, plexopathy, radiculopathy, or a contralateral disorder of the brainstem, thalamus, or cerebral cortex.

History Since many causes of peripheral neuropathy are hereditary, the patient should be asked about symptoms in family members. Patients should also be asked about other factors that can lead to neuropathy, such as alcohol use, exposure to toxins, medications, and other medical conditions. Common diseases that can lead to peripheral neuropathy include diabetes mellitus, hypothyroidism, and cancer (both the cancer itself and the treatments that are employed).

Physical examination Patients may present with weakness (especially distal), numbness or diminished sensation to light touch, pinprick, temperature and vibration (distal), and/or decreased deep tendon reflexes. Atrophy or weakness may be noted, again, usually in the more distal muscles. Romberg test (unsteadiness while standing with eyes closed) may be positive, as proprioception may be affected.

Diagnostic testing Electrodiagnostic testing is frequently crucial in the evaluation and categorization of a neuropathy. Electrodiagnostic testing can determine whether the neuropathy involves predominantly sensory fibers, motor fibers, or both. In addition, testing can determine if the involvement is primarily

NEUROPATHY

axonal, demyelinating, or both are affected. Finally, it should be determined if the neuropathy is segmental or uniform. The electrodiagnostic studies may help differentiate between congenital and acquired neuropathies. Different types of neuropathies are found in different conditions, and the type of neuropathy can help the clinician determine the underlying etiology (see Table 8.2). In addition, electrodiagnostic testing can help determine the severity of the neuropathy and if other nerve entrapments are present (entrapment neuropathies are more common in patients with peripheral neuropathy).

Special considerations Patients may suffer from autonomic neuropathies, which cannot be diagnosed by conventional electrodiagnostic testing (EMG/NCS).

Management (treatment) Treatment is aimed at controlling the underlying condition causing the neuropathy. In diabetic patients, improved glucose control can improve neuronal function.1 Symptomatic treatment of pain and dysesthesia (neuropathic pain) should be initiated. Pregabalin (Lyrica), duloxetine (Cymbalta), tricyclic antidepressants, gabapentin, carbamazepine, and diphyenylhydantoin have been used to reduce the symptoms of dysesthesia in patients with neuropathy. Physical therapy may help with strength, balance, and coordination. Assistive devices may be necessary to improve gait. Occupational therapy may provide adaptive equipment to assist in activities of daily living.

Complications/red flags Sensory axonal peripheral neuropathy should raise the suspicion for paraneoplastic syndrome. Patients with distal sensory peripheral neuropathy should be seen by a podiatrist for foot care to help prevent foot complications. It is important for these patients to inspect the bottoms of their feet daily using a long-handled mirror. Custom footwear may be indicated. Any patient with impaired sensation should be cautioned against using heat or cold on the distal extremities.

Further reading Weiss L, Silver JK, Weiss J (2004). Easy EMG. Boston: Butterworth Heinemann, pp. 161–166. 1 Tron,W, Cart Q, Cantello R, et al. (1984). Peripheral nerve function and metabolic control in diabetes mellitus. Ann Neurol 16:178–183.

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EMG finding

Uniform demyelinating mixed sensorimotor polyneuropathy

Segmental demyelinating motor > sensory polyneuropathy

Axon loss Sensory axon loss motor > neuropathy sensory polyneuropathy

Axon loss mixed sensorimotor polyneuropathy

Mixed axonal loss & demyelinating sensorimotor polyneuropathy

CMAP amplitude

Normal

Decreased secondary to dispersion or conduction block

Decreased

Normal

Decreased

Decreased

Increased

Normal

Normal

Normal

Increased

Motor conduction velocity

Decreased

Decreased

Normal

Normal

Normal

Decreased

Dispersion of CMAP

No

Yes

No

No

No

No

SNAP amplitude

Normal

Normal or decreased

Decreased (usually)

Decreased

Decreased

Decreased

SNAP conduction velocity

Decreased

Decreased (somewhat)

Normal

Normal

Normal

Decreased

Motor latency Increased

Neurological disorders

Table 8.2 Polyneuropathy

No (Normal)

Yes

No (Normal)

Yes

Yes

Common diseases

1. AIDP†: Guillain– Barré syndrome (ascending proximal weakness) 2. CIDP‡ (weakness of asymmetric low extremities) 3. Osteosclerotic myeloma 4. Leprosy 5. Acute arsenic polyneuropathy 6. Pharmaceuticals (Amiodarone Perhexiline) High dose Ara-c Carcinoma, AIDS

1. Paraneoplastic motor neuronopathy (distal weakness) 2. Porphyria 3. Axonal Guillain–Barré syndrome 4. Hereditary motor sensory neuropathy types II and V 5. Lead neuropathy 6. Dapsone neuropathy

1. Paraneoplastic (sensory, painful in distal extremities) 2. Hereditary sensory neuropathy types I–IV 3. Friedreich’s ataxia 4. Spinocerebellar degeneration 5. Abetalipoproteinemia (Bassen–Kornzweig disease) 6. Primary biliary cirrhosis 7. Acute sensory neuronopathy Cis-platinum toxicity

1. Alcoholic polyneuropathy (distal symmetric weakness) 2. Vitamin (thiamine, B12) deficiency (distal symmetric weakness) 3. Gouty neuropathy 4. Metal neuropathy (mercury, thallium, gold, etc.) 5. Sarcoidosis 6. Connective tissue diseases (rheumatoid arthritis, SLE, etc.) 7. Gastrectomy gastric restriction surgery for obesity

1. Diabetic polyneuropathy (distal symmetric weakness) 2. Uremia (distal symmetric weakness)

1. Hereditary motor sensory neuropathy type I, II, VI (distal weakness with little atrophy) 2. Metachromatic leukodystrophy 3. Krabbe’s leukodystrophy 4. Adrenomyeloneuropathy 5. Congenital hypomyelinating neuropathy 6. Tangier disease 7. Cockayne’s syndrome 8. Cerebrotendinous xanthomatosis

NEUROPATHY

Needle EMG No (Normal) Would fibs* & PSWs** likely be noted?

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EMG finding

Segmental demyelinating motor > sensory polyneuropathy

Axon loss Sensory axon loss motor > neuropathy sensory polyneuropathy 8. Lymphomatous sensory neuronopathy Chronic idiopathic ataxic neuropathy 9. Sjögren’s syndrome 10. Fisher variant Guillain–Barré syndrome 11. Paraproteinemias 12. Pyridoxine toxicity 13. Amyloidosis

* fbs:fibrillation potentials ** PSWs: positive sharp waves. † AIDP: acute inflammatory demyelinating polyneuropathy ‡ CIDP: chronic inflammatory demyelinating polyneuropathy

Axon loss mixed sensorimotor polyneuropathy 8. Chronic liver disease neuropathy of chronic illness 9. Hypothyroidism 10. Myotonic dystrophy 11. AIDS 12. Lyme disease 13.Vincristine neuropathy, etc. 14. Toxic neuropathy (acrylamide, carbon disulfide, carbon monoxide)

Mixed axonal loss & demyelinating sensorimotor polyneuropathy

Neurological disorders

Uniform demyelinating mixed sensorimotor polyneuropathy

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Table 8.2 (Contd.)

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Myopathy General description The diagnosis of myopathy or muscle disease includes a wide range of disorders characterized by weakness of skeletal muscle. The pathology is primarily of the muscle tissue. Myopathies may be congenital or acquired. There are a number of different causes and courses of myopathy, ranging from acute, subacute, to chronic. They usually affect the proximal muscles groups, although distal muscles can be affected as well. Some myopathies affect cardiac muscle, leading to a cardiomyopathy.

Clinical presentation Muscle weakness can be intermittent or persistent; pain, cramps, and stiffness are common complaints. Presentations and associated findings vary depending on the type of myopathy. They are difficult to categorize because of overlaps. However, for the sake of simplicity, the main categories include muscular dystrophies, congenital, metabolic (including mitochondrial), inflammatory, endocrine-related, and drug-induced myopathies. The most common ones are listed in Table 8.3.

Diagnostic testing The diagnosis of most myopathies, including muscular dystrophies, can be confirmed by muscle biopsy, genetic testing, various blood work and markers, and electrodiagnostic testing, including nerve conduction studies and needle EMG. These tests evaluate for the presence of disease, assist in diagnosis, and evaluate progression. Muscle biopsy is frequently used to determine if the cause of muscle weakness is of neuropathic or myopathic origin. Laboratory testing includes monitoring serum creatine kinase (CK). CK is sensitive but not specific for muscle disease.

Muscular dystrophies and myotonic syndromes A number of these syndromes are associated with clinical or electrical myotonia, tonic or temporary spasms. These disorders are further divided into myotonic dystrophies and “pure” myotonia. Almost all of the muscular dystrophies are characterized by a progressive course and early onset. Muscular dystrophies have classically been categorized by their distribution of weakness, age of onset, and inheritance pattern. Advances in molecular understanding of the muscular dystrophies have defined the genetic mutation and abnormal gene product for many of these disorders. The three most common muscular dystrophies will be discussed here. Duchenne muscular dystrophy (DMD) The etiology of DMD is an absence of dystrophin, a protein that helps keep muscle cells intact. The onset of DMD is most commonly seen in early childhood, about 2–6 years of age. The symptoms generally include generalized weakness and muscle wasting first affecting the muscles of the hips, pelvic area, thighs, and shoulders. Calves are often enlarged (pseudohypertrophy). Patients classically have what is known as the Gower sign—the

MYOPATHY

Table 8.3 Myopathic disorders Muscular dystrophies (MD)

• X-linked (dystrophinopathy, i.e., Duchenne or Becker MD) • Limb-girdle • Congenital • Facioscapulohumeral • Scapuloperoneal • Distal myopathy • Emery-Dreifuss MD

Congenital myopathies

• • • • • •

Central-core disease Nemaline myopathy Myotubular myopathy Centronuclear myopathy Desmin-related myopathy Other

Metabolic myopathies

• • • •

Glycogenosis Lipid storage myopathies Mitochondrial myopathies Periodic paralysis

Inflammatory myopathies

• • • •

Polymyositis Dermatomyositis Inclusion body myositis Other (e.g., viral)

Endocrine myopathies

• • • •

Thyroid Parathyroid Adrenal, steroid Pituitary

Drug-induced/toxic myopathies

• • • •

Myotonic syndromes Myotonic dystrophy (DM type 1) Proximal myotonic myopathy (PROMM; DM 2) Chloride channel myotonia (myotonia congenita Thomsen) • Sodium channel myotonia (paramyotonia congenita Eulenburg, hyperkalemic periodic paralysis) • Schwartz–Jampel • Drug induced

patient has to use his or her hands and arms to “walk” up the body from a squatting position because of lack of hip and thigh muscle strength. The progression of DMD eventually affects all voluntary muscles, as well as the heart and muscles of respiration. Up to 90% of patients with DMD have myocardial fibrosis. Survival is rare beyond the early 30s. The mode of inheritance is X-linked recessive.

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Becker muscular dystrophy (BMD) The etiology of BMD is insufficient production of dystrophin, a protein that helps keep muscle cells intact. The onset of BMD is commonly in adolescence or adulthood. Symptoms include generalized weakness and wasting first affecting the muscles of the hips, pelvic area, thighs, and shoulders. Calves are often enlarged. BMD is similar to Duchenne muscular dystrophy but often much less severe. Cardiac muscle may also be significantly affected. BMD progresses slowly, but it can affect all voluntary muscles. Most patients with BMD survive well into their mid to late adulthood. The mode of inheritance is X-linked recessive. Women can be carriers but usually exhibit no symptoms unless they are phenotypically recessive and display the trait. Facioscapulohumeral muscular dystrophy (FSH or FSHMD) Facioscapulohumeral muscular dystrophy (FSHMD), also known as Landouzy–Dejerine, is one of the most common types of muscular dystrophy. The etiology of FSHMD is a missing piece of DNA on chromosome 4. The onset of classic FSHMD is usually by the second or third decade. Facial muscles are involved initially with inability to shut the eyes tight and smile. Shoulder and upper arm muscles are also affected; marked atrophy of the biceps and triceps with relative preservation of the deltoid is classic. Disease progression is slow with intermittent periods of rapid deterioration. The mode of inheritance is autosomal dominant, or it may occur without a family history.

Congenital myopathies Congenital myopathies are typically slowly progressive or nonprogressive and usually present in the neonatal period. They are categorized by muscle biopsy and include central core disease, nemaline myopathy, centronuclear myopathy or myotubular myopathy, and desmin-related myopathy.

Metabolic myopathies Metabolic myopathies include muscle disorders that are secondary to inherited defects that lead to intracellular energy production abnormalities. They present clinically with cramps and myoglobinuria. Patients with these symptoms often have abnormalities in the glucose/glycogen metabolism pathway, lipid metabolism disorders, mitochondrial disorders (including the aerobic or anaerobic energy production pathways), or disorders involving adenine nucleotides. Symptoms may not be present at rest but may be induced after exercise or activity. Mitochondrial myopathies may also be a result of neurological syndromes involving the central nervous system.

Inflammatory myopathies Inflammatory myopathies are usually associated with infections or an immunological process and present with inflammatory changes in the muscles. They are further subdivided into polymyositis, dermatomyositis, and inclusion body myositis. They can present acutely or subacutely, and almost always have elevated serum creatine kinase (CK) levels.

MYOPATHY

Polymyositis and dermatomyositis have unknown etiology and are considered idiopathic inflammatory myopathies. They present as chronic muscle inflammation. Other forms of idiopathic inflammatory myopathy include inclusion body myositis and myositis that is seen with cancer or with other connective tissue diseases (e.g., scleroderma, systemic lupus erythematosus, and rheumatoid arthritis). These syndromes are diagnosed by a combination of clinical, laboratory, and pathological findings after all other forms of myopathy have been excluded. Dermatomyositis presents with a characteristic rash that includes scaly erythematous palpable eruptions over the metacarpophalangeal or interphalangeal joints, knees, elbows, or medial malleoli (Gottron’s papules) and/or a periorbital purplish discoloration (heliotrope rash). Idiopathic Inflammatory myopathy treatment is aimed toward decreasing the inflammation of affected tissues, relieving symptoms, increasing strength, and rebuilding endurance. Corticosteroids are the mainstay and first line of treatment. Other immunosuppressants and immunomodulators may be useful in severe or poor prognostic groups.

Endocrine and drug-induced myopathies Myopathies secondary to endocrine disorders can be attributed to disorders of the thyroid, parathyroid, adrenal (primary or iatrogenic), and pituitary glands. Except for myxedema and uremic hyperparathyroidism, CK levels are usually normal. One of the more common endocrine myopathies is related to excess glucocorticoids leading to Cushing’s syndrome, or from exogenous use of glucocorticoids. Myopathies from drugs, toxins, and nutritional disorders are more common. Alcoholic myopathy may be acute or chronic. Acute alcoholic myopathy is most likely to present after a drinking binge and presents as weakness, especially in the legs, with edema, swelling, and tenderness. Myoglobinuria and rhabdomyolysis may also follow. Hypokalemia from sweating, vomiting, or diarrhea may be a secondary effect. Chronic alcoholic myopathy may present with proximal muscle weakness, atrophy, and elevated CK levels, resembling polymyositis. Alcoholic myopathy may be distinguished from neuropathy because the myopathy results in proximal rather than distal muscle weakness (as seen in neuropathy). Rapid recovery usually occurs when alcohol is withdrawn. Alcohol abstinence is the only cure. Several medications have been suggested to cause drug-induced myopathies. The symptoms can develop acutely or subacutely and are characterized by pain, weakness, and sometimes myoglobinuria. Some of the most common drugs associated with myopathy include steroids, diuretics, colchicine, and chloroquine. Simvastatin and many other lipid-lowering agents have been associated with myopathy. Concomitant administration with immunosuppressive drugs such as cyclosporine has led to rhabdomyolysis. Both a deficiency and an excess of vitamin E have been implicated in causing myopathies. Critical-illness myopathy usually develops in a patient in the intensive care setting and is often considered when a patient is unable to be weaned off a ventilator. The etiology of the diffuse weakness is suspected to be secondary to prolonged daily use of either (often both) high-dose intravenous

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glucocorticoids (usually methylprednisolone) or nondepolarizing neuromuscular blocking agents (e.g., vecuronium). Affected patients often have had sepsis and multiorgan failure. Laboratory values reveal moderately elevated serum CK level, and EMG shows myopathic motor units (short duration, small amplitude, polyphasic units with early recruitment) and abnormal spontaneous activity (positive sharp waves and fibrillation potentials). The diagnosis can be confirmed by muscle biopsy, showing loss of myosin thick filaments on electron microscopy. Treatment is supportive after discontinuing the offending agents. Strength recovers over a period of weeks or months, and patients can usually be weaned off the ventilator. Critical-illness myopathy must be distinguished from critical-illness neuropathy and can occasionally coexist with it. In conclusion, myopathies have specific and distinct presentation patterns dependent on the mode of acquisition or inheritance. A meticulous, careful, and detailed history is of utmost importance for proper diagnosis to guide treatment. Rehabilitation and therapy are important in maintaining range of motion and preventing contractures during active disease. Exercise probably improves strength and endurance when it is initiated in a graded manner during periods of disease control.

Further reading Compeyrot-Lacassagne S, Feldman BM (2007). Inflammatory myopathies in children. Rheum Dis Clin North Am 33(3):525–553. Di Martino SJ, Kagen LJ, (2006). Newer therapeutic approaches: inflammatory muscle disorders. Rheum Dis Clin North Am 32:121–128. Ferri FF (2007). Practical Guide to the Care of the Medical Patient, 7th ed. St. Louis: Mosby. Fink MP, Abraham E, Vincent J-L, Kochanek P (2005). Textbook of Critical Care, 5th ed. Philadelphia: Saunders–Elsevier. Frontera WR, Silver JK, Rizzo TD (2008). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier. Goetz CG (2007). Textbook of Clinical Neurology, 3rd ed. Philadelphia: Saunders–Elsevier. Goldman L, Ausiello DA, Arend W, et al. (eds.) (2007). Cecil Medicine, 23rd ed. Philadelphia: Saunders–Elsevier. Harris E, Budd R, Firestein, G, Genovese G, Sergent J (2004). Kelley’s Textbook of Rheumatology, 7th ed. Philadelphia: Saunders–Elsevier. Khan J, Harrison TB, Rich MM (2008). Mechanisms of neuromuscular dysfunction in critical illness. Crit Care Clin 24(1):165–177. Kronenberg HM, Melemd S, Polonsky KS, Larsen PR (2008). Williams Textbook of Endocrinology, 11th ed. Philadelphia: Saunders–Elsevier. Muscular Dystrophy Association. Diseases in the MDA Program, July 2007. http://www.mda.org/ disease/40list.html Noble J (2001). Textbook of Primary Care Medicine, 3rd ed. St. Louis: Mosby. Rakel RE (2007). Textbook of Family Medicine, 7th ed. Philadelphia: Saunders–Elsevier.

Chapter 9

Rheumatological disorders Thomas Pobre Libi Rind Psoriatic arthritis 254 Rheumatoid arthritis 258 Juvenile rheumatoid arthritis 262 Ankylosing spondylitis 264 Gout 268 Joint replacement 274

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Rheumatological disorders

Psoriatic arthritis General description Psoriatic arthritis is an inflammatory arthritis associated with psoriasis. Together with ankylosing spondylitis, Reiter’s syndrome, and enteropathic arthritis, they form the group called spondyloarthropathies. The group shares the common characteristics of asymmetric peripheral joint arthritis, axial involvement, and usually absent rheumatoid factor.

Clinical manifestations The usual case is a patient with psoriasis presenting with complaints of inflammatory arthritis. The small joints of the hands and feet are the most commonly affected. Dactylitis, or “sausage digit,” and enthesitis (inflammation at the site of insertion of ligaments, tendons, joint capsule, or fascia to bone) involving the plantar fascia, Achilles tendon, quadriceps, and patellar tendon insertion are common features of early psoriatic arthritis. Spinal involvement similar to that found in ankylosing spondylitis occurs later in about a third of patients with an established diagnosis.

Differential diagnosis This includes osteoarthritis, rheumatoid arthritis, gout, and ankylosing spondylitis (see Table 9.1).

History Complaints of joint pain, swelling, morning stiffness, and fatigue by a patient with psoriasis should raise the index of suspicion for psoriatic arthritis.

Physical The physical examination should focus on assessment of joint involvement and psoriatic skin lesions. Joint involvement is typically asymmetrical and distal. Extra-articular findings include nail lesions, iritis, mouth ulcers, urethritis, and heel pain.

Diagnostic testing X-ray shows characteristic asymmetric joint involvement, classic “pencilin-cup” deformity of the distal interphalangeal joint (see Fig. 9.1), acroosteolysis, fluffy periostitis, and findings of enthesopathy. Findings in the axial skeleton include asymmetric sacroiliitis, vertebral syndesmophytes, paravertebral ossification, and calcification of the interspinous and anterior ligaments. There is no specific laboratory test for psoriatic arthritis. ESR may be elevated; low-titer rheumatoid factor and antinuclear antibodies are present in some patients.

Special considerations Up to 20% of patients with psoriatic arthritis do not have psoriasis when they initially develop inflammatory arthritis. Nail lesions, including pitting, ridging, and onycholysis, are the only clinical features of skin psoriasis that are significantly associated with the development of psoriatic arthritis.

PSORIATIC ARTHRITIS

Table 9.1 Differential diagnosis of psoriatic arthritis Signs and symptoms Peripheral disease Finger joint involvement

Psoriatic arthritis Asymmetric; oligoarthritis DIP

Sacroiliitis Asymmetric Joint stiffness Morning, peripheral joints, some spine Gender bias None

Rheumatoid arthritis Symmetric; polyarthritis MCP and PIP

Osteoarthritis Ankylosing spondylitis Monoarticular − to polyarticular DIP, PIP − − Worse after activity

Symmetric Spine

None

3:1, male to female None

−

B27

Osteophytes, subchondral sclerosis, and cyst. Joint space narrowing

Squaring of vertebral bodies, symmetric syndesmophytes, spinal osteopenia

Skin lesions

Psoriasis

Enthesitis Rheumatoid factor HLA association Radiographic changes

+ −

− Morning, peripheral joints 3:1, female to male Subcutaneous nodules − +

B27, Cw6

DR4

Erosions, Erosions, marginal, paramarginal, osteopenia absence of osteopenia, pencil-in-cup, asymmetric syndesmophytes

Heberden’s node − −

Figure 9.1 X-ray of patient with psoriatic arthritis.

+ −

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Management (treatment) The initial treatment is NSAIDs for joint disease and topical therapies for skin lesions. Second-line drugs are borrowed from the treatment of rheumatoid arthritis and include gold salts, antimalarial, D -penicillamine, methotrexate, and azathioprine. These drugs are effective, but usage is limited by toxicity. Newer therapeutic agents, such as the TNF-A agonists and other biological response modifiers, offer the potential for improved efficacy. Physical and occupational therapy is beneficial in preserving joint mobility and functional independence through range-of-motion exercises, activity modification, instruction in joint preservation techniques, and use of adaptive devices.

Further reading Gladman D, Chandran V (2009). Psoriatic Arthritis (the Facts). New York: Oxford University Press Kane D, Pathare S (2005). Early psoriatic arthritis. Rheum Dis Clin North Am 31:641–657. Mease P, Bernard SG (2005). Diagnosis and treatment of psoriatic arthritis. J Am Acad Dermatol 52:1–19. Ritchlin C. (2006). Newer therapeutic approaches: spondlyloarthritis and uveitis. Rheum Dis Clin North Am 32:75–90.

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Rheumatoid arthritis General description Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disorder that primarily affects smaller peripheral joints. Although research into the area of pathogenesis has shown the most progress in the last 10 years, the etiology remains unknown. Studies show that both genetic and environmental factors are involved. RA affects all racial and ethnic groups and the prevalence is variously estimated between 0.3% and 5%. Females are affected 2 to 4 times more than males.

Clinical manifestations Symmetrical peripheral polyarthritis affecting the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints of the hands, and sparing the distal interphalangeal (DIP) joints is the most common feature of early RA. Morning stiffness occurs in all inflammatory arthropathies, but stiffness lasting more than 1 hour rarely occurs in diseases other than RA. Other joints commonly affected include the wrist, elbow, ankle, and metatarsophalangeal and PIP joints of the feet. Rheumatoid nodules occurring over the posterior elbow and other pressure locations are highly specific for RA. Extraskeletal manifestations include acute pericarditis, rheumatoid pleural disease, mononeuritis multiplex, and Sjögren and Felty’s syndromes.

Differential diagnosis Acute viral polyarthritis, arthritis of connective tissue disease and sarcoidosis may be difficult to distinguish from early RA. Other differential diagnoses include osteoarthritis, psoriatic arthritis, gout, and Lyme disease. Malignancy, chronic infection, amyloidosis, and multicentric reticulohistiocytosis can all mimic the arthritis of RA.

History Symmetrical peripheral polyarthritis involving the small joints of the hands and feet, accompanied by morning stiffness lasting for more than 1 hour, strongly suggests RA. Involvement of a single large joint such as the knee or shoulder is less common.

Physical examination Tender fusiform appearance of the fingers due to swelling of the PIP joints and associated swelling of the MCP joints are typical early physical findings of RA. Soft tissue laxity results in ulnar deviation and palmar subluxation of the proximal phalanges. Swan-neck and boutonnière deformities (see Figs. 9.2 and 9.3) are common findings late in the course of the disease.

Diagnostic testing There is no single clinical, radiological, or serological test that can be used to diagnose RA with certainty (see Box 9.1). Rheumatoid factor is positive in 70%–80% of patients with RA; the usefulness, however, is limited by

RHEUMATOID ARTHRITIS

Figure 9.2 Swan -neck deformity in rheumatoid arthritis.

Figure 9.3 Boutineér deformity in rheumatoid arthritis.

the fact that rheumatoid factor is also positive in other disease conditions such as Sjögren’s syndrome and systemic lupus erythematosus (SLE) and in 5%–10% of healthy individuals. Antibodies to citrulline-containing protein (CCP) are found in most patients with RA and less in other diseases. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are much less specific but are useful in differentiating RA from noninflammatory arthritides and can be used to assess disease activity. X-ray of the involved joints shows erosion around the margins of the joint in 15%–30% of patient in the first year of disease. MRI is more sensitive in identifying bone erosions than is plain radiography.

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Box 9.1 American Rheumatism Association revised criteria for rheumatoid arthritis classification 1. Morning stiffness in and around joints lasting at least 1 hour before maximal improvement 2. Soft tissue swelling (arthritis) of three or more joint areas observed by a physician 3. Swelling (arthritis) of the proximal interphalangeal, metacarpophalangeal, or wrist joints 4. Symmetric swelling (arthritis) 5. Rheumatoid nodules 6. Presence of rheumatoid factor 7. Radiographic erosions and/or periarticular osteopenia in hand and/ or wrist joints Criteria 1 through 4 must have been present for at least 6 weeks. Rheumatoid arthritis is defined by the presence of four or more criteria, and no further qualifications (classic, definite, or probable) or list of exclusions is required.

Management (treatment) Joint damage from active synovial inflammation ultimately leading to poor outcomes occurs early in the course of the disease. Therefore, early aggressive treatment to suppress inflammation and prevent joint damage should be initiated. Disease-modifying anti-rheumatic drugs (DMARDs) should be offered as soon as possible after disease onset. Treatment of late-stage disease, where the joint is already damaged, is focused on pain relief and maintaining function. Physical and occupational therapy goals are pain relief and preservation of joint range of motion, mobility, and function.

Complications and red flags Neck pain radiating up the occiput should raise the suspicion of cervical subluxation in a patient with RA.

Further reading Arnett FC, Edworthy SM, Bloch DA, et .al. (1988). The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 31(3):315–324. Firestein GS, Budd RC, Harris ED, McInnis IB, Ruddy S (eds.) (2008). Kelley’s Textbook of Rheumatology, 8th ed. Philadelphia: WB Saunders.

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Juvenile rheumatoid arthritis General description Juvenile rheumatoid arthritis (JRA) is a chronic, idiopathic, inflammatory disorder that affects primarily larger joints in children before the age of 16. JRA has no relationship to adult-onset rheumatoid arthritis and is usually seronegative. Many authors prefer the term juvenile idiopathic arthritis (JIA) to emphasize that there is no relationship and also to include the condition with other arthritis in childhood. JRA has classically been divided into systemiconset JRA, pauciarticular-onset JRA, and polyarticular-onset JRA.

Clinical manifestations Systemic-onset JRA is formerly called Still’s disease. Males and females are equally affected. Intermittent spiking fever and macular salmon-pink rash may precede the development of arthritis. Daily or twice-daily fever that rapidly returns to baseline is characteristic. The rash is brought out by heat and fades as temperature returns to normal. The wrist, knee, and ankles are the joints typically involved. Pauciarticular-onset JRA includes those patients with involvement of four joints or less during the first 6 months of illness. Females are affected more than males. The peak incidence is at ages 2 and 3. Joint swelling, pain, and limping are the usual presenting signs and symptoms. Systemic findings other than uveitis are absent. The large joints (knee, ankle, elbow, and wrist) are typically involved. Polyarticular-onset JRA includes those patients with involvement of five or more joints during the first 6 months of illness. Females are affected more than males. The peak incidence is at ages 2 to 5 and between 10 and 14 years. In younger children the arthritis begins in one to two large joints, and has an indolent progressive course with apparent response to therapy and followed by relapse. Symmetrical joint involvement is usual. The older children usually have a rapid onset of involvement of multiple small joints of the hands and feet.

Differential diagnosis JRA must be distinguished from a variety of illnesses that present with arthritis in childhood. Children with arthritis involving the hips and enthesopathic symptoms have spondyloarthropathy and not pauciarticular-onset JRA. Serum sickness, viral infection, other forms of reactive arthritis, SLE, and systemic vasculitis may present with polyarticular-onset arthritis. Postinfectious and reactive arthritis may be associated with fever and rash that mimic systemic-onset JRA. Malignancies such as leukemia and lymphoma should also be ruled out.

History Patients with pauciarticular-onset JRA may be noted to limp without complaint; medical attention is often sought because of knee swelling. Younger children with polyarticular-onset JRA usually begin with symptoms similar to those of the pauciarticular-onset subtype. Older children have rapid onset of symptoms in multiple joints.

JUVENILE RHEUMATOID ARTHRITIS

Children with systemic-onset JRA often appear quite ill, with high fever and rashes at the onset. The correct diagnosis is often entertained after no response to antibiotic treatment.

Physical examination The involved joint is typically swollen and tender to palpation. The joint may be warm, but not erythematous. In systemic-onset JRA, daily or twicedaily spiking fever with rapid return to normal is characteristic. Macular salmon-pink rash (found in the axilla and around the waist) may be found anywhere in the body. The rash is most prominent when the child is febrile and it fades as the temperature returns to normal.

Diagnostic testing There is no specific diagnostic test for JRA. Rheumatoid factor is typically negative, save for a subset of polyarticular-onset JRA in older children. ANA is frequently positive in pauciarticular-onset JRA and is associated with an increased risk of iridocyclitis. Elevated ESR, leukocytosis, and anemia are marked in systemic-onset JRA.

Management (treatment) Pauciarticular-onset JRA usually responds to NSAIDs or selective COX-2 inhibitors. Intra-articular steroid injection has been shown to be of benefit and should be used more aggressively. It is rare for the first line of treatment, i.e., NSAID or COX-2 inhibitors, to control the inflammatory process of polyarticular JRA. The use of second-line drugs, referred to as disease-modifying antirheumatic drugs (DMARDs), should not be excessively delayed. Systemic corticosteroids should be used judiciously because of their side effects. Physical therapy goals are pain relief, preservation of joint range of motion, mobility, and function.

Complications and red flags Cataract and synechiae are complications of uveitis that occur more commonly with pauciarticular JRA. Macrophage activation syndrome (MAS), a life-threatening complication of systemic JRA, may occur with initiation of therapy. All NSAIDs and other anti-rheumatic medications, except corticosteroid and cyclosporine, should be held with MAS. Growth retardation, leg-length discrepancy, and osteoporosis are other complications.

Further reading Casssidy JT (2004). Juvenile rheumatoid arthritis. In Harris E, Budd R, Firestein, G, Genovese G, Sergent J (eds.) Kelley’sTextbook of Rheumatology, 7th ed, Philadelphia: WB Saunders. Criteria for the classification of juvenile rheumatoid arthritis. Bull Rheum Dis 1972; 23:712–715. Padeh S, Passwell JH (1998). Intraarticular corticosteroid injection in the management of children with chronic arthritis. Arthritis Rheum 41:1210–1214. Petty RE, Southwood TR, Baum J, et al. (1998). Revision of the proposed classification criteria for juvenile idiopathic arthritis: Durban, 1997. J Rheumatol 25:1991–1994. Prieur AM, Stephan JL (1994). Macrophage activation syndrome in rheumatic diseases in children. Rev Rheum Engl Ed 61:385. Wallace CA, Levinson JE (1991). Juvenile rheumatoid arthritis: outcome and treatment for the 1990s. Rheum Dis Clin North Am 17:891–905.

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Ankylosing spondylitis General description Ankylosing spondylitis (AS) is a chronic inflammatory disease that affects mainly the axial skeleton. The primary pathology is enthesitis (inflammation at the site of insertion of ligaments, tendons, joint capsule, or fascia to bone). Together with psoriatic arthritis, Reiter’s syndrome, and enteropathic arthritis, these conditions form the group of interrelated conditions called the spondyloarthropathies. There is strong association with the genetic marker HLA-B27, but the etiology is still unknown. The estimated prevalence rate ranges from 67.7 to 197 per 100,000 among whites and is rare in blacks. The diagnostic criteria for AS are noted in Box 9.2.

Clinical manifestations Deep, diffuse, achy back pain, insidious pain over the sacroiliac joints, morning stiffness, and relief of pain with physical activity are the usual presenting complaints. Chest pain accentuated with coughing and sneezing develops with the involvement of the costovertebral and costotransverse joints. Tenderness over entheses and girdle-joint involvement are not uncommon presenting symptoms. Fatigue, weight loss, and low-grade fever are common. Extraskeletal manifestations include acute uveitis, ascending aortitis, aortic valve insufficiency, conduction abnormalities, cardiomegaly, and fibrosis of the upper lobes of the lungs.

Differential diagnosis The differential diagnosis includes all causes of noninflammatory low back pain (lumbar strain, sacroiliac dysfunction, spondylosis, and spondylolysis), other spondyloarthropathies, and degenerative arthritides (see Table 9.1).

Box 9.2 Modified NY criteria for diagnosis of ankylosing spondylitis (1984) 1. Low back pain of at least 3 months duration improved by exercise and not relieved by rest 2. Limitation of lumbar spine in sagittal and frontal plane 3. Chest expansion decreased relative to normal values for age and sex 4. Bilateral sacroiliitis grade 2* 5. Unilateral sacroiliitis grade 3–4* Definite ankylosing spondylitis: • Unilateral grade 3 or 4 sacroiliitis and any clinical criterion • Bilateral grade 2 sacroiliitis and any clinical criterion * Grading of sacroiliitis: Grade 0 – Normal 1 – Suspicious 2 – Minimal sacroiliitis 3 – Moderate sacroiliitis 4 – Ankylosis

ANKYLOSING SPONDYLITIS

History The patient is an older adolescent or young adult with a complaint of back pain and the above-described inflammatory features. The disease is rare after the age of 40. A positive family history of AS increases the probability of the disease.

Physical examination Decreased lumbar spine mobility (positive modified Schober’s test) and decreased chest expansion are early signs of the disease. Tenderness may be elicited with palpation of the sacroiliac joints and involved entheses (ischial tuberosities, greater trochanters, spinous processes, costochondral junctions, iliac crests, achilles insertion, and plantar fascia). Schober’s test In a positive modified Schober’s test, the position of the fifth lumbar spinous process is marked with the patient standing upright. Additional marks are made 10 cm above and 5 cm below in the midline. With the patient bending forward, the distance between the upper and lower marks is measured. Normal individuals should have an increase of at least 5 cm between the lower and upper marks compared to when the patient was standing upright. Chest expansion Chest expansion (measured at the fourth intercostal space or just below the breast with the arms elevated over the head), as measured with maximal inspiration and maximal expiration, should be at least 2.5 cm.

Diagnostic testing The diagnosis is usually established by radiographic findings of bilateral sacroiliitis (see Fig. 9.4). Late radiographic findings include squaring of vertebral bodies and symmetric syndesmophytes (see Figs. 9.5 and 9.6). Tests for rheumatoid factor and ANA are negative. The diagnosis can be made without the HLA-B27 test.

Special considerations The course of AS is highly variable. It is generally mild and self-limited. Most patients can maintain good functional capacity and ability to work.

Management (treatment) The goals of treatment are to relieve pain, stiffness, and fatigue, to maintain good posture, and maintain good physical and psychosocial functioning. Treatments include NSAIDs, sulfasalazine, physical therapy, surgery, and topical corticosteroid for uveitis. Newer therapeutic agents, such as the TNF-A agonists and other biological response modifiers, have proven effective.

Complications and red flags The clinician should be alert to neurological complications that can occur with fractures, instability, compression, or inflammation.

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Figure 9.4 X-ray findings in ankylosing spondylitis. Note bilateral sacroiliitis.

Figure 9.5 Squaring of cervical vertebral bodies in ankylosing spondylitis.

ANKYLOSING SPONDYLITIS

Figure 9.6 Syndesmophytes in ankylosing spondylitis.

Further reading Ritchlin C (2006). Newer therapeutic approaches: spondlyloarthritis and uveitis. Rheum Dis Clin North Am 32:75–90, van der Linder S, Valkenburg HA, Cats A (1984). Evaluation of diagnostic criteria for ankylosing spondylitis: a proposal for modification of the New York criteria. Arthritis Rheum 27:361–368.

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Gout General description Gout is an inflammatory monoarticular arthritis caused by crystallization of monosodium urate in the joint spaces. It typically develops after 20–30 years of hyperuricemia and is often precipitated by sudden changes in serum urate levels. Ninety percent of cases are seen in men 30–60 years old. It is very rare in women and is almost never seen before menopause. Hyperuricemia is a hallmark feature of gout, but alone it is not enough to make a diagnosis, as most people with hyperuricemia never develop gout. Under-excretion of uric acid is responsible for 90% of cases of gouty arthritis. Common causes include chronic renal insufficiency, lead nephropathy, alcohol, diabetic ketoacidosis, and drugs (thiazide diuretics, nicotinic acid, and cyclosporine). Overproduction of uric acid is responsible for only 10% of cases. Causes include genetic factors (inborn errors of metabolism) or acquired (alcohol, hemolysis, neoplasm, psoriasis, sickle cell anemia). Factors predisposing to a gouty attack include intake of foods high in purines (cheese, meat), trauma, operation (most common on postoperative day 3), major medical illnesses, myocardial infarction, cerebrovascular events, fasting, alcohol, infection, and idiopathic causes.

Clinical manifestations There are three classic stages of the progression of gout. Acute gouty arthritis • It usually begins with sudden onset of excruciating pain, often waking the patient at night. • Initial presentation usually involves one joint, mostly the distal joints of the lower extremity. The metatarsophalangeal joint of the great toe is initially involved in 50% of patients. Other common sites are instep of the foot, ankle, knee, wrist, fingers, elbow, and olecranon bursa. • Rapid swelling, heat, redness, and exquisite tenderness are typical, and overlying skin may become tense, warm, shiny, and red or purplish. • Maximal intensity of pain occurs in the first 24 hours. • The first few attacks usually affect a single joint and typically resolve in a few days, but later attacks may affect several joints and last for up to 3 weeks if left untreated. Intercritical gout • Once the initial attack resolves, the patient enters the intercritical phase, which is often asymptomatic. • 75% of untreated patients will have a second attack within 2 years. • Periods between attacks tend to become shorter and attacks become more severe, prolonged, and polyarticular and may include fever. • Polyarticular flares can be migratory or involve a cluster of joints. • Tendons and bursa may also become involved. • Eventually the patient can develop tophi, which can be debilitating and cause deformities. • If left untreated, bony erosions and deformities develop, marking the end of the intercritical period.

GOUT

Chronic tophaceous gout • This occurs in patients with poorly controlled gout for 10–20 years. • It is characterized by areas of solid urate crystals surrounded by giant cells in connective tissues. • Clinically they are visible and/or palpable though typically non-tender. • Acute inflammation mimicking gouty arthritis may occur. • When the inflammation extends beyond a single joint, there is generalized enlargement of the digit similar to that seen in other disorders such as psoriatic arthritis and sarcoidosis.

Differential diagnosis Differential diagnosis of gout includes rheumatoid arthritis, osteoarthris, and septic arthritis, as well as pseudogout, soft tissue ankle injury, bursitis, cellulitis, joint dislocation, fracture, osteomyelitis, reactive arthritis, tenosynovitis, rheumatic fever, and Lyme disease6 (see Table 9.2).

Clinical presentation The patient will present with sudden onset of swelling in one joint, usually in the distal extremity. The joint will be inflamed (maximal inflammation occurring in the first 24 hours), red, warm, and exquisitely tender to even the slightest touch. Clinical diagnosis is made by presence of a triad of monoarticular arthritis, hyperuricemia, and positive response to colchicines, and confirmed by examination of synovial fluid.

Diagnostic testing Clinical suspicion of gout should be confirmed with needle aspiration of the affected joint fluid. Aspiration is best done during an acute attack, although even asymptomatic patients will show some crystals in previously affected joints. Aspirate will be sterile, containing inflammatory cells (typically between 5000 and 75,000/mm3 polymorphonuclear leukocytes [PMNs]) and crystals. Examination using polarized microscopy shows needle-shaped, negatively birefringent crystals. In chronic tophaceous gout with significant joint deformation, X-ray shows classic “rat-bite” deformity described as punched-out erosions with overhanging rim of cortical bone.

Other important points • Up to 20% of patients with acute gout will have normal uric acid levels at the time of diagnosis. • In elderly women with Heberden’s and Bouchard nodes who are taking thiazide diuretics, there have been many reported cases of superimposed gout. • A septic joint may trigger an attack of gout in people who are predisposed, so it is imperative to always Gram stain and culture the fluid in addition to looking for crystals. • 10% of patients with acute gout and 30% of patients with tophaceous gout will have a positive rheumatoid factor (RF).

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Table 9.2 Differentiating gout from other arthridities Gouty arthritis

Osteoarthritis Rheumatoid arthritis

Septic (nongonnococcal) arthritis

Onset

Sudden

Insidious

Sudden

Common locations

Great toe, ankles, knee, elbows

Weight-bearing Hands (PIP, joints (knees, MCP), knee, wrists, ankles hips, lumbar, hands)

Presence of inflammation

Yes

No

Insidious

Hip, knee, ankle, wrist

Yes

Yes

Radiographic Punched-out Narrowed joint space, erosions, changes or complications overhanging osteophytes rim of cortical bone

Narrow joint space, bony erosions

Rapid destruction of joint and other tissues if left untreated

Lab findings

None Crystals in joint, elevated PMNs

Elevated ESR, +RF, anemia

Leukocytosis, elevated ESR

Other features

Bouchard and May show systemic signs Heberden’s such as fever nodes or malaise, limited range of motion

Symmetrical, inflammatory polyarthritis, ulnar deviation, boutonniére deformity

Fever, malaise, hot or swollen joint, very limited range of motion

Aggravating and alleviating factors

Aggravated by weight bearing and early ambulation, improves with rest and NSAIDs

Worse in the morning, improves as day progresses

Aggravated by active or passive joint movement, improves with prompt antibiotic therapy and/or drainage

Aggravated by movement in weight bearing, alleviated by rest

Management NSAIDs • NSAIDs are the initial treatment of choice in an acute attack. • They are very effective in relieving pain, especially if started early; delay may decrease efficacy. Indomethacin is traditionally used, but others may be used as well. • Relative contraindications include congestive heart failure, active peptic ulcer disease, or renal insufficiency.

GOUT

• Do not use aspirin because it increases uric acid levels and may worsen the condition. Colchicine • This is an alternative for patients who cannot take NSAIDs or who do not respond to NSAIDs. • It is not the preferred choice because up to 80% of patients taking colchicine develop severe GI symptoms (nausea, vomiting, stomach cramps). • It is contraindicated in renal insufficiency and cytopenia. Corticosteroids • If NSAIDs or colchicines cannot be used or tolerated, a 7- to 10-day course of oral prednisone may be used. • Intra-articular steroid injections (if only one joint is involved) can provide dramatic relief of symptoms. • Do not administer allopurinol or probenecid during an acute attack as it may worsen the symptoms.

Prophylaxis Prophylactic treatment should not be started until the patient has had at least two attacks (within a year), as some patients do not have a second attack for years. If the patient requires long-term prophylaxis, a uricosuric or allopurinol will be used depending on whether uric acid is being overproduced or under-excreted, based on urine 24-hour uric acid excretion. Uricosurics (probenecid and sulfinpyrazone) are used for under-excreters. Allopurinol is used for overproducers.

Rehabilitation During an acute attack, use relaxation exercises to minimize pain and muscle guarding. Heat and cold may be used, ultrasound therapy or laser therapy as tolerated. Once an acute attack has resolved, the goal of therapy should be to minimize joint stiffness and maintain range of motion. Passive or active assist range of motion within limits of the pain. Gentle joint mobilization with traction may also be useful. The ultimate goal is to minimize muscle atrophy, prevent deformity, and maintain joint structure.

Complications Uric acid nephrolithiasis is more common in gout patients with reduced urine volume, increased uric acid excretion, and low urine pH. Chronic urate nephropathy resulting from sodium urate crystals deposition is currently uncommon.

Pseudogout (calcium pyrophosphate deposition disease) • Clinically presents very similarly to gout. • Calcium pyrophosphate crystals deposit in joints, causing inflammation. • It is commonly seen in elderly patients with degenerative joint disease, as crystal deposition is increased in the joints of these patients. • It most commonly affects only one joint, although it can affect several. Knees and wrists are most commonly affected.

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Diagnosis is confirmed by presence of weakly positive birefringent, rhomboidshaped crystals in synovial fluid. Imaging shows calcification of cartilage (chondrocalcinosis). Treatment is similar to that for gout (NSAIDs, colchicine, steroid injections). • Treat the underlying cause if one is present.

Further reading Ayala C, Spellberg B (2007). Boards and Wards. Baltimore: Lippincott Williams and Wilkins, pp. 61–63. Agabegi S (2008). Step up to Medicine. Cincinnati: Lippincott Williams and Wilkins, pp. 248–251. Beers M (2006). The Merck Manual. Hoboken, NJ: Wiley. Cohen M (2002). Mayo Clinic Internal Medicine Board Review. New York: Lippincott Williams and Wilkins, pp. 994–999. Kisner C (1990). Therapeutic Exercise Foundations and Techniques. Philadelphia: FA Davis, pp. 227–229.

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Joint replacement General description Joint replacement is an elective procedure whereby diseased articular surfaces are resected and replaced with metal and polyethylene prosthetic component. Total knee and total hip arthroplasty are the two most commonly performed orthopedic procedures at this time. It is estimated that more than 300,000 total knee and 150,000 total hip arthroplasties are performed in the United States annually. Shoulder and other smaller joint replacement are done with lesser frequency.

Indications The main indication for both hip and knee arthroplasty is relief of pain associated with joint disease that has failed conservative and prior surgical procedures. These conditions include degenerative, inflammatory, and post-traumatic arthritides, avascular necrosis, and late effects of developmental deformities. Correction of deformity and restoration of function should be considered secondary outcomes of the procedure.

Contraindications Active infection, local or systemic, is an absolute contraindication for joint replacement. Other contraindications include skeletal immaturity, existing significant medical problems, neurological disorders affecting the extremities such as paraplegia, and irreversible muscle weakness around the joint. Absent extensor mechanism and poor extremity circulation are contraindications for total knee arthroplasty. Relative contraindications include neuropathic (Charcot) joint, progressive neurological loss and morbid obesity. Age by itself is not a contraindication to joint replacement. However, longevity of the prosthesis and the activity level of the individual should be taken into consideration.

Preoperative management The physiatrist plays an important role in the identification of appropriate candidates for joint replacement. Conservative treatment that includes weight reduction, physical therapy, NSAIDs, COX-2 inhibitors, orthosis, and use of assistive devices should be tried and shown to fail before surgery is recommended. Patients should have a preoperative therapy session to provide instructions on how to transfer, use of assistive devices, stair negotiation, and hip precautions (in the case of total hip replacement).

Surgical considerations There are a large number of prosthesis designs and manufacturers for both total hip and total knee replacement. The multitude of choices reflects different philosophies regarding the type of fixation, design features, and materials. Of interest to the physiatrist is the type of fixation used and the surgical approach (in the case of total hip replacement). Fixation of prosthetic component to the bone is achieved either with the use of bone cement

JOINT REPLACEMENT

(polymethylmethacrylate) or through bony in-growth to a porous implant surface. The type of fixation generally determines the weight-bearing status of the limb postoperatively. Most of the total hip arthroplasties today are performed through a posterolateral or a direct lateral approach. The hip joint is entered and the femoral head dislocated posteriorly with the posterolateral approach. In the direct lateral approach, the joint is entered and the femoral head dislocated anteriorly. Although other factors such as prior hip surgery and implant position influence joint stability postoperatively, hip dislocation occurs more frequently with the posterolateral approach (hence the need for hip precautions).

Complications Intraoperative complications such as fracture, nerve injury, vascular injury, and cement-related hypotension are infrequent and are usually preventable. Venous thromboembolism, on the other hand, has been reported to occur in 2% of low-risk patients and in as many as 70% of high-risk patients. Perioperative mortality from pulmonary embolism occurs in 2%–3% of patient without prophylaxis. Prosthetic joint infection is another complication with devastating end result. Joint instability or dislocation, hematoma formation, and heterotrophic ossification are other postoperative issues that need vigilant attention. Long-term complications include polyethylene wear, osteolysis, aseptic loosening, periprosthetic fractures, and implant failure. Rarely, patients may have a significant leg length discrepancy after surgery, which may require the use of a shoe lift.

Postoperative management Prophylaxis against infection and venous thromboembolism, pain management, and an appropriate rehabilitation program are the main task of the postoperative period. Usually, 24 hours postoperative antibiotics are administered. Prophylaxis against venous thromboembolism with lowmolecular-weight heparin or warfarin is recommended. Compression stockings, mechanical intermittent compression device, and early mobilization are essential in the prevention of venous thromboembolism. Use of continuous passive motion (CPM) after total knee replacement, together with physical therapy, has been shown to result in greater knee flexion and shortened hospital stay. Hip precautions should be observed after hip replacement surgery when a posterolateral approach is used, to avoid the risk of dislocation. Such precautions include avoidance of hyperflexion, adduction, and internal rotation. These patients should be given an abduction pillow, adaptive equipment, raised toilet seats, and tub benches to enable greater compliance with hip precautions.

Outcome Reports on the result of joint replacements are generally excellent in attaining the goals of pain reduction and improved function. The result

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may vary depending on implant, fixation, surgical technique, surgeon, and patient factors. Survival analysis shows that 95% of total hip arthroplasties last for 15 years, and 85%–90% for more than 20 years.1,2 Total knee arthroplasty has survivorship of 91% at 10 years, 84% at 15 years, and 78% at 20 years.3

Further reading Canale TS, Beaty JH (2007), Campbell’s Operative Orthopaedics, 11th ed. St. Louis: Mosby. Horwitz, BR, Rockowitz, NL, Goll, SR, et al. (1993). A prospective randomized comparison of two surgical approaches to total hip arthroplasty. Clin Orthop 291:154–163. Morrey, BF (1997). Difficult complications after hip joint replacement. Dislocation. Clin Orthop 344:179–187. Paiement GD (1998). Prevention and treatment of venous thromboembolic disease complications in primary hip arthroplasty patients. Instr Course Lect 47:331. Saleh KJ, Kassim R, Yoon P, Vorlicky LN (2002). Complications of total hip arthroplasty. Am J Orthop 31:485–488. St. Clair SF, Higuera C, Krebs V, et al. (2006). Hip and knee arthroplasty in the geriatric population. Clin Geriatr Med 22:515–533.

1 Gaffey JL, Callaghan JJ, Pedersen DR, et al. (2004). Cementless acetabular fixation at fifteen years. A comparison with the same surgeon’s results following acetabular fixation with cement. J Bone Joint Surg [Am] 86-A:257–261. 2 Klapach AS, Callaghan JJ, Goetz DD, et al. (2001). Charnley total hip arthroplasty with use of improved cementing techniques: a minimum twenty-year follow-up study. J Bone Joint Surg [Am] 83-A:1840–1848. 3 Rand JA, Trousdale RT, Ilstrup DM, et al. (2003). Factors affecting the durability of primary total knee prostheses. J Bone Joint Surg [Am] 85-A:259–265.

Chapter 10

Prosthetics and orthotics Chioma Ezeadichie Jay M. Weiss Lyn Weiss Matthew J. Mikosz Adeel Popalzai Maryam Rafael Aghalar Amputation 278 Lower extremity prosthetics 282 Upper limb prosthetics (transradial), (transhumeral) 288 Ankle foot orthoses (AFO) 294 Knee ankle foot orthoses (KAFO) 298 Truncal and cervical orthoses 300

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Amputation Incidence and prevalence In 2005, 1.6 million amputees were living in the United States; approximately 50,000 new amputations are performed annually. By the year 2050, it is estimated that there will be approximately 3.6 million people living with an amputation. In the United States, 82% of amputations are due to vascular disease; the majority of the remainder are due to trauma, with malignancies and congenital deformities each accounting for about 1% of amputations.1 Regardless of the etiology, amputation remains a source of significant physical and psychological trauma in individuals facing limb loss (see Table 10.1). The lower limb amputation is much more common than the upper limb amputation. The ratio of upper limb to lower limb amputation is estimated at 1:4.9. In general, a longer stump (lower level of amputation), will result in greater leverage, strength, function, and lower energy requirement. However, extra-long amputations may actually impede proper fitting of a prosthesis (due to an extra-long lever arm or interference with a prosthetic joint or terminal device). To maintain function, the surgical reconstruction should consider how the prosthesis will fit on a residual limb, including consideration of any contractures, insensate areas, scars, graft sites, and length.

Rehabilitation after amputation Rehabilitation begins before amputation, if possible, and includes strengthening the residual muscles (especially upper extremities), psychological adjustment, and education about prosthetic options. Rehabilitation after the amputation should begin as soon as possible after surgery. The intensity can be increased as the patient’s condition improves. The success of rehabilitation depends on the level of amputation and type of amputation, any premorbid or resulting impairments and disabilities, the patient’s overall health, and family support. The goal of rehabilitation

Table 10.1 Causes of amputation Diseases

Peripheral vascular disease, diabetes, blood clots, osteomyelitis

Most common cause of lower extremity amputation

Injuries

Vascular injury

Most commonly the upper extremities

Surgery

Tumors of bones and muscles

1 Dillingham T, Pezzin L, MacKenzie E (2002). Limb amputation and limb deficiency: epidemiology and recent trends in the United States. South Med J 95(8):875–883.

AMPUTATION

is to maximize the patient’s capabilities, function, and independence, and is achieved as follows: • Postamputation care to promote wound healing and stump care, desensitization of the limb (a way to decrease the hypersensitivity that can often be experienced after limb amputation), reduce edema, shape the limb to fit a prosthesis, and prevention of contractures • Pain management for both postoperative and phantom pain (pain felt in the amputated area of the limb). Explain to the patient that phantom sensation is normal, whereas phantom pain is abnormal and needs to be addressed as soon as possible. Phantom sensation results because the neural pathways continue to tell the brain that the limb is still there. With time, there is “telescoping” of the sensation of the limb. Touching the residual limb will help with both phantom sensation and psychological adjustment to the amputation. • Exercise therapies that promote improvement of muscle strength, range of motion, endurance, and motor skills, restore activities of daily living (ADLs), and reach maximum independence • Determining home equipment needs (assistive devices) and coordinating outpatient rehabilitation services and community resources • Educating the patient and family or caretakers on proper skin care, proper nutrition, and home exercise program to maintain range of motion and prevent tightness in joints and muscles • Supporting the patient and the family as they learn to adjust to the patient’s physical limitations • Appropriate fitting of a prosthesis as well as training and follow-up

Energy expenditure Lower extremity amputation significantly affects the energy expenditure of ambulation (see Table 10.2). The energy cost of gait is usually measured in oxygen consumption. Individuals with amputations usually slow the cadence of gait to maintain the rate of oxygen consumption within a tolerable aerobic range. The amount of energy expended depends on a variety of factors, including length of the stump, the patient’s health, and the reason for the amputation.

Table 10.2 Energy expenditure by level of amputation Level of amputation

Increase in energy expenditure (above normal)

Transtibial

10%–40%

Bilateral transtibial

40% –100%

Transfemoral

60%–110%

Transtibial and transfemoral

~120%

Bilateral transfemoral

~200%

Wheelchair mobility

~9%

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For example, a traumatic long unilateral transtibial amputee uses about 10% more energy to walk the same distance as non-amputees. This energy expenditure increases to 60% for a traumatic unilateral transfemoral amputee. A short vascular transtibial amputee may use 40% more energy. An intact knee joint greatly reduces the energy expenditure (see Table 10.2). Depending on a patient’s cardiovascular status, the patient may not be a candidate for prosthetic use.

Further reading Braddom RL (2006). Physical Medicine and Rehabilitation. Philadelphia: WB Saunders, pp. 267–318. Ziegler-Graham K, MacKenzie EJ, Ephraim PL, Travison TG, Brookmeyer R (2008). Estimating the prevalence of limb loss in the United States: 2005 to 2050. Arch Phys Med Rehabil 89:422–429.

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Lower extremity prosthetics General description The rehabilitation goals of a lower extremity amputee may differ in individual patients, but in most circumstances they include restoring mobility for ambulation and transferring. The prosthetist and occupational and physical therapists should be considered an important part of the rehabilitation team. While the physician prescribes the prosthesis and its components, the prosthetist may have a more extensive knowledge of prosthetic components and may be helpful in optimizing function. Determination of the type of prosthesis and its components should be based on the patient’s individual status and potential. Some patients are not candidates for functional prosthetic use because of the increased energy expenditure required, poor healing, contractures, allodynia, or motivational or cognitive factors. In such cases, a cosmetic prosthesis may be appropriate. In general, transtibial (below-knee) amputees (BKA) are much more functional and have a better gait and lower energy expenditure than transfemoral (above-knee) amputees. A transtibial gait may be impossible to differentiate from that of a non-amputee. In contrast, a transfemoral amputee with an above-knee prosthesis will invariably have a noticeable gait. A transtibial amputation is also much easier to fit with a prosthesis. For these reasons, a transtibial amputation is far preferable to a transfemoral amputation (if ambulation is possibile). The rehabilitation process of an amputee can be divided into four phases: preprosthetic training, postoperative care, prosthetic fitting and training, and long-term follow-up care.1 Preprosthetic training In the preprosthetic stage, strength, endurance, range of motion, mobility and ambulation, and activities of daily living should be optimized to make the postoperative course smoother. Postoperative care The postoperative stage concentrates on wound management, edema reduction, and contracture prophylaxis as well as preservation of strength and mobility in the uninvolved limbs. Prosthetic fitting and training This involves making a cast of the residual limb and fabricating a prosthesis, taking into account the factors mentioned previously and using the appropriate components. It also requires active therapy to relearn how to walk and maximize function. Appropriate education in self-monitoring, skin care, and prosthesis maintenance is an important part of this stage. Long-term follow-up care Periodic follow-up and checking for complications occur during this phase. It also includes determining when a new prosthesis is required, the 1 DeLisa J, Gans BM, Walsh NE, et al. (eds.). (2004). Physical Medicine and Rehabilitation, Principals and Practice, 4th ed. Philadelphia: Lippincott Williams and Wilkins, pp. 1327–1331.

LOWER EXTREMITY PROSTHETICS

appropriate prescription at that stage, addressing changes to the residual limb or the patient’s physical and emotional status, and whether additional rehabilitation is required.

History In the nonpediatric population, most amputations are due to vascular disease (frequently complicated by diabetes mellitus) or trauma. The presence of neuropathy will predispose the patient to sensory abnormalities that can lead to potential skin breakdown in a prosthesis. Vascular disease and diabetes may contribute to poor healing and may be associated with cardiac problems, limiting the level of safe exertion. It is important to obtain a thorough past medical history to assess for these issues. When fitting any patient for a prosthesis, it is important to ask the patient what their goals are. The history should also assess the patient’s prior level of functioning, the types and extent of social supports, the physical barriers in the home, and the patient’s occupation (and whether they plan to return to work). Because prostheses are expensive, it is important to determine the patient’s insurance status, as well as any additional resources that are available.

Physical The length of the residual limb, the condition of the skin, the shape of the residual limb, and the integrity of the suture site should be assessed. Any redundant tissue or hypersensitive areas should be noted. The intact limb and the patient’s functional ability (transfers, bed mobility) should also be evaluated. Sensation should be assessed, as decreased sensation could lead to skin breakdown. The range of motion of the residual limb should be noted. Any contractures in the hip or knee could lead to difficulty with fitting a prosthesis and ambulation training. The patient’s coordination, strength, and cardiovascular status will affect prosthetic selection, fitting, and training and should be assessed.

Management The patient must be taught to be vigilant about skin inspection; a longhandled inspection mirror can aid in this process and the patient should have one. It is also important that the patient get used to touching the distal end of the residual limb as this helps the patient adjust psychologically to the amputation. It is normal for patients to experience the sensation that the distal limb is still intact (phantom sensation). Touching the stump will help reduce this sensation. The specifics of the prosthesis should be based on the patient’s goals. A patient who is not expected to be a community ambulator and uses the prosthesis for household transferring and ambulation will have different needs than a community ambulator, a construction worker, or an athlete. These factors, as well as cosmesis, need to be considered. The prosthetic prescription should include the diagnosis, type of prosthesis (with modifiers), socket type, liner, suspension method, type of foot, diagnostic or check socket, and supplies.2 Other factors, including the level 2 Frontera WR, Silver JK, Rizzo TD (2008). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier, pp. 599–603.

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of prosthetic use (i.e., home transfers and limited ambulation, limited community, community, heavy activity, or athletic), may also be appropriate and are frequently given in categories established by Medicare (referred to as “K” codes).

Components of the transtibial (BKA) prosthesis Socket The socket usually has a hard exterior with a soft liner. The socket is fabricated from a cast of the residual limb. Socks may be used under the liner to protect the skin and add bulk as the stump shrinks. The most common type of socket for a transtibial (below-knee) amputee is a patella tendon–bearing design. This puts most of the weight bearing on the patella tendon. The socket can be a total contact socket. This socket distributes pressure uniformly throughout the socket (instead of primarily on the patellar tendon) and commonly uses a gel liner. Supracondylar sockets have medial and lateral sidewalls that extend over the femoral condyles and provide good mediolateral stability. A total contact supracondylar–suprapatellar socket also extends anteriolaterally to give additional stability. Transtibial sockets are usually aligned in slight (5*) of knee flexion to enhance loading. This puts the quadriceps muscle at a mechanical advantage. Suspension The socket requires a type of suspension to keep it from falling off or extending during movement (pistoning). Common suspensions are a waist belt, thigh component, supracondylar cuff straps, gel liners, sleeves (neoprene, rubber or elastic), and a suction suspension. A popular suction suspension system uses a gel or silicone liner with a metal pin at the bottom that will lock in the prosthesis. Suction maintains the liner, while a mechanical lock connects the pin to the prosthesis. Foot The types of prosthetic feet are usually divided into categories by their functional features and include solid ankle, single axis, flexible keel, multiaxis, and dynamic response (energy storing). The type of foot should be based on the needs of the patient. Solid ankle A solid ankle cushion heel (SACH) is most commonly used in older patients. The advantages of a SACH foot are they are relative light weight and inexpensive and have no moving parts that may break. The foot is made of a wooden or composite (rigid) keel, compressible foam heel, and flexible toes. A forefoot rocker mechanism allows simulation of a normal foot. Single axis A single-axis foot permits movement in dorsiflexion and plantarflexion. Movement in theses planes is restricted by internal bumpers.

LOWER EXTREMITY PROSTHETICS

Flexible keel A flexible keel is similar to the SACH foot but has a flexible keel that helps to mimic forefoot rocker motion. The foot allows some inversion and eversion and gives a smoother rollover than that of a SACH foot. It is used in patients requiring a low to moderate activity level. Multiaxis A multiaxis foot can provide a more natural range of motion in dorsiflexion and plantar flexion, and inversion and eversion. This type of foot may be appropriate for an amputee who has to walk on uneven surfaces. Dynamic response (energy storing) Energy-storing prosthetic feet contain elements that store energy during the limb loading and mid-stance phases of gait and then return that energy during push-off. Examples of energy-storing prosthetic feet include the Flex-Foot, Carbon Copy II, Spring-lite foot, and the Seattle foot. They are used in younger, more active individuals and athletes. Socks Cotton socks of varying thickness (measured in ply) are used under the liner. The total number of ply is frequently increased as the residual limb shrinks (matures) with prosthetic use. Socks are not used in suction suspension.

Components of a transfemoral prosthesis (above-knee prosthesis) Socket The socket usually has a hard exterior with a soft liner. The socket is fabricated from a cast of the residual limb. Socks may be used under the liner to protect the skin and add bulk as the stump shrinks. The two main types of socket design for the transfemoral prosthesis are the quadrilateral socket and the ischial containment socket. Quadrilateral socket This socket has been in use for over 50 years. The primary area of weight bearing is on the ischial tuberosity. The posterior wall forms a “seat” for the ischial tuberosity to rest on. The anterior wall maintains posterior pressure on the thigh, keeping the ischial tuberosity in place. The medial and lateral walls also provide stability. The quadrilateral socket is used primarily by longer-term prosthetic users who are comfortable with the design. Newer transfemoral amputees are more often given an ischial containment socket. Ischial containment socket In this more recent design, the ischium is contained in the socket (rather than resting on it as in a quadrilateral socket). This socket has a narrower mediolateral dimension. Advantages of this design include better medial lateral stability (particularly in patients with short femurs), since the prosthesis has a greater area of contact due to its higher position on the femur and pelvis.

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Frequently there are cutouts made in the design of the hard exterior part of the socket for an inner flexible liner to allow for comfort without unduly sacrificing stability. Generally this is the prosthesis of choice for new transfemoral amputees. Suspension The transfemoral socket requires a type of suspension to keep it from falling off or extending during movement (pistoning). Suction sockets are commonly used, as well as suspension belts. Belts can be used in combination with other suspensions. Knee The knee can be a simple hinge (single axis) or polycentric, which can give a more natural gait. The knees can have a brake that will prevent flexion when weight bearing. Some knees can be manually locked for ambulation and released for sitting, which may provide more safety in certain patients where natural gait is not as important as added stability. Prosthetic knees will have some mechanism of providing friction to prevent excessive knee movement during gait. Simple mechanical friction is constant and may be more appropriate for lower-functioning, slowerwalking amputees. More active younger amputees may be better served by a knee with hydraulic or pneumatic friction. These can provide a variable resistance and a more natural gait, though they may be more expensive and heavier. More complex computer-controlled knee systems use an onboard microprocessor to vary resistance based on such factors as speed and terrain. They will respond differently to steps or uneven terrain. They can recognize a stumble and increase resistance to minimize the chance of a fall. Though more expensive, these may be covered by insurance carriers for more active amputees. Socks See Socks section, p. 285. Foot See Foot section, p. 284.

Special considerations The importance of cosmesis should be considered. Generally the exterior of the prosthesis can be covered to appear similar to the skin. While it is normal to have phantom sensation, phantom pain is abnormal and must be addressed as soon as possible. The volume of the residual limb will usually decrease greatly in the initial period of prosthetic use, and frequent follow-up and additional limb socks (stump socks) are necessary. The initial prosthesis is almost always a temporary prosthesis until the residual limb “matures” to close to its final dimensions. At that point, a more permanent replacement will be needed. Prosthetic life is variable, but without unusual factors a lifespan of 3–5 years is common.

LOWER EXTREMITY PROSTHETICS

Red flags and complications The underlying disease processes should be considered and patients (particularly those with vascular disease or neuropathy) should be vigilant for breakdown as they may require prolonged periods of non-weight bearing to heal. This vigilance should be increased after receiving a new prosthesis or after changes in the prosthesis are made.

Further reading Braddom R (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders–Elsevier, pp. 283–323. DeLisa, JA. Gans BM, Walsh NE, Bockenek WL, Frontera WR (eds.). (2004). Physical Medicine and Rehabilitation, Principles and Practice, 4th ed. Philadelphia: Lippincott Williams & Wilkins, pp. 1327–1331. Frontera WR, Silver JK, Rizzo TD (2008). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier, pp. 599–603.

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Upper limb prosthetics (transradial), (transhumeral) General description The upper limb amputee requires a thorough evaluation to fully assess their physical and functional needs and requirements. This assessment should include manual muscle testing of all joints bilaterally, range-ofmotion testing, sensation testing, a cognitive assessment, and a thorough evaluation of the limb to better understand what device or devices may be most suitable to meet the patient’s needs. There are several types of prostheses suitable for the transradial- and transhumeral-level amputee. These include passive, cable-operated, adaptive, and myoelectric prostheses. The physical exam will play a large part in selecting the most appropriate type of prosthesis for the individual.

Passive prosthesis These types of prostheses provide limited function but can be very cosmetically appealing. Although these devices provide limited function, they can have a considerable impact psychologically and help improve the individual’s self-esteem. The hand is typically in a fixed position and does not offer active grasp. The hand would be covered with a cosmetic glove that can vary significantly in appearance depending on the level of detail requested. Indications for a passive prosthesis The passive prosthesis is recommended for someone who is interested in using a lightweight cosmetic prosthesis. There are limited or no mechanical components in the prosthesis so the weight can be reduced considerably. Contraindications for a passive prosthesis The passive prosthesis provides limited function. If a functional prosthesis is required, this type of prosthesis would be contraindicated.

Cable-operated prosthesis The cable-operated or body-powered prosthesis is controlled through body motions such as glenohumeral flexion and biscapular abduction. A harness is required to control the prosthesis, which is anchored under the axilla. Indications for a cable-operated prosthesis The cable-operated or body-powered prosthesis is considered appropriate for someone with good strength and range of motion (ROM). These devices can also be constructed with heavy-duty components, so they would be suitable for heavy-duty type work. They can be extremely functional depending on the type of components that are used. Contraindications for a cable-operated prosthesis The cable-operated prosthesis is contraindicated for persons with limited strength and ROM, as it would be difficult for them to operate this type of device. A body-powered prosthesis is contraindicated for someone who could not tolerate pressure in the axilla or across the back.

UPPER LIMB PROSTHETICS

Adaptive prosthesis Adaptive prostheses are used for a specific activity. This type of prosthesis can be designed exclusively for a specific activity, or adaptive devices can be added to a passive, body-powered, or myoelectric prosthesis. Indications for adaptive prosthesis Adaptive prostheses would be indicated for someone wanting to use the prosthesis for a specific activity such as golf, weight lifting, etc. Contraindications for an adaptive prosthesis The main contraindication for a device specifically designed for an activity is that it would have limited function outside of that activity. Therefore, a passive, body-powered, or myoelectric prosthesis may be considered along with the specific attachments for the chosen activities.

Myoelectric prosthesis A myoelectric prosthesis uses surface EMG activity (from intact muscles) to control and operate a terminal device. Indications for a myoelectric prosthesis A thorough EMG test should be performed to check for viable EMG signals. If adequate signals are noted (at least 10 mV), the individual may be a suitable candidate for a myoelectric prosthesis. The clinician should assess two antagonist muscle groups. Ideally, one would want to see moderate to high signal strength with good separation between the two muscle sites. If only one viable muscle site is noted, a single-site myoelectric system could be considered. Myoelectric prostheses provide proportional control of the terminal device with increased grip strength compared to that with cable-operated prostheses. If the individual requires increased grip strength, a myoelectric prosthesis could be indicated. Contraindications for a myoelectric prosthesis A myoelectric prosthesis may be contraindicated for someone who is not compliant or does not have the cognitive ability to operate and maintain a myoelectric prosthesis. Also, if heavy-duty type activities are required, this type of prosthesis may not be the most suitable. Environmental factors such as extreme temperatures and moist or dirty environments may be contraindicated for this type of device. If no EMG signal is noted, then EMG control of the prosthesis would not be suitable. In that case, a switch-controlled electronic prosthesis could be an alternative option. This would still allow proportional control and grip strength through a linear pull of a switch.

Component options for transradial- and transhumeral-level amputees Hands Passive There are multiple options when selecting a prosthetic hand. Passive hands are lightweight and fixed in a relaxed position. A cosmetic glove would cover the hand to more closely resemble the individual’s sound side.

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There are also spring-loaded mechanical hands that can be used passively. These provide some grasp but require the intact hand to open the hand component. The spring would then close the hand. Cable operated Cable-operated hands can be either voluntary opening or voluntary closing, depending on the individual’s specific needs. The voluntary opening hand is opened by a pull on the cable through shoulder movement. A spring closes the hand. Grip force is limited by the amount of tension that the spring can provide. If increased grip strength is required, this type of hand may not be the best option. Voluntary closing hands are open at rest. A pull on the cable closes the hand. The individual can control grip strength by applying more or less pressure on the harness and cable. These hands can also incorporate a back-lock mechanism that allows the user to grab an object and maintain pressure on the object while relaxed. This way, the patient does not need to maintain tension on the cable to maintain grasp on an object. Electric Conventional electric hands operate in a three-jaw chuck grasp pattern. The speed is controlled by the EMG signal strength, called proportional control. The Sensor Hand from Otto Bock is a prosthetic hand with a sensor that can detect when an object is slipping. It will automatically adjust grip strength to maintain a secure grasp on the object. Most electronic hands can be controlled with either a single-site or dual-site EMG. New advances in technology have allowed for individually powered fingers and multipositional thumbs. The I-Limb is operated in a similar fashion as other myoelectric hands but offers the benefit of articulating fingers that conform around objects to provide a more secure grasp. The multipositional thumb allows for different grasping patterns, such as lateral, precision, and power grip. Hook-type prehensors (electronic hooks) Amputees can benefit from hook-type prehensors that allow for improved visibility of the object being held as well as finer grip prehension. The electronic terminal device (ETD) has hook-shaped fingers and is water resistant. The Greifer is a heavy-duty type electric hook prehensor that provides a claw-type grasp in which both fingers of the device close symmetrically and meet in the middle. The ETD has a stationary hook and the other hook closes down to it. All myoelectric devices have the option of a quick disconnect that can allow the individual to interchange devices if necessary. Wrists Passive Generally, when a passive device is requested, the main goal is to design the prosthesis to resemble the intact side and make it light in weight. This can be achieved by using a Delrin or plastic wrist, which is light and can be shaped to match the intact wrist dimensions. Other wrists can be used, but typically with this type of device the plastic wrist is most suitable.

UPPER LIMB PROSTHETICS (TRANSRADIAL), (TRANSHUMERAL)

Friction wrist Friction wrists can be used for passive or body-powered devices. These devices offer the user the ability to preposition the wrist manually by turning the wrist. The amount of friction can be adjusted to the specific requirements of the user. Quick disconnect wrist Quick disconnect wrists are widely used with the interchangeability of terminal devices. If the user has multiple terminal devices, they can quickly be interchanged by depressing a button on the wrist. These wrists offer manual rotation of the wrist and a positive lock. Quick disconnect friction wrists These wrists offer the quick disconnect feature but can be pre-positioned by manually rotating the wrist under friction. There is no positive lock with this type of wrist. Rotation wrist units This type of wrist allows the user to pre-position the terminal by a lever connected to the wrist by a cable. The wrist is spring loaded. When the lever is depressed, the wrist will rotate to the desired position. When the level is released, the wrist will lock into position. This may be beneficial for a bilateral amputee or patients with an impaired opposite side. Five-function wrist The five-function wrist offers flexion and extension, pronation and supination, and a quick disconnect feature. These actions can be performed by a lever, a cable, or a combination of both. This type of wrist is also beneficial for the individual who has bilateral upper limb amputations or an impaired opposite side. Electronic wrists In an above-elbow or short transradial amputee, an electronic wrist may be used. This can allow wrist rotation as well as flexion and extension. This added motion will permit the user to function more effectively at midline or near their mouth. Electronic wrists commonly employ a quick disconnect feature. Elbows Passive Passive elbows can be used to reduce the overall weight of the prosthesis for persons with amputation at the transhumeral or higher level. These elbows are manually positioned and can be locked in various positions. These elbows can be manually positioned in flexion and extension and also internal and external rotation. Body powered There are several types of body-powered elbows currently available. These elbows are controlled by body motion through cables or manually with the other limb. They can perform flexion and extension, and internal and external rotation. The typical motions used to operate the elbow are glenohumeral flexion and biscapular abduction.

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When considering whether this type of elbow is appropriate for a patient, certain criteria need to be considered. Adequate ROM and strength must be present to operate this type of elbow. These elbows can be locked and unlocked by a cable connected to the harness. Hybrid elbows The hybrid elbow is used when a body-powered elbow and an electronic terminal device is being considered. This type of elbow is operated in a similar fashion as the body-powered elbow but allows for the connection of electronic components. If EMG or switch control of the terminal device is a viable option, the electrodes and/or switch and battery supply can be connected to the elbow turntable so there are no wires exposed externally. An electronic elbow lock feature is also an option with this type of elbow. Electric elbows There are currently several electronic elbows available that offer motorized flexion and extension of the elbow. These elbows can be controlled by EMG signals or electronic switches. They can be operated sequentially or simultaneously with the terminal device. Speed and lifting force vary among electronic elbows. The average weight of an electronic elbow is approximately 2 pounds. The electronic elbow can be proportionally controlled depending on the rate of the EMG signal or the amount of pull on the electronic switch.

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Ankle foot orthoses (AFO) General description An ankle foot orthosis (AFO) is a brace worn on the lower leg and foot. It can be used as an assistive device to provide mediolateral stability to the foot and ankle, compensate for weak muscles, and improve gait by controlling ankle motion. AFOs can be beneficial by providing support to weak or wasted limbs or by positioning a lower limb with tight, contracted muscles into a more natural position. AFOs can also be used to immobilize the ankle and lower leg in the presence of arthritis or fracture.

Indications AFOs are commonly used in the treatment of disorders that affect lower extremity muscle function. Such disorders can alter the stability of the foot and ankle or can affect the biomechanics of gait, creating problems with dorsiflexion, plantar flexion, and movement around the subtalar joint. Some common indications for AFOs include the following: • Foot drop or foot slap (due to dorsiflexion weakness) • Plantar spasticity • Stroke • Spinal cord injury • Muscular dystrophy • Cerebral palsy • Polio and post-polio syndrome • Multiple sclerosis (MS)

AFO design types Plastic AFOs Plastic AFOs are the most commonly used AFOs because of their low cost, cosmetic appeal, light weight, practical ability to fit within shoes, and similar structural support as that of metal AFOs. Plastic AFOs can be custom molded to fit the individual. The components of plastic AFOs include the foot component, which may be extended to reduce spasticity. Hinges can also be placed at the ankle, which can allow limited or complete ankle motion depending on the severity of the foot disorder. The calf shell covers most of the lower portion of the leg over the calf and provides added stability. Structural support of an AFO depends on the design of the trim line as well as the foot plate. Common designs for plastic AFOs include the following: • The solid plastic AFO is the most commonly prescribed plastic AFO. Solid refers to being made of a single piece of plastic. It is used for patients who have severe plantar spasticity, plantarflexion weakness, foot drop, or Charcot joint, and for postoperative immobilization of the foot. Solid AFOs have no ankle joint and can vary in the degree of flexibility, depending on the level of spasticity. • The posterior leaf spring (PLS) is the most flexible plastic AFO with a thin plastic band behind the ankle. The design is used for flaccid

ANKLE FOOT ORTHOSES (AFO)

foot drop and is set in dorsiflexion to provide spring assist during the swing phase of gait. The PLS is appropriate with isolated dorsiflexion weakness with intact plantarflexion. • The semi-rigid plastic AFO provides functional alignment for flaccid extremities, resistance to mild extensor spasticity, and mediolateral support for ankle instability. It is positioned in dorsiflexion with a trim line behind the malleoli. It is commonly used for foot drop and mediolateral instability at the ankle. Metal AFOs Metal AFOs are used much less commonly than plastic AFOs. They are made up of a proximal calf band, two metal uprights, ankle joints, and an attachment to the shoe. Stirrups are used to anchor the uprights to the shoes between the sole and the heel. Metal AFOs are used for patients with foot drop or insensate foot due to peripheral neuropathy, and in patients with fluctuating edema. These are frequently used in older patients who are comfortable with this style of brace and have been using it for years. Ankle joints The ankle joint consists of pins and springs to assist ankle joint motion. Different ankle joint mechanisms allow for fixed, limited, or full dorsiflexion and plantar flexion. Different hinged ankle joints can be used with both plastic and metal AFOs (although many plastic AFOs do not use a separate ankle joint). They include the following types: • The Klenzak ankle joint allows ankle dorsiflexion assistance with the inclusion of a spring, and prevents rapid plantar flexion. It is used for flaccid foot drop and knee hyperextension. • A plantar stop (posterior stop) is used to control plantar spasticity and to help stretch plantar contractures. This type of ankle joint restricts plantar flexion, but allows full dorsiflexion. • A dorsiflexion stop (anterior stop) substitutes for the function of the gastrocnemius–soleus complex. It allows full plantar flexion while limiting dorsiflexion and can be used to aid weak calf muscles. • The T-strap is used with double metal upright AFOs to provide medial or lateral stability to the ankle. A medial T-strap is used for valgus deformity, and a lateral T-strap is used for varus deformity. Patellar tendon–bearing AFOs are designed to transfer weight from the foot and ankle on to the patellar tendon and tibial flares, with the load being transmitted to the shoe via metal uprights. This type is used for tibial fractures, diabetic foot ulcers, and painful heel conditions such as calcaneal fractures and avascular necrosis of the foot or ankle. Pressure-relief AFOs eliminate weight bearing with a heel cutout and by using a hinged lever arm posteriorly that can be adjusted medially or laterally to prevent malleolar pressure sore development. This type is used for pressure relief and contracture prevention.

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Contraindications and complications Certain conditions such as severe spasticity, ankle edema, and diabetic neuropathy with ulceration are considered relative contraindications to AFO use. Proper sensation and proprioception in the lower limbs is vital. The skin must be observed to prevent skin breakdown. In addition, all AFOs should terminate least 1 inch below the fibular neck in order to prevent a compressive common peroneal neuropathy. Metal AFOs are contraindicated in children, as the weight of the brace can cause external tibial rotation.

Further reading Braddom RL. (ed.). (2006). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders– Elsevier, pp. 347–355. Cuccurullo SJ. (2004). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical, pp. 467–469. DeLisa JA. Gans BM, Walsh NE, Bockenek WL, Frontera WR (eds.). (2004). Physical Medicine and Rehabilitation, Principles and Practice, 4th ed., Vol. 2. Philadelphia: Lippincott Williams & Wilkins, pp. 1383–1385. Edelstein J, Bruckner J (2002). Orthotics: A Comprehensive Clinical Approach. Thorofare, NJ: Slack, pp. 39–50.

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Knee ankle foot orthoses (KAFO) General description A knee ankle foot orthosis (KAFO) is an extension of an ankle foot orthosis (AFO). It is comprised of the same components as the AFO with the addition of a knee joint, thigh uprights, and a proximal thigh band. KAFOs provide stability during ambulation at the knee, ankle, and subtalar joints. KAFOs are used to control instabilities of the lower limb, specifically knee instability and knee flexion spasticity. It can also be used in cases of knee extensor or hamstring weakness.

Indications KAFOs are used to primarily control knee motion and alignment. Several disorders can alter the stability of the knee and lower limb. KAFOs are commonly used to control disorders such as genu recurvatum and genu valgum. They also provide support following surgery or fractures that result in knee instability and weakness. Among the indications for KAFOs, muscle weakness and paralysis of the leg are the most frequently identified. KAFOs are used most frequently for muscle weakness secondary to the following pathologies: • Spinal cord injury • Poliomyelitis • Multiple sclerosis • Muscular dystrophy

KAFO design types Designs are differentiated by differing knee joints and knee locks. The choice of knee joint or lock is dictated by the level and severity of injury. The mechanical knee joint can be polycentric or single axis. Polycentric knee joints are used to aid knee motion whereas single-axis joints are used to provide more knee stabilization. In addition, if the knee extensor muscles are weak, a knee lock may be indicated. Knee joints Free motion knee joint This type of joint provides unrestricted knee flexion and extension with a stop to prevent hyperextension. It is used for genu recurvatum and mediolateral instability. Offset knee joint This KAFO is prescribed for patients with weak knee extensors and some hip strength. It provides free flexion and extension of the knee during the swing phase of gait. It has a hinge that is placed posterior to the knee joint so the patient’s weight line falls anterior to the offset joint, stabilizing the knee during early stance on level surfaces. Knee locks Ratchet lock This is the most commonly prescribed lock. It has a catching mechanism with 12* increments that allows stabilized knee extension and prevents the knee from going into flexion when arising from a seated to standing

KNEE ANKLE FOOT ORTHOSES (KAFO)

position. The mechanism is then released by using a lever arm to allow knee flexion. Drop ring lock Knee flexion is controlled with the assistance of gravity, which brings the ring into the locked position when the user stands with the knee in full extension. Manual assistance is then used to allow flexion. The disadvantage of this mechanism is that, unlike the ratchet lock, there is no locking mechanism until the knee is in full extension. Pawl lock with bail release This knee lock uses a manual lock-and-unlock mechanism. Lifting up the bail lever posteriorly will release the knee joint and permit knee flexion, whereas a spring-loaded projection helps lock the knee into extension. Scott–Craig orthosis This design consists of an ankle joint with anterior and posterior adjustable stops, a pretibial band, a posterior thigh band, an offset knee joint with bail lock, and a T-shaped foot plate for mediolateral stability. The ankle joint functions with a dorsiflexion stop, allowing a swing-to gait with crutches and a posterior stop to prevent drag. This KAFO is used to facilitate standing and ambulation in patients with paraplegia due to spinal cord injury at the L1 level or higher. Contraindications and complications General contraindications to the use of a KAFO include the patient’s inability to meet energy demands (i.e., lack of adequate strength to control standing balance). In addition, an open wound or pressure sore in the area of the orthotic is a contraindication. Proper sensation and proprioception in the lower limbs is vital, especially in patients with spinal cord injury. Weak upper body strength along with weak trunk control is a relative contraindication if these muscles are needed to help the patient ambulate. The offset joint should not be used in patients with knee or hip flexion contracture. In addition, locked knee joints are contraindicated for patients with knee contracture.

Further reading Braddom RL (ed.). (2006). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders– Elsevier, pp. 355–358. Cuccurullo SJ. (2004). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical, pp. 469–470. DeLisa JA. Gans BM, Walsh NE, Bockenek WL, Frontera WR (eds.). (2004). Physical Medicine and Rehabilitation, Principles and Practice, 4th ed., Vol. 2. Philadelphia: Lippincott Williams & Wilkins, pp. 1385–1386. Edelstein J, Bruckner J (2002). Orthotics: A Comprehensive Clinical Approach, Thorofare, NJ: Slack, pp. 61–70.

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Truncal and cervical orthoses General description In contrast to limb orthoses, which usually provide mechanical assistance, truncal and cervical orthoses are used to support, align, prevent, or correct deformities of a body part. This may be accomplished by resisting motion or protecting certain body parts. While cervical and lumbar braces may be frequently used, their efficacy has not been established for muscular neck and back pain.1,2 The U.S. government’s Agency for Health Care Policy Research’s review panel on this topic concluded, “There is no evidence that lumbar corsets or support belts are effective for treating acute low back problems and conflicting evidence on whether lumbar corsets and support belts are effective for preventing or reducing the impact of low back problems in subjects who do frequent lifting at work.”3 For muscular neck pain, “collars may promote inactivity, which can delay recovery in patients with WAD” (whiplash-associated disorders) and have not been shown to be beneficial.4,5 Finally, patients can develop a psychological dependence on the orthosis. Lumbar orthoses may be beneficial in pain due to spinal fracture (especially osteoporotic compression fractures) and in cases of spinal instability. Spine surgeons may use bracing after spine surgery (especially stabilization and fusion). Spinal bracing can also be used in scoliotic patients.

Possible complications Because these orthoses may cover vital structures, it is important not to obstruct chest tubes, colostomies, tracheostomies, and dressings, etc. As with any orthosis, care must be taken to avoid skin breakdown. Long-term use of truncal orthoses can lead to abdominal muscle atrophy. An orthosis can cause an increase in motion in the segments above or below the areas confined by the orthosis.

Thoracolumbosacral (TLS) orthoses TLS corset This soft orthotic has an axillary strap attached to a posterior thoracic section. The front is fitted from the xiphoid process to the pubic symphysis. The posterior aspect of the orthosis extends to the apices of the buttocks. It can have a groin strap or a garter to help maintain placement. For women, a brassiere can be incorporated into the orthosis. 1 Shen FH, Samartzis D, Andersson GB (2006). Nonsurgical management of acute and chronic low back pain. J Am Acad Orthop Surg 14(8):477–487. 2 Patel AT, Ogle AA (2000). Diagnosis and management of acute low back pain. Am Fam Physician 61:1779–1786, 1789–1790. 3 AHCPR Archived Clinical Practice Guidelines 14. Acute Low Back Problems in Adults. www.ncbi. nlm.nih.gov/books/bv.fcgi?rid=hstat6.section.26067. 4 Spitzer WO, Skovron ML, Salmi RL, et.al. (1995). Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining “whiplash” and its management. Spine 20(8 Suppl):1S–73S. 5 Rodriquez AA, Barr KP, Burns SP (2004). Whiplash: pathophysiology, diagnosis, treatment, and prognosis. Muscle Nerve 28:768–781.

TRUNCAL AND CERVICAL ORTHOSES

The TLS corset increases intra-abdominal pressure and provides minimal restriction against trunk flexion and hyperextension. This orthosis can be used to help control pain in generalized osteoporosis, metastatic malignancy, myeloma, and thoracic osteoarthritis. TLS flexion extension control orthosis: Taylor brace (Taylor–Knight) This rigid orthotic has a pelvic band, posterior uprights that extend right above the scapular spines connected by an interscapular band, an abdominal apron attached to the posterior uprights, and axillary straps. (The Taylor–Knight has an additional thoracic band connected to the pelvic band via two lateral uprights). This orthosis limits trunk flexion and extension (and lateral motion if using the Taylor–Knight). It may be used for postsurgical support of traumatic fractures, stable osteoporotic fractures, spondylolisthesis, scoliosis, spinal stenosis, and herniated disks. It is contraindicated for unstable fractures (which require more stabilization). TLS flexion extension lateral rotary control orthosis This is the most restrictive TLS orthosis. It is commonly referred to as a “body jacket.” Premade versions can be used and fitted, but usually this orthosis is a plastic jacket custom made for each patient. It usually extends from the upper chest to the groin area. The orthosis limits flexion, extension, lateral bending, and rotation. It is usually indicated for the treatment or post surgical management of traumatic or pathological spinal fractures in the mid to low thoracic and lumbar region. It is also used after surgeries for spondylolisthesis, scoliosis, spinal stenosis, herniated disks, and disc infections.

Lumbosacral (LS) orthoses LS corset/belt The corset is made of a soft fabric that encircles the torso. Anteriorly, it extends from the level of the xiphoid process to the pubic symphysis. Posteriorly, it extends from just below the inferior angles of the scapulae to the apices of the buttocks. Adjustments can be made to custom fit different body shapes and sizes. Metal bars can be inserted into the cloth for extra restriction of flexion and extension. The LS belt is more comfortable since it does not extend up and down as much as the corset. This orthosis increases intra-abdominal pressure and it is postulated to decrease spinal load. As noted previously, there is controversy in the literature on the use of these types of orthoses for back pain, with some clinicians arguing they can do more harm than good. Nevertheless, they sometimes provide warmth and psychological comfort in patients with low back pain associated with many disorders such as herniated disks, lumbar muscle strain, or osteoarthritis. This type of brace is also sometimes used for immobilization after lumbar laminectomy. LS flexion extension control orthosis: chairback brace (chairback–Knight) This type of lumbar orthosis has a thoracic and pelvic band connected by two posterior uprights and an abdominal apron. The thoracic band is

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positioned just below the scapulae and extends laterally to the mid-axillary line. The pelvic band lies just over the apex of the buttock and extends laterally to the mid-trochanteric line. The posterior uprights lie over the paraspinal muscles. The abdominal apron extends from the xiphoid process to the pubic symphysis. The brace can also have a lateral upright for lateral control, which is also called the chairback–Knight brace. The orthosis restricts L1–4 flexion and extension and some lateral movement (if it has the lateral uprights). This also increases intra-abdominal pressure. It is usually indicated for spondylolisthesis, postoperative lumbar laminectomies, fusions, or diskectomies. LS extension lateral control orthosis: William brace This orthosis has a pelvic band, thoracic band, and lateral uprights. Instead of posterior uprights, it has a pair of oblique uprights that extends from the pelvic band to the lateral upright. In front is an elastic abdominal apron connected to the lateral uprights. The brace limits extension and lateral trunk movement but allows forward flexion. It prevents hyperlordotic posture and thus is generally used for spondylolysis and spondylolisthesis. Contraindications for use are spinal compression fractures. Rigid LS orthosis This is a custom-made plastic orthosis that is molded for an improved fit. Indications include postsurgical lumbar immobilization and treatment of lumbar compression fractures.

Scoliosis braces (Milwaukee, Boston, Wilmington, Charleston, Providence) These braces are used to prevent progression of scoliotic curves and to correct the curve. They work by applying force on the convex side at the apex of the curve and on the concave sides above and below that point. The most successful (and cumbersome) of these is the Milwaukee brace, which has extensions up to the head for the chin and occiput. These can be uncomfortable and cosmetically undesirable. The other braces represent efforts to control the spinal curve without the chin and head components. These braces are generally used between 8 hours/day and 23 hours/day (full-time).

Other orthoses Sacroiliac corset/belt This orthosis encircles the lower torso. The top portion sits just below the level of the iliac crests, and the bottom edge is at the level of the inguinal ligaments. Groin straps for men and garters for women are added to help keep it from moving upward. The belt provides sacroilliac joint stability. It can reduce sacroiliac diastasis or pubic symphysis separation, which can happen during pregnancy or trauma. (They are also used by construction workers, weight lifters and others who lift heavy objects, to prevent low back strain.)

TRUNCAL AND CERVICAL ORTHOSES

Cervical orthoses Foam (soft) collars The simplest cervical device is the soft foam collar. These are foam rubber with a cotton cover. This may promote inactivity; however it does not sufficiently restrict motion to prevent injury in cases of instability. Hard collars (including Philadelphia collar) These are two-piece collars made of hard plastic or similar material. They are more restrictive than soft collars but are not adequate in cases of spinal instability. These may be used for prehospital immobilization after injuries or as “step-down” braces after a more restrictive halo orthosis. Stabilizing orthoses (cervicothoracic orthosis) These are the most limiting orthoses for the cervical spine. Their aim is to fasten the head to the chest, thereby immobilizing the cervical spine. Two common examples of these are the SOMI (sternal, occipital, mandible, immobilizer) and the Halo. The Halo vest has a ring fixed to the skull by pins that go into the skull. The ring is attached to a rigid plastic vest.

Further reading DeLisa JA, Gans BM, Walsh NE, Bockenek WL, Frontera WR (eds.). (2004). Physical Medicine and Rehabilitation, Principles and Practice, 4th ed. Philadelphia: Lippincott Williams & Wilkins, pp. 694–697, 1355–1365.

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Chapter 11

Spinal cord injury Jay M. Weiss General facts: epidemiology and demographics 306 Function by level 310 Management and medications 314 Complications 318

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General facts: epidemiology and demographics General description Spinal cord injuries (SCI) represent a complex disorder with many different clinical pictures depending on the level and the completeness of the injuries. In general, rehabilitation and management of spinal cord injuries is a relatively recent phenomenon. Decades ago, patients didn’t survive the injuries that caused spinal cord injuries. Those that did survive would have drastically shortened life spans due to the many medical complications associated with SCI. With the improvements in recognition of spinal trauma and medical care, many more patients survive these injuries than in years past. Depending on the completeness and level of injury, patients have varying functional potential. This affects their level of independence in activities of daily living (ADLs) and other (vocational, recreational) activities. A lawyer or accountant with paraplegia may have no significant change in his or her employability, whereas a construction worker is unlikely to be able to return to his or her previous job.

Epidemiology Spinal cord injuries occur disproportionately in males, with a 4:1 male to female ratio. The incidence (number of new cases in a year) is 30 to 60 per million population, with a prevalence (number of cases at any time) of 700 to 900 per million. The most common causes are motor vehicle collisions (including motorcycles), followed by falls, violence, and sports injuries.

Demographics SCI patients are more likely to have lower levels of education than the uninjured population. They have a higher (pre-injury) unemployment rate. They are more likely to be single (never married, divorced, or separated) than the uninjured population. These demographic factors are enormously important in the rehabilitation of SCI. In addition to the medical aspects, there are significant psychological, social, vocational, and financial implications to these injuries. The proper assessment of a patient’s medical, psychological, and vocational rehabilitation needs is expensive. The proper implementation of rehabilitation in those areas requires support systems (family, friends, and caregivers) in addition to money. Unfortunately, the demographics of SCI patients put them at significant disadvantages in all of these areas. They are less likely to be employed or have insurance coverage at the time of injury. They have a lower education level and thus may have less employability in nonphysical jobs compared to the uninjured population. They are more likely single, lacking a spouse caregiver to help with the medical and psychological aspects of their condition. They are less likely to be able to afford the equipment or therapies necessary to optimize their function.

GENERAL FACTS: EPIDEMIOLOGY AND DEMOGRAPHICS

Clinical assessment The SCI patient can be evaluated on the basis of the American Spinal Injury Association (ASIA) scoring system (see Fig. 11.1). This requires a motor assessment, a sensory assessment, and assessment of rectal tone and voluntary sphincter contraction. An initial medical and urological assessment is also appropriate. The motor assessment requires examination of key muscles from each myotome in the upper and lower extremities. Muscle strength is graded on a commonly used 0–5 scale. The sensory assessment is based on a 0–2 scale (0, absent sensation; 1, decreased or altered; 2, normal or spared). Motor and sensory are assessed bilaterally, as there can be side-to-side differences. This would yield a left motor level, a left sensory level, and a right motor level and sensory level. The neurological level is based on the lowest level with normal motor and sensory function bilaterally. It is especially important to document all of these (L and R, motor and sensory) levels when there are motor or sensory or side-to-side discrepancies. In these cases, the ASIA neurological level alone may not show a complete picture of function. In addition to establishing a neurological (functional) level, the ASIA system requires an impairment assessment. This is based on the completeness of the injury (see Fig. 11.1).

Partial spinal cord lesions In certain incomplete lesions of the spinal cord, certain patterns may occur depending on the location of the damage. Two (relatively) common classes of incomplete spinal cord lesions are central cord syndrome and Brown– Sequard syndrome. In central cord syndrome, the injury is to the center of the cervical cord. This is the location of fibers that innervate the upper extremity muscles. The lower extremity corticospinal tracts are more lateral and spared (or relatively spared) in these lesions. This syndrome gives a “paradoxical” spinal cord picture in which the upper extremity motor function is affected more than lower. In Brown–Sequard syndrome, there is a lesion to one side of the spinal cord. Because different spinal tracts cross the midline at different levels, a patchy picture will occur with findings on both sides of the body. There is motor and sensory loss on the side of the lesion (ipsilateral) and pain and temperature sense loss on the opposite (contralateral) side.

Diagnostic testing Spinal imaging, including X-rays (at times including flexion/extension views), MRI, and CT will generally be necessary at an early stage in diagnosis. These studies may be helpful in assessing stability and the need for surgery. The functional (ASIA) level, however, may not correspond to the radiological level of injury or findings. Laboratory testing, pulmonary function tests, and urological studies are frequently necessary depending on individual circumstances.

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Examiner Name

Date/Time of Exam

C2

STANDARD NEUROLOGICAL CLASSIFICATION OF SPINAL CORD INJURY

C2

SENSORY LIGHT TOUCH R L

Elbow flexors Wrist extensors C2 Elbow extensors Finger flexors (distal phalanx of middle finger) C3 C4 Finger abductors (middle finger) C5 UPPER LIMB C6 ⫹ ⫽ TOTAL C7 (MAXIMUM) (25) (25) (50) C8 T1 Comments: T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L2 Hip flexors L4 Knee extensors L3 L5 Ankle dorsiflexors L4 S1 Long loe extensors L5 Ankle plantar flexors S1 S2 S3 Voluntary anal contraction S4-5 (Yes/No) LOWER LIMB TOTAL

⫹

(MAXIMUM) (25)

⫽ (25)

TOTALS

with normal function

R

L

C4

C5

0 ⫽ absent 1 ⫽ impaired 2 ⫽ normal NY ⫽ not testable

T2

T3 T4 T5 T6 T7 T8 T9

T1 C6

C5

T1 C6

T10 T11

S3

T12

S4-5 L1

L1

Palm L L 2 2 L L 3 3

S2

L 4 S1

Palm

S2

L 4

L2

L2

L3

L3

L5 L4

COMPLETE OR INCOMPLETE?

⫹

⫽ ⫽

Key Sensory Points

L4

L5

⫹

Dorster

Dorster S1

L5

(MAXIMUM) (56) (56)

(50)

NEUROLOGICAL LEVEL SENSORY The most caucla segment MOTOR

T2

C7 C5 C6

C5 C6 C7 C8 T1

KEY SENSORY POINTS

PIN PRICK R L

C7 C8

(scoring on reverse side)

C4

Spinal cord injury

KEY MUSCLES

L

R

C3

C3

MOTOR

L5

Any anal sensation (Yes/No) PIN PRICK SCORE (max: 112) LIGHT TOUCH SCORE (max: 112)

(56) (56)

Incomlete = aaa sensory cv motor function ps 54–55

ZONE OF PARTIAL PRESERVATION

ASIA IMPAIRMENT SCALE

Casual extent of partialy annenrated segments

R SENSORY MOTOR

This form may be copied freely but should not be allered without premission from the American Spinel Injury Association.

L

S1

S1 S1

CHAPTER 11

Patient Name

MUSCLE GRADING 0

total paralysis

1

palpable or visible contraction

2

active movement, full range of motion, gravity eliminated active movement, full range of motion, against gravity

4

active movement, full range of motion, against gravity and provides some resistance

5

active movement, full range of motion, against gravity and provides normal resistance

5* muscle able to exert, in examiner’s judgement, sufficient resistance to be considered normal if indentifiable inhibiting factors were not present NT not testable. Patient unable to reliably exert effort or muscle unavailable for testing due to factors such as immobilization, pain on effort or confracture.

A = Complete: No motor or sensory function is preserved in the sacral segments S4–S5. B = Incomplete: Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4–S5. C = Incomplete: Motor function is preserved below the neurological level, and more than half of key muscles below the neurological level have a muscle grade less than 3.

D = Incomplete: Motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more. E = Normal: Motor and sensory function are normal.

CLINICAL SYNDROMES (OPTIONAL) Central Cord Brown-Sequard Anterior-Cord Conus Medullaris Cauda Equina

STEPS IN CLASSIFICATION The following order is recommended in determining the classification of individuals with SCI. 1. Determine sensory levels for right and left sides. 2. Determine motor levels for right and left sides. Note: in regions where there is no myotome to test, the motor level is presumed to be the same as the sensory level. 3. Determine the single neurological level. This is the lowest segment where motor and sensory function is normal on both sides, and is the most cephalad of the sensory and motor levels determined in steps 1 and 2 4. Determine whether the injury is Complete or Incomplete (sacral sparing) If voluntary and contraction = No AND all S4-5 sensory scores = 0 AND any anal sensation = No, then injury is COMPLETE. Otherwise injury is incomplete. 5. Determine ASIA Impairment Scale (AIS) Grade: Is injury Complete? If YES, AIS = A Record ZPP (For ZPP record lowest dermatome or NO myotome on each side with some (non-zero score) preservation) Is injury motor incomplete? If NO, AIS = B (Yes=voluntary anal contraction OR motor YES function more than three levels below the motor level on a given side.) Are at least half of the key muscles below the (single) neurological level graded 3 or better? NO YES AIS = C

AIS = D

If sensation and motor function is normal in all segments, AIS = E Note: AIS E is used in follow up testing when an individual with a documented SCI has recovered normal function. If at initial testing no deficits are found, the individual is neurologically intact,; the ASIA Impairment Scale does not apply.

Figure 11.1 ASIA standard neurological classification of spinal cord injury. American Spinal Injury Association: International Standard for Neurological Classification of Spinal Cord Injury, revised 2002. Chicago, IL. Reprinted with permission.

GENERAL FACTS: EPIDEMIOLOGY AND DEMOGRAPHICS

3

ASIA IMPAIRMENT SCALE

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Function by level The recovery after an SCI can be variable, and early on an accurate prognosis cannot always be established. In the acute phase, “spinal shock” may be present. This state is characterized by a lower motor neuron appearance including flaccidity that may last days to weeks. After this phase, a more characteristic “upper motor neuron” picture featuring hyperreflexia will be present. Partial return below the level of the lesion can occur. Depending on the degree of partial return, an individual patient may have significantly greater function than predicted, based on their level. Due to the relative uniformity of innervations by spinal level, some generalizations of function can be made. The following function by level is expected in a complete (ASIA A) SCI (see Table 11.1).

Table 11.1 Spinal cord injury function by level Last level spared

Muscles spared

Sensation spared

Head, some of C2–C4 Cranial nerves, some neck (high tetraplegia) respiratory muscles, no upper or lower extremity muscles

Mobility and ambulation

Functional level

Dependent in Powered wheelchair (may transfers, all be able to control ADLs, will require some respiratory with mouth assistance controls)

C5 tetraplegia

Some shoulder and bicep function

Head, neck, Powered some shoulder wheelchair

Dependent in transfers, may assist in feeding with setup and equipment, respiratory independent

C6 tetraplegia

Shoulder muscles, elbow flexion and wrist extension

Shoulder, some hand

Powered wheelchair, they may be able to assist with transfer

Should be able to perform some ADLs (feeding and grooming) with proper setup and adaptive equipment

C7 tetraplegia

Above, plus Lateral hand triceps and and forearm more finger flexion

May be able to perform sliding board transfer, more likely to propel manual wheelchair

Likely to perform intermittent catheterization, more ADL independence

FUNCTION BY LEVEL

Table 11.1 (Contd.) Last level spared C8 tetraplegia

Muscles Sensation spared spared Most of upper Most of extremities upper extremities spared spared with more normal hand function (some intrinsics may be impaired)

Mobility and ambulation Manual wheelchair, more likely to perform sliding board transfer

Functional level More ADL independence, may be able to drive with hand controls, still requires extensive trunk support in wheelchair, likely able to selfcatheterize

Thoracic paraplegia

Upper extremity spared, varying trunk strength depending on level

Manual wheelchair (less bracing at lower levels), more transfer independence

ADL independence at wheelchair level including catheterization, driving more likely, improved autonomic function at lower levels

Upper lumbar paraplegia

Sparing of Trunk, prox L1 or L2 thigh may give hip flexion or some knee extension

Independent in transfers and wheelchair mobility

As above, good trunk balance. Independent in ADLs, may require household help and shopping and cooking assistance

Lower lumbar paraplegia

Sparing of L3 and L4 can give functional knee extension

Upper extremities, trunk sensation depends on level

Hip flexors, More likely to knee extensors have functional ambulation with bracing

As above

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Tetraplegia (last functioning level above T1) The term tetraplegia replaces the older term quadriplegia. In these cases there is at least some impairment to the upper extremities and generally loss of lower extremity functioning.

High tetraplegics (above the C5 level) These patients will have no significant upper or lower extremity strength. Depending on the level between C2 and C4, there will be some respiratory involvement. Higher levels will require ventilators, and tracheostomies are common in this group. These patients are dependent in all activities of daily living (toileting, eating, bathing, and transferring). Mobility is by powered wheelchair. They may be able to control a motorized wheelchair with mouth controls. They may require diaphragmatic pacing. An indwelling urinary catheter is frequently necessary.

C5 tetraplegia At this level, some shoulder and bicep function is expected, leading to some upper extremity function. These patients are generally dependent in all activities of daily living, but with a balanced forearm orthosis (a device to hold the arms up and eliminate gravity on elbow movement) they may be able to assist in feeding and grooming with proper setup. Breathing is independent and they can usually operate a power wheelchair.

C6 tetraplegia In general, every additional level of preservation in the cervical spinal cord yields very significant functional advantages. C6 preservation allows wrist extension that gives passive grip (tenodesis effect) and therefore provides some functional hand use. Some individuals may be able to assist in transfers and manual wheelchair propulsion. With setup and adaptive equipment, they should be independent in feeding and grooming. Some males may be able to self-catheterize.

C7 tetraplegia At this level, significant triceps function can permit independence in sliding board transfer. These individuals are more likely to be able to intermittently catheterize than those with C6 tetraplegia.

C8 tetraplegia More normal hand functioning (active finger flexion) should give more functioning and a higher degree of grooming and feeding independence without adaptive equipment. Driving (with hand controls) is more likely at this level, as is independence in wheelchair propulsion.

T1–T12 thoracic paraplegia These lesions are characterized by intact upper extremity function and absent lower extremity function. The thoracic nerves give truncal sensation and stability but have no limb innervations (except for T1, which is

FUNCTION BY LEVEL

spared in a T1 paraplegia). Additional levels of preservation give greater truncal stability and sensation. From a functional standpoint, lower thoracic–level paraplegics may have similar levels of independence but require less wheelchair bracing (due to better trunk control). A very significant factor is autonomic function. Patients with lesions at and below the T6 level are unlikely to develop autonomic dysreflexia and orthostatic hypotension (see Complications). With T8 preservation, thermoregulation (temperature control) is usually preserved.

Lumbar paraplegia Upper lumbar neurological levels may allow some hip flexion or even quadriceps strength (knee extension). Sparing of L1 or L2 (in complete lesions) may allow ambulation with a knee ankle foot orthosis (KAFO), but this is generally not considered community ambulation and these individuals will likely be dependent on a manual wheelchair for mobility. Lower-level lesions will give more quadriceps function, and functional or community ambulation (generally with bracing) is likely. The spinal cord ends around the L2 vertebra, and the continuing fibers of the cauda equina are lower motor neurons (peripheral nerve fibers from an anterior horn cell that will exit the spine and innervate muscle). Upper motor neuron signs, such as spasticity and detrussor sphincter dyssynergia, would be absent (see Complications).

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Management and medications Bladder management SCI patients should have urodynamic studies as a baseline and be followed regularly by an urologist. Most paraplegic and tetraplegic patients will have an upper motor neuron bladder with increased detrussor muscle tone. When this increased bladder pressure is combined with inability to relax the sphincter, the resultant detrussor sphincter dyssynergia can cause ureteral reflux and potentially damage the kidneys. When feasible, intermittent straight catheterization and medications to relax the bladder wall are employed. In high tetraplegics, the patient may not be able to perform intermittent catheterization alone and indwelling catheters (Foley or suprapubic) may be necessary (though they carry an increased risk of infection). Generally, urine volumes should be monitored and intake should be restricted to keep catheterization volumes below 500 cc. Straight catheterization should occur 4 times a day. Some fluid restriction can be employed in the evening to permit a schedule that avoids a middle-of-the-night catheterization. Clean technique (not sterile) is usually adequate. In conjunction with catheterizations, anticholinergic agents (such as oxybutynin chloride) are used to decrease bladder tone. Cranberry juice and vitamin C are commonly used to acidify the urine to minimize bacterial growth. Sterile urine is usually not feasible in the SCI patient. When a clinical sign of infection occurs (fever, autonomic dysreflexia, increased WBC, foul smell or urinary change) these infections should be treated. Adult diapers may be necessary for urine (and stool leakage).

Bowel management SCI patients can lose normal bowel motility as well as the sensation that the rectal vault is full and that defecation will occur. Pain medications can also decrease GI motility (primarily opioid analgesics). A bowel program must be individualized, as bowel patterns vary greatly in the uninjured population. Bowel programs include adequate fluid intake, stool softeners, timed evacuations, adequate fiber, bulk-forming preparations, stimulants, and irritants. Through time, the SCI patient can learn how to optimize his or her bowel patterns. Frequently, after eating, a gastrocolic reflex will stimulate defecation. This can be augmented by digital stimulation to initiate defecation. A complication of retained stool is impaction, which can lead to autonomic dysreflexia (see Complications, p. 318).

Skin management (decubiti prevention) Due to the loss of sensory input, SCI patients are at increased risk for pressure ulcers. Depending on patients’ positioning and function, these can occur in various areas. In bedridden patients, pressure ulcers can develop in the sacrum and buttocks, but can occur in any pressure-bearing area. Pressure-reduction mattresses and frequent position changes, as well as frequent skin checks can prevent these complications.

MANAGEMENT AND MEDICATIONS

For paraplegics and tetraplegics in a wheelchair, pressure relief can be in the form of special cushions and position changes (wheelchair pushups should be encouraged in those who are capable). The skin should be checked and maintained in a clean and dry environment. There are numerous dressings available for decubitus ulcer treatment. Pressure relief is necessary for any healing.

Contracture prevention SCI patients may be wheelchair bound for prolonged periods of time. They may also have spasticity, which will also increase the likelihood of contractures. The most common lower extremity contractures are ankle plantar flexion, hip flexion, and knee flexion. To prevent a contracture, joints should be carried through their full range of motion several times per day. If the patient is capable of ambulating (with bracing) this will also help prevent or minimize hip flexion, knee flexion, and ankle plantar flexion contractures.

Deep vein thrombosis (DVT) prophylaxis Due to the loss of muscle pumping in the legs, SCI patients are at increased risk for DVT and thromboembolic events. Preventative measures should include compressive stockings, an anticoagulant (low-molecular-weight heparin is generally preferable over Coumadin or subcutaneous heparin), and intermittent compression devices. For those at significant risk of DVT, an inferior vena cava filter may be also used.

Spasticity management In some SCI patients, spasticity may not be a significant problem. Furthermore, some patterns of spasticity can increase function (especially extensor patterns in the lower extremities). In many instances, spasticity can be irritating and painful, and clonus may occur with certain movements. In spasticity management a combination of medications, positioning, nerve blocks, neuromuscular junction blocks (phenol or botulinum toxin), intrathecal baclofen, and, in rare cases, surgery is used. Generally, antispasmodics such as baclofen or tizanidine are employed as first-line medications.

Autonomic management Due to autonomic nervous system disruption, SCI patients are at risk of hypotension at rest and orthostatic hypotension with sitting or standing, as well as impaired thermoregulation. Compressive stockings will help somewhat, but other treatments may be necessary. Some physical modalities such as gradually changing position from lying to standing will help compensate for these problems. Frequently, adrenergic medications or mineralocorticoids are necessary to maintain blood pressure. The risk of hypertension with these, however, requires careful titration.

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Common SCI medications and their uses Bladder • Oxybutynin chloride (Ditropan): anticholinergic, decreases detrussor muscle tension • Tamsulosin (Flomax): alpha-antagonist, decreases smooth muscle contraction • Vitamin C, cranberry juice: acidifies urine, may have a bacteriostatic effect Bowel • Docusate sodium (Colace): stool softener • Psyllium powder (Metamucil): bulk-forming agent • Senna (Senokot): stimulates peristalsis • Bisacodyl suppository (Dulcolax): stimulates peristalsis • Glycerin suppositories: draws water into colon Spasticity • Tizanidine (Zanaflex): alpha-2 agonist • Baclofen (Lioresal): GABA analog that can be used orally or intrathecally • Diazepam (Valium): potentiates GABA, CNS depressant Autonomic • Fludrocortisone acetate (Florinef): mineralocorticoid increases sodium resorption • Ephedrine sulfate: a sympathomimetic agent (an alpha- and betaagonist) raises blood pressure. DVT prophylaxis • Enoxaparin (Lovenox): low-molecular-weight heparin (generally preferred) • Coumadin • Subcutaneous heparin Autonomic dysreflexia • Nitroglycerine (sublingual or nitropaste) • Procardia 10 mg (chewed or punctured) • Clonidine 0.1–0.2 mg PO • IV hydralazine (10 mg push over 30 seconds) or nipride

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Complications General There are several complications of SCI that are common and that the clinician must be aware of. Some, such as decubiti and contractures, result from loss of sensation and mobility limitations in large part due to abnormalities of the somatic nerves. Others, such as orthostatic hypotension and autonomic dysreflexia, are abnormalities primarily of the autonomic nervous system (sympathetic and parasympathetic fibers). Other complications, such as detrussor sphincter dyssynergia, are related primarily to disruption of both sympathetic and somatic nerve function. Avoidance of complications requires constant vigilance by the patient and caregivers.

Autonomic dysreflexia Autonomic dysreflexia is an emergent and potentially life-threatening situation that physicians and SCI patients must be aware of. It is unlikely to occur in lesions below T6. It generally occurs from noxious stimuli below the level of the injury and leads to an overflow of sympathetic activity. This can result in severe hypertension, which is frequently accompanied by severe headache and sweating. The cause of the stimulus should be removed immediately. If no other obvious cause is present, straight catheterize to reduce a full bladder. The patient should be checked for stool impaction or skin lesions (decubiti, ingrown toenails, etc.). Because autonomic dysreflexia can be life threatening, blood pressure should be monitored. Proper positioning (sit patient up, remove compressive stockings and abdominal binder) and medications (nitroglycerine, nitropaste, Procardia) to rapidly decrease blood pressure should be immediately instituted. Symptoms • Headache • Hypertension • Sweating • Blurry vision Common potential causes (causes of noxious stimuli below level of lesion) • Urinary distension • Infection • Fecal impaction • Skin lesion • Other Treatment • Straight catheterize • Sit patient up • Remove compressive stockings and abdominal binder • Check for cause and remove irritating stimulus • Monitor BP

COMPLICATIONS

• If systolic BP remains over 150 mmHg, institute antihypertensive medications • Antihypertensive medications: nitroglycerine paste, Procardia, clonidine, hydralazine (IM or IV), amyl nitrate (inhaled)

Heterotopic ossification The formation of bone in soft tissues can lead to contractures and pain. Heterotopic ossification is common and can occur in up to 50% of SCI patients (although it may not be clinically significant). Range of motion can help prevent joint contractures. The diagnosis can be made by radiological studies, including X-rays and bone scan. Etidronate disodium can decrease the amount of bone produced. Surgery is rarely indicated.

Further reading DeLisa JA, Gans BM, Walsh NE, Bockenek WL, Frontera WR (eds.). (2004). Physical Medicine and Rehabilitation, Principles and Practice, 4th ed. Philadelphia: Lippincott Williams & Wilkins pp. 1715–1751. Kirshblum S. et al. (2004). Spinal cord injuries. In Cucurillo S (ed.). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical Publishing, pp. 489–551. Nesathurai S (2000). The Rehabilitation of People with Spinal Cord Injury, 2nd ed. Boston: Blackwell Science, pp. 1–122.

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Chapter 12

Traumatic brain injury Ricardo Cruz

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Traumatic brain injury Definition Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain, possibly leading to permanent or temporary impairments of cognitive, physical, and psychosocial functions with an associated diminished or altered state of consciousness.

Introduction According to the National Institutes of Health (NIH), TBI is a major public health problem, especially among • Male adolescents and young adults ages 15–24 years old • Elderly people of both sexes age 75 years and older • Children aged 5 and younger Based on NIH data: • Approximately 1.4 million people experience a TBI. • Approximately 50,000 people die from head injury. • Approximately 1 million head-injured people are treated in hospital emergency rooms. • Approximately 230,000 people are hospitalized for TBI and survive. The financial cost is estimated at approximately $4 billion per year. This estimate includes loss of potential income of the patient and relatives who may need to become caregivers, cost of acute care, and other medical expenses such as continuous ambulatory and rehabilitation care.

Causes of TBI • Skull fractures (e.g., depressed or penetrating) • Diffuse axonal injury (e.g., coup/contrecoup injuries, shaken baby syndrome) • Hemorrhage (e.g., epidural, subdural, subarachnoid, intracerebral hemorrhage) • Anoxia/hypoxia (e.g., post-cardiac arrest, near-drowning)

Classification of TBI based on Glasgow Coma Scale Based on the Glasgow Coma Scale score (within 48 hours post-injury): • Severe TBI = 1–8 • Moderate TBI = 9–12 • Mild TBI = 13–15

Glasgow Coma Scale The Glasgow Coma Scale (GCS) defines severity of TBI within 48 hours of injury. Three determinants of GCS • Motor response • Eye opening • Verbal response

TRAUMATIC BRAIN INJURY

Eye opening • Spontaneous = 4 • To speech = 3 • To painful stimulation = 2 • No response = 1 Motor response • Follows commands = 6 • Makes localizing movements to pain = 5 • Makes withdrawal movements to pain = 4 • Flexor (decorticate) posturing to pain = 3 • Extensor (decerebrate) posturing to pain = 2 • No response = 1 Verbal response • Oriented to person, place, and date = 5 • Converses but is disoriented = 4 • Says inappropriate words = 3 • Says incomprehensible sounds = 2 • No response = 1

Symptoms of TBI Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain. Symptoms of mild TBI may include headache, dizziness, sensory problems, fatigue, change in sleep patterns, and behavioral, mood, and cognitive changes. Sensory problems include blurring of vision, tinnitus or a bad taste in the mouth. Cognitive changes include problems with memory, concentration, and attention. Moderate or severe TBI may show similar symptoms and may include persistent and/or worsening headache, nausea and vomiting, seizures, anisocoria, slurring of speech, ataxia, weakness, numbness in the extremities. and altered mental status. Mental status and behavioral changes can range from confusion, restlessness, and agitation to a vegetative state or coma.

Ranchos Los Amigos Scale The severity of deficit in cognitive functioning can be defined by the Ranchos Los Amigos Scale. The levels are based on observations of the patient’s response to external stimuli. They provide a descriptive guideline of the various stages a patient with brain injury will experience as he or she progresses through recovery. An understanding of the eight levels provides insight into the progression through recovery and rehabilitation. 8 levels of Ranchos Los Amigos Scale • Level I = no response • Level II = generalized response • Level III = localized response • Level IV = confused–agitated

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Traumatic brain injury

Level V = confused–inappropriate Level VI = confused–appropriate Level VII = automatic–appropriate Level VIII = purposeful–appropriate

Posttraumatic amnesia (PTA) PTA occurs in all patients when they emerge from coma. Disorientation to time, place, and person occurs. Patients can have a confused state, diminished memory, and reduced ability to attend and respond to environmental cues. PTA duration has clinical significance and prognostic implications.

Galveston Orientation and Amnesia Test (GOAT) The duration of PTA can be reliably and quickly assessed with the Galveston Orientation and Amnesia Test (GOAT). A score of 76 or more on three consecutive occasions is considered to indicate that the patient is out of PTA. The test should be administered daily.

Complications of TBI • Seizures • Depression • Heterotopic ossification • Hydrocephalus • Deep venous thrombosis (DVT) • Spasticity • GI complications: bowel incontinence, stress ulcer • GU complications: urinary incontinence, urinary tract infection

Principles of treatment Moderately to severely injured patients may receive treatment and care in an ICU of a hospital. When the patient becomes stable, the patient may be transferred to an acute rehabilitation center or acute rehabilitation unit of the medical center where aggressive multidisciplinary rehabilitation (MDR) can be provided. MDR involves individually tailored treatment programs in the areas of physiatry, physical therapy, occupational therapy, speech/language therapy, nutrition, psychology and psychiatry, rehabilitation nursing, social work and support, and recreational therapy. From the acute rehabilitation facility, the patient may be discharged to: • Home with home care services and therapy • Subacute facility or skilled nursing facility • Outpatient rehabilitation • Supportive and vocational living programs • School-based programs for children The TBI patient, the family, and the rehabilitation team members should work together to find the best place for the patient to recover.

TRAUMATIC BRAIN INJURY

Medications used in TBI Anti-anxiety agents and agents to control agitation (benzodiazepines) • Ativan (lorazepam) • Xanax (alprazolam) Antidepressants SSRIs • Lexapro (escitalopram) • Paxil (paroxetine) • Zoloft (sertraline) TCAs • Elavil (amitriptyline) • Pamelor (nortriptyline) Anti-seizure medications • Depakote (valproate) • Dilantin (phenytoin) • Keppra (levetiracetam) • Neurontin (gabapentin) • Tegretol (carbamazepine) Anti-spasticity agents Systemic • Lioresal (baclofen) • Zanaflex (tizanidine) Local • Botox (botulinum toxin injection) • Intrathecal baclofen (ITB pump) • Phenol (peripheral nerve blocks) Attentional agents • Provigil (modafinil) • Ritalin (methylphenidate) Sleep agents • Desyrel (trazodone) • Restoril (temazepam)

Prognosis Indicators to predict the level of a patient’s recovery are as follows: • Duration of coma • Severity of coma in the first few hours after the injury (based on GCS) • Duration of PTA • Severity of contusions and hemorrhages in the brain • Severity of other injuries sustained The duration of PTA is the best indicator of the extent of cognitive and functional deficits after TBI. The GCS gives a prognosis for survival rather than for functional outcomes. Patients with additional hypoxic or ischemic injury usually have a worse outcome for the same duration of coma.

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Further reading Baguley IJ, Cameron ID, Green AM, Slewa-Younan S, Marosszeky JE, Gurka JA (2004). Pharmacological management of dysautonomia following traumatic brain injury. Brain Injury 18(5):409–417. Brown AW, Malec JF, McClelland RL, et al. (2005). Clinical elements that predict outcome after traumatic brain injury: a prospective multicenter recursive partitioning (decision-tree) analysis. J Neurotrauma 22(10):1040–1051. Bushnik T, Englander J, Duong T (2004). Medical and social issues related to posttraumatic seizures in persons with traumatic brain injury. J Head Trauma Rehabil 19(4):296–304. Cifu DX, Kaelin DL, Wall BE (1996). Deep venous thrombosis: incidence on admission to a brain injury rehabilitation program. Arch Phys Med Rehabil 77(11):1182–1185. Davis DP, Serrano JA, Vilke GM, et al. (2006). The predictive value of field versus arrival Glasgow Coma Scale score and TRISS calculations in moderate-to-severe traumatic brain injury. J Trauma 60(5):985–990. Dikmen SS, Bombardier CH, Machamer JE, et al. (2004). Natural history of depression in traumatic brain injury. Arch Phys Med Rehabil 85(9):1457–1464. Greenwald BD, Burnett DM, Miller MA. (2003). Congenital and acquired brain injury. 1. Brain injury: epidemiology and pathophysiology. Arch Phys Med Rehabil 84(3 Suppl 1):S3–S7. Harrison-Felix C, Whiteneck G, Devivo MJ, et al. (2006). Causes of death following 1 year postinjury among individuals with traumatic brain injury. J Head Trauma Rehabil 21(1):22–33. Jordan B (200)). Cognitive rehabilitation following traumatic brain injury. JAMA 283:3123–3124. Jorge RE, Robinson RG, Moser D, et al. (2004). Major depression following traumatic brain injury. Arch Gen Psychiatry 61(1):42–50. Khan F, Baguley IJ, Cameron ID (2003). Rehabilitation after traumatic brain injury. Med J Aust 178(6):290–295. Khateb A, Ammann J, Annoni JM, Diserens K (2005). Cognition-enhancing effects of donepezil in traumatic brain injury. Eur Neurol 54(1):39–45. Langlois JA, Rutland-Brown W, Thomas KE (2006). Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention. Lu J, Marmarou A, Choi S, et al. (2005). Mortality from traumatic brain injury. Acta Neurochir Suppl 95:281–285. Melamed E, Robinson D, Halperin N, et al. (2002). Brain injury-related heterotopic bone formation: treatment strategy and results. Am J Phys Med Rehabil 81(9):670–674. Parcell DL, Ponsford JL, Rajaratnam SM, Redman JR (2006). Self-reported changes to nighttime sleep after traumatic brain injury. Arch Phys Med Rehabil 87(2):278–285. Smith DH, Meaney DF, Shull WH (2003). Diffuse axonal injury in head trauma. J Head Trauma Rehabil 18(4):307–316. Solomon S (2001). Posttraumatic headache. Med Clin North Am 85(4):987–996. Whitnall L, McMillan TM, Murray GD, Teasdale GM (2006). Disability in young people and adults after head injury: 5–7 year follow up of a prospective cohort study. J Neurol Neurosurg Psychiatry 77(5):640–645. Zafonte RD, Mann NR, Millis SR, et al. (1997). Posttraumatic amnesia: its relation to functional outcome. Arch Phys Med Rehabil 78(10):1103–1106.

Chapter 13

Stroke Ricardo Cruz Andrew Galmer

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Stroke

Stroke Introduction A stroke by definition is a neurological deficit caused by a defect in vascular flow to a certain portion of the brain. There are two major categories of stroke: ischemic and hemorrhagic. Ischemia is caused by a decreased blood supply to the brain, while hemorrhage is considered to be large amounts of blood within a closed cranial cavity. Strokes present clinically in many ways given the different areas of the brain that are affected.

Ischemic stroke Ischemic stroke occurs when there is a disruption of the vascular flow to a region of the brain, usually because of occlusion of an intracranial vessel. Ischemic strokes may occur due to thrombosis, embolism, or shock. A lack of blood supply to a portion of the brain can lead to death of brain tissue in that area, resulting in focal neurological defects. A stroke is considered a medical emergency that must be quickly diagnosed and treated. Transient ischemic attacks (TIA) Episodes of TIAs are stroke symptoms that last for less than 24 hours. Most symptoms, however, will last for less than 1 hour. TIAs can result from emboli that travel into the brain or from intracranial vessel thrombosis. During a TIA, the occlusion is only temporary and neurological function is fully restored. Rapid improvement of symptoms is a contraindication to thrombolysis therapy; however, acute antiplatelet therapy is recommended. There are three subtypes of brain ischemia. Thrombosis • Local obstruction of an artery is usually due to arteriosclerotic lesions of the neck (from carotid artery disease) or in medium-sized arteries of the brain, most commonly originating from the middle cerebral artery. • Patients classically present with neurological deficits after waking up and onset may be either rapid or stepwise. • Lacunar stroke is caused by small vessel thrombotic disease most commonly affecting the subcortical structures but sparing the cerebral cortex. Patients usually have a history of hypertension along with diabetes. Embolism • Embolic events occur when particles from distant sources travel to block arterial perfusion to brain tissue. Emboli most commonly originate from a mural thrombus within the heart in a patient with atrial fibrillation. Other sources of emboli include the internal carotid artery, aorta, and blood clots from the periphery that pass through septal defects (paradoxical emboli). • The onset of embolic stroke is fast, occurring in just seconds with maximal deficits noticed immediately.

STROKE

Systemic hypoperfusion • Decreased systemic perfusion leads to more widespread effects. Hypoperfusion can be due to low cardiac output, pulmonary embolism, or hypoxemia. • Watershed infarcts may occur along bordering cerebral arteries after a prolonged period of hypotension. Signs and symptoms Symptoms of ischemic stroke tend to present rapidly and are dictated by the area of the brain that is affected, along with the severity of the event. Patients with acute stroke frequently do not seek medical attention because they do not experience pain and they may lose the ability to recognize that something is wrong. Often it is a family member that calls for help. Patients may present with the following: • Paresthesias of face, arm, or leg on same side • Difficulty speaking or understanding • Visual disturbances • Confusion, vertigo, disequilibrium, trouble walking • Sudden onset of headache Differential diagnosis: Other causes can mimic stroke in the sudden onset of neurological symptoms (see Box 13.1). These must be considered before initiation of treatment. History and physical High suspicion for stroke should be considered in patients presenting with an acute onset of neurological deficits and/or altered levels of consciousness.

Box 13.1 Disorders that may present similar to stroke • • • • • • • • • • • • • • • • • •

Seizure Intracranial tumor Migraine Metabolic encephalopathy Multiple sclerosis Hypoglycemia Systemic infections Toxic metabolic cause Hyponatremia Positional vertigo Syncope Subdural hematoma Herpes encephalitis Transient global amnesia Demyelinating disease Myasthenia gravis Hypertensive encephalopathy Conversion disorder

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• Clinically, hemorrhagic strokes present more often with nausea, vomiting, and headache, whereas ischemic strokes typically do not. • Patients will present with a combination of symptoms including paresis, vision loss, visual field deficits, ataxia, and aphasia. • Timing of the onset of symptoms is important for meeting the time restrictions for the initiation of thrombolytic therapy (typically therapy must be initiated within 3 hours of the event). Physical examination should focus on detection of extracranial causes, ruling out other pathologies, and a complete neurological examination. An examination should include the following: • Examination of the head and neck for trauma, infectious processes, fundal examination, cardiovascular examination for murmurs, auscultation for carotid bruits, and palpation of the peripheral pulses • Neurological status should be thoroughly yet quickly assessed, including mental status, level of consciousness, cranial nerves, motor and sensory function, and cerebellar function. A stroke scale such as the National Institutes of Health Stroke Scale (NIHSS) can be used to analyze the neurological deficits and to follow the patient’s progression (see Table 13.1). The location of the lesion will determine specificity of symptoms (see Table 13.2). The NIHSS has a total of 42 points, with small strokes having a score less than 5. Specific stroke syndromes Gerstmann syndrome • Anatomy: cerebral hemisphere—dominant parietal lobe • Artery: middle cerebral artery • Symptoms: acalculia • Agraphia • Finger agnosia • Right and left disorientation Anton syndrome • Anatomy: cerebral hemispheres—bilateral occipital lobes • Artery: posterior cerebral artery (bilateral basilar artery) • Symptoms: visual loss—bilateral • Unawareness or denial of blindness Weber syndrome • Anatomy: midbrain–base • Artery: posterior cerebral artery (penetrating branches to midbrain) • Symptoms: contralateral hemiparesis • Ipsilateral lateral gaze weakness Dejerine–Roussy syndrome • Anatomy: thalamus • Artery: posterior cerebral artery—penetrating branches to thalamus • Symptoms: hemisensory loss—all modalities • Hemi-body pain

STROKE

Table 13.1 National Institutes of Health Stroke Scale (NIHSS) 1a. Level of consciousness (LOC)

0 = alert and responsive; 1 = arousable to minor stimulation; 2 = arousable to painful stimulation; 3 = reflex responses

1b. LOC questions: Ask patient’s age and month. Must be exact

0 = both correct; 1 = one correct; 2 = neither correct

1c. Commands: Open/close eyes, 0 = both correct; 1 = one correct; grip and release nonparetic hand. 2 = neither correct 2. Best gaze: Horizontal extraocular 0 = normal; 1 = partial gaze palsy; movement by voluntary or abnormal gaze in one or both eyes; doll’s eye 2 = forced eye deviation or total paresis that cannot be overcome by doll’s 3. Visual field: Use visual field threat if necessary. If monocular, score field of good eye.

0 = no visual loss; 1 = partial hemianopsia, quadrantanopsia, extinction; 2 = complete hemianopsia; 3 = bilateral hemianopsia or blindness

4. Facial palsy: If stuporous, check symmetry of grimace to pain. Paralysis (lower face)

0 = normal; 1 = minor paralysis (normal-looking face, asymmetric smile); 2 = partial, 3 = complete paralysis (upper and lower face)

5. Motor arm: Arms outstretched 90º (sitting) or 45* (supine) for 10 seconds. Encourage best effort, note paretic side.

0 = no drift; 1 = drift but does not hit bed; 2 = some antigravity effort, but cannot sustain; 3 = no antigravity effort, but even minimal movements count; 4 = no movement at all; X = unable to assess due to amputation, fusion, etc.

6. Motor leg: raise leg to 30* supine for 5 seconds 7. Limb ataxia: Check finger–nose– finger; heel–shin; score only if out of proportion with paresis.

0 = no ataxia (or aphasic, hemiplegic); 1 = ataxia in upper or lower extremity; 2 = ataxia in upper & lower extremity; X = unable to assess as above

8. Sensory: Use safety pin. Check grimace or withdrawal if stuporous. Score only strokerelated losses.

0 = normal; 1 = mild to moderate unilateral loss but patient aware of touch (or aphasic, confused); 2 = total loss, patient unaware of touch. Coma, bilateral loss

9. Best language: Describe cookie jar picture, name objects, read sentences. May use repeating, writing, stereognosis

0 = normal; 1 = mild–moderate aphasia (comprehensible); 2 = severe aphasia (almost no information exchanged); 3 = mute, global aphasia, coma

10. Dysarthria: Read list of words.

0 = normal; 1 = mild–moderate slurred; 2 = severe, unintelligible or mute; X = intubation or mechanical barrier

11. Extinction/neglect: Simultaneously touch patient on both hands, show fingers in both visual fields, ask about deficit, left hand.

0 = normal, none detected (or visual loss alone; 1 = neglects or extinguishes to double simultaneous stimulation in any modality; 2 = profound neglect in more than one modality

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Table 13.2 Examples of location-specific lesions Lesion

Symptoms

Temporal lobe

Wernicke’s aphasia: patient has fluent speech but is incomprehensible, wordy

Frontal lobe

Broca’s aphasia: unable to verbalize, broken speech

Cortical

Decorticate posturing: flexion of arms

Midbrain/lower lesion

Decerebrate posturing: extension of arms

Anterior cerebral artery

Contralateral lower extremity weakness and/ or sensory disturbance, disinhibition and speech perseveration, primitive reflexes, impaired judgment

Middle cerebral artery

Aphasia, contralateral hemiparesis, contralateral hypesthesia, ipsilateral hemianopsia. Arm/face weakness > leg weakness

Posterior cerebral artery Altered vision and thought: contralateral homonymous hemianopsia, cortical blindness, visual agnosia, altered mental status, impaired memory Vertebral/basilar

Ipsilateral cranial nerve deficits and contralateral motor deficits

Lacunar strokes

Motor, sensory, and ataxic hemiparetic strokes. Usually do not lead to impairments in cognition, memory, speech, or level of consciousness

Locked-in syndrome • Anatomy: bilateral ventral pons • Artery: basilar artery • Symptoms: paralysis of both upper and lower extremities • Paralysis of both sides of the face • Intact vertical gaze and blinking Millard–Gubler syndrome • Anatomy: unilateral ventrocaudal pons • Artery: basilar artery—short circumferential branches Basilar artery—paramedian branches • Symptoms: contralateral upper and lower extremity weakness • Ipsilateral facial weakness • Ipsilateral lateral gaze weakness Wallenberg syndrome • Anatomy: posterior lateral medulla • Artery: posterior inferior cerebellar artery • Symptoms: loss of pain and temperature sensation on the ipsilateral face and contralateral body • Ipsilateral Horner’s syndrome, ataxia, dysphagia, hoarseness, nystagmus, vertigo Dejerine syndrome • Anatomy: medial medulla

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Table 13.3 Commonly used testing in ischemic stroke Test

Results

CT scan head (no contrast)

• This is the first imaging study that should be ordered. • Differentiate between ischemic and hemorrhagic infarction. • Ischemic areas will appear dark whereas hemorrhagic areas will be white. • CT identifies 95% of subarachnoid hemorrhages.

MRI of brain

• More sensitive than CT scan • Not used in emergency setting

ECG

• Identifies cardiac causes such as MI or atrial fibrillation

Carotid duplex

• Analyzes percentage of carotid stenosis

Magnetic resonance arteriogram

• Identifies head and neck vessel stenosis and aneurisms

• • • •

Artery: anterior spinal artery Symptoms: contralateral hemiparesis Contralateral sensory loss (vibration and proprioception sense) Ipsilateral hypoglossal palsy

Diagnostic tests in the workup of ischemic stroke can include head CT, brain MRI, ECG (halter monitor), carotid duplex, and magnetic resonance angiogram. Other tests to order in the emergency department include CBC, PT/PTT, serum electrolytes, blood glucose, and echocardiogram (see Table 13.3). Special considerations • Risk factors for stroke include age, hypertension, smoking, diabetes mellitus (DM), hyperlipidemia, atrial fibrillation, septal defects, coronary artery disease, family history of stroke, previous stroke, and carotid bruits. • Risk of stroke in a patient with a TIA is about 10% per year, 30% in 5 years. • Younger patients prone to stroke include those using oral contraceptives and those with a hypercoaguable state, sickle cell disease, polycythemia vera, or cocaine use. • Special attention should be paid to amaurosis fugax (monocular blindness) during a TIA, as it may indicate carotid stenosis or local ophthalmic artery disease. • Consider endarterectomy for patients with >70% occluded carotid artery with symptoms. Management (treatment) The goal of treatment of ischemic stroke is to increase cerebral perfusion and prevent complications such as infections and DVT. • Supportive treatment is started immediately, including establishing an airway, oxygen, and IV fluids.

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• Blood pressure control should be initiated if systolic reading is >220, diastolic BP >120, MAP >130, or patient has an indication for therapy and/or is receiving thrombolytic therapy to prevent bleeding. • There is a clear benefit for administration of IV recombinant Alteplase (rtPA) in patients with acute stroke. Clinical outcome was improved if patients received rtPA within 3 hours of onset of ischemic stroke (National Institute of Neurological Disorders and Stroke) (see Table 13.4). • Within 3 hours of onset of stroke, rtPA is administered at a dose of 0.9 mg/kg IV—10% of total dose as a bolus and the rest of the total dose within 1 hour. Complications and red flags • Neurological insult can worsen. • Cerebral edema is seen 1–2 days after onset of symptoms for up to 10 days. High intracranial pressures may result and must be controlled with mannitol. • Hemorrhage into infarction • Seizures Medical care Medical care for acute ischemic stroke occurs on a continuum, beginning in the prehospital setting and ending at home after discharge. Stroke centers and organized protocols for the acute and in-house treatment of stroke patients have been shown to decrease morbidity and mortality associated with stroke. Prehospital care personnel are critical elements in the acute ischemic stroke chain of survival. Emergency medical services (EMS) personnel should begin with the ABCs (airway, breathing, circulation) and, once the patient’s condition is stable, should perform a more directed assessment and administer supportive treatment. Prehospital stroke assessment tools, such as the Cincinnati Prehospital Stroke Scale or Los Angeles Prehospital Stroke Scale, identify patients with Table 13.4 Indications and contraindications for rtPA Indications for rtPA therapy Clinical diagnosis of stroke Onset of symptoms to administration of rtPA <3 hours CT scan is negative for hemorrhage or edema 18 years of age or older Consent Contraindications to rtPA therapy BP over 185/110 not responding to medical treatment Platelets <100,000; Hct <25%; glucose <50 or >400 mg/dL Heparin use within 48 hours, prolonged PTT, elevated INR Rapid improvement of symptoms Stroke, head injury, intracranial hemorrhage within 3 months Major surgery within 2 weeks Gastrointestinal bleeding within 3 weeks Recent myocardial infarction Coma or stupor

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potential stroke. Providing supplemental oxygen when indicated, establishing IV lines, measuring serum glucose, and administering glucose in hypoglycemic patients are elements of prehospital stroke care. Equally important is prehospital triage and notification of a potential stroke patient. This allows for early mobilization of necessary resources, such as a stroke team, radiology, and pharmacy. With the creation and certification of primary stroke centers, regional health-care systems should determine the best triage policy for potential stroke patients in their area. The goal of acute stroke management in the emergency department is rapid and efficient care. Continuing from assessment of the ABCs, stroke patient evaluation and, if eligible, fibrinolytic therapy should be administered within 1 hour from presentation, as shown in Table 13.5. Stroke management is a team effort with nursing and medical staff working closely together. General stroke care issues are outlined in Table 13.6.

Table 13.5 NINDS recommended stroke evaluation time benchmarks for potential thrombolysis candidate Time interval

Time target

Door to doctor Access to neurologic expertise Door to CT scan completion Door to CT scan interpretation Door to treatment Admission to monitored bed

10 minutes 15 minutes 25 minutes 45 minutes 60 minutes 3 hours

Table 13.6 General management of patients with acute stroke Blood glucose

Treat hypoglycemia with D50 Treat hyperglycemia with insulin if serum glucose >200 mg/dL

Blood pressure

See recommendations for thrombolysis candidates and noncandidates (see Table 13.7)

Cardiac monitor

Continuous monitoring for ischemic changes or atrial fibrillation

Intravenous fluids

Avoid D5W and excessive fluid administration IV isotonic sodium chloride solution at 50 mL/hr unless otherwise indicated

Oral intake

NPO initially; aspiration risk is great, avoid oral intake until swallowing assessed

Oxygen

Supplement if indicated (SaO2 <90%, hypotensive, etc.)

Temperature

Avoid hyperthermia, oral or rectal acetaminophen as needed

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Fibrinolytic therapy of IV recombinant Alteplase activator (rtPA) for appropriate patients within 3 hours from symptom onset remains a Class I recommendation by the American Stroke Association. Hypoglycemia and hyperglycemia need to be identified and treated early in the evaluation. Not only can both produce symptoms that mimic ischemic stroke, but they also can aggravate ongoing neuronal ischemia. Administration of glucose in hypoglycemia produces profound and prompt improvement, while insulin should be started for patients with stroke and hyperglycemia. Ongoing studies will help determine the optimal level of glycemic control. Hyperthermia is infrequently associated with stroke but can increase morbidity. Administration of acetaminophen, by mouth or per rectum, is indicated in the presence of fever (temperature >100.4°F). Supplemental oxygen is recommended when the patient has a documented oxygen requirement. To date, conflicting evidence exists that supernormal oxygenation improves outcome. Optimal blood pressure targets remain to be determined. Many patients are hypertensive on arrival. Recent American Stroke Association guidelines have reinforced the need for caution in lowering blood pressures acutely. Table 13.7 shows current recommendations for both candidates and noncandidates for thrombolytic therapy. In the small proportion of patients with stroke who are relatively hypotensive, pharmacologically increasing blood pressure may improve flow through critical stenoses. Surgical care Surgical intervention is rarely required urgently in acute ischemic stroke; however, current recommendations suggest that neurosurgical care should be available within 2 hours when needed, e.g., to evaluate surgical options in hemorrhagic transformation following t-PA or in the management of life-threatening elevations of intracranial pressure (ICP). Increased ICP is a life-threatening event occurring in as many as 20% of all strokes; it is more common in large, hemispheric strokes. Edema and herniation are the most common causes of early death in patients with hemispheric stroke. Patient position, hyperventilation, hyperosmolar therapy, and rarely, barbiturate coma may be used, as in patients with increased ICP secondary to closed head injury. Recent reports of hemicraniectomy to treat life-threatening ICP have suggested that these patients have shorter ICU stays and a lower mortality rate if surgery is performed before clinical deterioration. One randomized clinical trial did not confirm these benefits. Selected patients with either hemorrhagic transformation or intracerebral hemorrhage after thrombolytic therapy may benefit from surgical evacuation of the hematoma. If neurosurgical care is not available in-house, a transfer policy is encouraged to expedite patient transfer when neurosurgical expertise is needed.

Hemorrhagic stroke Hemorrhagic stroke occurs when a blood vessel in the brain ruptures or leaks. There are two main types of hemorrhagic strokes, which refer to

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Table 13.7 Blood pressure management in patients with stroke* Candidates for fibrinolysis

Blood pressure

Treatment

Pretreatment SBP >185 or DBP >110 mmHg

Labetalol 10–20 mg IVP 1–2 doses or Enalapril 1.25 mg IVP

Post-treatment DBP >140 mmHg

Sodium nitroprusside (0.5 mcg/kg/min)

SBP >230 mmHg or DBP 121–140 mmHg

Labetalol 10–20 mg IVP and consider labetalol infusion at 1–2 mg/min or nicardipine 5 mg/hr IV infusion and titrate

SBP 180–230 mmHg or DBP Labetalol 10 mg IVP, may repeat and double every 10 105–120 mmHg minutes up to maximum dose of 150 mg Noncandidates for fibrinolysis

DBP >140 mmHg

Sodium nitroprusside 0.5 mcg/kg/min; may reduce approximately 10%–20%

Labetalol 10–20 mg IVP over SBP >220 or DBP 121–140 mmHg or MAP >130 mmHg 1–2 minutes; may repeat and double every 10 minutes up to maximum dose of 150 mg or nicardipine 5 mg/hr IV infusion and titrate SBP <220 mmHg or DBP 105–120 mmHg or MAP <130 mmHg

Antihypertensive therapy indicated only if acute MI, aortic dissection, severe CHF, or hypertensive encephalopathy present

*Adopted from 2005 Advanced Cardiac Life Support (ACLS) guidelines and 2003 American Stroke Association Scientific Statement.

location of the insult: intracerebral hemorrhage and subarachnoid hemorrhage (SAH). Intracerebral hemorrhage A primary intracerebral hemorrhage consists of bleeding into the brain parenchyma, leading to brain damage directly at the site of the hemorrhage by compression of the surrounding tissue. • Bleeding is usually the result of rupture of arterioles, with hematoma formation and accumulation of blood over minutes to hours. The hematoma spreads and enlarges until it is limited by increasing pressure or is decompressed by entering into the nearby ventricular system or into the cerebrospinal fluid (CSF). • Common causes include hypertension, trauma, bleeding diatheses, amyloid angiopathy, amphetamines, and cocaine use. • Ischemic stroke can convert into hemorrhagic stroke. • Common areas affected include basal ganglia, pons, cerebellum, and cortical areas.

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• It is associated with a 50% mortality rate in 30 days, and significant morbidity for survivors. Signs and symptoms Patients will present with the following: • Focal neurological deficits that worsen over minutes to a few hours (as compared to embolism or SAH, in which effects are abrupt and maximal initially) • Altered level of consciousness • Headache and vomiting • Increased intracranial pressure • Earliest symptoms relate to the portion of the brain that is affected by the hemorrhage (see Tables 13.2 and 13.8). History and physical • It is important to rule out other pathologies that may mimic hemorrhagic stroke (see Box 13.1). • Hypertension, fever, or cardiac arrhythmias should be ruled out. • Nuchal rigidity may be present. • Subhyaloid retinal hemorrhages may be present. • Altered level of consciousness • Anisocoria (pupils of unequal diameter) Diagnostic tests CT scanning can be diagnostic 95% of the time depending on the size of the bleed. Analyze for the following: • Hematoma volume • Displacement of tissue • Edema Blood studies include CBC, platelets, and coagulation panels, serum electrolytes; order a toxicity screen if findings are suspicious. Special considerations Prognosis depends on age, smoking history, and location of the aneurysm. Table 13.8 Findings in specific hemorrhagic lesions Lesion

Findings

Pons

Pinpoint pupils

Thalamus

Decreased reactivity of pupils, contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

Putamen

Dilated pupils, contralateral limb motor and/or sensory signs

Cerebellum

Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, miosis, or decreased level of consciousness

Left temporal lobe

Aphasia

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• Smokers have a worse prognosis. • Anterior circulation aneurysms carry a more favorable prognosis. Management It is important to establish a diagnosis of hemorrhagic stroke before treatment is started. Admit the patient to the ICU and establish airway, breathing, and circulation. • Blood pressure treatment with nitroprusside must be started if systolic BP is >160 or diastolic BP is >105. • Hyperventililation, mannitol, and diuretics should be started if ICP is increased. • Anticonvulsant medications for seizure activity or lobar hemorrhage • Surgical decompression of cerebellar hematomas (>3 cm) may be indicated (not indicated for intracerebral hemorrhage).

Subarachnoid hemorrhage Subarachnoid hemorrhage (SAH) occurs when there is a hemorrhage into the CSF outside of the brain parenchyma. SAHs are caused either by a rupture of arterial aneurysms near the base of the brain or by vascular malformations near the pial surface. Blood is released into the CSF and rapidly increases the ICP, causing death if bleeding is severe. SAH is most commonly caused by a ruptured berry aneurism near the bifurcation of arteries at the Circle of Willis. Signs and symptoms • Patients with SAH experience a very abrupt onset of severe headache described as “the worst headache of my life.” • Absence of focal neurological signs initially (unless bleeding occurs into brain simultaneously) • 50% experience loss of consciousness • Vomiting • Loss of memory • Retinal hemorrhages • Late onset of meningial irritation (neck stiffness, photophobia, and low back pain) and photophobia Diagnosis • Order the following lab studies: serum chemistry panel, CBC count, PT/PTT, and blood typing/screening tests. • Noncontrast CT of the head is the most sensitive imaging study (it can be negative in 10%). • Grading SAH • Grade I: no subarachnoid blood seen on CT scan • Grade II: diffuse or vertical layers of SAH <1 mm thick • Grade III: diffuse clot and/or vertical layer >1 mm thick • Grade IV: intracerebral or intraventricular clot with diffuse or no subarachnoid blood • Look for evidence of hydrocephalus. • Lumbar puncture (LP) to evaluate CSF if the CT is negative with high clinical suspicion • Blood in the CSF increases suspicion for SAH.

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• Xanthochromia, or yellowish discoloration of the CSF from red blood cell lysis is diagnostic for SAH. • Patients with negative CT and LP findings have a good prognosis. • Cerebral angiogram to detect for bleeding site Complications Rerupture • Incidence is greatest in the first 2 weeks. • The peak is within 24–48 hours following initial SAH (approximately 6%), with a rate of 1.5% per day for the next 12–13 days. Vasospasm • Can occur in 50%, leading to ischemic events • Most common cause of death and disability following aneurysmal SAH Hydrocephalus • Acute: may present within the first 7 days, usually due to interference of CSF outflow (obstructive mechanisms) • Delayed: insidious presentation • Seizures • Syndrome of inappropriate antidiuretic hormone secretion (SIADH) Treatment The goal of treatment of SAH is to identify the source of bleeding and quickly treat it to prevent rebleeding. Medical treatment • The patient should be placed in a quiet room and given mild sedation if agitated and IV fluids. • Elevate head of bed to 30° to increase venous drainage. • Stool softeners (docusate sodium, senna) to prevent elevation of ICP associated with Valsalva maneuver • Pain control • Nifedipine can be given to prevent vasospasm and ischemia. • Phenytoin or phenobarbitol can prevent recurring seizures and terminate electrical seizure activity. • Blood pressure should be controlled within a range that allows for cerebral perfusion yet limits risk of rebleeding (nitroprusside, labetalol) Surgical treatment • Berry aneurisms are clipped surgically to prevent rebleeding. • Endovascular techniques can be used as an alternative to clipping (with reduced morbidity and mortality compared to clipping).

Stroke rehabilitation Stroke rehabilitation settings Inpatient rehabilitation is defined as “rehabilitation performed during an inpatient stay in a freestanding rehabilitation hospital or a rehabilitation unit of an acute care hospital. The term inpatient is also used to refer generically to programs where the patient is in residence during treatment, whether in an acute care hospital, a rehabilitation hospital, or a nursing facility.”

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Nursing facility rehabilitation is defined as “rehabilitation performed during a stay in a nursing facility. Nursing facilities vary widely in their rehabilitation capabilities, ranging from maintenance care to comprehensive and intense rehabilitation programs.” Outpatient rehabilitation is defined as “rehabilitation performed in an outpatient facility that is either freestanding or attached to an acute care or rehabilitation hospital. Day hospital care is a subset of outpatient rehabilitation in which the patient spends a major part of the day in an outpatient rehabilitation facility.” Home-based rehabilitation is defined as a “rehabilitation program provided in the patient’s place of residence.”1 Principles of stroke rehabilitation • Successful rehabilitation of a stroke patient includes early enrollment into a customized, comprehensive, multidisciplinary program including a physiatrist, physical, occupational and speech therapy programs, the patient, his or her family, psychologist, and vocational counselor. • Emphasis should be placed on education of the patient and family members about prevention of stroke by controlling blood pressure and diabetes, and eliminating risk factors including smoking, obesity, high cholesterol, and poor diet. • Physical therapy has been shown to recruit unused neural pathways that eventually improve long-term neural recovery. Therapeutic exercises to improve cortical reorganization may include robot-assisted exercise training, neurodevelopmental techniques, constraint-induced movement therapy (CI movement therapy involves forced used of the involved upper extremity and discourages use of the unaffected extremity), and treadmill training with the body weight partially suspended (promotes symmetrical removal of body weight to facilitate locomotor abilities after stroke). Neurodevelopmental techniques for motor recovery focus on a progression of movement through the developmental sequence, inhibition of primitive reflexes and spasticity, and facilitation of higher-level control. • Strength, range of motion, gait, and sensation should be analyzed with aims to develop an individual regimen. • Transcutaneous electrical nerve stimulation (TENS) is used to encourage brain reorganization and recovery of function using a small electrical probe to stimulate nerve activity in stroke-impaired limbs. • Occupational therapy is used for ADLs such as feeding, dressing, toileting and bathing. • The patient needs to relearn skills such as personal grooming, preparing meals, and housecleaning. • Speech–language pathologists help the patient relearn language, improve swallowing abilities, and develop problem-solving skills. • Stroke patients must be warned about aspiration as they may have difficulty swallowing. 1 Gresham GE, Duncan PW, Stason WB, et al. Post-Stroke Rehabilitation. Clinical Practice Guideline, No. 16. Rockville, Md: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research; May 1995. AHCPR Publication No. 95–0662.

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• Repeated treatments of botulinum toxin after a stroke help to reduce spasticity and reduce pain in the arms and hands. • Phenol block has been shown to be effective in reducing spasticity. • Bracing may be helpful to restore mobility and ambulation. • Splinting may assist with appropriate positioning, decrease spasticity, decrease contractures, and improve functional ability. • Visual and spatial neglect should be treated by functional adaptation measures such as visual scanning, environmental adaptation and modification, and patient and caregiver education. • Assistive devices are used to improve ambulation and mobility and promote independence in ADLs. • It is important to treat post-stroke depression because it can impact the patient’s participation in therapy and delay recovery. Post-stroke management includes pharmacotherapy such as SSRIs and TCAs. Cognitive-behavioral therapy techniques and brief supportive therapy may also be beneficial. • Stroke rehabilitation should also focus on minimizing disability and preventing complications such as deep vein thrombosis, contractures, pain, complex regional pain syndrome or reflex sympathetic dystrophy, immobility, pneumonia, decubiti, shoulder subluxation, pain, incontinence, sexual dysfunction, brachial plexus injury, frozen shoulder, dysphagia, bowel and bladder dysfunction, depression, spasticity, and seizures.

Further reading Adams HP, Adams RJ, Brott T, et al. (2003). Guidelines for the early management of patients with ischemic stroke: a scientific statement from the Stroke Council of the American Stroke Association. Stroke. 34(4):1056–1083. Agabegi S (2008). Step Up to Medicine. Cincinnati: Lippincott Williams and Wilkins. Ayala C, Spellberg B (2007). Boards and Wards. Baltimore: Lippincott Williams and Wilkins. Fauci A, Braunwald E, Kasper D, Hauser S (2008). Harrison’s Principles of Internal Medicine, 17th ed. New York: McGraw-Hill. Goldstein LB, Samsa GP (1997). Reliability of the National Institutes of Health Stroke Scale. Extension to non-neurologists in the context of a clinical trial. Stroke 28:307–310. Kirazli Y, On AY, Kismali B, Aksit R (1998). Comparison of phenol block and botulinus toxin type A in the treatment of spastic foot after stroke: a randomized, double-blind trial. Am J Phys Med Rehabil 77:510–515. Lincoln NB, Flannaghan T, Sutcliffe L, Rother L (1997). Evaluation of cognitive behavioural treatment for depression after stroke: a pilot study. Clin Rehabil. 11:114–122. Mathiowetz V, Haugen JB (1994). Motor behavior research: implications for therapeutic approaches to central nervous system dysfunction. Am J Occup Ther 48:733–745. On AY, Kirazli Y, Kismali B, Aksit R (1999). Mechanisms of action of phenol block and botulinus toxin type A in relieving spasticity: electrophysiologic investigation and follow-up. Am J Phys Med Rehabil 78:344–349. Visintin M, Barbeau H, Korner-Bitensky N, Mayo NE (1998). A new approach to retrain gait in stroke patients through body weight support and treadmill stimulation. Stroke 29:1122–1128. Zoltan B (1996). Vision, Perception and Cognition: A Manual for the Evaluation and Treatment of the Neurologically Impaired Adult. Thorofare, NJ: Slack.

Chapter 14

Pulmonary and cardiac rehabilitation Jay M. Weiss Lyn Weiss Pulmonary rehabilitation 344 Cardiac rehabilitation 348

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Pulmonary rehabilitation General description Pulmonary rehabilitation is the process of evaluating and improving pulmonary function. Success depends on understanding and managing the cause of the dysfunction and designing a program to improve endurance and independence. The underlying pulmonary disorder should be identified. In cases of inadequate pulmonary function this can be due to intrinsic diseases of the lung such as chronic bronchitis, asthma, emphysema, or cystic fibrosis (frequently causing chronic obstructive pulmonary disease, or COPD) or factors extrinsic to the lungs such as general muscle weakness (ALS, myopathy, disorder of the diaphragm or nerves supplying the muscles). Most of the intrinsic disorders of the lung cause air trapping from either loss of elasticity or obstruction of the airways due to spasm or secretions. Some of these factors can be reversed or improved with medications. The most important and correctable cause of COPD is cigarette smoking. The incidence of COPD increases with increases in the number of pack-years smoked.1 Pulmonary rehabilitation has been shown to improve function and endurance and decrease hospitalization. However, it has not been shown to significantly improve pulmonary function tests (PFTs).

Clinical manifestations Patients with COPD, including emphysema and chronic bronchitis, are most commonly smokers. Obviously, smoking cessation in these individuals is an important component of the patient’s care.

History Shortness of breath may occur with activity. In more severe cases, this may occur with minimal exertion or at rest. In intrinsic disorders of the lung, a smoking history will most commonly be elicited. The severity of the symptoms commonly increases over time. In extrinsic disorders, there will usually be a medical reason (Guillain– Barré, spinal cord injury, muscular dystrophy, etc.) that should be thoroughly detailed.

Physical In COPD patients, the physical examination may reveal labored breathing, pursed-lip breathing (an effort to increase expiratory pressure to prevent airway collapse), use of accessory muscles of respiration, cyanosis, or a barrel chest. Auscultation may reveal signs of airway secretions including rales and wheezing. Sputum production may be appreciated.

Diagnostic testing Baseline pulmonary function tests are necessary in patients with dyspnea.1 The FEV1 (amount of air exhaled in 1 second with maximum effort) is one 1 Qaseem A, Snow V, Shekelle P, et al. (2007). Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians, Ann Intern Med 147(9):633–638.

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of the most important measures. Oxygen saturation is not a substitute for spirometry, but can be used during the rehabilitation process as it is easier to measure than arterial PO2 and can be easily done with a pulse oximeter during exercise.

Management (treatment) Treatment for stable COPD should be reserved for patients with respiratory symptoms and FEV1 <60%.1 Medications can include beta-agonists, anticholinergics, and steroids (inhaled or oral) depending on the underlying lung pathology and response. Medications should be optimized prior to start of a pulmonary rehabilitation program. Supplemental oxygen should be prescribed for patients with PaO2 of 55 mmHg or less.1 Oxygen should also be used in patients whose O2 saturation drops below 90% during exercise.

Pulmonary rehabilitation The goal of pulmonary rehabilitation programs is to improve function by increasing endurance and oxygen extraction and decreasing or expelling secretions. After an assessment, certain techniques can be used to optimize air movement and minimize air trapping. These include instruction in diaphragmatic breathing (to retrain the patient to use the diaphragm more than the chest muscles). Positioning changes can be used to address ventilation and perfusion mismatches and to help with postural drainage. More efficient coughing techniques can be taught to help expel secretions. This will help prevent pooling of secretions, subsequent infections, or air trapping. Manual chest therapy, including percussion or a vibrator, can help mobilize secretions. A pulmonary rehabilitation program should include endurance and/or reconditioning exercises. For these the therapist needs to monitor the patient’s heart rate and oxygen saturation. The heart rate should be limited, generally as a percentage of an age-adjusted maximal heart rate (this is especially important for patients with additional cardiac disease). Oxygen saturation should be monitored as well as the patient’s perceived exertion. Exercise should be discontinued for O2 saturation below 90%, significant increases in exertion or dyspnea, chest pain, or tachycardia or irregular heart rate. Therapy should be performed 3–5 days per week. Walking is a fundamental part of a pulmonary rehabilitation, and patients should be encouraged to walk outside of therapy (with appropriate precautions and oxygen supplementation if required). An exercise bicycle may also be beneficial for home use. An important part of therapy is for patients to learn their abilities and limitations so they can safely exercise at home. Physical or occupational therapists should also help develop an upper body exercise program. Occupational therapists may be helpful in assessing activity of daily living (ADL) impairments and with prescribing assistive devices. Respiratory

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therapists can help instruct patients in the proper use of medications and mobilization of secretions and teach them breathing techniques. In pulmonary patients, nutritional evaluations may also be needed.

Further reading Bach JR (2007). Respiratory rehabilitation. In O’Young B, Young M, Stiens S (eds.). Physical Medicine and Rehabilitation Secrets. St. Louis: Mosby, pp. 195–203. Bach JR (2008). Pulmonary rehabilitation. In Frontera WR, Silver JK, Rizzo TD (eds.). Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: Saunders–Elsevier, pp. 823–831. Gonzalez P, Cuccurullo S (2004). Pulmonary/cardiac/cancer. In Cuccurullo S (ed.). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical, pp. 585–644.

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Cardiac rehabilitation General description The goal of cardiac rehabilitation is to restore and maintain an optimal physiological, psychological, social, vocational, and emotional status in patients with cardiovascular disease.

Phases of cardiac rehabilitation Engery expenditure is often calculated in metabolic equivalents (METs). MET is a measure of total energy expenditure (based on Calories); 1 MET corresponds to 1.2 Calories/minute. A person at rest is using 1 MET. The intensity of exercise or exertion is commonly estimated in METs. The phases of cardiac rehabilitation depend on the timing of cardiac events Phase I In phase I, the patient is hospitalized. This phase is divided into the acute and subacute phases. Acute This is the phase of rehabilitation when the patient is hospitalized. During the acute period, when the patient is still in the coronary care unit (CCU), the goal is to prevent deterioration. Activities of 1–2 METS are performed. Isometrics should be avoided, as this increases heart rate. Valsalva maneuvers should not be performed, as this could increase the likelihood of arrhythmias. The legs should not be raised above the head because this can increase preload demands. While the patient is in the CCU, a bedside commode should be used so there is less of a cardiac demand (3.6 METS for a commode vs. 4.7 METS for a bedpan). Constipation should be avoided to reduce the risk of Valsalva maneuver. Subacute During this phase of rehabilitation the patient is transferred to the telemetry or medical ward. Early ambulation is encouraged, and the patient should be performing activities at about the 3–4 MET level. Phase II This is the supervised ambulatory outpatient phase; it lasts about 3–6 months. ECG stress is typically performed during this phase to guide further rehabilitation. Phase III This is the intermediate phase and is not as intensely monitored. Phase IV The goal is to improve physical fitness and decrease risk factors for cardiovascular disease

Outcomes of cardiac rehabilitation • Improved exercise tolerance • Improvement of symptoms • Decreased angina

CARDIAC REHABILITATION

• • • • •

• Decreased heart failure in patients with left ventricular systolic dysfunction • Improved measures of myocardial ischemia (MI) Improved psychosocial well-being Improved blood lipid levels Stress reduction Decreased cigarette smoking Decreased cardiovascular mortality

History The patient must be asked about reversible and irreversible risk factors for cardiovascular disease. Reversible risk factors include hypertension, cigarette smoking, hypercholesterolemia, obesity, sedentary lifestyle, diabetes mellitus, and hypertriglyceridmia. Irreversible risk factors include age, male gender, family history of coronary artery disease, and a past history of coronary artery disease, peripheral vascular disease, or congestive heart failure (CHF).

Exercise intensity Ideally, the intensity of an exercise program should be great enough to produce a training effect, yet low enough that it does not overload the cardiopulmonary system. No ECG or blood pressure abnormalities should be noted as a result of the exercise training. The intensity and duration of exercise may be determined by several methods. The most common is the target heart rate, which is calculated as 220 minus the patient’s age; 80% of this number would be considered the target heart rate. Those with low fitness levels or patients taking betablockers may require a lower level of intensity. Other ways to measure exercise intensity include the METs level of activity, rating of perceived exertion (the Borg scale is a 10- or 15-grade scale of perceived exertion), or oxygen consumption (as measured by expired gases). Patients will get the most consistent benefit from exercising is if they exercise at least 3 times per week for at least 1/2 hour per session.

Exercise in specific populations Amputees Energy costs for patients with prostheses should be taken into consideration when ascertaining if a patient could benefit from a prosthesis. There is a 50%–75% increase in the energy cost of ambulation with crutches, whereas a unilateral below-knee prosthesis increases the energy cost of ambulation by only about 9%–28% (see Chapter 10, Amputation). Sexual activity Many patients are reluctant to return to sexual activity after a cardiac event for fear of damaging the heart. Normal sexual intercourse among normal middle-aged couples is about 3–4 METs. Therefore, if patients can achieve a physical activity of 5 METs or more, it is safe to resume sexual activity (i.e., about the same amount of energy required to ascend and descend two flights of stairs).

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Extramarital sex or sex preceded by heavy eating or drinking may place more demands on the heart. Cardiac rehabilitation and the physically disabled Modifications to exercise programs should be made to accommodate the physically disabled. For example, in a hemiplegic patient who wishes to exercise, the paretic leg can be strapped to a stationary bicycle pedal (or the paretic arm to a handlebar). Upper extremity cycling can be performed on an upper extremity ergometer by patients with lower extremity weakness or limited range of motion.

Complications and red flags Absolute contraindications to exercise testing and training for patients with MI include acute MI, unstable angina, moderate to severe aortic stenosis, resting systolic blood pressure above 200 mmHg or diastolic pressure above 110 mmHg, uncontrolled arrhythmias, tachycardia above 100 beats/ minute, symptomatic CHF, third-degree heart block (without pacemaker), active pericarditis or myocarditis, recent embolism or thrombophlebitis, uncontrolled diabetes, or resting ST displacement >3 mm. Relative contraindications include significant arterial or pulmonary hypertension, moderate valvular or myocardial heart disease, electrolyte abnormalities, left main coronary obstruction, hypertrophic cardiomyopathy, and psychiatric disease.

Suggested reading Balady GJ, Fletcher BJ, Froelicher EF, et al. (1994). Cardiac rehabilitation programs: a statement for healthcare professionals from the American Heart Association. Circulation 90:1602–1610. Leon AS, Franklin BA, Costa F, et al. (2005). Cardiac rehabilitation and secondary prevention of coronary heart disease. Circulation 111:369–376. Stukel TA, Alter DA (2009). Analysis methods for observational studies: effects of cardiac rehabilitation on mortality of coronary patients. J Am Coll Cardiol 54(1):34–35

Chapter 15

Pediatrics Thomas Pobre Rebecca Trangco-Evans Rafael Abramov Prematurity 352 Cerebral palsy 354 Spina bifida 360

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Prematurity Background Prematurity is defined as a birth before 37 weeks of gestation. It accounts for about one-third of all infant deaths in the United States and half of children with cerebral palsy. The degree of prematurity is defined by gestational age or birth weight. Complications of prematurity increase with the degree of prematurity. Extremely preterm infants have about 50% mortality rate and have the greatest risk of impairment if they survive.

Classification • Based on gestational age • Late preterm birth: 34 to <37 weeks • Very preterm birth: <32 weeks • Extremely preterm birth: <25 weeks • Based on birth weight • Low birth weight: <2500 grams • Very low birth weight: <1500 grams • Extremely low birth weight: <1000 grams

Complications of premature infants Risk of complications of the preterm infant increases with severity of prematurity. Complications can be divided into short term and long term. Short-term complication occurs in the neonatal period and results from anatomic and functional immaturity. These include hypothermia, respiratory distress, symptomatic patent ductus arteriosus, hypotension, hypoglycemia, infection, and intracranial hemorrhage. Survivors of preterm birth are more likely to have neurodevelopmental and chronic health problems. Increased prevalence of impaired cognitive skills, motor deficits, cerebral palsy, sensory impairment including vision and hearing losses, and behavioral and psychological problems have been documented in survivors of premature birth.

Developmental Intervention Different schools of thought exist on the intervention for premature infants. One school argues that intervention should be aimed at simulating the intrauterine environment. The other school believes that the preterm differs substantially from the fetus and requires intervention similar to that for the term infant. There is, however, an agreement that early recognition of and intervention for children with developmental disabilities is needed. The Individuals with Disabilities Education Act (IDEA) mandates early intervention for eligible patients between birth and the age of 3 years. Each state is required to develop a program to identify patients that are eligible and to provide intervention.

Therapeutic exercise Premature infants are at higher risk of having neuromuscular dysfunction. Management includes positioning to prevent exaggeration of abnormal tone, reflexes, and postures. Most studies evaluating the effectiveness

PREMATURITY

of early intervention for motor dysfunctions are anecdotal reports and personal experiences. Many methods of therapeutic exercises have been developed. • Proprioceptive neuromuscular facilitation (PNF) recommends resistive exercises to facilitate movement by increased proprioceptive input. This is applicable to the older child. • Rood advocates activating muscles through sensory receptors following a sequence of developmental patterns. Treatment is aimed at awareness of normal patterns. • Brunnstrom recommends facilitating a predictable synergistic pattern to produce purposeful motion. • Neurodevelopmental treatment (NDT), developed by Bobaths, is based on the premise that impaired postural mechanism is responsible for abnormal movement. The aim is to alter abnormal postures, improve balance in antigravity postures, and develop movement patterns following the normal developmental sequence. This is the most widely use method. Other methods include biofeedback therapy and conductive education.

Long-term neurodevelopmental outcome Improvement in neonatal care over time has resulted in improved patient survival and possibly improved neurodevelopmental outcomes. Changes in practice that could help bring about the improvement include the use of antenatal glucocorticoid, surfactant and breast milk, and decreased use of postnatal corticosteroid and high-frequency ventilation. Despite the increased risk of disability, studies done in Canada and England have shown that adult survivors of preterm births may overcome their neurodevelopmental deficit and function comparable to those born full term.

Further reading Taggart PJ, Matthews DJ (1992). Developmental intervention and therapeutic exercise. In Molnar GE (ed.) Pediatric Rehabilitation. Philadelphia: Williams & Wilkins.

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Cerebral palsy General description Cerebral palsy (CP) consists of a heterogeneous group of nonprogressive disorders of motor and postural impairment resulting from an injury to the developing brain. It is considered the most common physical disability in childhood and has an incidence of 2.5 per 1000 live births in the United States. There is an increased chance of developing CP in premature and low-birth-weight infants.

Clinical manifestations CP has a wide variability of presentation, ranging from mild motor disturbance to severe global mental and physical dysfunction (see Table 15.1). Early detection is by demonstration of persistence of primitive reflexes or a delay in their disappearance. The Moro reflex cannot be elicited in the first months of life in most patients with CP, whereas the presence of the Babinski sign can be a reliable tool for early diagnosis of spastic CP. Voluntary movement is described as uncoordinated and requires marked effort and concentration. There is co-contraction of agonist and antagonist muscles with mass movements during motor activity. The disordered movements result in developmental delay of gross motor skills. There may be a combination of weakness, lack of coordination, and/or presence of abnormal tone in certain group of muscles.

Differential diagnosis This includes global developmental delay, autism, muscular dystrophies, spinal muscular atrophy, Down syndrome, spinal cord injuries, arginase deficiency, glutaric aciduria type 1, juvenile neuronal ceroid-lipofuchinosis (Vogt–Spielmeyer disease), juvenile variant of metachromatic dystrophy, Lesch–Nyhan syndrome, mitochondrial disorders, Niemann–Pick disease type C, Pelizaeus–Merzbacher disease, and Rett syndrome.

History The injury to the central nervous system may occur in the prenatal, perinatal, or postnatal periods. Prenatal (70%–80%) • Excessive maternal weight gain • Diabetes • Lupus • Seizure disorder • Placental insufficiency • HIV • TORCH • Illegal drug use • Prescription medication use • Alcohol and tobacco use • Multiple gestation Perinatal • Low birth weight • Intraventricular hemorrhage

CEREBRAL PALSY

Table 15.1 Classification of cerebral palsy and major causes Motor syndrome

Associated features

Neuropathology

Major causes

1. Spastic type Spastic diplegia: legs > arms

Normal intelligence Minimal seizures

Periventricular leukomalacia (PVL), particularly the internal capsule

Prematurity Ischemia Infection Endocrine/metabolic (thyroid)

Spastic quadriplegia: all four extremities are equally involved

High association with mental retardation and seizures

PVL Multicystic encephalomalacia Malformations

Intrapartum ischemia/anoxia (32%) Infection Endocrine, metabolic Genetic, developmental

Spastic hemiplegia: one- sided involvement, arm > leg, Double hemiplegia: both sides, arms>legs

Seizure disorder in 30% Mental retardation in 25%

Stroke in utero or neonatal Calcifications associated with congenital infections CT/MRI shows atrophic contralateral cerebral hemisphere with dilated lateral ventricle

Thrombophilic disorders: anticardiolipin antibodies Infection Genetic or developmental Periventricular hemorrhagic infarction

Lesions in putamen, globus pallidus, thalamus, basal ganglia

Birth asphyxia Kernicterus Mitochondrial Genetic/metabolic

2. Extrapyramidal Less common (10%–20%) (athetoid, dyskinetic) Negative upper motor neuron sign Intellect preserved Seizures uncommon 3. Ataxichypotonic

Rarest form (5%–10%) Wide-based gait, intention tremor Impaired balance and coordination

Cerebellar hypoplasia Cerebral dysgenesis Granule cell deficiency Joubert syndrome

Mixed type

Spastic and dystonic

Lesions in deep gray Asphyxia matter structures Toxins

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• • • • •

Pediatrics

Cyanotic heart disease Perinatal asphyxia Prolonged ventilation Tracheostomy Metabolic disorders

Postnatal • Bacterial meningitis • Viral encephalitis • Hyperbilirubinemia • Motor vehicle collisions • Falls • Child abuse

Physical Spastic hemiplegia • Hand preference at an early age • Delayed walking, circumductive gait, toe walking, weak dorsiflexors • Growth arrest in the hand and thumbnail of affected limb • Spastic equinovarus deformity of the foot • Ankle clonus, Babinski sign on affected side Spastic diplegia • Drags the legs during crawling • Excessive adduction of hips in severe cases • Scissoring posture of lower limbs • Tiptoe walking, equinovarus • Unable to sit if paraspinal muscle weak • Bilateral Babinski sign Spastic quadriplegia • Marked motor impairment • Swallowing difficulties leading to aspiration pneumonia • Decreased spontaneous movements • Generalized spasticity • Flexion contractures of knees and elbows in late childhood • Speech and visual impairment Extrapyramidal: athetoid/choreoathetoid • Hypotonic infants with poor head control, marked head lag • Variable tone with rigidity and dystonia over several years • Feeding difficulty, (+) tongue thrust, drooling • Speech absent or sentences slurred, voice modulation impaired • Abnormally slow writhing movements of the hands, feet, arms, or legs that are exacerbated during periods of stress and absent during sleep Positive signs of spastic CP • Spastic hypertonia • Hyperreflexia caused by hyperexcitability of the stretch reflex • Extensor plantar responses • Clonus

CEREBRAL PALSY

Negative signs of spastic CP • Slow, effortful voluntary movements • Impaired fine motor function • Difficulty in isolating individual movements • Fatigability

Diagnostic testing • Cranial ultrasound to assess hemorrhagic or hypoxic injury • MRI of the brain to determine location and extent of structural lesions or associated congenital malformations • MRI of the spinal cord to rule out spinal cord injury • Audiology, visual examination • Genetic evaluations, chromosomal studies, blood chemistries • Developmental screening tools

Special consideration Although CP is a nonprogressive condition, the clinical expression of the neuropathological lesions may change over time as the brain matures, with a changing course of function and dysfunction over the years of growth and development. Secondary conditions such as lack of mobility, joint contractures, malnutrition, incontinence, and relative social isolation may be addressed. The strongest predictor of mortality is intellectual impairment. Death before age 40 is usually due to respiratory problems. Over 30 years of age, causes of death are cancers and diseases of the circulatory system. In the older age group the cause of death is usually from diseases of the digestive and nervous systems.

Management A multispecialty management team is needed to address the wide variety of conditions in CP. The team should include a pediatrician, orthopedist, physiatrist, neurologist, physical therapist, occupational therapist, orthotist or prosthetist, speech and language pathologist, social worker, psychologist, and educator. Physical therapy • Muscle strengthening, stretching of tight muscle groups • Constraint therapy in hemiplegia • Gait and posture training • Assistive device training Occupational therapy • Neurodevelopmental treatment (Bobath) • Fine motor skills • Adaptive devices for ADLs Orthotist Bracing includes AFO, hip abduction braces, hand and wrist splints, and spinal braces or jackets. In addition to therapies, bracing, and medical equipment used in CP, medications can have an important role in decreasing spasticity and increasing functions (see Table 15.2). Orthotic and neurosurgical interventions also may be employed (see Box 15.1 and Table 15.3).

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Table 15.2 Common medications for treatment of spasticity Drug

Mechanism of action

Side effects

Pharmacology and dosing

Baclofen

GABA agonist, binds to GABAB receptors of lamina I–IV of spinal cord, presynaptic inhibition of monoand polysynaptic reflexes

Sedation, confusion, nausea, dizziness, muscle weakness, ataxia, paresthesia. Withdrawal can produce seizures, rebound hypertonia, fever, and death.

Oral and intrathecal. Mean half-life is 3.5 hours Metabolized in kidney Intrathecal route: minimum body weight 15 kg Oral dose: start at 2.5–5 mg/day, increase to 30 mg/day (2–7 years old) or 60 mg/ day (age ≥8)

Dose-dependent decrease in stretch reflex and grip strength with diffuse weakness, sedation, nausea, vomiting, diarrhea, paresthesia, hepatotoxicity

Half-life is 15 hours, metabolized in the liver Pediatric dose: 0.5 mg/kg bid, up to 3 mg/ kg qid

Dantrolene Inhibits release sodium of calcium at the sarcoplasmic reticulum

Clonidine

Nausea, vomiting, Alpha-2 agonist, bradycardia, decreases hypotension, dry tone through hyperpolarization of mouth, drowsiness, dizziness, constipation, motoneurons Has antinociceptive depression effect through release of substance P

Mean half life: 5–19 hours Metabolized in liver and kidney Dose: start 0.05 mg bid, titrate until side effects limit tolerance

Tizanidine

Same as clonidine Alpha-2 agonist. Same as clonidine No studies clearly demonstrated use in children with CP

Half-life is 2.5 hours Extensive first-pass metabolism in liver Start at 2 mg at bedtime until max 36 mg/day

Botulinum toxin

Acts on motor end plate by blocking release of neurotransmitter acetylcholine and inhibiting muscle contraction

Increased stumbling, leg Onset of action in cramps, leg weakness, 12–72 hours, peak at calf atrophy, pain during 1–3 weeks, lasts 2–6 months injection, infection, bleeding, rash, allergic Dose usually <20 U/ reaction, bruising, kg body weight temporary incontinence, pneumonia, and constipation

Diazepam

Facilitates postsynaptic binding of GABA in brainstem, reticular formation

CNS depression, sedation, Mean half-life: 20–80 memory loss, impaired hours attention, decreased Metabolized in the motor coordination. Limit liver Dose 0.12–0.8 use to severely involved mg/kg/day in divided children doses

CEREBRAL PALSY

Box 15.1 Orthopedic intervention in CP • • • •

Adductor tendon release Pelvic osteotomy for hip subluxation Muscle-tendon lengthening procedure Capsulotomies, osteotomies for rigid deformities

Table 15.3 Neurosurgical interventions in CP Procedure

Use

Drawbacks

Selective neurectomy

Focal hypertonia

Large scar, excess weakening

Selective dorsal rhizotomy

Generalized spasticity legs

Focal sensory loss Risk of bladder dysfunction Perioperative bronchospasm Degenerative spine

Selective dorsal root entry zone lesioning

Generalized spasticity of arms

Focal sensory loss Degenerative spine

Intrathecal baclofen

Generalized hypertonia Generalized spasticity, being used functionally Mixed hypertonia

Wound healing Infection Catheter obstruction Catheter leakage/breakage Respiratory collapse from overdose

Deep brain stimulation

Dystonic CP

Unclear efficacy Infection Intracranial bleeding

Further reading Abbott R (2004). Neurosurgical management of abnormal muscle tone in childhood. Pediatr Clin North Am 51(2):457–475. Green L, Greenberg GM, Hurwitz E (2003). Primary care of children with cerebral palsy. Clin Fam Pract 2(2):467–491. Hutton JL (2006). Cerebral palsy life expectancy. Clin Perinatol 33(2):545–555. Johnston MV (2007). Encephalopathies. In Kliegman RM, Behrman RE, Jenson HB, Stanton B (eds.). Nelson Textbook of Pediatrics, 18th ed. Philadelphia: Saunders. Krigger KW (2006). Cerebral palsy: an overview. Am Fam Physician 73:91–100. Liptak GS, Accardo PJ (2004). Health and social outcomes of children with cerebral palsy. J Pediatr 145(2 Suppl):S36–S41. Miller G (2007, May 30). Clinical features and diagnosis of cerebral palsy. UpToDate. Sawyer JR (2007). Cerebral palsy. In Canale ST, Beaty JH (eds.). Campbell’s Operative Orthopaedics, 11th ed. Verrotti A, Greco R, Spalice A, Chiarelli F, Iannetti P (2006). Pharmacotherapy of spasticity in children with cerebral palsy. Pediatr Neurol 34:1–6.

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Spina bifida General description Spina bifida is a group of congenital neural-tube malformations affecting the posterior spinal elements that occur during the neurulation process at 24–28 days of gestation. It consists of three entities classified according to degree of the defect (see Fig. 15.1). Spina bifida occulta In this type there is failure of fusion of posterior vertebral arches. It is the mildest form of the disease, discovered by incidental finding. The most common area of defect is S1, followed by S2. It is covered by normal skin. The true incidence is unknown because of its benign nature. Meningocele This is a defect in vertebral bony structure with herniation of meninges and cerebrospinal fluid. It is usually covered with normal skin. Myelomeningocele The defect occurs in the vertebral bony structure with herniation of the spinal cord, nerves, meninges, and CSF. It is usually an open sac. This is most common type of known incidences of spinal dysraphism and is the most debilitating. The most common site is the lumbar spine.

Etiology The etiology of spina bifida is multifactorial: environmental, genetic, geographic, racial, ethnic, and socioeconomic. The U.S. Public Health Service recommendation of 400 mcg folic acid daily for females of child-bearing age greatly reduces the incidence of spina bifida, which suggests that folic acid deficiency is an etiologic factor for spina bifida.

Clinical manifestations The clinical features depend on the level of the lesion, which can occur anywhere along the spine. This affects the degree of neurological and physical impairments.

History The diagnosis is usually made during the prenatal period. Higher prevalence of spina bifida is seen with other genetic diseases (usually trisomy), gestational diabetes, maternal hyperthermia, and use of folate antagonists (phenobarbital, phenytoin, etc.) during the first month of gestation.

Physical Myelomeningocele is confirmed at birth with a visible sac (with or without skin break) at any level of the spinal cord. Uncomplicated spina bifida oculta can present as a patch of hair, birthmark, or skin dimple in the defected area. It is very important to perform a thorough neurological, orthopedic, and physiatric examination on the patient with spina bifida to assess the degree of paralysis, sensory loss, bladder and bowel dysfunction, and bone and/or soft tissue abnormalities.

SPINA BIFIDA

Figure 15.1 Three types of spina bifida (from left to right): spina bifida occulta, meningocele, and myelomeningocele.

Diagnostic testing • Maternal serum alpha-fetoprotein (AFP) screening is done at 15–20 months of gestation. Elevated levels are seen in open neural defects as well as some non-neural anomalies. • Ultrasound markers can detect Arnold–Chiari malformations, which are very common in spinal dysraphism.

Management A multidisciplinary approach to treatment is essential. Neurosurgical intervention to close the lesion is required in the first 48 hours of life. Any associated defects must be managed appropriately. Hydrocephalus This is due to Arnold–Chiari malformation. The lower the vertebral defect, the higher the likelihood of hydrocephalus after surgical closure of the defect. Hydrocephalus requires shunting and frequent monitoring of the patient. It can be a great source of morbidity and is directly associated with mobility impairments. Arnold–Chiari 2 malformation Herniation of the fourth ventricle and lower medulla occurs below the level of foramen magnum. This is associated with spina bifida and requires prompt neurosurgical evaluation. Bladder dysfunction Urinary tract infection (UTI) is a frequent cause of hospital admission and renal failure, which is the most common cause of death in patients with spina bifida. Medication, catherization, and/or surgery may be required. Bowel incontinence It is important to implement a bowel program (scheduled and predictable bowel movement).

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Mobility Only 4% of patients with a lesion at L2 or higher can ambulate. Iliopsoas strength grade of 0–3 is associated with partial or complete use of a wheelchair.

Complications • Tethered cord syndrome: tissue attachment to defect causing abnormal stretching of spinal cord • Musculoskeletal • Fractures • Kyphosis • Scoliosis • Hip dislocations • Club foot • Pressure ulcers and burns due to insensate limbs • Latex allergy is increased in patients with spina bifida

Special considerations The following procedures require more research before they can be recommended: • Surgical closure of the spinal defect in utero may be associated with a decrease in hydrocephalus and Chiari malformations. • Cesarean section to prevent damage to the tissue as the fetus passes through the vaginal canal

Further reading Dicianno BE, Kurowski BG, Yang JM, et al. (2008). Rehabilitation and medical management of the adult with spina bifida. Am J Phys Med Rehabil 87(12):1027–1050. Botto LD, Moore CA, Khoury MJ, Erickson JD (1999). Neural-tube defects. N Engl J Med 341(20):1509–1518.

Chapter 16

Common complications Lyn Weiss Teena Varghese Matthew M. Shatzer Shimon Y. Blau Robert A. Domingo Samantha Mendelson

Heterotopic ossification 364 Bladder dysfunction 368 Spasticity 374 Pressure ulcers 378 Venous thromboembolism 382 Swallowing disorders 388 Sexuality and the disabled 396 Immobility syndrome 398

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Heterotopic ossification General description Heterotopic ossification (HO) is defined as an abnormal formation of lamellar bone within extraskeletal soft tissue, most frequently around a joint. As the bone matures it becomes encapsulated and is not connected to the periosteum. HO is also commonly known as myositis ossificans, paraosteoarthropathy, ectopic ossification, osteosis neuratica, para-articular bone formation, and neurogenic ossifying fibromyopathy. One possible mechanism for HO is altered control of differentiation from pluripotent mesenchymal stem cells into osteoblasts, which form new bone. Another proposed mechanism is a decrease in tissue oxygenation, which may induce changes in multipotential connective tissue cells so that the new bone forms between layers of connective tissue. Heterotopic ossification of the hip is most commonly classified using the Booker system (see Fig. 16.1): • Grade 1: Islands of bone lie within the soft tissues about the hip. • Grade 2: Bony spurs protrude from either the femur or the pelvis, with a gap of >1 cm between opposing bony ends. • Grade 3: The gaps between the spurs are <1 cm. • Grade 4: Apparent ankylosis of the hip is noted due to the heterotopic ossification.

Incidence Spinal cord injury (SCI) The incidence of HO in patients with SCI has been reported to be 16%–57%. HO occurs below the level of injury unless there is a confounding factor (such as burn or traumatic brain injury [TBI]). The most common joint in which HO is found is the hip (anterior > posterior), followed by the knee, shoulder, and elbow. Risk factors include spasticity, complete injury, trauma or prior surgery to the joint, and pressure ulcers near the joint.

C16.F2

Figure 16.1 Heterotopic ossification, grades 1–4 (left to right).

HETEROTOPIC OSSIFICATION

Traumatic brain injury (TBI) The incidence of HO in TBI has been reported to be 11%–76%. HO is found in the upper extremity as frequently as in the lower extremity. Commonly affected joints include the hip, elbows, shoulders, and knees. Risk factors include prolonged coma, immobility, increased tone and limb spasticity, long bone fractures, pressure ulcers, and edema. The time of greatest risk is 3–4 months after injury. Burn The incidence of HO in burn patients is as high as 23%. The most commonly affected joint is the elbow. Risk factors include full-thickness burn to the upper extremities, >20% of total body surface burns, immobility, and repeated minor trauma. Stroke HO is infrequently seen in patients with CVA. HO may be found in the elbow (on the extensor side) or shoulder. Joint replacement The reported incidence of HO after joint replacement varies from 3% to 90%. Risk factors after hip replacement include male gender, older age, previous history of HO, pre-existing hip fusion, ankylosing spondylitis, Paget’s disease, post-traumatic arthritis, osteonecrosis, and rheumatoid arthritis.

Clinical manifestations Patients may present with local edema, erythema, or warmth over the joint, muscle guarding, low-grade fever, lymphedema, and nerve or vascular compression.

Differential diagnosis • • • • • •

DVT Cellulitis Fracture Septic joint Tumor Hematoma

Diagnostic testing • Triple-phase bone scanning is the most sensitive test for early detection; a positive result may precede X-ray findings by 7–10 days. HO may be seen within 2–4 weeks after injury in phase I (the bloodflow phase) or phase II (blood-pool phase). For phase III the static/ delayed images may become positive in 4–8 weeks. • X-rays may take 3 weeks to 2 months to reveal HO, but this modality is useful to confirm bone maturation (which may take up to 1 year). • Serum alkaline phosphatase (SAP) is the earliest indicator (may be elevated at 2 weeks post-injury) but has low specificity. • Osteoclastic and osteoblastic markers (CTX-1 and P1NP) may be elevated as early as 1 week after joint replacement.

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Prevention • Gentle range of motion exercises, control of increased tone • NSAIDs • Radiation treatment is used perioperatively on patients with total hip replacement. It is not practical for TBI patients, as this treatment carries some increased risk of neoplasm and would require total body radiation in this population. Radiation is given either <4 hours preoperatively or within 72 hours postoperatively. The mechanism is believed to be inhibition of rapidly dividing osteoprogenitor cells that are present within the first week but later differentiate into mature cells such as osteoblasts. • Use of bisphosphonates has been discontinued as they only postpone ossification until treatment is stopped.

Management (treatment) • Disphosponates and NSAIDs (indomethacin) have questionable efficacy. • ROM is used prophylactically and as treatment for developing HO. • Surgery is used for removal of HO if increased function is the goal. This is usually done after 12–18 months to allow for bone maturation. The bone scan must show no acute changes, and SAP must be within normal limits. • Manipulation under anesthesia: risk includes fracture of bone since HO is stronger than osteoporotic bone.

Complications Peripheral nerve entrapment, loss of function, ankylosis, predisposition for skin breakdown, and ulceration secondary to poor positioning are all complications of HO.

Further reading Board T (2007). The prophylaxis and treatment of heterotopic ossification following lower limb arthroplasty. J Bone Joint Surg 89-B:434–440. Cuccurullo S (ed.). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical Publishing, pp. 66–67. DeLisa J, Gans BM, Walsh NE, Bockenek WL, Frontera WR (eds.) (2005). Physical Medicine and Rehabilitation, Principals and Practice, 4th ed. Philadelphia: Lippincott Williams and Wilkins, pp. 1726–1727. Young MA, Stiens SA, O’Young B (1997). PM&R Secrets, 2nd ed. Philadelphia: Hanley & Belfus, pp. 456–460.

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Bladder dysfunction General description Bladder dysfunction is seen commonly in traumatic brain injury (TBI), spinal cord injury (SCI), and elderly patients. In the United States, approximately 13 million individuals are afflicted with urinary incontinence. This chapter discusses bladder dysfunction with a focus on neurogenic bladder (dysfunctional bladder secondary to a neurological disorder) and urinary incontinence.

Normal neurophysiology Figure 16.2 illustrates the anatomy and physiology of the bladder. In the normal, neurologically intact individual, the neurophysiology is as follows: In the bladder-filling phase, the sympathetic nerves (T11–L2) via the hypogastric nerve relax the detrusor muscle (by inhibiting contractions via beta-adrenergic receptors at the fundus) and contract the internal sphincter (via alpha-adrenergic receptors at the bladder neck). Somatic nerves (via the pudendal nerve) contract the external sphincter and pelvic floor muscles. During this filling phase, continence is maintained because the pressure within the bladder is less than that within the urethra. As the bladder distends, stretch receptors send signals to the pons and then the frontal lobe, where the urge to void is perceived. The first sensation of bladder filling occurs at about 100 mL of urine and bladder fullness occurs at about 350 mL. If urination is deemed appropriate by the brain, excitatory signals are sent to the pontine and sacral micturition centers, resulting in sympathetic and pudendal nerve inhibition and parasympathetic nerve stimulation. This causes detrusor muscle contraction and urethral sphincter relaxation, allowing the bladder to empty in a coordinated manner.

Neurogenic bladder pathophysiology Neurogenic bladder can occur whenever a lesion blocks the pathway between the brain and bladder as outlined in Table 16.1.

Sympathetics (T11-L2) via hypogastric n. act on beta-adrenergic receptors (b) in detrusor muscle and alphaadrenergic receptors (a) in the internal sphincter

C16.F1

M

b

a

Parasympathetics (S2-4) act via pelvic nerves on muscarinic receptors (M) in detrusor muscle

Somatics (S2-4) via pudendal n. act on the external sphincter

Figure 16.2 Bladder anatomy and physiology. Created by Teena Varghese, M.D.

BLADDER DYSFUNCTION

Table 16.1 Bladder lesions: causes and effects Lesion

Causes

Bladder effects (initial)

Bladder Effects (Delayed)

Suprapontine CVA, TBI, tumor, Parkinson’s disease, Shy–Drager syndrome

Detrusor areflexia (retention due to acute cerebral shock post-CVA)

Detrusor hyperreflexia (frequency and urgency)

Spinal cord

Trauma, multiple sclerosis (MS), tumor Lesions above T6: Bladder distention can result in autonomic dysreflexia, presenting with sweating, headache, hypertension, and/ or reflex bradycardia. Treat with bladder decompression. Lesions below T6: Detrusor sphincter dyssynergia with detrusor hyperreflexia (DSD-DH) may occur. Patient has the urge to void, but difficulty emptying bladder completely because of simultaneous contractions of the bladder and urethral sphincter.

Detrusor areflexia (flaccid bladder due to spinal shock for 6–12 weeks)

Detrusor hyperreflexia

Peripheral nerve

Diabetic cystopathy, tabes dorsalis, herpes zoster, herniated disc, pelvic surgery

Detrusor areflexia

Detrusor areflexia

Clinical manifestations of urinary incontinence Patients with incontinence may have symptoms of urine leakage, frequency, and urgency. The different types of urinary incontinence are as follows: • Stress: occurs when transient increases in intra-abdominal pressure overcome the urethral sphincter (e.g., with sneezing or coughing) • Urge: the sudden desire to empty the bladder (due to uninhibited bladder contractions or detrusor over activity) when the bladder is not filled to capacity • Mixed: symptoms of both stress and urge due to a combination of urethral sphincter impairment and detrusor overactivity

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• Overflow: occurs when incomplete bladder emptying causes overflow leakage of urine due to impaired detrusor muscle contraction or bladder outlet obstruction; seen in men with benign prostate hypertrophy • Reflex: seen in neurological impairment of the central nervous system (e.g., MS, CVA, Parkinson’s disease, spinal cord injury)

Differential diagnosis of urinary incontinence This includes urinary tract infection (UTI), diabetes with hyperglycemia, pregnancy, urethritis, medications, and prostatic enlargement.

History and physical The following components must be obtained during a thorough history taking: time of onset, symptoms of frequency, urgency, hesitancy, severity of leakage, interference with daily activities, prior surgeries, obstetrical history, past medical history of illness such as brain or spinal disease/injury, and current medication usage. Medications that can cause symptoms of incontinence include alcohol, diuretics, caffeine, antidepressants, antipsychotics, sedatives, narcotics, alpha- or beta-adrenergic agents, and calcium channel blockers. The initial physical exam should focus on findings of fecal impaction (which places pressure on the bladder), atrophic vaginitis, prostate nodules, severe pelvic prolapse, and abnormalities suggesting neurological diseases or spinal cord lesions.

Diagnostic tests • Lab tests: urinalysis and basic metabolic profile should be obtained first to rule out other causes (i.e., hyperglycemia, UTI, renal dysfunction). • Post-void residual volume (PVR) detects urinary retention (i.e., overflow); it may be tested via catheterization or ultrasound. In general, a PVR greater than 200 mL suggests insufficiency, due to either detrusor weakness or obstruction. PVR test is recommended in men with moderate to severe symptoms of benign prostatic hypertrophy (BPH), SCI, and Parkinson’s disease. • Urodynamic testing is the diagnostic gold standard test but is invasive, expensive, and not always necessary to make the diagnosis. It is useful if surgery is being considered, such as a sphincterotomy, augmentation, continent diversion, or transurethral resection of the prostate (TURP). • Urinary flow rate is measured by a flowmeter. This is used to evaluate bladder outlet obstruction. • Urine cystoscopy should be considered if there is hematuria or pelvic pain; it allows for visual assessment. • Cystogram is used to assess stress incontinence; open bladder neck can also be detected. • Abdominal leak-point pressure is used to diagnose stress incontinence. The patient is asked to bear down and the lowest pressure to generate leakage is recorded. • Filling cystometrogram (CMG) measures bladder capacity and detrusor over activity. A two-channel catheter is placed in the bladder, one for

BLADDER DYSFUNCTION

filling and one for recording. The bladder is then filled with liquid or gas and the patient is asked to suppress voiding. • Voiding CMG (pressure-flow study) evaluates outlet obstruction by comparing detrusor pressure and rate of urinary flow during voiding. • Sphincter electromyography (EMG): periurethral recordings are preferred. EMG activity should increase with increased filling of the bladder. Low levels of EMG activity are common in complete spinal cord injury. This EMG helps to distinguish between coordinated and uncoordinated voiding.

Management Behavioral and mechanical therapy (first line) • Bladder training, for urge incontinence and mixed incontinence, involves frequent timed, voluntary voiding to keep the urinary volume low and train the CNS and pelvic muscles to inhibit detrusor contractions. Successful training may take several weeks. • Kegel exercises and pelvic weights are used for stress incontinence. Kegel exercises consist of contracting and relaxing the pelvic floor muscles as if trying to control urination or defecation with minimal abdominal muscle involvement. This is found to help younger, premenopausal women. • Biofeedback is used for stress, urge, and mixed incontinence. It involves using an electronic device and computer to provide immediate information about the pelvic muscles. • Intermittent catheterizations are for overflow incontinence and neurogenic bladder. It can be based on bladder volume or timed voiding, for example, every 6 hours, and adjust frequency according to amount drained. • Crede’s maneuver: another individual applies pressure over the lower abdomen to push urine out mechanically. Pharmacological therapy The medications commonly used for bladder dysfunction are listed by category in Table 16.2. Surgical therapy • For stress incontinence the goal is to increase urethral outlet resistance with bladder neck suspension, periurethral bulking therapy, or a pubovaginal sling. • For urge incontinence the goal is to increase bladder compliance with sacral nerve modulation, injection of neurotoxins such as Botox, or bladder augmentation.

Complications of urinary incontinence Urinary incontinence can have a significant impact on patients’ quality of life. It can result in complications such as urinary tract infections, vesicoureteral reflux, pyelonephritis, hydroureter, renal failure, contact dermatitis, decubitus ulcers, prolonged hospital stay, increased mortality, psychosocial distress from loss of self-esteem, depression, and restriction of social and sexual activities.

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Table 16.2 Medications for bladder dysfunction Category

Medications

Indications

Side effects

Anticholinergics/ antispasmodics

Oxybutynin (Ditropan) Tolterodine (Detrol) Vesicare Enablex

Urge incontinence, overactive bladder, urgency, frequency

Dry mouth, blurry vision, tachycardia, drowsiness, constipation, confusion

Alpha-agonists

Pseudoephedrine

Open bladder neck

Hypertension, agitation, dizziness, palpitations

Norepinephrine Tricyclic antidepressants

Amitriptyline

Conjugated estrogen

Premarin

Imipramine

Mixed incontinence; Cardiac issues, pelvic floor muscle e.g., arrhythmias, dysfunction QT prolongation, postural hypotension Stress or mixed incontinence

Nausea, vomiting, hypertension, gallstones, fluid retention

Alpha-antagonists Flomax

BPH, urinary retention

Orthostatic hypotension, syncope

Cholinergic

Urinary retention

GI discomfort, salivation, flushing, diaphoresis, miosis, bronchospasm, urgency

Bethanecol

Further reading Cardenas D, Mayo M (2006). Management of bladder dysfunction. In Braddom R (ed.). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders–Elsevier. pp. 617–636. Kirschblum S, Gonzalez P, Cuccurullo S, Lucianon L (2004). Spinal cord injuries. In Cuccurullo S (ed.) Physical Medicine and Rehabilitation Board Review. New York: Desmos Medical Publishing, pp. 516–525. Weiss BD (1998). Diagnostic evaluation of urinary incontinence in geriatric patients. Am Fam Physician 57(11):2675–2674.

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Spasticity General description Spasticity is defined as a velocity-dependent increased resistance to passive stretch, associated with exaggerated tendon jerks. Spasticity, along with hyperreflexia, is what is known as a positive symptom of the upper motor neuron syndrome. The negative symptoms include weakness and poor dexterity. Spasticity is a condition that may be present in any insult to the brain or spinal cord, such as the following: • Spinal cord injury • Brain injury • Multiple sclerosis • Brain tumor • Cerebral palsy This condition must be differentiated from hypertonia, in which resistance to joint movement occurs at very low speeds and does not depend on imposed speed. Spasticity was initially described by British physician William John Little in 1861 when he described congenital cerebral spastic paralysis.

Clinical presentation The noted “pattern” of spasticity will frequently be determined by the associated diagnosis. Patterns associated with spinal cord involvement may be more variable. However, there are frequently more specific patterns seen in patients with brain pathology as follows: Upper extremity • Shoulder: internal rotation; adduction • Elbow: flexion • Forearm: pronation • Wrist: flexion • Finger: flexion • Thumb: adduction Lower extremity • Hip: flexion and adduction • Knee: extension • Ankle: plantarflexion; equinovarus posture • Toe: flexion The above patterns of spasticity can help determine treatment options (discussed under Treatment).

Physical examination The clinician will note increased resistance while assessing range of motion. Measurement of spasticity is primarily by means of the Modified Ashworth Scale, shown in Box 16.1.

SPASTICITY

Box 16.1 Modified Ashworth Scale Ashworth 0 Ashworth 1 Ashworth 1+ Ashworth 2 Ashworth 3 Ashworth 4

No increase in tone Slightly increased tone with a “catch–release” at terminal ROM Slightly increased tone with a catch followed by resistance through less than half the ROM Increased tone throughout most of ROM with affected part easily moved Considerably increased tone; passive movement difficult Affected part appears rigid

There are other methods of assessing spasticity, primarily for research purposes, as follows: • Tardieu Scale • Physicians Rating Scale • H-reflexes • F-waves • Surface EMG

Treatment of spasticity In some cases, spasticity may be beneficial, thus there is no need for treatment. Spasticity may • Provide strength and help with transfers, walking, or grip • Improve blood flow and minimize edema or prevent DVT • Reduce the risk of osteoporosis (Wolff’s law) However, spasticity often requires treatment for problems it can cause: • Mobility impairment • ADL impairment • Skin breakdown • Pain • Orthopedic limitations (hip dislocation, contractures) • Insomnia • Weight loss In such cases, spasticity needs to be treated. Nonpharmacological treatment • A stretching program with ROM exercises is the cornerstone of any program to treat spasticity; this “resets” muscle spindle. • Splints and casting must be used with caution; evaluate for skin breakdown. • Cryotherapy reduces hyperexcitability of muscle stretch reflex and reduces nerve conduction velocity. Pharmacological treatment Commonly used medications for the treatment of spasticity are listed in Table 16.3.

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Table 16.3 Medications for treatment of spasticity Medication

Mechanism

Baclofen

Not fully known, Start 5 mg tid. Titrate likely GABA to max 20 agonist mg qid

Dosage

Indication

Adverse reactions

Spasticity due to spinal etiology

Drowsiness, dizziness, N/V, CNS depression

Clonidine

Central alphaagonist

Diazepam

Postsynaptic 2–10 mg GABA facilitator bid–qid

Dantrolene

Reduces sarcoplasmic reticulum Ca release

Tizanidine

Central alpha-2 Start 2 mg Spasticity due Fatigue, weakness, agonist qhs; titrate to brain or hypotension to 4 mg tid spinal etiology

Botulinum toxin

Blocks release Varies by To selectively Weakness, flu-like of acetylcholine muscle and decrease symptoms, pain, type used spasticity antibodies to toxin in targeted muscles

0.1–0.2 mg Spasticity TTS due to spinal etiology Spasticity due to spinal etiology

Start 25 mg Spasticity qd, titrate due to brain to max 400 etiology mg/day

Hypotension, fatigues, limb pain Sedation, dizziness, ataxia, hypotension, confusion Elevated LFTs, weakness

bid, twice daily; CNS, central nervous system; LFTs, liver function tests; N/V, nausea/vomiting; qd, every day; qhs, at night; qid, 4 times daily; tid, 3 times daily; TTS, transdermal therapeutic system.

Botulinum toxin injections into spastic muscles Botulinum toxin has been increasingly used in specific muscles to reduce spasticity. The mechanism of action is blocking acetylcholine (ACh) release presynaptically. The advantage of botulinum toxin over oral agents is the focal treatment of spasticity without systemic effects. In addition, the effects wear off after time (which can be both an advantage and a disadvantage). The onset of action after injection is usually 24–72 hours, with a peak effect in 2–6 weeks. The injections usually produce a clinical response for about 3–4 months before another injection is required. The predominant adverse reaction is pain at the site of the injection. Patients may develop antibodies to botulinum toxin. Injections should not be done more frequently than every 3 months, to prevent formation of antibodies. Dosage is variable and depends on the size of the muscle. The different botulinum toxin preparations use different doses (in units). Units given here are for botulinum toxin A (Botox). Generally, no more than 100 units are injected into one muscle. If >50 units are being injected into one muscle, it should be done into more than one site. Usually, an injection involves several muscles and total injection dosage rarely exceeds 400 units.

SPASTICITY

Surgical management Implantation of an intrathecal baclofen pump may be useful in patients with intractable spasticity or those who cannot tolerate the side effects from antispasticity medication. Other surgical procedures that can be considered (once other treatments for spasticity have failed) include rhizotomy, myelotomy, tendon lengthening, and joint fusion.

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Pressure ulcers General description A pressure ulcer is a localized injury to the skin and/or underlying tissue, usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction.1 The mechanism of tissue ischemia results when prolonged pressure over bony prominences exceeds arteriolar perfusion pressure (32 mmHg). It should be noted that less pressure is needed the longer the pressure is maintained.2 For example, 70 mm of Hg over 2 hours may result in occlusion of the microvessels of the dermis. However, if the pressure is 100 mmHg, only 1 hour may be required before tissue damage occurs.

Staging of pressure ulcers The staging system developed by Shea divided the extent of tissue damage into four categories. Stage 1 involves the superficial epidermis and dermal layers. Stage 2 extends to adipose tissue. Stage 3 involves full thickness of the skin down to and including muscle. Stage 4 involves the destruction of tissue down to bone and or joint structures. In 2007, the National Pressure Ulcer Advisory Panel updated these stages and added two more categories.1 Stage 1 Stage 1 involves intact skin with nonblanchable redness of a localized area, usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler compared to adjacent tissue. Stage I may be difficult to detect in dark-skinned individuals. Stage 2 Stage 2 involves partial-thickness loss of dermis presenting as a shallow, open ulcer with a red-pink wound bed, without slough. This may also present as an intact or open/ruptured serum-filled blister. The ulcer may present as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation. Stage 3 Stage 3 involves full-thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, and/or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. This stage may include undermining and tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue and stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Bone or tendon is not visible or directly palpable.

1 National Pressure Ulcer Advisory Panel (2007). Updated staging system. www.npuap.org/pr2.htm. 2 Kosiak M (1961). Etiology of decubitus ulcers. Arch Phys Med Rehabil 42:19–29.

PRESSURE ULCERS

Stage IV Stage 4 involves full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Stage IV ulcers often include undermining and tunneling. Stage 4 ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule), making osteomyelitis possible. Exposed bone or tendon is visible or directly palpable. Unstageable This entails full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and thus stage, cannot be determined. Suspected deep tissue injury This involves damage to underlying tissue, yet the skin is intact. The intact skin may be discolored or blistered.

Risk factors Ischemia, pressure, shearing, friction, elevated tissue temperature, immobility, maceration, malnutrition, anemia, smoking, poor nutritional status, altered sensation, and altered mental status are all risk factors in the development of pressure ulcers.

Prevention Pressure ulcers can be avoided by meticulous attention to minimizing the extrinsic factors (pressure, maceration, shear and friction). The patient who is immobilized should be turned and positioned every 2 hours to minimize pressure forces. Appropriate beds or wheelchair cushions can also help decrease pressure over vulnerable areas. If necessary, pressure measurement testing will help localize the areas at highest risk. Patients who are able to should perform wheelchair pushups in order to relieve the pressure while sitting (every 30 minutes is recommended). The common areas at risk for increased pressure include the heels, sacrum, greater trochanter, ischium, malleoli and, especially in children, the occiput. The shoulder, elbow, knee, and ear can also be vulnerable areas in patients who are in bed. Patients confined to a wheelchair may also develop pressure ulcers over the scapula and the ball of the foot. Different tissues are more sensitive to developing pressure ulcers. Muscle is more susceptible to pressure than skin. Subcutaneous fat is less susceptible than muscle, but more susceptible than skin. Friction affects the skin by separating the epidermis from the basal cell layer.

Physical It is essential to examine all areas of the skin (including the sacrum) in patients at risk. Staging (described above) must be performed and communicated to all treating members of the team. The description of the pressure ulcer must also include the location, size, and depth of the ulcer.

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Diagnostic testing If osteomyelitis is suspected, a bone biopsy should be considered. Leukocyte count, ESR, and plain films may be useful but only have a positive predictive value of 69% when all three are positive.3 Bone scans may be used but have a high false-positive rate if there is a pressure ulcer.

Special considerations Since muscle is more sensitive to pressure than skin, sustained high pressure over a bony prominence may lead to tissue ischemia that is worse at the muscle–bone interface. The skin may appear indurated, erthematous, or warm, but the skin may be intact. Several days later, the wound may open, revealing a deep (stage 4) wound. Therefore, it is important to inspect and suspect.

Management (treatment) Treatment depends on the extent and location of the pressure ulcer. Prevention is always preferable to treatment. Prone positioning should be considered for patients with sacral or ischial tuberosity ulcers. If spasticity is present, controlling it will help decrease both shear and pressure. It is important to be meticulous about bowel and bladder management to avoid contamination and maceration of the ulcer. The goal is to keep the wound clean, moist, debrided, and free from infection. Any eschar (tough, dry matter covering a wound) must be removed for healing to take place. Eschar can harbor bacteria and prevent granulation and epithelialization of the wound. Debridement may be sharp (surgical), mechanical (wet-to-dry dressings, hydrotherapy), or enzymatic debridement (for noninfected wounds). Cytotoxic agents (Povidine, acetic acid) should never be used on healthy tissue. A moist environment promotes healing by providing for cell migration and mitosis, but maceration must be avoided. There must be adequate oxygenation; hyperbaric oxygen may be used to promote wound healing. To heal a wound, there must also be a sufficient blood supply, and occasionally bypass grafting is required. Systemic antibiotics are rarely needed unless there are signs of sepsis. If a purulent wound is not healing within 2–4 weeks of treatment, a topical antibiotic may be helpful (i.e., silver sulfadiazine or triple antibiotic ointment). The patient’s nutritional and hydration status must be maintained to ensure appropriate healing. Myocutaneous flaps may be needed to provide well-vascularized tissue to fill the space left after resection of a pressure ulcer.4

Complications and red flags Osteomyelitis can occur if the underlying bone becomes infected. Cellulitis and sepsis are also possible. Dehydration may occur as a consequence of fluid loss through the wound (the skin is the primary barrier to maintaining adequate hydration). Sinus tracts may develop and communicate with abdominal viscera. 3 Lewis, VL, Bailey MH, Pulawski G, et al. (1988). The diagnosis of osteomyelitis in patients with pressure sores. Plast Reconstr Surg 81:229–232. 4 Priebe MM (1997). Pressure ulcers. In Young MA, Stiens SA, O’Young B (eds.). PM&R Secrets. Philadelphia: Hanley & Belfus, p. 494.

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Venous thromboembolism General Deep venous thrombosis (DVT) is a potentially serious complication in hospital patients. It can be community acquired, but hospital or nursing home patients who are bedridden are at increased risk. The factors predisposing for venous thrombosis are venous stasis, vascular endothelial damage, and hypercoagulability (referred to as Virchow’s triad). Any patient on bed rest is at increased risk and prophylaxis should be considered unless contraindicated. The presence of one or more risk factors (some of which are hereditary, whereas others are acquired and can be modified or eliminated) increases the likelihood of DVT. The principal danger of DVT is embolization from the thrombosis, most often to the lungs.

Risk factors for venous thromboembolism Hereditary • Factor V Leiden mutation • Prothrombin gene mutation: Factor V Leiden deficiency and prothrombin gene mutation account for 50%–60% of cases. Although they are associated with a lower risk of thrombosis than that of other hereditary causes, they are more common in the general population. • Activated protein C resistance (90% caused by Factor V Leiden deficiency) • Protein C deficiency • Protein S deficiency • Antithrombin deficiency • Elevated levels of factors VIII, IX, and XI • Dysfibrinogenemia • Hyperhomocysteinemia • Plasminogen deficiency • Increased levels of thrombin-activatable fibrinolysis inhibitor • Possibly elevated levels of lipoprotein(a) Acquired • Fracture (hip or leg) • Hip or knee replacement • Major surgery (especially orthopedic, major vascular, neurosurgery, and cancer surgery) • Major trauma • Spinal cord injury • Central venous lines or pacemaker • Chemotherapy • Congestive heart or respiratory failure • Hormone replacement therapy • Malignancy • Oral contraceptive therapy (risk increases with concomitant smoking) • Neurological disease with extremity paresis • Institutionalization within previous 90 days

VENOUS THROMBOEMBOLISM

• • • • • • • • • • • • • • • •

Presence of acute infectious disease Pregnancy and postpartum Previous venous thromboembolism Bed rest >3 days Immobility Increasing age Obesity Superficial vein thrombosis Varicose veins (risk associated with varicose veins diminishes with age) Systemic lupus erythematosus (SLE) Antiphospholipid antibody syndrome Smoking Inflammatory bowel disease Chronic renal disease Myeloproliferative disease Tamoxifen therapy

Diagnosis of deep venous thrombosis History The presenting complaint may be calf pain or foot or ankle swelling. There may be a history of hospitalization or a long period of immobilization. Patients may be asymptomatic until embolization. Physical examination There may be tenderness in the calf, or swelling or warmth. Redness may be present. A swollen vein (cord) may be palpable in the calf. There may also be superficial venous dilation. Homan’s sign may be present, which is the production of pain in the posterior calf after sudden passive dorsiflexion of the ankle joint with the knee flexed to 30*. It must be stressed that the clinical examination is notoriously unreliable; diagnosis should be based on further studies.

Differential diagnosis The differential diagnosis of a swollen limb includes cellulitis, chronic venous insufficiency, lymphedema, congestive heart failure, varicose veins, and superficial phlebitis. Other disorders that may cause a similar picture include arthritis, neuropathy, arterial occlusion, and muscle tear or strain.

Prophylaxis Early ambulation, graduated compression stockings, intermittent pneumatic compression, and anticoagulation can help prevent thrombosis. Prophylactic anticoagulation is usually low-molecular-weight heparin (i.e., enoxaparin), low-dose unfractionated heparin, and fondaparinux sodium (Arixtra)

Diagnostic tests (see Table 16.4) Other tests Computed tomography Consider CT if workup includes a pulmonary angiogram to rule out pulmonary embolism (PE) as no additional contrast medium is needed.

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Table 16.4 Diagnostic testing for DVT Imaging modality

General

Advantages

Disadvantages

Contrast venography

Gold standard for diagnosis, but rarely performed because of its limitations and accuracy of noninvasive testing. Reserved for cases where noninvasive studies are nondiagnostic or impossible to perform

Sensitive Specific Generally available Acute vs. chronic DVT Less operator dependent than ultrasound Most accurate test for calf DVT

Invasive Expensive Contraindications: Renal insufficiency Severe contrast allergy Adverse effects (pain, DVT) Not portable

Compression ultrasound with venous imaging (venous Doppler)

Initial test of choice. Combined with Doppler, referred to as duplex ultrasound

Noninvasive Safe Available Relatively inexpensive Portable Few contraindications No radiation Symptomatic proximal DVT Upper extremity DVT May diagnose other pathology Numerous clinical trials to date

Operator dependent Less accurate for chronic DVT, Symptomatic or asymptomatic proximal DVT Less useful for pelvic DVT and asymptomatic proximal DVT May not be possible in massive obesity, severe edema, casts or immobilization devices

Impedance plethysmography

May be considered for initial test, but less commonly used than ultrasound because of lower sensitivity, common inter-observer disagreements, lack of availability, and limitations of false positives

Noninvasive Safe Inexpensive Portable Symptomatic proximal DVT Recurrent DVT No radiation Numerous clinical trials to date

Operator dependent Asymptomatic proximal DVT Calf DVT Nonobstructing thrombi Potential falsepositive tests Not useful for upper extremity DVT Casts or immobilization devices preclude use Not useful for alternative diagnoses

VENOUS THROMBOEMBOLISM

Table 16.4 (Contd.) Imaging modality

General

Advantages

Disadvantages

MRI

Accuracy equals that of contrast venography for diagnosis of DVT. Reserved for situations where contrast venography cannot be performed (e.g., contrast allergy)

Sensitive Specific Safe Available Pelvic/IVC DVT Upper extremity DVT Bilateral examination Alternative diagnoses No ionizing radiation Contrast unnecessary Repeat/detailed examination of questionable areas Potentially useful for acute vs. chronic DVT Potentially useful for diagnosing PE

Claustrophobia Cost Not portable Calf DVT Metallic devices Massive obesity Reader expertise required

D-dimer • Not specific. • >500 ng/mL of fibrinogen equivalent units

Complications of deep vein thrombosis The main complication of DVT is PE. Over 90% of these originate from proximal lower extremity veins. A “saddle” PE is one at the bifurcation of the main pulmonary artery extending into the left and right pulmonary arteries. These can cause pulmonary hypertension, cor pulmonale, right ventricular failure, dysfunction, and death. Right ventricular dysfunction is associated with increased mortality. The primary presenting signs of a PE are dyspnea, tachypnea, and tachycardia. Other symptoms and signs include orthopnea, angina-like pain, fever, wheezing, cyanosis, hypotension, hemoptysis, decreased breath sounds, and jugular distension. The differential diagnosis of PE include, pneumonia or bronchitis, pericardial tamponade, asthma, lung cancer, chronic obstructive pulmonary disease (COPD) exacerbation, primary pulmonary hypertension, myocardial infarction (MI), rib fracture, pulmonary edema, pneumothorax, anxiety, costochondritis, aortic dissection, and musculoskeletal pain.

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Tests used for the diagnosis of PE include arterial blood gas (ABG), ECG, chest X-ray, spiral CT, pulmonary angiography (which is considered the gold standard) and ventilation/perfusion (V/Q) scan. The ABG may show hypoxemia, hypocapnia, and respiratory alkalosis, and in massive PE it may show hypercapnia and combined respiratory and metabolic acidosis. ESR, lactate dehydrogenase (LDH), AST, brain natriuretic peptide (BNP), troponins, and D-dimer may be abnormal. EKG changes may show T-wave inversion, ST changes, axis deviation, and right bundle branch block. The V/Q scan may show a ventilation and perfusion mismatch. Chest X-ray changes may also be seen in PE. Echocardiography may show nonspecific findings for PE, but may aid in assessing for right ventricular dysfunction.

Treatment of DVT and PE Anticoagulation is indicated for treatment of both DVT and PE. The options for anticoagulation include subcutaneously (SC) administered lowmolecular-weight heparin (LMWH), intravenous (IV) unfractionated heparin (UFH), and SC UFH. Fondaparinux sodium (Arixtra) is used for DVT and not for PE. Patients can be switched to warfarin and when the INR is therapeutic (>2.0). LMWH, UFH, or fondaparinux can be discontinued. In patients with a high degree of clinical suspicion, treatment may be started while awaiting test results. See Table 16.5 for treatment duration. Mechanical or surgical thrombectomy is rarely necessary. An IVC filter is indicated in patients with a contraindication for or complication of anticoagulation therapy, as well as in those with recurrent thromboembolism despite anticoagulation therapy.

Table 16.5 Treatment duration for DVT Patient factors

Duration

• • • •

3 months 6–12 months Indefinite‡ 12 months

First episode DVT/PE with transient (reversible) risk factor* First episode of idiopathic DVT/PE DVT/PE in presence of cancer† First episode of DVT/PE with documented antiphospholipid antibodies or 2 or more thrombophilic conditions (e.g., combined factor V Leiden and prothrombin gene mutation) • First episode of DVT/PE with documented deficiency of antithrombin, protein C or S, factor V Leiden, or prothrombin gene mutation, homocysteinemia, or high factor VIII levels • 2 or more episodes of DVT/PE, 1 episode of life-threatening thrombosis, 1 episode of thrombosis in unusual site, other high-risk patients

6–12 months

Indefinite

* Applies to proximal vein thrombosis and symptomatic DVT confined to calf veins. † Recommended first 3–6 months of long-term anticoagulation therapy with LMWH. ‡ Or until cancer resolves.

VENOUS THROMBOEMBOLISM

IV thrombolysis, percutaneous mechanical thrombectomy, or surgical thrombectomy is not indicated for most patients with DVT or PE. Consider it in selected patients such as those with massive iliofemoral DVT at risk of gangrene secondary to venous occlusion. In patients with hemodynamically unstable PE and a low risk of bleeding, consider thrombolytic therapy as a first approach.

Further reading Alikhan R, Cohen AT, et al. (2004). Risk factors for venous thromboembolism in hospitalized patients with acute medical illness: analysis of the MEDENOX Study. Arch Intern Med 164:963–968. Anderson FA, Spencer FA (2003). Risk factors for venous thromboembolism. Circulation 107(23 Suppl 1); I:9–I16. Buller HR, Agnelli G, et al. (2004). Antithrombotic therapy for venous thromboembolic disease: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 126(3 Suppl):401S–428S. Crowther MA, Kelton JG (2003). Congenital thrombophilic states associated with venous thrombosis: a qualitative overview and proposed classification system. Ann Intern Med 138:128–134. Fields JM, Goyal M (2008). Venothromboembolism. Emerg Med Clin N Am 26(3):649–683. Goldhaber SZ (1998). Pulmonary embolism. N Engl J Med 339:93–104. Heit JA, Silverstein MD, et al. (2000). Risk factors for deep vein thrombosis and pulmonary embolism: a population-based case-control study. Arch Intern Med 160:809–815. Kahn SR (1998). The clinical diagnosis of deep venous thrombosis: integrating incidence, risk factors, and symptoms and signs. Arch Intern Med 158:2315–2313. Stein PD, Henry JW (1997). Clinical characteristics of patients with acute pulmonary embolism stratified according to their presenting syndromes. Chest 112:974–979. Stein PD, Terrin ML, et al. (1991). Clinical, laboratory, roentgenographic and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest 100:598–603. Tapson VF, Carroll BA, et al. (1999). The diagnostic approach to acute venous thromboembolism. Am J Respir Crit Care Med 160(3):1043–1066.

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Swallowing disorders Introduction Eating and drinking are about as natural as breathing for a human being. Therefore, when something occurs that can affect how well a person consumes food, liquid, or medication, patients and/or family members may be left feeling quite debilitated. They may be frustrated by the condition they find themselves in and frightened by its consequences. Will the patient ever be able to eat again? Swallowing disorders are referred to as dysphagia. It commonly occurs in approximately half the patient population that has suffered from a stroke and remains the most common subgroup of illnesses that can produce a swallowing disorder. According to the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), 27%–50% of stroke patients will develop dysphagia. Further, 43%–54% of stroke patients with dysphagia will experience aspiration and, of these, 37% will develop pneumonia. Finally, if not part of a dysphagia diagnosis and treatment program, 3.8% of dysphagia patients with pneumonia will die.1 To a less severe degree, other adverse effects of swallowing disorders may include malnutrition and increased length of hospital stay. Other conditions that may result in dysphagia include but are not restricted to traumatic brain injury, Parkinson’s disease, advanced stages of multiple sclerosis, motor neuron disease, myasthenia gravis, the different muscular dystrophies, and the natural outcome of the aging process. When patients become unable to swallow foods, liquids, or medications safely by mouth, poor prognoses may be rendered. For this reason, early identification of a swallowing disorder is of great importance. According to the JCAHO, “screening for dysphagia should be performed on all ischemic/hemorrhagic stroke patients before being given food, fluids, or medication by mouth.”1 By extension, patients suffering from any of the other aforementioned disease processes, in addition to stroke, should be evaluated for their swallowing capabilities as soon as possible during their hospitalization.

Normal swallowing In all people, swallowing occurs in three distinct stages: the oral stage, the pharyngeal stage, and the esophageal stage. The oral stage is the first component of swallowing and consists of the preparatory and transport phases. The preparatory phase, or the time it takes for individuals to bite, chew, taste, etc. prior to bolus transport, will vary across individuals and food textures. In healthy individuals, the time it takes for the food to move from the mouth to the throat after it has been sufficiently chewed, mixed with saliva, and formed into a bolus is 1 second. This is known as the transport phase, which occurs at the tail end of the oral stage of swallowing. During the pharyngeal stage of swallowing, many things occur simultaneously to ensure the safe passage of the bolus: true vocal fold closure and 1 Swigert N, Steele C, Riquelme L (2007). Dysphagia screening for patients with stroke: challenges in implementing a Joint Commission guideline. ASHA Leader 12(3):28–29.

SWALLOWING DISORDERS

ventricular (false vocal fold) closure, retroflexion of the epiglottis, and elevation and forward movement of the larynx, all for the purpose of airway protection. In addition, the nasopharynx will close to prevent the possibility of nasal regurgitation. Finally, the esophagus will inflate as the upper esophageal sphincter relaxes, to accept the food bolus. All these separate but coordinated movements that occur in the pharynx take an additional 1 second to accomplish in healthy individuals. During the esophageal stage of swallowing, bolus motility through the esophagus may take anywhere from 8 to 20 seconds to accomplish in healthy people. Peristalsis, or the sequential contraction and relaxation of the muscles of the proximal, middle, and distal segments of the esophagus, then occurs, moving the bolus toward the lower esophageal sphincter and stomach. To summarize the timing elements of swallowing: • Oral stage (preparatory time: varies by individual and food texture; transport time: 1 second) • Pharyngeal stage (transport time: 1 second) • Esophageal stage (transport time: 8–20 seconds)

Signs and symptoms of disordered swallowing Clinicians need to be mindful of what to look for across the different stages of the swallowing process in order to make a proper diagnosis and initiate the appropriate treatment. Oral stage Initially, an examination of the orofacial region needs to be conducted to determine if any asymmetry exists as a result of a cerebrovascular accident (CVA) with accompanying hemiplegia or hemiparesis. Any sort of asymmetry or weakness detected in the oral region may have an affect on how well the patient can handle foods or liquids during the oral preparatory or transport phases of swallowing. For example, the patient may have difficulty placing or holding foods and liquids in their mouth because of poor lip compression or be unable to detect the presence of food or liquid residue at the lips or within the oral cavity itself due to sensory difficulties. The patient may also have problems with forming food into a bolus (including breaking the food into smaller particles, mixing crumbs with saliva to form a cohesive bolus, and gathering food particles into a central location on the mid-section of the tongue blade) or moving the tongue in an upward–backward sweeping motion to properly sweep the bolus toward the faucial pillars, where the pharyngeal stage of swallowing is triggered. Some patients demonstrating difficulty with bolus formation end up with food particles being deposited on the palate or in the buccal or cheek cavities, and because of accompanying sensory deprivation, they are often unaware that the residue exists. As a result, such patients may exhibit tracheal penetration of the undetected food residue minutes or even hours after the meal has concluded. Pharyngeal stage Following an examination of the structures and functions of the oral cavity, the clinician needs to examine what happens during the key pharyngeal

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swallowing stage. One of the most telling signs that a patient is having difficulty moving food or liquid through the pharyngeal cavity is the presence of a wet, often “gurgly” voice with accompanying cough at the completion of a swallow. A moist vocal quality is generally associated with the presence of either food or liquid residue in the area of the vocal folds, generally in the vallecular space or bilateral pyriform sinuses. A cough response, by contrast, is indicative of actual penetration of residue into the laryngeal vestibule and trachea. The cough is elicited when foreign matter enters the trachea and is detected by sensory cells designed to expel debris as needed and to keep the airway clear and protected. Unfortunately, clinicians cannot always count on the presence of a cough reflex to indicate that penetration of residue has occurred. In some individuals, the cough reflex may be missing because of the illness suffered and/or because of normal aging. In such cases, a patient may initially appear to be eating or drinking well with no apparent distress, only to exhibit delayed signs of aspiration after some time has elapsed. These signs include oral cavity residue, pharyngeal stridor detected via cervical auscultation, a persistent wet vocal quality, re-swallowing a bolus without success, or a spiking temperature, suggesting aspiration and development of pneumonia. Some patients present with a history of recurrent pneumonia, which should serve as a red flag alerting the clinician to a pending poor prognosis. Finally, some individuals may complain of pain on swallowing that may reflect problems with the mechanics of laryngeal structure movements. Esophageal stage During the final stage of swallowing food into the stomach, patients may present with various signs and symptoms indicating difficulty with the task. For example, a patient may report an unjustified feeling of fullness before completion of a meal. Often, this observation may be directly attributable to a bolus motility problem through the esophagus itself. This manifests as delayed or halted movement of the bolus toward the stomach, as well as proximal escape or backward flow of the bolus toward the pharynx. These symptoms can occur as a result of various esophageal conditions, including strictures, which are a narrowing of the esophageal lumen. They may also result from achalasia or the failure of the lower esophageal sphincter to relax. In some patients, backflow could result from a condition called “corkscrew” or presbyesophagus, generally associated with persons of advancing age. One of the most common afflictions to affect the ability to swallow is gastroesophageal reflux disease (GERD). This ailment is associated with poor containment of stomach contents secondary to lower esophageal sphincter (LES) dysfunction, or the inability of the LES to contain stomach contents. As a result, partially digested foods exposed to stomach acids re-enter the esophagus and flow backward toward the pharynx, causing great pain and/or a burning sensation. These patients may also exhibit frequent coughing or gagging. Fistulas, or small holes connecting the esophagus to the trachea, may develop in some cases, creating an easy avenue for food or liquid to escape into the airway after it has been safely swallowed. The symptoms suffered

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by these patients are similar to those experienced by patients who aspirate after swallowing from other causes (discussed earlier). An additional condition that could lead to aspiration is Zenker’s diverticulum, or small pockets that form when muscles in the pharynx and/ or esophagus herniate, causing materials to pool within the small space. At the conclusion of a swallow, the material that had pooled within the diverticulum usually will empty and, as a result, may fall into the airway, causing an aspiration. Speech–language pathologists who serve primarily as swallow clinicians in a hospital setting may be limited in their ability to work with patients who suffer from dysphagia, depending on the source or underlying etiology. Generally, if the swallowing problem results from a condition that can be localized to either the oral or pharyngeal cavities, a swallow clinician may be able to enact appropriate treatment strategies. However, if a swallowing problem is discovered as being primarily esophageal in nature, speech–language pathologists may be limited in what they can do, short of recommending a change in diet consistency or suggesting that patients alternate food swallows with liquids to help flush residue and aid in motility. In cases when a fistula or diverticulum is diagnosed as a result of a diagnostic procedure (modified barium swallow; fiber-optic endoscopic evaluation of swallowing), they may need to refer the patient for an appropriate medical or surgical consult.

Diagnostic procedures Various diagnostic procedures are employed to evaluate the ability of a patient to safely swallow. A quick and effective method for ascertaining the ability of an individual to safely consume food, liquid, and medication is the bedside evaluation, which is often the first step before more comprehensive examinations are used. Examples of these include the modified barium swallow and the fibeoptic endoscopic evaluation of swallowing, with or without sensory testing. Bedside evaluation This is the most frequently used assessment procedure in most facilities that provide care and treatment for those with dysphagia. It begins with an examination of the patient’s chart to learn of any underlying or contributive diseases or significant history of past aspirations, followed by screening of the patient’s ability to consume various food and liquid textures presented at bedside. But before feeding the patient, the speech–language pathologist first conducts the patient interview to determine what problems exist in terms of food and liquid management. If the patient is unable to participate in the interview process, the swallow clinician may ask questions of the nurse or physician assigned to the case or ask members of the family empowered to speak on behalf of the patient. In the course of speaking to the patient, the speech–language pathologist is seeking to determine the cognitive, linguistic, and behavioral attributes of the patient. It is important to determine if the patient has the capacity to understand language, as they will be asked to participate in the screening procedure to the best of their ability. If the patient doesn’t have the

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requisite cognitive abilities to follow a conversation and/or simple instructions (e.g., because of dementia, or aphasia), or does not exhibit adequate verbal communicative abilities to answer or ask questions during the bedside procedure (e.g., English is their second language), results may not be accurate or represent a patient’s true ability with swallowing. One of the first things to be done during a bedside evaluation is to examine the oral cavity. A swallow clinician must be able to determine if a patient has the potential ability to swallow or not, and a visual inspection of the oral cavity can reveal much. The presence of dried secretions that require swabbing to eliminate, the appearance of food particles or the remains of medication previously given, and mouth breathing (which prevents a patient from engaging in overly long bolus preparation intraorally because of the shortness of breath that occurs when their mouth is closed for too long) all contribute to the prognosis ultimately rendered. After the visual inspection is completed, the speech–language pathologist may be better informed as to which consistencies of food or liquid should be used or avoided in the screening procedure. At bedside, the more typically used consistencies are a mechanical soft food that requires some amount of chewing (usually a graham cracker or pretzel); a softer, more puree-like food that requires little chewing (pudding, applesauce), and different grades of liquids, including honey and nectar-thickened juices, and water, a thin liquid. Each of these foods and liquids may be used or not, depending on preliminary results of the patient interview. Once the food is offered, the clinician will observe the ability of the patient to prepare and transport the bolus through the oral and pharyngeal cavities. This can be directly observed visually as materials contained in the mouth move toward the pharynx, or it can be indirectly observed once materials have entered the throat itself. For example, the swallow clinician can watch the patient for signs of chewing efficiency, length of chewing pattern, time spent in moving the bolus through the mouth, food spillage from the oral cavity, if any, and laryngeal elevation once the pharyngeal stage of swallowing has been triggered. In addition, the clinician can listen to the sound of the swallow via cervical auscultation with use of a stethoscope placed at the patient’s neck at the moment of swallowing. In a healthy individual, a loud gulp (described as a “clunk”) can be detected. Other sounds indicating swallowing problems include multiple swallows, termed “piecemeal” (reflecting vallecular pooling), or “stridor”, indicative of residue. After providing foods and liquids, the clinician may ask the patient to vocalize in order to observe the condition of their voice. A wet, hoarse vocal quality is what may be noted in cases of food or liquid residue in the pharynx. Another commonly used bedside procedure used with patients with tracheosotomy tubes is the blue-dye procedure, which often requires nursing and/or respiratory therapy staff together with a speech–language pathologist. The procedure involves deflation of the patient’s cuff, followed by an initial suctioning of the trachea and/or oropharynx. Once the patient has been sufficiently prepped, he or she is provided a blue-dyed substance by mouth, either a liquid or solid, depending on the patient’s current level of swallowing ability, followed by resuctioning at the trachea and oropharynx.

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If the patient spills any blue-tinged material from the trachea, this generally indicates that the material provided by mouth has penetrated the trachea, placing that person at risk for aspiration. However, if no blue dye is noted, the patient is considered able to swallow and can start on a particular diet that initially may include fluids only, followed by more consistent food items as the patient continues to progress. Modified barium swallow (MBS) Considered by many to be the gold standard in terms of examining a person’s ability to swallow safely through use of instrumentation, the modified barium swallow is widely used. Also referred to as video fluoroscopy, this technique employs use of radiological equipment and video recording to examine the oral, pharyngeal, and esophageal cavities while the patient is provided various food and liquid barium consistencies. This procedure helps to define the etiology of aspiration by providing the clinician with information concerning the patient’s speed of swallow through the three swallow stages and, through visualization, helps to identify and define any anatomical or physiological abnormalities that could cause the dysphagia symptoms reported. For example, the MBS could provide information on bolus transport times through the mouth or throat, motility issues as the bolus moves through the esophagus, or any aspiration that occurs. The MBS provides relatively low doses of radiation and allows for a visualization of the oral cavity while the patient is chewing. It also shows the triggering of the pharyngeal swallow in relation to position of bolus and reveals the various motor aspects of the pharyngeal swallowing stage, which include movements of larynx, hyoid, tongue base, pharyngeal walls, and cricopharyngeal region. Fiber-optic endoscopic evaluation of swallowing Known as FEES (or FEESST, if one were to incorporate the additional diagnostic technique of sensory testing to assess arytenoid cartilage function), this procedure has gained in popularity and use over the past several years. Employing an endoscopic tube with a light source and video camera, a clinician with specific training can examine the larynx during the pharyngeal stage of swallowing. Introducing the endoscope through the nose and positioning it just above the larynx, different foods and liquids with either a blue or green coloring are introduced, which the patient is instructed to chew and swallow. Given that the endoscope is situated above the laryngeal vestibule, neither the oral cavity nor the esophagus can be visualized. However, the clinician can see the top of the larynx and observe if aspiration occurs once the pharyngeal stage of swallowing is triggered. The clinician might also be able to observe if premature spillage from the oral cavity occurs, which may reflect the inability of the patient to form a cohesive food bolus. This is easily visualized if blue- or green-tinged food comes into view and pools within the laryngeal vestibule, vallecular space, and/or pyriform sinuses before the pharyngeal swallow stage is triggered. In other cases, a clinician might notice the occurrence of reflux as it backflows from the esophagus into the pharyngeal cavity.

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Clinicians do not always agree which procedure, the MBSs or the FEES, is more revealing or diagnostic. While the MBS can provide the clinician with a visual representation of all three swallowing stages, the FEES provides an actual image compared to a radiographic image (although the image provided only incorporates the second swallow stage). The MBS does expose the patient to low doses of radiation, whereas the FEES is considered a more intrusive procedure because of the transnasal introduction of the fiber-optic endoscopic tube. A patient needs an appointment to have an MBS conducted, as a radiological suite needs to be booked, along with a radiologist. The FEES procedure can be conducted at bedside, as long as the equipment and the ability to transport it safely is established, and the speech–language pathologist can act independently, given the correct training. The debate continues, as do both procedures in different facilities.

Results of assessment Following assessment of a patient’s swallowing ability, a number of different recommendations may be made. However, the assessment should be based on the specific abilities and needs of the individual tested. For some patients who present with a worst-case scenario, the ability to swallow may not exist. Any attempt to feed the patient by mouth would result in the possibility of penetrating into the trachea, followed by aspiration into the lungs. Such an individual should be made NPO and receive nothing by mouth. In lieu of oral nutrition, some alternative means of getting nourishment and hydration into the system may include intravenous (IV) feedings, use of nasogastric (NG) tubes, percutaneous endoscopic gastrostomy (PEG) tubes, or jejunostomy (J) tubes. With the exception of IV feeding, which supplies the patient with IV solutions, each of the tubes mentioned feed the patient a specially prepared liquid diet containing the nutrients and essential ingredients required by that individual. The main difference between the tubes is their point of insertion (NG is through the nose and into the stomach; PEG is through the abdomen and into the stomach; J-tube is through the abdomen and into the jejunum of the intestine). Some patients may not initially have the ability to consume solid foods safely, so for them a full liquid and/or thickened liquid diet may be the appropriate recommendation following testing. For others, soft solid foods or puree textures may be the proper recommendation, as they may have difficulty with bolus preparation of more solid consistencies. Still others may be appropriately nourished through a range of mechanical soft food consistencies, which are foods that differ slightly from regular foods. Some may be chopped and others may come with more natural moisture added to aid in bolus preparation and transport. Finally, some persons may pass all aspects of swallow testing and be awarded the regular diet at the conclusion of testing. For any patient exhibiting a disorder of swallowing, not only can appropriate diet recommendations be made in conjunction with a dietician, but additional measures can also be taken to help patients improve their overall swallow function. Speech–language pathologists have specific training in the areas of oral motor development and voice production, which

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intersect quite naturally in the area of swallowing. Swallow clinicians may determine which of the patients examined for swallowing deficits may benefit from dysphagia therapy and work to help these individuals make improvements in this area.

Conclusions The importance of performing a proper diagnostic evaluation to ascertain the legitimate swallowing abilities of a patient cannot be overstated. The effects of correct diagnosis and treatment for patients with dysphagia are far-reaching and include several key areas: • Respiratory—the prevention of aspiration pneumonia and other aspiration sequela • Nutritional—the prevention of malnutrition and dehydration associated with swallowing inefficiency and weakness • Financial—the limiting of health-care expenditures for the preventable consequences of dysphagia • Physiological—the restoration of normal swallowing physiology • Quality of life—the restoration of normal mealtime participation and enjoyment thereof for the patient and family

Further reading Dikeman K, Kazandjian M (2003). Communication and Swallowing Management of Tracheostomized and Ventilator-Dependent Adults, 2nd ed. Clifton Park, NY: Thomson-Delmar Learning. Logemann J (1998). Evaluation and Treatment of Swallowing Disorders, 2nd ed. Austin, TX: Pro-Ed Publishers. Perlman A, Schulze-Delrieu K (1997). Deglutition and Its Disorders, San Diego: Singular Publishing Group.

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Sexuality and the disabled Overview Sexuality is often a subject that physicians are uncomfortable talking to their patients about. However, it should be considered in the same manner as other bodily functions and discussed with the patient before discharge. Successful return to sexual activity will depend on the patient’s impairment, self-image, and previous functional status, and on the attitude of the partner. While physical aspects of altered sexual function need to be addressed, the emotional issues need to be considered as well. The issues in sexuality are compounded by possible fertility issues (spinal cord injury, neuropathy), erectile dysfunction (spinal cord injury, vascular disorders, medication, stroke, neuropathy, psychological disorders), urinary catheters (incontinence), cultural issues, mobility (almost any physical impairment), physical changes (amputations, burns), cardiac concerns, (post-CABG), age, fatigue, privacy issues (especially in institutions), fear of further injury, cognitive issues (TBI), pain, depression, and hypersexuality (TBI, stroke).

Cardiac Cardiac patients, in general, should be instructed that sexual relations with a stable partner require about 3–5 METs. This is the equivalent of going up and down two flights of stairs. If the patient can tolerate this activity, he or she should be encouraged to resume sexual activity. The patient should be reminded that sexual relations with a new partner or outside of the relationship cause higher energy demands.

Medication While depression can lead to altered sexual function, the treatment of depression can lead to altered sexual function as well. Medications for depression that do not affect sexual function, such as bupropion, mirtazapine, and nefazodone, should be considered.1 Testosterone has been used to treat hypoactive sexual desire in both males and females. Medications used to achieve erection include sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis). Estrogen or vaginal lubricants have been used to improve lubrication in females.

Devices to achieve erection Vacuum-assisted devices can be used to achieve erection. Either a manual pump or a battery-operated device is used to create a vacuum, which pulls blood into the penis. A constriction band at the base of the penis maintains the blood in the penis, and keeps it erect. Penile injections involve injecting medications (papaverine, phentolamine, and/or prostaglandin E) into the cavernous spaces.

1 Hirschfield RM (1999). Care of the sexually active depressed patient. J Clin Psychiatry 60 (Suppl 17):32–35.

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Problems with penile injections include pain, fibrosis, hematoma, scarring and permanent curvature of the penis, priapism, and adversity to self-administering an injection. Penile prostheses are usually used as a treatment of last resort, as complications are common (infection, ulceration, sensory changes, mechanical failure).

Further reading Branco F, Sipski M, Sherman A (2007). Sexuality issues in persons with disabilities. In Braddom R (ed.). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders–Elsevier, pp. 667–684.

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Immobility syndrome General description Unwittingly, the health-care system tends to promote immobility in our patients. Care patterns that keep patients in their beds promote dependence on physician and nursing staff. Patients are frequently restrained by either physical restraints (poseys), chemical restraints (medication), or treatment restraints (IV, oxygen, catheters). Deconditioning occurs at a faster rate than reconditioning.

Clinical manifestations Immobility affects most of the organ systems in the body. Cardiovascular • Increased heart rate • Secondary to increased sympathetic nervous system activity • With complete bed rest, the resting pulse rate increases 1 beat/ minute every 2 days. • Along with increased heart rate is a decrease in diastolic filling time and a decreased systolic ejection time. • Decreased cardiac reserves • Decreased diastolic filling time (with corresponding decreased coronary blood flow and decreased O2 available to cardiac muscles) • Decreased cardiac output • Decreased stroke volume • Decreased left ventricular function • Orthostatic hypotension (begins after 3 weeks of bed rest and is secondary to excessive pooling of blood in the lower extremities and decreased circulating blood volume) • 20 days of bed rest may lead to a 25% decrease in stroke volume and a 20% increase in heart rate. Joints • Immobilization can induce cartilage degeneration. • Opposing joint surfaces that contact each other can lead to pressure necrosis and erosion or fissure development. • The body attempts to repair joints through cartilage proliferation, osteophyte formation, and fibrofatty infiltration of the joint cavity. Bone • Loss of bone mass due to increased bone resorption • Loss of trabecular bone more than cortical bone (almost 1% loss of vertebral mineral content per week) • Increased risk of fracture, dorsal kyphosis, and chronic back pain • Wolff’s law states that the ratio of formation to resorption of bone is influenced by the stressors that the bone is subjected to. Since weight bearing is the primary stress on most bones (as well as the pull of muscles), immobility greatly increases the resorption of bone relative to the formation of bone, leading to osteoporosis and an increased fracture risk.

IMMOBILITY SYNDROME

Connective tissue • Contractures (contributing factors include spasticity, improper bed positioning, and maintaining the limb in a shortened position) • Muscles that cross two joints are at increased risk for contractures. Musculoskeletal • Loss of muscle strength (to maintain muscle strength, all that is needed is a daily muscle contraction of 20% or more of maximum tension for several seconds) • Decreased endurance • Muscle atrophy (begins after 1 day of immobilization. Muscles may lose half of their bulk after 2 months) • Decreased flexibility Central nervous system • Sensory deprivation • Mental deterioration • Behavior disturbances • Dependency • Decreased balance and coordination (increase the likelihood of falls) • Anxiety • Sleep disturbances • Depression Peripheral nervous system • Compression neuropathies Gastrointestinal • Anorexia • Constipation • Malnutrition Endocrine and renal • Decreased basal metabolic rate (which can lead to diuresis, natriuresis, and fluid shifts) • Negative nitrogen balance • Glucose intolerance • Hypercalcemia (symptoms of hypercalcemia include anorexia, abdominal pain, nausea, malaise, headache, polydipsia, polyuria, lethargy, and coma). Symptoms may occur within 2–4 weeks. Hypercalcemia is especially common in adolescent males with traumatic brain injury. • Decreased parathyroid hormone • Increased plasma renin activity • Increased aldosterone secretion • Altered growth hormone production • Altered spermatogenesis and androgen secretion • Altered circadian rhythm • Renal stones Pulmonary • Decreased tidal volume • Decreased minute ventilatory volume

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• Decreased ability to contract ventilatory muscles sufficiently to accomplish full inspiration • Decreased strength of respiratory muscles • Decreased respiratory capacity • Increased respiratory rate to compensate for decreased respiratory capacity • Decreased ventilation and increased perfusion lead to arteriovenous (AV) shunting and decreased arterial oxygenation. • Decreased ability to clear secretions • Accumulation of secretions in the lower bronchial tree, which can block airways, cause atelectasis and increase the risk of pneumonia. Skin • Localized areas of cellular necrosis • Complications of decubiti (infection, periostitis, sinus formation, osteomyelitis, septic arthritis, septicemia, heterotopic ossification, protein loss, and anemia) • Prevention of decubiti consists of turning the patient every 2 hours, prone lying when possible, avoiding the semirecumbent position, avoiding use of doughnuts, adequate nutrition, proper mattress, and decreasing friction, spasticity, shear, and excess moisture. Venous thromboembolism • Due primarily to venous stasis and may be due to increased blood coagulability • Length of bed rest is directly related to the likelihood of DVT Genitourinary system • Decreased voiding • Increased post-void residual volume • Increased risk of urinary tract infections • Increased risk of calculus formation • Decreased glomerular filtration rate

Chapter 17

Rehabilitation issues Lyn Weiss Dennis J. Dowling Robert A. Domingo Lynn A. Schaefer Vladimir Salomon Elizabeth Flynn Carol Kave Chamoff Thomas Pobre Burns 402 AIDS/HIV-associated conditions 406 Cancer rehabilitation 408 Communication disorders 412 Neuropsychological assessment and treatment 416 Osteopathic manipulation 420 Gait 424 Wheelchair prescriptions 428 Assistive devices 432 Adaptive devices 434 Resources for the physiatrist 438

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Burns General description A burn is a permanent destruction of tissue secondary to an external agent. Among the many agents that can cause burns are heat (thermal), cold (frostbite), electrical, chemical, and radiation energy. Burns can not only affect the skin but also cause complex systemic responses involving most organs. The skin protects the body against the environment, prevents evaporation of fluid, and helps to maintain thermoregulation. Burn rehabilitation should be initiated as early as possible to prevent deformities and functional impairment.

Classification Burns are classified by the degree of tissue damage: • First degree: injury to the outer layer of the epidermis. There is erythema, but no blistering. • Second degree superficial (partial thickness): injury to the epidermis, but the basal layer remains intact. Blistering of the skin is noted. • Second degree deep (partial thickness): injury to the dermis. The basal layer lining the skin appendages is intact. Blistering of the skin is noted. • Third degree (full thickness): injury to the epidermis and dermis. Burns are also classified according to the percentage of body surface area affected. The rule of 9’s is used to estimate the area burned (each of the following areas is estimated as having 9% of the total body surface area: each upper limb, the front of each lower limb, the back of each lower limb, the anterior trunk (2 units or 18%), the posterior trunk, and the head).

Body’s reaction to burns The response to a burn depends on the type of burn, duration, intensity and amount of tissue destroyed. Shortly after the insult, histamine is released, which causes vasoconstriction. Within a few hours, vasodilatation and increased capillary permeability occur, allowing plasma to escape into the wound. Platelets and leukocytes aggregate, causing thrombotic ischemia and further damage. There is a large fluid loss through the wound. Evaporation causes heat loss. Patients are prone to contamination of the wound and sepsis, as the skin is the body’s primary protection from infection. Acutely, the patient is at risk for hypovolemia, shock, upper airway obstruction, cardiac and pulmonary complications, and deep venous thrombosis (DVT). Immediate measures address the patient’s survival and include resuscitation and wound coverage. An escharotomy (incision through the burned tissue to relieve increased tissue pressure) may be necessary to preserve limb function.

Factors affecting burn recovery A patient’s ability to recover from a burn injury depends on the patient’s age, any associated medical conditions, the total body surface area affected, any associated injuries, as well as burn depth. Burn recovery will also depend on the type of burn.

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Radiation therapy may result in delayed healing or chronic wounds. Chemical burns can cause liquefaction necrosis (alkali burns) or coagulation necrosis (acid burns). Electrical burns cause a disproportionate amount of morbidity and mortality due to the depth of tissue damage.

Grafting Grafting is a method to achieve wound coverage by transferring tissue from an uninjured area of the body (autograft) or from tissue not originating from the patient (allograft). It is usually required for full-thickness wounds and deep partial-thickness wounds that are slow to heal. Grafting should be performed as soon as the patient is medically stable enough to undergo the procedure. Any burn that does not heal in 18–21 days will usually require skin grafting. Grafts should be immobilized for a minimum of 3–5 days after surgery to improve the ability of the graft to take.

Goals of burn rehabilitation The goals of rehabilitation of the burn patient are to promote wound healing, prevent complications, and restore function. Wound healing initially includes removal of dead tissue and maintaining a moist, clean environment to promote tissue growth. Sharp (scalpel) or mechanical (forceps or wet to dry dressings) debridement can be used. Hydrotherapy can also be used to debride devitalized tissue. Enzymatic debridement can be used, but not over intact skin. Surgical debridement may include tangential, fascial, or full-thickness excisions. Burn complications include joint contracture, weakness, infections, pruritus, scarring, pain, and medical complications (decreased pulmonary and cardiac function, endocrine dysfunction). The patient must be positioned and splinted carefully to maintain range of motion (ROM) and avoid compression neuropathies. In general, the affected tissue should be kept in an elongated state. Positioning and splinting should keep the upper extremities supinated, with shoulders at 90* abduction and externally rotated. Hand splints should position the wrist in extension, 60–80* of metacarpophalangeal flexion, full interphalangeal extension, and thumb abduction.1 The lower extremities should be positioned with the ankles at 90* of dorsiflexion, and no flexion at the knees and hips. Exposed tendons should be splinted in a slack position to prevent rupture. Serial plaster casts can be used, especially in children and noncompliant adults. However, the cast must be changed frequently (every 3 days) and inspected. New graft sites should be protected from shear or stress. Scarring occurs quickly and must be minimized. Pressure garments facilitate appropriate orientation of collagen as the scar matures, and should be continuous (worn 23 hours a day) and provide at least 25 mmHg of pressure. They must be changed approximately every 3 months, as they lose elasticity, and smaller garments are needed as edema and scarring are controlled. They are usually worn for 12–24 months. 1 Brammer C, Spires MC (2002). Manual of Physical Medicine and Rehabilitation. Philadelphia: Hanley & Belfus, p. 26.

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Restoration of function includes early mobilization. Patients should begin ambulation as soon as their medical condition allows. Patients with lower extremity burns should not ambulate until circulation to the graft site is established. If a burn is over a joint, ROM exercises are usually held for 3 days for a meshed graft and 5 days for a sheet graft. Once the graft appears healthy, active ROM exercises can be initiated. The graft must be inspected after exercises to ensure that there is no disruption to healing. Range of motion exercises should be performed 3–4 times per day. It is best to instruct the patient and family in these exercises so they can be performed at home. Burns and scars near the mouth can result in microstomia (loss of normal mouth opening). Custom mouth splints should be used to prevent the loss of the normal mouth aperture. The device must be worn at all times except during eating and oral hygiene. Restoration of function must include attention to cosmesis and the patient’s adjustment to his or her disability. Depression, post-traumatic stress disorder, sexual dysfunction, lower self-esteem, adjustment disorder, and delirium are all common in burn patients.

Management (treatment) First- and second-degree burns can be extremely painful, and the pain must be managed. Third-degree burns are usually not as painful as the nerve endings have been destroyed. Pain control is especially important in the early stages of burn management as it can increase heart rate, blood pressure, and metabolic rate. Early mobilization may be limited by poor pain control. Narcotics are used primarily. Patient-controlled analgesia (PCA) should be considered with severe pain. Edema is common due to seepage of fluids and electrolytes, as well as obstruction of local lymphatic vessels. The patient’s hydration status must be monitored and maintained. The limb should be elevated and splinted to prevent deformity. Posttraumatic stress disorder is common in burn victims and must be addressed. Nutritional support is required in burn patients both to promote healing and to compensate for protein and electrolytes lost to fluid shifts. There is an increased metabolic demand from healing and warding off infection. Caloric needs are thus increased in these patients. Pruritus is common in full-thickness burns, as the oil and sweat glands are damaged, leaving the patient with dry and friable skin. Scarring must be kept to a minimum. External vascular support garments and moisturization will help prevent scarring. If scarring does develop, scar mobilization and massage should be employed. Infection is a serious and common complication, since the body’s primary natural defense against infection is compromised. Surgery may be indicated in management of the patient with chronic burns. Simple releases (Z-plasty) may be used for contracted skin. Reconstruction (for cosmesis) or repeat skin grafting may be necessary.

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Complications and red flags Electrical burns can be deceptively deep and cause damage to internal organs (due to resistance, conductivity, and heat production). After an electrical burn to the head or shoulders, or visual exposure to the flash, cataracts can form within 1 month to 3 years. Up to 23% of burn patients may develop heterotopic ossification (HO).2 The location of the HO does not necessarily correlate with location of the burn. Active ROM therapy within the pain-free arc should be employed. Peripheral neuropathy occurs in 15%–30% of burn patients (more commonly in patients with more than 20% total surface area burns2). The etiology of peripheral neuropathy may be infectious, metabolic, nutritional, toxic, or drug induced. Localized neuropathy may also be due to traction or stretching of a nerve (as during positioning, sometimes presenting as a brachial plexopathy) or local scarring. In the pediatric burn population, professionals must be aware of child abuse and have a low threshold for suspicion. Burns to the hands, feet, or genitalia in a child are considered especially suspicious. Long-term disabilities in burn patients include heat and cold sensitivity, pruritus, weakness, contractures, scarring, sensory impairment, fatigue, sleep disturbances, decreased endurance, psychological disorders, intolerance to sun, perfumes, and other chemical irritants, and gait disturbances.

2 Rivers E, Fischer S (1997). Burn rehabilitation. In Young MA, Stiens S, O’Young B (eds.). (2007). PM&R Secrets. Philadelphia: Hanley & Belfus, pp. 421–422.

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AIDS/HIV-associated conditions General description Human immunodeficiency virus (HIV) was first described in 1985. It is now considered a pandemic, with 59 million people who have been infected, including 20 million who have died.1 The ensuing disability and death have led to tremendous physical, psychological, and financial burdens on patients, families, and the health-care system. HIV represents a spectrum of diseases. Acquired immune deficiency syndrome (AIDS) is the presence of one or more AIDS-defining illnesses or a cluster determinant 4 (CD4) count below 200/mm3. Transmission of the disease is primarily by sexual contact (84%), although it can also occur via infected blood or blood products, IV drug abuse, needle stick, and perinatally.

Clinical manifestations HIV is classified by stages of primary infection with seroconversion, clinical latency, early symptomatic disease, and AIDS. The clinical manifestations depend on the patient’s staging. Patients with HIV can present with numerous complications as a result of their disease and their disease treatments. Neuropathies are common, and can result from the disease itself or a side effect of medications. The types of neuropathies include Guillain–Barré, distal symmetric polyneuropathy, inflammatory demyelinating polyneuropathy, motor neuron disease, autonomic neuropathy, compression neuropathies, polyradiculopathy, and mononeuritis multiplex. Patients usually become debilitated as their disease progresses From 7% to 20% of patients develop myelopathy,2,3 which may be a result of opportunistic infections, HIV myelitis, or vacuolar myelopathy. Progressive chronic myelopathy can occur in patients with human T-lymphotropic virus type 1.4 Patients with AIDS have a higher propensity than the general population to develop malignancies (especially non-Hodgkin lymphoma, primary brain lymphoma, and Kaposi sarcoma), pneumonia, opportunistic infections, tuberculosis, myalgias, arthralgias, and encephalopathy. Patients are also at increased risk for neuropsychiatric disorders, especially depression.

Special considerations Weight loss and tissue wasting (usually a result of malnutrition, anorexia, infection, hypogonadism, and/or an HIV-induced hypermetabolic state) affect many of these patients. Treatment with viral suppression through antiretroviral agents is the first approach. In patients with weight loss, 1 UNAIDS (2004). Report on the Global AIDS Epidemic, 2004. Bangkok, Thailand. 2 Di Rocco A (1999). Diseases of the spinal cord in human immunodeficiency virus infection. Semin Neurol 19:151–155. 3 Quencer RM, Post MJ (1997). Spinal cord lesions in patients with AIDS. Neuroimaging Clin North Am 7:359–373. 4 Braddom R (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders–Elsevier, p. 1301.

AIDS/HIV-ASSOCIATED CONDITIONS

protein and caloric supplements should be encouraged. Increased exercise (combined with steroid hormones in patients with low serum testosterone) may be beneficial.

Management (treatment) The course of the illness is variable and depends on such factors as viral load, comorbid conditions, access to health care, and timing and types of treatment. Treatment plans should maximize nutrition, cardiovascular conditioning, endurance, and functional independence. The clinician should try to intervene early to reduce the effects of comorbid conditions and debility. Because more patients with HIV/AIDS are living longer as a result of antiretroviral agents and improved medical care, the challenges of treating the disease in an aging population (and the associated co morbidities) have increased.

Complications and red flags Patients with HIV are at increased risk for infectious and neoplastic disorders, pain, debility, and nervous system disorders (both peripheral and central). A patient with complaints of a change in symptoms should be evaluated as soon as possible. Physicians need to educate their patients about the disease and how to avoid transmission to others. Health-care providers are at risk for disease transmission if care is not taken with bodily fluids. Universal precautions should always be used, especially when handling a needle or bodily fluids. However, if the patient has no open wounds and there is no anticipated contact with bodily fluids, there is no need to use any different precautions than those used with other patients (i.e., there is no need for gloves, gown, etc.).

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Cancer rehabilitation General description The rehabilitation of patients with cancer varies widely and depends on the type, location, and staging of the cancer, treatments given, prognosis, and comorbid conditions. Almost all physiatric issues may complicate the treatment of a patient with cancer. These include psychological factors (depression, change in body image), edema, amputation, pain, speech and swallowing disorders, debility, sexual dysfunction, fractures, nutrition, surgery, bowel and bladder continence, mobility, activities of daily life, neuropathies affecting peripheral nerves or nerve roots or plexus, myopathy, autonomic neuropathy, weakness, myelopathy, constipation, sleep disturbances, orthostatic hypotension, malnutrition, cognitive and brain dysfunction, contractures, decubitis ulcers, and, most importantly, quality of life. As with most rehabilitative issues, the team approach, including the patient and his or her family, is the most likely to yield a positive result. With improvements in the early identification and treatment of cancers, more patients are achieving long-term survival.

Clinical manifestations Cancer can affect any organ in the body. The clinical manifestations will depend on the type of cancer.

Differential diagnosis When treating a patient with a history of malignancy, the differential diagnosis of any physical findings must include a complication from the primary tumor, metastasis, remote effects (paraneoplastic syndrome), or a reaction to treatments (radiation, chemotherapy, etc.).

History The history must include a detailed description of the type of tumor, staging, and any treatments performed, including surgeries, chemotherapy, or radiation therapy. It is helpful to get a report from the oncologist, as the patient may not know all of the information. The physician must also get information on the patient’s nutritional status, prior functional history, and the patient’s goals for rehabilitation. A psychological assessment is helpful to screen for depression. It is important to assess the patient’s pain level and determine if the patient feels the pain is being managed. Since these patients are often on chronic pain medications, the side effects from narcotics (constipation, nausea, lethargy, etc) need to be assessed. Nutritional factors such as weight loss and appetite should also be addressed.

Physical examination The physical examination of a patient with cancer should include an assessment of the patient’s general physical condition and of any effects of the cancer specifically. Special attention must be paid to common complications of cancers, including nutritional status, hydration, swallowing, maneuvers that cause pain, edema, neuropathy, and cognition. The physician must

CANCER REHABILITATION

be concerned about DVT, pathological fractures, and the patient’s cardiac and respiratory function.

Diagnostic testing Specific diagnostic testing depends on the type of cancer, the typical locations for metastasis, and the treatments performed.

Special considerations Paraneoplastic syndrome is especially prominent in patients with small cell lung cancers (1%–3% of patients with small cell lung carcinoma will develop paraneoplastic syndrome). Paraneoplastic syndrome may present as neuropathy, myasthenia gravis, Lambert–Eaton myasthenic syndrome, neuromyotonia, or dermatomyositis. Patients with cancer may also develop coagulopathies and be at increased risk for DVT and PE. Most of the chemotherapeutic agents have significant side effects that can include anorexia, nausea, anemia, weakness, and peripheral neuropathy. Before starting a patient on a therapy program, consider the patient’s cardiac and respiratory status. Some cancers are more likely to metastasize to bone. These include breast, lung, kidney, prostate, colon, melanoma, lymphoma, and multiple myeloma. In patients with suspected metastasis to bone, consider bone scanning. Pain may be a result of either the direct effects of the tumor or complications of treatment. Either way, pain must be adequately addressed.

Management (treatment) Although management will depend on the patient’s particular disability, general conditioning exercises will benefit most patients. Increased levels of physical activity may be associated with a decreased risk of both diseasespecific and overall mortality in patients with colorectal cancer.1,2,3 Exercise appears to have a beneficial impact on cardiopulmonary function, mood, fatigue, and quality of life, in addition to its effect on survival in breast cancer patients.1,4–8 1 Malhotra V, Perry MC (2007). Various rehabilitation issues in patients treated for cancer. UpToDate. 2 Meyerhardt JA, Giovannucci EL, Holmes MD, et al. (2006). Physical activity and survival after colorectal cancer diagnosis. J Clin Oncol 24:3527–3534. 3 Meyerhardt JA, Heseltine D, Niedzwiecki D, et al. (2006). Impact of physical activity on cancer recurrence and survival in patients with stage III colon cancer: findings from CALGB 89803. J Clin Oncol 24:3535–3541. 4 Courneya KS, Mackey JR, Bell GJ, et al. (2003). Randomized controlled trial of exercise training in postmenopausal breast cancer survivors: cardiopulmonary and quality of life outcomes. J Clin Oncol 21:1660–1668. 5 Daley AJ, Crank H, Saxton JM, et al. (2007). Randomized trial of exercise therapy in women treated for breast cancer. J Clin Oncol 25:1713–1721. 6 McNeely ML, Campbell KL, Rowe BH, et al. (2006). Effects of exercise on breast cancer patients and survivors: a systematic review and meta-analysis. CMAJ 175:34–41. 7 Mutrie N, Campbell AM, Whyte F, et al. (2007). Benefits of supervised group exercise programme for women being treated for early stage breast cancer: pragmatic randomised controlled trial. BMJ 334:517. 8 Pinto BM, Trunzo JJ (2004). Body esteem and mood among sedentary and active breast cancer survivors. Mayo Clin Proc 79:181–186.

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Quality-of-life issues are important, and pain must be adequately managed. Nonopiod analgesics should be used for mild pain. Opiod analgesics are employed for moderate to severe pain. Adjuvant drugs or other therapeutic modalities should be considered to supplement analgesics or treat side effects. In patients with chronic pain, it is better to dose the patient around the clock rather than prn. Rescue doses should be available for breakthrough pain. As a general rule, dosing of rescue medication is 1/6 of the 24-hour total daily dose. The patient’s general nutritional status, weight, albumin levels, hydration, and ability to swallow must also be assessed. Referral to a dietician and/or speech pathologist should be made when indicated.

Complications and red flags Myelopathy must be diagnosed early and treated aggressively. DVT and/ or pulmonary embolism (PE) must be considered in patients with cancer. Indications of brain metastasis may include headache, seizures, or weakness. If lytic lesions to the bones are considered unstable, surgical intervention is warranted. In general, lytic lesions in the femur are considered unstable if there is cortical destruction of >1.3 cm. in the femoral neck, >2.5 cm elsewhere in the femur, >60% of the bone width is affected, or >50% of the cortex is affected.9 Heat (or thermal modalities such as ultrasound) should not be used over tumor or radiated sites, as increased blood flow is suspected to accelerate tumor growth and promote metastatic spread, and radiated skin has reduced circulation.

9 Cuccurullo S (ed.). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical Publishing, p. 635.

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Communication disorders Introduction Verbal communication, or the ability to convey information and ideas from one person to another through use of speech, sets us apart from every other species on Earth. Without any formal training, children who develop typically with no medical, cognitive, or perceptual problems can learn to speak by simply attending to the signs and signals that surround them in the home setting. Through the social environment in which they are raised, children learn to “crack the code” and acquire a native language for the expression of thoughts and ideas, using arbitrary linguistic symbols while abiding by the rules that govern how these symbols are combined. Through speech they express their thoughts, using a finely tuned coordination of the neuromuscular complex. This complex involves four separate subsystems for speaking: respiration, phonation, resonance, and articulation. Each of these systems involves specific motor activities that result in the production of speech sounds that can then be interpreted by the speakers of the language to represent different concepts. The major function of all this coordinated effort is communication, which involves both a speaker and a listener in a mutually negotiated interchange of information in a sociolinguistic context. Deficits in communication may be determined to be either speech or language problems or both, and must be differentially diagnosed.

Cerebral localization In terms of cortical function, the role that the different lobes play in the control of different activities is well documented. The frontal lobe, the largest part of the cortex, is primarily responsible for voluntary motor function or muscle movement, which includes volitional movements of the head, neck, trunk, and four extremities as well as verbal speech production. The parietal lobe is primarily responsible for sensory function or the interpretation of sensory information that it receives from the environment through the sense organs of the body. Among other things, this includes the sense of touch as it relates to the articulation of sounds in the oral cavity. The temporal lobe is mostly responsible for hearing and long-term memory storage. When information is heard through our ears, data get transmitted to the temporal lobe for perception and interpretation, or the attachment of meaning. The auditory data that people receive may include words that contain meaning, or sounds with inherent meaning attached (e.g., sirens or car alarms). Finally, the occipital lobe is responsible for the interpretation of visual information. When our eyes see, the visual data are sent to the occipital lobe where it is perceived in the form of a picture. Visual data or symbols may come in a variety of different forms, such as printed words (e.g., “Do Not Enter”); colors that have meaning (e.g., a red light to imply “stop”); or even stick figures (e.g., caricature in skirt to represent “ladies room”).

COMMUNICATION DISORDERS

The cerebellum (“small cerebrum”) is considered the most recent evolutionary development in human neurology. This part of the brain is responsible for balance and coordination. In terms of the oral movements involved in speech production, a person would not be able to perform rapid and repetitive transitioning of the tongue, jaw, and soft palate without it. The cerebellum also helps individuals to judge the distance, speed, and power of a voluntary muscle movement, which helps to maintain the correct amount of muscle tone needed for the synergistic coordination of breathing, voicing, resonating, and articulating involved in speech production. Finally, the brain stem serves as a connecting pathway between the brain above and the spinal cord below.

Speech and language problems When patients suffer from some sort of brain damage, it may leave them with the inability to either formulate words (a language problem) or verbally produce them (a speech problem). These inabilities need to be differentiated. Language disorders include aphasia, a disorder in which patients may suffer either in the ability to encode a message (deciding how or what to say before they produce any verbal speech) or in decoding the message heard (perceiving the signal through the auditory channel and attaching meaning). However, with speech disorders that result from brain injury, the problems in communication may be more motorically rather than cognitively based in terms of how patients actually perform certain muscle movements to produce the speech sounds needed in a message. Such speech disorders are classified as dysarthria, a term for a collection of motor speech disorders due to an impairment originating in the central or peripheral nervous systems. Aphasia is one of the most common problems of communication confronted by a patient in an acute care setting. This disorder of language is caused by brain injury that results in a range of symptoms. In some patients, all aspects of language comprehension (the ability to perceive or understand) and production (the ability to express thoughts or ideas) may be impaired. In others, fewer aspects of comprehension and/or production may be lost or affected. The most common cause of aphasia is a cerebrovascular accident (CVA).

Types of aphasia Broca’s aphasia This type of aphasia is considered a nonfluent language disorder in that the person who suffers from it is unable to speak in a flowing or connected way. The patient with this type of aphasia has sustained some degree of injury to the third frontal convolution of the left, or language-dominant, hemisphere, or Broca’s area. The speech of these patients is characteristically “choppy,” with many occurrences of the patient not being able to remember the words he or she is trying to say.

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Wernicke’s aphasia Wernicke’s aphasia results from injury to the posterior portion of the superior temporal gyrus in the left, or language-dominant, hemisphere, or Wernicke’s area. This type of aphasia is considered a fluent aphasia in which the patient is capable of speaking in a connected or fluent manner. However, the spontaneous speech of these patients is also spliced with jargon or nonsense utterances, referred to as paraphasias. Most Wernicke aphasics are unaware of the speech errors they commit in connected speech and may act surprised that people do not understand them when they speak. They may feel paranoid, homicidal, suicidal, and depressed, and may at times be confused with psychiatric patients. Wernicke’s aphasia has also been referred to as word deafness, syntactic aphasia, or central aphasia. Anomic aphasia This variety of fluent aphasia may be caused by lesions in different regions of the brain, including the angular gyrus, the second temporal gyrus, or at the juncture of the temperoparietal lobes. With this type of language disorder, a patient is typically unable to produce the names of things whereas most other language functions besides naming are relatively intact (e.g., such patients exhibit good auditory comprehension ability). Conduction aphasia This type of fluent aphasia results from damage done to the arcuate fasciculus, or bundle of neurons that connect both Broca’s and Wernicke’s areas within the same hemisphere. It is also linked to lesions located deep in the supramarginal gyrus of the parietal lobe. Speech is usually fluent but with frequent paraphasias noted. Overall, the patient’s comprehension is considered good, though verbal imitation is quite poor. Conduction aphasia is similar to Wernicke’s aphasia with one main exception: conduction aphasics have relatively good auditory comprehension. Global aphasia Considered a nonfluent type of language disorder, global aphasia is marked by severe deficits in both comprehension and production of language. The brain damage is usually severe, with lesions in the frontal, temporal, and parietal lobes, and with damage extending to subcortical regions of the brain as well. Both Broca’s and Wernicke’s areas of the brain may be involved. Such patients often require assistance to speak, in the form of augmentative communication devices.

Types of dysarthria Spastic dysarthria This type of dysarthria is associated with a bilateral lesion of the upper motor neuron and characterized by imprecise articulation, a monotone pitch, and mono-loudness, as well as poor prosody or rhythm of speech.

COMMUNICATION DISORDERS

Flaccid dysarthria Associated with disorders of the lower motor neuron, this type of dysarthria is marked by mild to moderate hypernasality paired with nasal emissions, secondary to impaired velopharyngeal function. Ataxic dysarthria This dysarthria is associated with damage to the cerebellar system. The speech errors that result relate essentially to timing, syllabic stress, and articulatory proficiency. Hyperkinetic dysarthria Because of damage done to the extrapyramidal system and basal ganglia, such patients may exhibit involuntary movements due to abnormal muscle tone, ranging from hypertonic to hypotonic. Hyperkinetic dysarthria is marked by disorders of loudness, rate, and inappropriate interruptions of phonation or voicing. Examples of patients who exhibit too much tone accounting for their hyperkinetic dysarthria include persons with chorea or Tourette syndrome. Patients with too little tone may have athetosis or dystonia. Hypokinetic dysarthria This type of dysarthria is also associated with disorders of the extrapyramidal system and is characterized by monotone pitch or loudness, reduced stress, and imprecise consonant articulation. Any brief description of motor speech disorders would be incomplete without mention of apraxia (from the Latin for “lack of motion”). Apraxia involves the disruption of voluntary or purposeful programming of muscular movements while involuntary movements remain intact (Nicolosi et al., 1996). This motor speech disorder differs from the condition of dysarthria in that it results from faulty motor planning at the level of the cortex. Dysarthria, by contrast, results from poor motor execution at the level of the speech musculature itself for breathing, phonating, resonating, or articulating.

Conclusion The importance of conducting a timely, proper diagnosis of the communicative abilities of an individual following brain damage cannot be minimized. Once it is known what residual speech–language skills are preserved, an appropriate means of restoring communication skills to a more functional level can be conducted. A speech–language pathologist, as part of the rehabilitative multidisciplinary team, must be contacted immediately so the work of recovery can commence.

Further reading Brookshire R (1992). An Introduction to Neurogenic Communication Disorders, 4th ed. St. Louis, MO: Mosby Year Book. Nicolosi L, Harryman E, Kresheck J (1996). Terminology of Communication Disorders, 4th ed. Baltimore, MD: Williams & Wilkins. Roseberry-McKibbin C. Hegde M (2006). An Advanced Review of Speech–Language Pathology, 2nd ed. Austin, TX: Pro-Ed Publisher.

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Neuropsychological assessment and treatment Introduction Psychological factors are particularly relevant in rehabilitation, as they can impede a patient’s acceptance of goals, their progress toward those goals, and, ultimately, their outcome. In addition, brain injury and stroke give rise to cognitive, behavioral, and emotional sequelae that can have a profound effect on the patient’s rehabilitation and functioning. These are also arguably the most distressing symptoms for the family, the most difficult to treat, and the least understood in the rehabilitation setting. Psychologists, and neuropsychologists in particular, are therefore an essential part of the rehabilitation team. They can help the patient (as well as the patient’s family) understand their condition, manage emotions, and cope with stressors and pain. They also inform the team and contribute to goal setting and discharge planning. Neuropsychologists have specialized training in brain–behavior relationships, and can perform cognitive evaluations in addition to treatment.

Emotional and behavioral problems Patients in a rehabilitation setting can exhibit emotional and behavioral difficulties as reactions to the injury or operation that brought them to rehabilitation in the first place and/or as a result of the experience of hospitalization, including loss of independence, separation from loved ones, and frustration over wanting to go home. Patients often have many practical concerns and anxieties about their functioning, such as who is paying the bills while they’re hospitalized, when they can return to work, and whether they will need continued help at home. Pain, which is common in this population, can induce or exacerbate emotional symptoms. In addition, patients with brain injury must cope with cognitive and physical limitations and the very real possibility that their lives will not to return to the way they were. Emotional and behavioral sequelae can also be the direct result of underlying neurological impairment. For example, patients with left frontal strokes or those localized to subcortical areas of the brain can experience an “organic depression.” Alternatively, damage to frontal areas may also result in behavioral disturbances such as disinhibition, impulsivity, abulia (lack of initiation), and emotional lability. Some common emotional problems include the following: • Depression, often with feelings of sadness, hopelessness, worthlessness, irritability, and disturbed sleep, appetite, and activity • Anxiety, including obsessive thinking, fears, and worry; low selfconfidence • Post traumatic stress disorder (PTSD), with hypervigilance and reliving of the trauma • Adjustment disorder • Denial (to be differentiated from organic unawareness of deficit, or anosognosia, which may result from right hemisphere dysfunction)

NEUROPSYCHOLOGICAL ASSESSMENT AND TREATMENT

A psychologist or psychiatrist, preferably one familiar with emotional and behavioral manifestations following brain injury, should evaluate the patient to determine the correct diagnosis. Management and treatment may include psychotherapeutics, medication, and/or environmental modification. Mood disorders are often overdiagnosed in the brain-injured population, as physical symptoms thought to be from depression may be secondary to the brain injury itself.

The neuropsychological evaluation A neuropsychological evaluation is a comprehensive assessment of cognitive, behavioral, and emotional and personality functions. This involves a clinical interview, behavioral observations, and a wide variety of standardized tests (primarily paper–pencil tests), most of which are done sitting at a table or at bedside in a hospital. Evaluations can vary from less than 1 hour to 6–8 hours of face-to-face contact, depending on the information sought (and the patient’s stamina). Neuropsychological evaluations are tailored to the individual patient and frequently done as an outpatient (after acute hospitalization). An estimate of the patient’s premorbid functioning is part of the evaluation. A neuropsychological evaluation can help with diagnosis, guidance of treatment, tracking of treatment progress, establishment of a baseline (as in prior to brain surgery), and assessment of psychological factors impacting rehabilitation. It can also be used for disability, return to work or school, driving, or legal purposes.

Specifics of a neuropsychological evaluation An evaluation can assess orientation, awareness, attention, memory and learning, language, perceptual and visuospatial functions, planning, problem solving, multitasking, intelligence, academic skills, and motor skills. Some of the tests measure consistency of effort or attempts to deceive (malingering). Among the more commonly used tests are the Mini Mental Status Examination, Minnesota Multiphasic Personality Inventory (MMPI), Wechsler Adult Intelligence Scale, and many others. The battery of tests chosen should be individualized. Other commonly used tests are listed in Table 17.1, including tests for the evaluation of memory, attention, and executive functioning, as well as mood and personality. The evaluation of language difficulties is covered in Communication disorders (p. 396).This list is by no means exhaustive (see Lezak et al., 2004; Strauss et al., 2006).

Special assessment considerations Commonly, questions arise as to whether and when a patient may return to work or to driving. As these are extremely complex tasks, requiring numerous cognitive skills, the assessment of readiness for these functions requires evaluation of various cognitive areas underlying these abilities. Predictors of driving ability include evaluation of vision, hearing, reaction time, processing speed, attention, concentration, visuospatial skills, judgment, ability to multitask, memory, and motor control. A road test or driver training is frequently necessary. Similar assessments need to be made for return to work (which should be job specific).

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Table 17.1 Examples of neuropsychological tests by domain Cognitive domain

Examples of neuropsychological tests

Intelligence

Wechsler Adult Intelligence Scale (WAIS)

Attention

Trail Making Test A Visual Cancellation Tests Continuous Performance Test Paced Auditory Serial Addition Test

Mood

Beck Depression Inventory Beck Anxiety Inventory

Executive functioning

Trail Making Test B Category Test Wisconsin Card Sort Test Delis–Kaplan Executive Function System Clock Drawing

Learning and memory

Wechsler Memory Scale (WMS) California Verbal Learning Test Rey Osterrieth Complex Figure

Personality

Minnesota Multiphasic Personality Inventory (MMPI)

Studies have shown that the best time to attempt return to work following a brain injury is 6–18 months post-injury. Returning to work too quickly can result in failure, which may inhibit further attempts. Ideally, if the patient can return to their previous employer with ongoing supervision and support, outcomes appear better. In sum, no one test or test battery can accurately predict how a person who has sustained a brain injury will drive or function in everyday settings or vocational settings. Predictions are made on the basis of multiple tests that closely match the skill subsets required to perform the task(s). The closer that testing can simulate the demands required, the more accurate the predictions will be.

Interventions and treatment Psychotherapy In an acute setting, psychotherapy is likely to be of short duration, supportive in nature, and more problem-focused in orientation. Cognitivebehavioral techniques appear to be efficacious. Psychotherapy with brain-injured patients may also involve a degree of awareness orientation, with a careful and titrated explanation of their injury and resultant deficits. Support groups, family therapy, stress management, and relaxation skills all may play a role in treating brain-injured patients.

NEUROPSYCHOLOGICAL ASSESSMENT AND TREATMENT

Cognitive remediation Treatment of cognitive and behavioral sequelae of brain injury is known as cognitive remediation. Cognitive remediation achieves functional change by reinforcing, strengthening, or restoring previously learned patterns of behavior and establishing new patterns of cognitive activity or compensatory mechanisms for impaired neurological systems. When performed by neuropsychologists, this is based on theories of cognitive psychology, learning, and neuropsychology and is approached systematically to provide an empirical measure of change. With regard to compensation, a neuropsychologist should be able to make suggestions for structuring the environment and the patient’s support system to compensate for the brain injury. External prostheses (i.e., planners, calendars, recording devices, timers, pagers, etc.) and internal cueing strategies (i.e., developing mnemonics or an internal checklist) are also taught and their use is reinforced. Education plays a large part in cognitive remediation. Patients often benefit from being told their diagnosis, resultant disabilities, and prognosis. Some elementary review of the parts of the brain and where theirs has been affected can go a long way toward relieving uncertainty and anxiety, and reassuring patients that they are not “going crazy.” Patients with poor awareness can also benefit from a consistent review of their areas of strengths and weaknesses, as well as orientation training (date, time, names, etc.). Cognitive remediation can occur individually and/ or in group settings.

Conclusions Psychological factors are critically important in rehabilitation, yet can be overlooked. These may include mood changes such as depression or anxiety, behavioral dysfunction such as agitation, poor initiation, or wandering, and/or cognitive deficits (i.e., in memory, language, attention, or executive functioning), particularly in brain-injured or stroke patients. The neuropsychologist thus plays a critical role as part of the multidisciplinary rehabilitation team. Neuropsychologists are directly involved in assessment and treatment of psychological and cognitive disorders and assist in determination of rehabilitation goals, education of patients and staff, and discharge planning.

Further reading Folstein MF, Folstein SE, McHugh PR (1975). “Mini Mental State”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 12:189–198. Langer KG, Laatsch L, Lewis L (eds.). (1999). Psychotherapeutic Interventions for Adults With Brain Injury or Stroke: A Clinician’s Treatment Resource. Madison, CT: Psychosocial Press. Lezak MD, Howieson DB, Loring DW. (2004). Neuropsychological Assessment. New York: Oxford University Press. Strauss E, Sherman EMS, Spreen O (2006). A Compendium of Neuropsychological Tests: Administration, Norms, and Commentary. New York: Oxford University Press. Tyerman A, King NS (eds.). (2008). Psychological Approaches to Rehabilitation after Traumatic Brain Injury. Malden, MA: Blackwell Publishing.

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Osteopathic manipulation Osteopathic manipulation is an interventional approach to the treatment of patients in health and disease that is practiced primarily by osteopathic physicians (D.O.s). Although all D.O.s learn osteopathic manipulative treatment (OMT) as part of their medical school training, many do not use it in their respective specialties. Osteopathic physicians are gravitating toward the specialty of physical medicine and rehabilitation in increasing numbers. This relationship is probably due in no small part to the extensive education that D.O.s receive in their predoctoral education of neuromusculoskeletal medicine. Those who specialize in OMT may take additional residency or fellowship training in neuromusculoskeletal medicine/osteopathic manipulative medicine and receive certification from the American Osteopathic Board for Neuromusculoskeletal Medicine (AOBNMM). All physicians, D.O. or M.D., can legally practice manipulation by virtue of their medical license. The philosophical principles of osteopathy, although clarified over the last 100 years, have remained mostly unchanged: • Structure and function are interrelated. • The person is a unit and is composed of integrated organ systems that comprise the mind, body, and spirit. • The body has an inherent ability to regulate itself, adapt to changes, compensate when regulation and adaptation are inadequate, defend itself, and repair itself when damaged. • Disease or dysfunction of the body is the interaction of the person and an activating event. • Disease occurs when the body is overwhelmed or underprepared • Rational treatment is based on these principles and the treatment decision is based on proper history, examination, experience, and knowledge. • The function of the physician is to facilitate the body’s inherent capacities and to minimize the effects of disease. Osteopathic manipulation is the physical application of forces, primarily by use of the practitioner’s hands, to the patient with the intent of improving and facilitating function. It can be used alone or in conjunction with other recognized interventions. The use of any specific technique must be guided by the physician’s palpatory and other diagnostic appreciation of the patient’s condition as well as knowledge of anatomical form and function, and must be individualized to the patient’s ability to benefit from and tolerate the treatment. When disease or injury occurs, either primarily or secondary, soft tissue alterations occur as well as decreased motion regionally or throughout the body. These are typically described as “somatic dysfunction,” which is “impaired or altered function of related components of the somatic (body framework) system: skeletal, arthrodial and myofascial structures, and their related vascular, lymphatic, and neural elements.”1 1 Glossary of Osteopathic Terminology, AOA Yearbook and Directory of Osteopathic Physicians AOA, Chicago, 2002.

OSTEOPATHIC MANIPULATION

The physician searches for several visible, palpable, and motion findings that can be summarized by the mnemonic STAR (Sensitivity to pressure or movement that should not otherwise provoke the response; Tissue texture alterations, including sudomotor, erythema, bogginess, ropiness, and temperature changes; Asymmetry of position and/or structure; and Restriction of motion). The concept of barrier must also include an understanding of the physiological, anatomical, restrictive, and pathological barriers. When somatic dysfunction exists, the motion barrier that occurs does not allow motion approximating the physiological or pathological barriers (pathological barriers can exist where there has also been a change in structure, such as hypertrophy or erosion, which occurs in such conditions as arthritis). These limitations are known as restrictive barriers. Diagnosis is not necessarily a distinctive element that occurs only prior to treatment, as the physician must monitor throughout the process and reassess following the treatment. Every modality has relative indications and contraindications that also depend on the skill and experience of the practitioner. As with any intervention, there can be side effects, such as soreness and fatigue, that are not atypical but are usually transient, well tolerated, and usually only experienced early in the process. Certain disease conditions (i.e., osteoporosis) carry firmer contraindications to some modalities but may be amenable to others. There are many types of individual techniques that fall into a four-boxed grid categorizing how barriers to motion are engaged (direct— barrier engaged; indirect—relative freedoms engaged) and whether there is participation by the patient in the process (active—the patient follows directions to move or resist forces; passive—the patient remains relaxed for part or all of the manipulative technique). ACTIVE

PASSIVE

DIRECT INDIRECT Often, the lines between one technique and another are blurred, as well as the classification of the technique, especially when an experienced practitioner is performing the treatment. However, there are many described techniques. Among the most common are the following: • Articulatory treatment system (ART): A low-velocity/moderateamplitude technique, sometimes repetitive, whereby a joint is carried through its full motion through the restrictive barrier. • Balanced ligamentous tension (BLT): Forces are guides to reduce the tension on the ligaments and related myofascial structures. • Chapman reflex: Diagnostic points in the body, similar to those used in acupuncture, are determined and treated with rhythmic pressure to affect visceral diagnoses.

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• Counterstrain (CS): A system of diagnosis and treatment that locates tender points within muscles and ligaments (strain). The patient is passively positioned to shorten the extremity or region for a period of time (90–120 seconds) to reduce the contraction and reflex activity. • Cranial treatment (CR) or cranial osteopathy: A system of diagnosis and treatment addressing the restrictions and motions of the head and related structures. • Facilitated oscillatory release technique (FOR): A technique intended to normalize neuromuscular function by applying a manual oscillatory force, combined with any other ligamentous or myofascial technique. • Facilitated positional release (FPR), a system in which the region of the body is placed into a neutral position, diminishing tissue and joint tension in all planes, and an activating force (compression or torsion) is added. • Fascial release (FR) treatment or myofascial release (MFR): A system of diagnosis and treatment that engages continual palpatory feedback to achieve release of myofascial tissues. • Functional method: An indirect treatment approach that involves applying an indirect guiding force, holding the position, or adding compression to exaggerate position and allow for spontaneous release. • High-velocity/low-amplitude technique (HVLA): A technique employing a rapid, low force of brief duration and short distance or rotation within the anatomical range of motion of a joint, and that engages the restrictive barrier in one or more planes of motion to elicit release of restriction. It is also known as thrust technique. • Inhibitory pressure technique: The application of steady pressure to soft tissues to reduce reflex activity and produce relaxation. • Ligamentous articular strain technique (LAS): A manipulative technique in which the goal of treatment is to balance the tension in opposing ligaments where there is abnormal tension present. • Lymphatic techniques and lymphatic pump: Terms used to describe the impact of intrathoracic or other bodily regional pressure changes, with the emphasis on improving lymphatic flow. • Muscle energy (ME) or muscle energy technique (MET): A system of diagnosis and treatment in which the patient actively moves the body as specifically directed against a defined resistance. • Progressive inhibition of neuromuscular structures (PINS): A system of diagnosis and treatment in which two anatomically related points are located and inhibitory pressure is exerted to the intervening series of sensitive points. • Springing technique: A low-velocity/moderate-amplitude technique whereby the restrictive barrier is engaged repeatedly to produce an increased freedom of motion. • Still technique: A specific nonrepetitive articulatory method that is indirect and then direct. • Visceral manipulation (VIS): A system of diagnosis and treatment directed to the viscera to improve physiological function. Some of the conditions for which osteopathic manipulation are used include disc herniations, spinal stenosis, cervicalgia, low back pain, headache,

OSTEOPATHIC MANIPULATION

neuropathic pain, carpal tunnel syndrome, lateral and medial epicondylitis, plantar fasciitis, adhesive capsulitis, sprains and strains, costochondritis, and temporomandibular joint dysfunction. The extent of the effectiveness may be limited by the chronicity, extent of structural and pathological deformation, comorbid conditions, and skill of the physician.

Further reading Carey TS, Motyka TM, Garrett JM, Keller RB (2003). Do osteopathic physicians differ in patient interaction from allopathic physicians? An empirically derived approach. J Am Osteopath Assoc 103:313–318. DiGiovanna EL (2001). An Encyclopedia of Osteopathy. Indianapolis: American Academy of Osteopathy. Dowling DJ (2006). The 2005 T. L. Northup Lecture: What if. The AAO Journal 16(1):11–21. Dowling DJ, Martinke DJ (2004). The philosophy of osteopathic medicine. In DiGiovanna E, Schiowitz S, Dowling DJ (eds.). An Osteopathic Approach to Diagnosis and Treatment, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, pp. 10–15. Gevitz N (1988). Other Healers: Unorthodox Medicine in America. Baltimore: Johns Hopkins University Press Gevitz N (2004). The DOs: Osteopathic Medicine in America, 2nd ed. Baltimore: Johns Hopkins University Press. Hulet GD (1922). A Text Book of the Principles of Osteopathy, 5th ed. Pasadena, CA: A.T. Still Research Institute. Hurwitz EL, Aker PD, Adams AH, Meeker WC, et al. (1996). Manipulation and mobilization of the cervical spine: a systematic review of the literature. Spine 21(15):1746–1756 Johnson SM, Bordinat D (1998). Professional identity: key to the future of the osteopathic medical profession in the United States. J Am Osteopath Assoc 98:325. Littlejohn JM (2000). The principle of osteopathy. J Am Osteopath Assoc 7(6):237–246 reprinted in J Am Osteopath Assoc 100:191–200. Peterson B (1998). A compilation of the thoughts of George W. Northrup, DO, on the philosophy of osteopathic medicine. J Am Osteopath Assoc 98:53–57. Seffinger MA, Hruby RJ (2007). Evidence-Based Manual Medicine: A Problem-Oriented Approach. Philadelphia: Saunders Elsevier. Seffinger MA, King HH, Ward RC, Jones JM, Rogers FJ, Patterson MM (2003). Osteopathic philosophy. In Ward RC (ed.). Foundations for Osteopathic Medicine, 2nd ed. Philadelphia: Lippincott, Williams & Wilkins, pp. 3–18. Still AT (1899). The Philosophy of Osteopathy. Kirksville, MO. Still AT (1902). The Philosophy and Mechanical Principles of Osteopathy. Kansas City, MO: HudsonKimberly. Still AT (1950). Autobiography of A. T. Still. In Truhlar RE. Doctor A.T. Still in the Living, Privately published by the author, Cleveland. Ward RC (ed.) (2003). Foundations for Osteopathic Medicine, 2nd ed. Philadelphia: Lippincott, Williams & Wilkins.

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Gait Normal gait cycle An assessment of normal gait is necessary to understand the differences that occur in abnormal gait.

Definitions Stride length: measured distance from heel strike of one foot to heel strike of that same foot. Step length: measured distance from heel strike of one foot to heel strike of the opposite foot (usually approximately 15–20 inches) Gait cycle: the entire sequence of movement of one leg during walking. Gait cycle is divided into two main phases: Stance phase: component of gait phase in which the foot contacts the ground (approximately 60% of the cycle time during walking). The stance phase is divided into the following: • Initial contact, when the foot contacts the ground. Eccentric contraction is noted in the gluteus maximus, gluteus medius, hamstring, quadriceps, and pretibial muscles. • Loading response, the time from foot flat to the time that the opposite foot begins the swing phase. • Mid-stance, the time from when the opposite foot begins the swing phase to the time that the tibia is vertical. • Terminal stance, the time from heel rise until the opposite foot makes contact with the ground. • Preswing, the time from when the opposite foot contacts the ground, ending with toe off. Swing phase: component of gait phase in which the foot is in the air (approximately 40% of the cycle time during walking). This is divided into the following phases: • Initial swing: the time from when the foot leaves the floor to when the foot is in alignment with the opposite foot. • Mid-swing: the time from when the foot is in alignment with the opposite foot to when the tibia is vertical. • Terminal swing: the time from when the tibia is vertical to the time the foot contacts the ground. Step: the time from an occurrence (such as heel strike) in one foot to the time of the same event in the other foot. There are two steps in each gait cycle (one for each foot). Stride: the time from initial contact of one foot to next the initial contact of that same foot. Cadence: the number of steps per minute (average in the adult is 90–120 steps per minute). Base of support: the distance between the feet during stance phase.

GAIT

Determinants of gait There are six determinants of gait, which basically work to maintain the center of gravity as the body moves in space. This provides for a smoother, more efficient gait pattern. • Pelvic rotation (about 4* in either direction) essentially lengthens the limb and therefore raises the center of gravity. • Pelvic tilt occurs in mid-stance and lowers the center of gravity. • Knee flexion: 15* of knee flexion in mid-stance lowers the center of gravity. • Foot motion: the ankle pivots on the posterior heel at initial contact, which lowers the center of gravity. • Late knee motion: 30–40* of knee flexion during the last part of the stance phase lowers the center of gravity. • Pelvic lateral displacement: positioning the feet closer together (distance less than the width of the pelvis) decreases excursion of the center of gravity.

Abnormalities of gait (see Table 17.2) Table 17.2 Some common abnormalities of gait Gait abnormality

Cause

Effect

Corrective measure

Antalgic gait

If ambulation causes pain, the gait is modified so as to reduce weight bearing on the affected side.

Gait is slow and steps are short

Use a cane in the contralateral hand.

Steppage gait

If a limb is Excessive flexion functionally of the hip and elongated (as knee may be the case with dorsiflexor weakness, gastrocsoleus spasticity, or ankle plantarflexion deformity), there is excessive flexion of the hip and knee to clear the foot.

Correct the cause of the functional limb elongation (i.e., AFO, baclofen injections, physical therapy).

Foot slap

Due to mild (strength grade 3 to 4/5) dorsiflexion weakness, the foot moves rapidly from initial contact to loading response.

Strengthening of the ankle dorsiflexors and/or an AFO (with dorsiflexion assist or plantarflexion stop)

An audible slap may be heard as the weak foot hits the floor.

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Table 17.2 (Contd.) Gait abnormality

Cause

Effect

Corrective measure

Gait changes in To improve balance the elderly and stability, the stride length is shortened and more time spent in the double support stance phase. Degenerative changes in the hips and knees lead to mild flexion of trunk.

Decreased walking speed and shorter stride length with stooped posture

An assistive device such as a walker will help the patient with stability. Trunk extension exercises should be performed to avoid stooped posture.

Trendelenburg Hip pain or weak gait hip abductors (gluteus medius and minimus) will reduce external hip movement. To maintain the center of gravity above the hip joint, the trunk will bend toward the affected side.

Lateral trunk bending toward the affected limb during stance phase (compensated Trendelenburg) or dropping of the unaffected hip during stance phase of the affected side (uncompensated Trendelenburg)

Use a cane in the contralateral hand during the stance period on the affected side.

Genu recurvatum (knee hyperextension)

Causes include quadriceps weakness, plantar flexion contracture, laxity of knee ligaments, plantar flexion spasticity, heel cord contracture, and quadriceps spasticity

Hyperextending the knee helps to prevent buckling by causing an extension moment in front of the knee. However, this can lead to pain, ligamentous laxity, and bony deformity (by stressing the capsular and ligamentous structures of the posterior aspect of the knee)

Some patients use the recurvatum to their advantage. Patients without abnormal knee external movement may not require correction. Setting an AFO in ankle dorsiflexion will help establish a flexion moment at the knee. If the problem is plantar flexion spasticity, that should be addressed. Knee braces may have to be employed.

Circumduction of the hip

Weak hip flexion causes physiological lengthening of the limb

Compensatory hip external rotation or circumduction

Use a shoe lift on the contralateral limb (to create functional lengthening).

GAIT

Further reading Braddom R (ed.). (2007). Physical Medicine and Rehabilitation, 3rd ed. Philadelphia: Saunders, Elsevier, pp. 93–110. Cuccurullo S (ed.) (2004). Physical Medicine and Rehabilitation Board Review. New York: Demos Medical Publishing, pp. 409–416. O’Young B, Young M, Stiens S (1997). PM&R Secrets. Philadelphia: Hanley & Belfus. 1997, pp. 107–111.

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Wheelchair prescriptions Goals The goals of an appropriate wheelchair prescription are as follows: 1. Maximize efficient independent mobility 2. Prevent and minimize deformity or injury and provide stable positioning 3. Maximize independent functioning 4. Project a healthy, vital, and attractive body image 5. Minimize short- and long-term equipment costs

Proper sitting position When a patient is seated in the wheelchair, the following should be noted: • Head in midline • Trunk erect • Hips flexed to 90*, knees at 90–100* • Feet in neutral position, with the spine stable and the pelvis level

Important measurements Seat width The seat width is measured across the widest point of the hips (with clothing and any braces or orthosis). Add 1 inch (1”) to this measurement for the total seat width. If the wheelchair is too narrow, transfers and access to the chair are difficult and pressure skin breakdown is more likely to develop. If the seat is too wide, truncal support is compromised, leading to scoliosis, back pain, and difficulty with wheelchair propulsion. Seat depth The seat depth is measured from the dorsal buttocks to the popliteal fossa; 2–3” is then subtracted from this measurement. If the seat depth is too shallow, ischial pressure is increased and stability of the chair decreased. If the backrest is cushioned, the thickness of the cushion must be added. Seat height The seat height is measured from the bottom of the heel to the posterior thigh. Two inches is added to compensate for leg rest clearance. Consider the cushion thickness and its relative additional height. Foam cushions compress to half their normal size. Variations on seat height measurements are needed for the foot drive, or hemiplegic, chair, which is designed with the seat closer to the floor to allow the unaffected leg to propel the chair. Backrest Seat backs vary according to the patient’s needs. The backrest should be high enough to support the patient, but not inhibit movement. If the patient has good trunk control and can propel a wheelchair, 3” is subtracted from this measurement. If the patient has poor trunk muscles but can still propel a wheelchair, 2” is subtracted from this measurement. If the patient has no upper extremity strength and poor trunk control, a full measurement is taken with the possible addition of a headrest and recliner mechanism.

WHEELCHAIR PRESCRIPTIONS

Armrests The arm height is measured from the buttocks to the bottom of the patient’s bent elbow at 90*. The measurement must be taken with the cushion; 1” is added to this measurement. Fixed armrests are lighter but not usually prescribed, secondary to interference with transfers and activities of daily living. • They do not add width to the chair. • Removable armrests are for patients who are close to being independent with transfers. • With removable armrests, seat width is increased by 2''. • With removable armrests, weight is also increased.

Recliner and tilt mechanisms Indications Patients prone to skin pressure breakdown, who cannot sit fully erect or have poor sitting balance, poor endurance, orthostasis, or respiratory needs, or who otherwise need to be able to adjust the backrest may benefit from a recliner or tilt mechanism. This type of wheelchair may have manual or power controls. These systems add weight and bulk and require a longer wheel base to maintain adequate stability when the chair is reclined. In addition, shear forces are usually increased. Types of recliners • Semi-recliner can be adjusted to 30*. The chair is 3” longer and is more difficult to propel. Shear forces are increased when reclined. • Full recliner reclines to 90* and is 6” longer than the standard chair. • There are low and “zero” shear recliners; however, no system will completely eliminate shear forces. • Power recliner • Advantages include independent pressure relief and the ability to assist in orthostatic episodes. It allows for passive range of motion (PROM) of hip and knee, makes it easier to perform catheterization, and can help mobilize secretion. • Disadvantages include increased shear forces and possibly increased spasticity. It also has a greater turning radius. • Tilt-in-space • Alternative to recliner system • Entire seat and back are tilted as a unit • Angle does not change • Advantages include decreased shear forces and it maintains seating positions during weight shift. It also has a tight turning radius. • Disadvantages are that it has no ROM benefits, makes catheterizations difficult to perform, and doesn’t have as much pressure relief as full recliners.

Wheels Standard wheels are 20–24 inches in diameter. Mag wheels are the most common wheels. They are made from plastic or metal, but were initially made from magnesium, thus their name. Mag wheels require less maintenance than spoke wheels. Spoke wheels are lighter, easier to propel, and

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have improved shock absorbance. However, they are prone to bending and loosening. Wheel axle position Posterior position • Greater rolling resistance • More energy required for propulsion • Greater turning radius • More stable chair Anterior position • Less rolling resistance • Less energy required to propel • Smaller turning radius • Less stable chair • More maneuverable

Safety equipment • A seatbelt is not only for safety but also to maintain the body in good position. • Brakes or parking locks • Grade aides assist pushing the wheelchair on inclines or hills. • Anti-tipping devices prevent the chair from falling backward or forward.

Handrims • These are attached to the driving wheels to allow propulsion and control safety without touching the tire directly, to avoid soiling the hands. • Larger-diameter handrims are easier to grasp and propel but are heavier and cause decreased distance with each stroke.

Casters • Casters allow steering of the wheelchair and are available in 8”, 5”, and 2” size. • The smaller and narrower the caster, the lighter and more maneuverable the chair. • Smaller casters allow a shorter turning radius but perform poorly on outdoor surfaces and on carpets, causing the chair to wobble on uneven surfaces.

Front rigging • This term is used to describe the footrest and leg rest collectively. • Disadvantages are aggravation of hip deformities, pressure lesions on the lateral aspects of the leg, and interference with side transfers if the legs are jammed in one place. • Footrests are usually adjustable and should have 2” of clearance from the floor. • Elevating leg rests help with decreasing dependent edema and come with a calf support for the lower leg.

WHEELCHAIR PRESCRIPTIONS

• Elevating leg rests are essential for patients with a below-knee amputation and for patients with knee extension contractures or other joint abnormalities.

Camber • Camber is the wheel angle against the vertical axis (the further the bottom of the wheel is moved outward, the greater the camber and stability). • Camber makes the wheelchair easier to propel (especially at higher speeds), increases stability, and tightens the turning radius. • It is useful in sport chairs. • The disadvantages are increased overall width of the chair, increased tire wear, and lower seat height, which may increase wear and tear of the shoulder joint.

Manual vs. power chairs Manual wheelchairs are lighter, easier to transport, require less maintenance, and encourage exercise. Power chairs can be used for patients with limited strength, coordination, or ability. These chairs are heavier, require more maintenance, and are usually more expensive.

Conclusion Any prescription for a wheelchair has to take into consideration the patient’s physical status, medical status, environment, and goals for mobility. The best approach is a team approach, consisting of the physician, therapist, wheelchair vendor, and, most importantly, the patient.

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Assistive devices General description Assistive devices are used during ambulation to reduce weight bearing on a lower extremity or to provide greater stability for patients with weakness or balance deficits. They enhance the patient’s ability to ambulate safely and independently by increasing the base of support, thereby improving balance. They also decrease the demand on the lower extremities, which may help alleviate pain during ambulation or compensate for lower extremity weakness. There are several factors to take into account when determining which assistive device is appropriate for the patient. These include weight-bearing status, pain, strength, balance, confidence level of the patient, and home situation.

Walkers A walker is the most stable ambulatory device. It consists of a metal or aluminum frame that provides four points of contact with the ground, thus giving a wide and stable base of support. Walkers are indicated for patients with restricted weight bearing, those having weakness in one or both lower extremities, or patients with balance and coordination deficits who are unsafe walking with crutches or a cane. Walkers come in different sizes and types and are relatively easy to use. Before using any type of walker, it is imperative that it be properly fitted to the patient’s height and weight. The top of walker should reach the height of the greater trochanter when the patient is standing upright, and there should be approximately 30* of elbow flexion. Walkers also come in narrow and wide widths, for varying size and weight of patients. A standard walker is stable and often the first choice when beginning gait training after an injury. The patient must be able to pick up the walker and place it forward to ambulate, which can be a disadvantage for elderly or severely deconditioned patients. They are very difficult to manage with stairs. Standard walkers also promote a step-to-gait pattern, which is a disadvantage when teaching a patient to increase weight shift toward the affected extremity. A rolling walker has front wheels that eliminate the need to pick up the walker and place it forward. This is a good choice for elderly patients who need the stability of a walker but do not have the upper body strength or balance and coordination required to lift a standard walker. A rolling walker also allows the patient to ambulate with equal step lengths and a continuous gait pattern. A disadvantage is that it can’t be used on carpets. A platform can be added to any walker for patients who are unable to weight bear through the wrist or hand due to weight-bearing restrictions, pain, or significant weakness. The forearm is strapped to a platform attached to the side of the walker, allowing weight bearing through the elbow rather than the wrist and hand. Reverse walkers are a type of walker generally used by the pediatric population. The child pulls the walker from behind them while they walk. Reverse walkers help to provide a wide base of support while promoting a more upright posture.

ASSISTIVE DEVICES

Crutches Axillary crutches are indicated for patients with weight-bearing restrictions. However, they are less stable than a walker and require more upper extremity strength, coordination, and balance. Axillary crutches are typically used by younger, more agile patients and are ideal for use on stairs. The top of the axillary pads should be two finger widths below the axilla and the crutch tips should be 6" anterior and 6" lateral to the body. Loftstrand crutches consist of a cuff that fits just below the elbow, a handgrip, and a metal shaft with one rubber tip touching the ground. They are lightweight but less restrictive and therefore not appropriate for patients with poor trunk stability.

Canes Canes are used for balance and stability, but do not offer bilateral support and thus cannot be used for patients with weight-bearing restrictions. Canes can be used when the patient requires additional support for balance or if the patient is able to fully weight bear but has difficulty due to apprehension, pain, or weakness in the lower extremity. For proper fit, the top of the cane handle should be at wrist level when the patient is standing upright with the arm relaxed at their side. The cane is held in the arm opposite the involved lower extremity. During ambulation, the cane is moved forward simultaneously with the affected lower extremity, which helps to promote a normal reciprocal gait pattern and arm swing. There are several types of canes. A straight cane has one point touching the ground and is the least supportive of the ambulatory devices. Straight canes are primarily for patients with minor balance or coordination deficits, or patients who lack the confidence to ambulate without a device for long distances. Straight canes can be helpful in decreasing the weight on an arthritic joint (most commonly a hip or knee). When a person ambulates with a straight cane, the weight that is transmitted through the arm decreases the weight passed through the knee or hip. Use of a straight cane can dramatically reduce hip pain. Assume the right hip is osteoarthritic. When the left leg is in the air (swing phase), the weight passing through the right hip is actually far greater than the actual body weight. Gravity would cause the unsupported left pelvis to drop. In order to counteract this drop of the pelvis, the abductors of the right hip (primarily gluteus medius) must fire strongly. As the center of gravity of the body is further away from the right hip joint than the abductors are, the abductors must contract with a force much larger than the actual body weight. This means that the force on the right hip joint during stance phase is several times that of the body weight. If a cane is used in the left hand, the force of contraction of the right gluteus medius (to keep the pelvis level) is greatly reduced. Thus a straight cane in the opposite hand can mean >50% reduction in stress on the affected hip joint and lead to a dramatic decrease in pain and an increase in function. A quad cane has a square base with four points that touch the ground. The base can be narrow or wide, depending on the amount of support needed for the patient. A quad cane provides more support than a straight cane and is easy to use on stairs.

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Adaptive devices General description Occupational therapists address the functional consequences of illness or injury. To that end, they may develop a program of exercises and/or therapeutic activities designed to help the individual regain or improve lost capabilities such as muscle strength, range of motion, motor function, balance, and endurance, as well as perceptual and cognitive skills. This approach to rehabilitation is known as a restorative or remedial approach in that it focuses on the specific impairments underlying the individual’s disability.1 Another approach to rehabilitation often used by occupational therapists is known as the adaptive approach, which stresses training in specific occupations, such as basic activities of daily living (BADL), and facilitates improved function through the use of compensation.1 Compensation strategies frequently taught by occupational therapists include modifications to the environment or the method being used, obtaining specific assistance from another person, or the provision of adaptive devices.2 Adaptive devices can enable an individual to achieve independence when lost capabilities may be unlikely or slow to return. They can also enable individuals to perform specific activities with greater safety and less effort or discomfort. Many adaptive devices are commercially available; however it is sometimes necessary for a therapist to design a special device or piece of equipment. In fact, many of the devices that are commercially available today were originally conceived of and made by occupational therapists and their patients.1,3 For rehabilitation to be successful, the selection of appropriate adaptive devices must be a collaborative effort between the patient and the occupational therapist. The safe and effective use of adaptive devices often requires a significant amount of training and practice. This chapter will present some of the most frequently used adaptive devices prescribed by occupational therapists to enable individuals to compensate for lost or impaired skills. The devices presented are those most commonly used to promote independence in BADLs. However, there are also a wide variety of adaptive devices prescribed by occupational therapists to promote independence in instrumental activities of daily living (IADLs), such as cooking, laundry, money management, and computer use, as well as play and leisure activities and vocational tasks. Feeding (see Fig. 17.1) • Elongated handle utensils are used when upper extremity range of motion is limited (Fig. 17.1A). • Weighted utensils are used to promote stabilization for patients with poor coordination (Fig. 17.1B). 1 Zoltan B (2007). Vision, Perception and Cognition: A Manual for the Evaluation and Treatment of the Adult with Acquired Brain Injury, 4th ed. Thorofare, NJ: Slack. 2 Unsworth C (1999). Cognitive and Perceptual Dysfunction: A Clinical Reasoning Approach to Evaluation and Intervention. Philadelphia: F.A. Davis. 3 Pedretti LW, Zoltan B (1990). Occupational Therapy Practice Skills for Physical Dysfunction, 3rd ed. St. Louis, MO: Mosby.

ADAPTIVE DEVICES

A

B

E C

D

Figure 17.1 Feeding adaptive equipment. (A) elongated utensil; (B) weighted utensil; (C) built-up utensil; (D) universal cuff; (E) rocker knife

• Built-up handle utensils are used when grasp is limited or weak (Fig. 17.1C). • A universal cuff with utensil holder is used when grasp is not possible. The cuff fits around the hand and has a pocket for a utensil (Fig. 17.1D). • A rocker knife is used for one-handed food cutting (Fig. 17.1E). • Mobil arm supports and suspension slings are used to facilitate upper extremity function when there is proximal weakness. • Lightweight utensils are used when there is limited upper extremity strength or pain. • A plate guard is used to prevent food from being pushed off the plate for the patient eating with one hand or with poor coordination. • Non-skid mats are used to stabilize the plate on the table for the patient eating with one hand or with poor coordination. • Covered cups and glasses help prevent spillage for the patient with poor coordination. • Cups and mugs with T-shaped handles or elongated handles are for those with weak grasp. • Straws with a one-way valve are used to facilitate drinking for those with weak sipping ability. • A liquid level indicator helps facilitate pouring for those with vision impairment. It hooks onto the side of a glass or cup and emits a sound when the liquid level is approaching the rim.

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Grooming • An extended-handle comb or brush is for those with limited range of motion. • A universal cuff is used to hold a toothbrush or safety razor when grasp is not possible. • Built-up toothbrushes, safety razors, and brushes are for those with weak grasp. • An electric razor holder straps to an electric razor and has a hand cuff for those unable to grasp. • A hair dryer holder holds an electric hair dryer in place for one-handed hair styling. • Wall-mounted or table-based magnifying mirrors facilitate hair grooming and makeup application for those with impaired vision.

Bathing/tub or shower transfers • Tub or shower seats and benches facilitate bathing while seated for those with impaired balance, back or leg pain, or limited endurance (available with padding, back supports, and suction cups). • A hand-held shower hose facilitates bathing while seated. • Safety rails firmly attached to walls or the side of a tub are for those with impaired balance to ensure safety when entering or exiting the tub or shower. • A long-handled bath sponge or brush is for reaching the back or feet when range of motion, strength, or balance is limited, or when bending is painful or contraindicated (total hip precautions). • Terry cloth bath mitts are useful when grasp is not possible. • Soap on a string or mounted liquid soap pumps ensure easy availability of soap.

Toileting and toilet transfers • A dressing stick or reacher facilitates pulling up clothing when bending is difficult or contraindicated. • Grab bars and safety frame facilitate safe transfers on and off the toilet. • A raised toilet seat or 3-in-1 commode facilitates rising off of the toilet, especially when sitting on low surfaces is contraindicated (total hip precautions). • Wiping tongs hold toilet paper and extend reach when range of motion is limited or for the very obese patient. • Bidet toilet seats eliminate wiping by hand.

Dressing (see Fig. 17.2) • A reacher facilitates threading legs into pants and skirts and positioning of clothing when bending is contraindicated or difficult because of impaired balance, range of motion or strength, or pain (Fig. 17.2A). • A dressing stick (a long rod with a hook attached at the ends) is used to facilitate lower extremity dressing when bending is contraindicated or difficult because of impaired balance, range of motion, strength, or endurance, or pain. It also helps for reaching hangers in the closet (Fig. 17.2B).

ADAPTIVE DEVICES

• A sock aide facilitates donning of socks when bending is contraindicated or difficult because of impaired balance, range of motion, strength, or endurance, or pain (Fig. 17.2D). • Long-handled shoe horns and elastic shoe laces enable putting on and fastening shoes when bending is contraindicated or difficult with impaired balance, range of motion, strength, or endurance, or pain (Fig. 17.2C). • Button hooks and zipper pulls are for patients with impaired coordination or prehension (Fig. 17.2E, F). • Velcro clothing fasteners (shoes, pants, shirts, bras) can replace regular fasteners, for those with impaired coordination or prehension.

A

B

C E F D

Figure 17.2 Dressing adaptive equipment. (A) Reacher; (B) dressing stick; (C) long shoe horn; (D) sock aide; (E) button hook; (F) zipper pull.

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CHAPTER 17

Rehabilitation issues

Resources for the physiatrist There are a multitude of resources available to professionals in the field of PM&R. Below is a list of some of the resources that may be of interest to physiatrists. Many of the organizations below have extensive Web sites with links to practice resources, CME, and educational opportunities and podcasts.

Books Physical Medicine and Rehabilitation: Principles and Practice (2 volume set) by Joel A. DeLisa, Bruce M. Gans, Nicolas E. Walsh, and William L. Bockenek (hardcover, Sep 1, 2004). Physical Medicine and Rehabilitation by Randall L. Braddom (hardcover, Aug 31, 2006). Essentials of Physical Medicine and Rehabilitation by Walter R. Frontera, Julie K. Silver, and Thomas D. Rizzo (hardcover, May 13, 2008). Electrodiagnostic Medicine by Daniel Dumitru, Anthony A. Amato, and Machiel Zwarts (hardcover, Sep 4, 2001). Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice by Jun Kimura (hardcover, Feb 15, 2001). Easy EMG by Lyn Weiss, Julie Silver, and Jay Weiss (Paperback, April 20, 2004). Easy Injections by Weiss, Silver, Lennard and Weiss (2007) Philadelphia: Butterworth-Heinemann/ Elsevier. Pediatric Rehabilitation (Rehabilitation Medicine Library) by Gabriella E. Molnar (hardcover, Feb 1992). Physical Medicine & Rehabilitation Secrets by Bryan J. O’Young, Mark A. Young, and Steven A. Stiens (paperback, Sep 21, 2007). Essentials of Musculoskeletal Care (3rd edition) by Walter Greene and Letha Yurko Griffin (hardcover, Sep 2005). Physical Examination of the Spine and Extremities by Stanley Hoppenfeld, Richard Hutton, and Hugh Thomas (hardcover, Jun 5, 1976). Injection Techniques in Orthopaedics and Sports Medicine with CD-ROM: A Practical Manual for Doctors and Physiotherapists by Stephanie Saunders and Steve Longworth (spiral-bound, Aug 21, 2006).

Journals American Journal of Physical Medicine & Rehabilitation: www.amjphysmedrehab.com Archives of Physical Medicine & Rehabilitation: http://www.archives-pmr.org/ New England Journal of Medicine: http://www.nejm.org Physical Medicine and Rehabilitation Clinics of North America

Online Ebsco online: http://ejournals.ebsco.com/ eMedicine: http://www.emedicine.com/ Harvard Radiology database and teaching: http://eradiology.bidmc.harvard.edu/ International Spine Intervention Society: www.spinalinjection.com MD Consult: http://home.mdconsult.com/ Medscape: http://www.medscape.com/home Musculoskeletal ultrasound: http://www.med.umich.edu/rad/muscskel/mskus/index.html National Center for Biotechnology Information: http://www.ncbi.nlm.nih.gov/ National Library of Medicine: http://www.nlm.nih.gov Pain education: http://www.painedu.org/ Regional anesthesia procedure videos: http://www.anesth.uiowa.edu/rasci/movies.html Shoulder examination tests: http://www.shoulderdoc.co.uk/article.asp?article=614§ion=497 Society of Skeletal Radiology: http://www.skeletalrad.org/resources/web_resources.aspx Ultrasound Guided Regional Anesthesia Web: http://www.usgraweb.hk/

RESOURCES FOR THE PHYSIATRIST Ultrasound imaging: http://nerveatlas.ucsf.edu/index.html UpToDate online: http://uptodateonline.com/

Physical medicine and rehabilitation organizations American Academy of Physical Medicine and Rehabilitation (AAPM&R) American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) American Board of Physical Medicine and Rehabilitation (ABPMR) Foundation American Congress of Rehabilitation Medicine (ACRM) American Paraplegia Society (APS) American Spinal Injury Association (ASIA) Association of Academic Physiatrists (AAP) Foundation for Physical Medicine and Rehabilitation International Society of Physical and Rehabilitation Medicine (ISPRM)

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Index A 75% rule 8–9 abdominal leak point pressure 370 aberrant behavior and opioids 220 acetaminophen 216–17, 222 achilles tendon 51, 154 acromioclavicular joint 199 activities of daily living (ADL) 11, 74, 434 activity 13 activity limitation 12 Actonel (risedronate) 40 acute inflammatory demyelinating polyneuropathy 240–1 Adams test 44 adaptive devices 434–7 adhesive capsulitis 86–7 admission, reasons for 4 adrenocorticotropic hormone (ACTH) 168 Agency for Health care Policy Research 300 AIDS/HIV-associated conditions 406–7 alendronate (Fosamax) 40 Allen test 111 allopurinol 226, 271 alpha-agonists 372 alpha-antagonists 372 amantadine 225, 229 American Academy of Neurolgy 187 American Academy of Physical Medicine and Rehabilitation (AAPM&R) 8–9, 187 American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) 187 American college of Rheumatology 166 American Medical Association (AMA) 10–4, 166 American Osteopathic Board for Neuromusculoskeletal Medicine 420 American Rheumatism Association 260

Americans with Disabilities Act (ADA) 10–4 American Spinal Injury Association 307 amitriptyline 169, 223, 372 amplitude 186 amputation 278–80 amputees and exercise 349 amyotrophic lateral sclerosis (ALS) 236, 237, 238 analgesics 216–19, 410 acetaminophen 216–17 anti-inflammatory drugs 217–19 patient-controlled 404 preemptive 216 rotation 221 tramadol 219 anatomic loss 11 ankle 152–9 achilles tendon 51, 154 foot orthoses (AFO) 294–6 muscles involved in ankle and foot pain 153 retrocalcaneal and achilles bursitis 152–3 solid prosthesis 284 see also ankle sprains; knee ankle foot othorses ankle sprains: anterior drawer test 154 cotton test 155 external rotation stress test 156 grades 157 Kleiger’s test 155 lateral ankle sprain 157–63 medial ankle sprain 158–63 squeeze test 155 syndesmosis/anterior ankle sprain 159 talar tilt test 154 ankle sprains 154–63 ankylosing spondylitis 264–7, 255 anosognosia 416 anterior cruciate ligament injury 144–5 anterior drawer test 145, 154 anterior talofibular ligament (ATFL) 154 anti-anxiety agents 325

anticholinergics 229, 372 antidepressants 222–3, 325 see also tricyclic antidepressants antidromic impulse 187 anti-inflammatory drugs 217–19 antiseizure/antiepileptic medications 223–4, 325 antispasmodics 224, 325, 372 Anton syndrome 330 anxiety 416 aphasia 332, 413–14 Apley test 147 Arnold-Chiari 2 malformation 361 arterial disease, peripheral 58 arthritis: acute gouty 268, 270 psoriatic 254–6 septic (nongonnococcal) 270 see also osteoarthritis; rheumatoid articulatory treatment system (ART) 421 ASIA standard neurological classification 308–9 aspirin 218 assessment 5 assistive devices 432–3 asymmetry, hand 110 ataxic-hypotonic motor syndrome 355 attentional agents 325 attention 418 autonomic dysreflexia 316, 318–19 autonomic management 315 autonomic medications 316

B baclofen (Lioresal) 224, 316, 358, 376 balanced ligamentous tension (BLT) 421 base of support 424 basic activities of daily living (BADL) 434 bathing/tub or shower transfers 436

442

INDEX Becker muscular dystrophy (BMD) 250 behavioral and mechanical therapy and bladder dysfunction 371 behavioral problems 416–17 benzodiazepines 325 best gaze 331 best language 331 beta-blockers 225 bethanecol 372 bicipital tendonitis 92–3 bilateral internuclear ophthalmoplegia 231–2 biofeedback 371 bisacodyl suppository (Dulcolax) 316 bisphosphonates 226 bladder anatomy and physiology 368 bladder dysfunction 361, 368–72 clinical manifestations of urinary incontinence 369–70 complications of urinary incontinence 371–2 diagnostic tests 370–1 differential diagnosis of urinary incontinence 370 general description 368 history and physical 370 lesions: causes and effects 369 management 371 medications 372 neurogenic physiology 368 normal neurophysiology 368 bladder management 314 bladder medications 368 blue-dye procedures 392 body function 11 body structure 11 bones and immobility syndrome 398 Boston brace 302 botulinum toxin 358, 376 bounce home test 147 boutonnière deformity 258, 259–76 bowel incontinence 361 bowel management 314 bowel medications 316 bradykinesia 228 Bragard sign test 147 Brown-Sequard syndrome 23, 307 bupropion 223, 396 burns 365, 402–5

C C5-C8 nerve roots 19 cadence 424 calcaneal apophysitis 152 calcaneofibular ligament (CFL) 154 calcitonin (Miacalcin) 40, 226 calcium pyrophosphate deposition disease (pseudogout) 271–2 cancer 408–10 canes 433 capsaicin 181 capsular injuries 116–17 carbamazepine 223, 243 carbidopa 229 cardiac patients and sexuality 396 cardiac rehabilitation 348–50 cardiovascular factors and immobility syndrome 398 carisoprodol 225 carpal tunnel syndrome (CTS) 100–2, 189 catheterizations, intermittent 371 cauda equina syndrome 23, 60–1 caudal epidural nerve block 204, 205 Centers for Medicare and Medicaid Services (CMS): Final Rule 8 central cord syndrome 23, 307 central nervous system and immobility syndrome 399 central slip disruption 114 cerebellum 413 cerebral localization 412–13 cerebral palsy 354–9 classification and major causes 355 clinical manifestations 354 common medications for spasticity treatment 358 diagnostic testing 357 differential diagnosis 354 general description 354 history 354–6 management 357–9 neurosurgical interventions 359 orthopedic intervention 359 physical 356–7

spastic 356, 357 spastic hemiplegia 355, 356 spastic quadriplegia 355, 356 spastic type spastic diplegia 355, 356 special considerations 357 cervical auscultation 392 cervical epidural nerve blocks/cervical and lumbar epidural nerve blocks 202, 203, 204 cervical myofascial pain 28–9 cervical orthoses 303 cervical pain 16–17 cervical radiculopathy 18–20 cervical spondylosis 24–5 cervical sprain and strain 26–7 cervicothoracic orthosis 303 chairback brace (chairbackKnight) 301–2 Chapman reflex 421 Charleston brace 302 chest expansion 265 Childress test 147 chlorzoxazone 225 cholinergics 372 chronic obstructive pulmonary disease (COPD) 344, 345 Cialis (tadalafil) 396 clonidine 316, 358, 376 Cobb angle 42, 43, 44, 45 codeine 222 cognitive remediation 419 colchicine 226, 271 cold 212 collateral ligament injury 114, 142–3 commands 331 communication disorders 412–15 complex regional pain syndrome (CRPS) 176–8 complications 363–400 heterotopic ossification 364–6 immobility syndrome 398–400 pressure ulcers 378–80 sexuality and the disabled 396–7 spasticity 374–7 see also bladder dysfunction; swallowing disorders; venous thromboembolism

INDEX compound muscle action potential (CMAP) 186, 187 compression fractures 34–5 compression/grind test 111 compression ultrasound with venous imaging 384 COMT inhibitors 229 conduction block (neurapraxia) 186 connective tissue and immobility syndrome 399 contrast venography 384 conus medullaris syndrome 23, 60–1 Copaxone (glatiramer acetate) 232 corticosteroids 119, 225, 226, 251, 271 corticotropin-releasing hormone (CRH) 168 cortisol 168 cotton test 155 counterstrain (CS) 422 cranberry juice 316 cranial treatment (CR) 422 Crede’s maneuver 371 crutches 433 cryotherapy 212 cubital tunnel syndrome 94–5 Current Opioid Misuse Measure (COMM) 220 cyclobenzaprine 169, 225 cyclooxygenase (COX) enzymes 217,3] cyclosporine 251 Cymbalta (duloxetine) 169, 243 cystogram 370

D dantrolene 224, 358, 376 deep vein thrombosis (DVT) 316, 385–6 prophylaxis 315, 316 Dejerine-Roussy syndrome 330, 332–3 denial 416 Department of Veterans Affairs 187 depression 416 De Quervain’s tenosynovitis 106 deep vein thrombosis (DVT) 385–7 dermatomal distribution of nerve roots 18 dermatomyositis 250 desipramine 223

Detrol (telterodine) 372 dextromethorphan 225 diagnostic test results 4 diathermy 213–14 diazepam (Valium) 225, 316, 358, 376 diphyenylhydantoin 243 disability 11–12, 13–14 and cardiac rehabilitation 350 and sexuality 396–7 significant 12 true 12 Ditropan (oxybutynin) 316, 372 docusate sodium (Colace) 316 dopamine agonists 229 dorsal (posterior) cord syndrome 23 dorsal ulnar cutaneous nerve 95 dorsiflexion stop (anterior stop) 295 doxepin 223 dressing devices 436–7 drop arm maneuver 75 drop ring lock 299 Duchenne muscular dystrophy (DMD) 248–9 Dulcolax 316 duloxetine (Cymbalta) 169, 243 dynamic response (energy storing) 285 dysarthria 331, 413, 414–15

E edema 404 elbows (prostheses) 291–2 elderly, gait changes in 426 electrodiagnosis 184–90 conditions evaluated by testing 185 electromyography testing 184 inclusions in report 190 insertional activity and activity at rest 188 limitations of test 190 needle electromyography examination 187–8 nerve conduction studies 186–7 overview 184 specific disorders and their findings 189–90 why electromyography testing is performed 185

electromyography (EMG) 371 see also electrodiagnosis electrotherapy 214 El Escorial criteria 237 emobolism 328 emotional problems 416–17 empty can maneuver/ test 75, 92 enablex 372 endocrine factors and immobility syndrome 399 energy expenditure and amputation 279–80 enoxaparin (Lovenox) 316 ephedrine sulfate 316 epicondylitis 86–7 epidural nerve blocks, cervical and lumbar 202, 203, 204 erection devices 396–7 ergotamines 225 estrogen 40, 396, 372 Evista (raloxifene) 40 executive functioning 418 exercise 349–50 external rotation stress test 156 extinction/neglect 331 extrapyrimidal: athetoid/ choreoathetoid 356 extrapyrimidal motor syndrome 355 eye opening 323

F FABERs test 123 facet joint injection 206–7 facet syndrome 51 facial palsy 331 facilitated oscillatory release technique (FOR) 422 facilitated positional release (FPR) 422 facioscapulohumeral muscular dystrophy 250 fascial release (FR) 422 feeding devices 434–5 fentanyl 222 fiber-optic endoscopic evaluation of swallowing 393–4 fibromyalgia 166–70 background 166 clinical presentation 168 definition 166 diagnosis 169 differential diagnosis 169 epidemiology 168 etiology 168

443

444

INDEX laboratory analysis 169 management: 169–70 pathophysiology 166–8 tender-point sites for classification criteria 167–81 filling cystometogram (CMG) 370 filuzole 237 Finkelstein test 105, 106, 107, 111 flexible keel prosthesis 285 flexor carpi radialis (FCR) 187 Flomax (tamsulosin) 316, 372 fludrocortisone acetate (Florinef) 316 fluidotherapy 213 fluoxetine 169 foam (soft) collars 303 Food and Drug Administration (FDA) 223, 232–3, 237 foot 160–3 motion 425 prosthesis 284–5 slap 425 see also knee ankle foot orthoses Forteo (teriparatide) 40 Fosamax 40 Frenkel’s Exercises for Ataxic conditions 233 Froment’s sign test 95 frontal lobe 412 ’frozen shoulder’ see adhesive capsulitis 86–7 functional electrical stimulation (FES) 214 functional history 4 functional loss 11 functional method 422 function by level and spinal cord injury 310–3 C2-C4 (high tetraplegia) 310 C5 tetraplegia 310, 312 C6 tetraplegia 310, 312 C7 tetraplegia 310, 312 C8 tetraplegia 311, 312 high tetraplegia (above the c5 level) 312 lower lumbar paraplegia 311, 313 tetraplegia (last functioning level above T1) 32 thoracic paraplegia (T1-T12) 311, 312–13 upper lumbar paraplegia 311, 313 F waves 187

G gabapentin 181, 223, 243 gain 186 gait 424–7 Galveston Orientation and Amnesia Test (GOAT) 324 ganglion cyst 108 gastroesophageal reflux disease (GERD) 390 gastrointestinal factors and immobility syndrome 399 genitourinary system and immobility syndrome 400 genu recurvatum (knee hyperextension) 426 Gerstmann syndrome 330 GI prophylactic agents 218 Glasgow coma Scale 322–3 glatiramer acetate (Copaxone) 232 glenohumeral joint 197, 198 glycerin suppositories 316 goals 5 gout 226, 268–72 Gower sign 248 grafting 403 greater trochanteric bursa 195, 196 grooming devices 436 growth hormone, decreased 167 Guillain-Barré syndrome 240–1

H Haglund’s deformity 152 hallux rigidis 161 hallux valgus 161 hand 110–1 prostheses 289–90 handicap 12–13, 13–14 hard collars (including Philadelphia collar) 303 Hawkins-Kennedy test/ Hawkins impingement sign 78 Hawkin’s maneuver 75 headache 30–2 medications 225 head and neck 15–32 cervical myofascial pain 28–9 cervical pain 16–17 cervical radiculopathy 18–20 cervical spondylosis 24–5

cervical sprain and strain and whiplash 26–7 headache 30–2 myelopathy 22–3 heat 212–14 heterotopic ossification 319, 364–6, 405 high-velocity/low-amplitude technique (HVLA) 422 hip: circumduction 426 osteoarthritis 122–4 histamine type 2 receptor (H) blockers 18 home-based rehabilitation and stroke 341 horizontal coordinate 186 hot packs 212 H reflexes 187 human herpes virus 3 180 hydralazine 316 hydrocephalus 340, 361 hydrotherapy 213 hyperalgesia, opioidinduced 221 hypersensitivity to pain 166–8

I ibandronate 40 iliotibial band 195, 197 imipramine 223, 372 immobility syndrome 398–400 impairment 10–1, 13–14 impedance plethysmography 384 inclusion body myositis 250 increased insertional activity 188 Individuals with Disabilities Education Act (IDEA) 352 inhibitory pressure technique 422 initial contact 424 inpatient rehabilitation and stroke 340 inteferons 232 intelligence 418 interferential stimulation 214 International classification of Functioning, Disability and Health (ICF) 10–14 International classification of Impairments, Disabilities and Handicaps (ICIDH) 10–14 interventional spinal procedures 202–10

INDEX caudal epidural nerve block 204, 205 cervical and lumbar epidural nerve blocks 202, 203, 204 facet joint injection 206–7 intrathecal pumps 210 nucleoplasty 209 radiofrequency ablation (RFA) 208–9 sacroiliac joint injection 204–6 selective nerve root blocks (SNRB) 207–8 spinal cord stimulators (SCS) 209–10 vertebroplasty/ kyphoplasty 209 intracerebral hemorrhage 337–8 intrafusal muscle fibers 192 intrathecal pumps 210 intravenous (IV) feeding 394 iontophoresis 214 ischemic stroke 328–36 blood pressure management 337 commonly used testing 333 complications and red flags 334 disorders presenting similar to stroke 329 general management for acute stroke 335 history and physical 329–30 indications and contraindications for rtPA 334 location-specific lesions 332 management (treatment) 333–4 medical care 334–6 National Institutes of Health Stroke Scale 331 NINDS recommended stroke evaluation time benchmarks for potential thrombolysis candidate 335 signs and symptoms 329 special considerations 333 specific stroke syndromes 330–3 surgical care 336 transient ischemic attacks (TIA) 328–9 ischial containment socket prosthesis 285–6

J jejunostomy tubes 394 Jobe’s (empty can) maneuver 75 Joint commission on Accreditation of Healthcare Organizations 388 joint range of motion in hand 110 joint replacement 274–6, 365 joints and immobility syndrome 398 ’jumpers knee’ 140–1 juvenile rheumatoid arthritis 262–3

K Kegel exercises 371 ketamine 225 Kleiger’s test 155 Klenzak ankle joint 295 knee 128–30 ankle foot othorses (KAFO) 298–9 bursitis 136–8 flexion 425 joint 194–5 motion, late 425 osteoarthritis 132–4 prosthesis 286 kyphoplasty 35, 209

L L1 55 L2 55 L3 55 L4-5 50, 64 L4 64 L5 68 L5-S1 64 lab tests and bladder dysfunction 370 Lachman test 145 lamictal 226 lamogrigine 224 Landouzy-Dejerine 250 language problems 413 lateral collateral ligament injuries 142–3 lateral pivot shift test 145 learning and memory 418 level of consciousness 331 levodopa 229 lidocaine 181, 224 ligamentous articular strain technique (LAS) 422

limb ataxia 331 Lioresal (baclofen) 224, 316, 358, 376 loading response 424 local anesthetic 173 locked-in syndrome 330–2 Lovenox (enoxaparin) 316 low back pain 50, 51, 52, 64, 65 lower esophageal spincter (LES) dysfunction 390 lower extremity 121–63 anterior cruciate ligament injury 144–5 foot 160–3 knee bursitis 136–8 knee 128–30 knee osteoarthritis 132–4 medial and lateral collateral ligament injuries 142–3 meniscal injuries 146–8 osteoarthritis of hip 122–4 patellar and quadriceps tendonitis and Osgood Schlatter 140–1 patellofemoral pain 150–1 spasticity 374 trochanteric bursitis/ greater trochanter pain syndrome 126–7 see also ankle; lower extremity prosthetics lower extremity prosthetics 282–7 general description 282–3 history 283 management 283–4 physical 283 red flags and complications 287 special considerations 286 transfemoral prosthesis (above-knee) 285–6 transtibial (BKA) prosthesis components 284–5 lumbar epidural nerve blocks 202, 203, 204 lumbar paraplegia, lower 311, 313 lumbar radiculopathy 54–6 lumbar spinal stenosis 58–9 lumbar spondylosis 62–3 lumbar sprain and strain 50–2 lumbosacral (LS) orthoses 301–2 lymphatic techniques 422 Lyrica (pregabalin) 181, 169, 224, 243

445

446

INDEX

M McMurray test 145, 147 mallet finger 112–13 medial ankle sprain 158–63 medial collateral ligament injuries 142–3 median nerve 110–1, 101 medical conditions requiring intensive rehabilitation services 9 Medicare 8–9 medications: contributing to bone loss 37 see also procedures and medications medrol 225 memantine 225 membrane stabilizers 224 meningocele 360, 361 meniscal injuries 146–8 menisci, knee 128 metabolic equivalents (METs) 348, 349–50, 396 Metamucil (psyllium powder) 316 metatarsalgia 161 methadone 222 methocarbamol 225 methylprednisolone 252 mexiletine 224 Meyerding technique 65 Miacalcin (calcitonin) 40, 226 microwave diathermy 214 mid-stance 424 migraine, characteristics of 31 Millard-Gubler syndrome 332 Miller-Fisher syndrome (MFS) 240 milnacipran (Savella) 169 Milwaukee brace 45, 302 Mini Mental Status Examination 417 Minnesota Multiphasic Personality Inventory 417 mirtazapine 223, 396 misoprostol 218 mitoxantrone (Novantrone) 232 mobility and spina bifida 362 Modified Ashworth Scale 374–5 modified barium swallow (MBS) 393, 394 monoamine oxidase (MAO) B inhibitors 229

mood 418 Morton’s neuroma 162 motor arm/leg 331 motor nerve studies 186 motor neuron disease 189 motor response 323 motor syndrome 23 motor unit disorders 236–8 motor unit morphology and recruitment 188 multiaxis prosthesis 285 multidisciplinary rehabilitation (MDR) 324 multiple sclerosis 230–4 muscle energy (ME) or muscle energy technique (MET) 422 muscle relaxants 224–5 muscles involved in ankle and foot pain 153 muscles, knee 130 muscular dystrophies 248–50 musculoskeletal factors and immobility syndrome 399 musculoskeletal injection and aspiration 194–9 acromioclavicular joint 199 glenohumeral joint 197, 198 greater trochanteric bursa 195, 196 iliotibial band 195, 197 knee joint 194–5 pes anserine bursa 195, 196 prepatellar bursa 197, 198 subacromial space 199, 200 myelomeningocele 360, 361, 360 myelopathy 22–3, 410 myofascial pain syndrome 172–4, 192 myofascial release (MFR) 422 myopathy 189, 248–52 alcoholic 251 clinical presentation 248 congenital 249, 250 critical-illness 251 diagnostic testing 248 drug-induced/toxic 249, 251–2 endocrine 249, 251–2 general description 248 inflammatory 249, 250–1 metabolic 249, 250

muscular dystrophies and myotonic syndromes 248–50 myositis 251 myotonic syndromes 248–50

N narcotics 404 nasogastric (NG) tubes 394 natalizumab (Tysabri) 232 National Institutes of Health Stroke Scale 330, 331 National Pressure Ulcer Advisory Panel 378–9 neck see head and neck Neer impingement sign 78 Neer’s maneuver 75 nefazodone 223, 396 nerve conduction studies 186–7 nerve growth factor, increased 168 nerve roots, dermatomal distribution of 18 neurodevelopmental outcome, long-term and prematurity 353 neurogenic claudication 58 neuroleptic malignant syndrome 226 neuroleptics 226 neurological assessment of hand 110–1 neurological disorders 227–52 Guillain-Barré syndrome 240–1 motor unit disorders 236–8 multiple sclerosis 230–4 neuropathy 242–3 Parkinson’s disease 228–9 see also myopathy neuropathy 189–90, 242–3 neuropsychological assessment and treatment 416–19 neurosurgical interventions and cerebral palsy 359 NINDS recommended stroke evaluation time benchmarks for potential thrombolysis candidate 335 nitroglycerine 316 N-methyl-D-aspartic acid (NMDA) receptor antagonists 220 non-steroidal antiinflammatory drugs 226, 270

INDEX norepinephrine 372 nortriptyline 223 Novantrone (mitoxantrone) 232 nucleoplasty 209 nursing facility rehabilitation and stroke 341

O occipital lobe 412 occupational therapy and cerebral palsy 357 O’Donoghue test 147 olecranon bursitis 98 opioid therapy 181, 219–22 aberrant behavior 220 abuse 219–20 addiction 220 analgesic rotation 221 opioid-induced hyperalgesia 221 Opioid Risk Tool 220 practice guidelines 221 side effects 221–2 tolerance 220 withdrawal 220 optic neuritis 231–2 orthodromic studies 186 orthopedic intervention and cerebral palsy 359 orthotics see prosthetics and orthotics Osgood Schlatter 140–1 osteoarthritis 255, 270 hip 122–4 knee 132–4 osteopathic manipulative treatment 173, 420–3 osteoporosis 36–41 clinical manifestation 36 diagnostic testing 36–8 differential diagnosis 36 general description 36 history 36 management 38–41 medical conditions increasing fracture risk 37 medications contributing to bone loss 37 pharmacological treatment 40 physical 36 special considerations 38 therapy guidelines 39 outpatient rehabilitation and stroke 341 oxcarbazepine 224 oxybutynin (Ditropan) 316, 372

P pain: acute 216 cervical 16–17 chronic 216 hypersensitivity 166–8 see also pain pharmacology; pain syndromes painful arc maneuver 75, 78 pain pharmacology 216–26 analgesic categories 216–19 antidepressants 222–3 antiseizure/antiepileptic medications 223–4 corticosteroids 225 headache medications 225 membrane stabilizers 224 muscle relaxants 224–5 opioid therapy 219–22 preemptive analgesia 216 types of pain 216 uricosuric agents and gout 226 pain syndromes 165–81 complex regional pain syndrome (CRPS) 176–8 myofascial pain syndrome 172–4 postherpetic neuralgia 180–1 see also fibromyalgia papaverine 396 paraffin bath 212 paraneoplastic syndrome 409 parietal lobe 412 Parkinson’s disease 228–9 paroxetine 223 participation restriction 13 patellar tendonitis 140–1 patellofemoral pain 150–1 patient-controlled analgesia 404 Patrick’s test 123 pawl lock with bail release 299 Payr sign 147 pediatrics 351–62 prematurity 352–3 spina bifida 360–2 see also cerebral palsy pelvic lateral displacement 425 pelvic rotation 425 pelvic tilt 425 pelvic weights 371 percutaneous endoscopic gastrostomy (PEG) 394

peripheral nerve lesion 369 peripheral nervous system and immobility syndrome 399 personality 418 pes anserine bursa 195, 196 phalanx dislocations 114–15 Phalen test 100, 105, 111 phentolamine 396 phenytoin 223 phonophoresis 213 physiatric history and physical 4–5 physiatry 2 physical examination 4–5 physical modalities 212–14 physical therapy 173, 357 plantar fasciitis 160–3 plantar stop (posterior stop) 295 plexopathies 189 polymyositis 250 polyneuropathy 244–5 positive sharp waves (PSWs) 188 posterior tibial tendonitis 161 postherpetic neuralgia 180–1 post-traumatic amnesia 324 post-traumatic stress disorder 404, 416 post-void residual volume (PVR) 370 pramipexole 225 preemptive analgesia 216 pregabalin (Lyrica) 181, 169, 224, 243 premarin 372 prematurity 352–3 prepatellar bursa 197, 198 pressure ulcers 378–80 preswing 424 PRICE treatment 138 probenecid 226 procardia 316 procedures and medications 183–226 physical modalities 212–14 trigger point injection 192 see also electrodiagnosis; interventional spinal procedures; musculoskeletal injection and aspiration; pain pharmacology progesterone 40 progressive inhibition of neuromuscular structures (PINS) 422 prostaglandin E 396

447

448

INDEX prosthetics and orthotics 35, 277–303 amputation 278–80 ankle foot orthoses (AFO) 294–6 cerebral palsy 357–9 cervical orthoses 303 knee ankle foot othorses (KAFO) 298–9 truncal and cervical orthoses 300–3 see also lower extremity prosthetics; upper limb prosthetics proton pump inhibitors (PPIs) 218 Providence brace 302 pruritus 404 pseudoephedrine 372 pseudogout (calcium pyrophosphate deposition disease) 271–2 psoriatic arthritis 254–6 psychosocial history 4 psychotherapy 418 psyllium powder (Metamucil) 316 Public Health Service 360 pulmonary embolism 386–7 pulmonary factors and immobility syndrome 399–400 pulmonary rehabilitation 344–6

Q quadriceps tendonitis 140–1 quadrilateral socket prosthesis 285

R radial nerve 111 radial tunnel syndrome 96–7 radiculopathy 189 radiofrequency ablation (RFA) 208–9 raloxifene (Evista) 40 Ranchos Los Amigos Scale 323–4 range of motion (ROM) 118, 403, 405 ratchet lock 298–9 rehabilitation issues 401–39 adaptive devices 434–7 AIDS/HIV-associated conditions 406–7 assistive devices 432–3

burns 402–5 cancer 408–10 communication disorders 412–15 gait 424–7 neuropsychological assessment and treatment 416–19 osteopathic manipulation 420–3 resources for physiatrist 438–9 wheelchair prescriptions 428–31 remedial approach 434 renal factors and immobility syndrome 399 renal toxicity 218 rerupture 340 resources for physiatrist 438–9 responses, late 187 restorative approach 434 retrocalcaneal and achilles bursitis 152–3 rheumatoid arthritis 255, 258–60, 270 juvenile 262–3 rheumatological disorders 253–76 ankylosing spondylitis 264–7 gout 268–72 joint replacement 274–6 juvenile rheumatoid arthritis 262–3 psoriatic arthritis 254–6 rheumatoid arthritis 255, 258–60 rigidity 228 risedronate (Actonel) 40 root level and corresponding muscle groups 54 ropinirole 225 rotator cuff surgery and rehabilitation 82–4

S S1 55 sacroiliac corset/belt 302 sacroiliac joint dysfunction 51 sacroiliac joint injection 204–6 Savella (milnacipran) 169 scaphoid compression test 105 scarring prevention 404 Schober’s test 265 scoliosis 42–6

adolescent idiopathic (10 years to maturity) 45–6 braces 302 cauda equina and conus medullaris syndrome 60–1 classifications 43–70 clinical manifestations 42 Cobb angle determination 44 differential diagnosis 42 etiologies 42 general description 42 infantile idiopathic (0–3 years) 4 juvenile idiopathic (3–10 years) 44–5 lumbar radiculopathy 54–6 lumbar spinal stenosis 58–9 lumbar spondylosis 62–3 lumbar sprain and strain 50–2 spondylolisthesis 64–6 spondylolysis 68–70 thoracic radiculopathy and thoracic intervertebral disc herniations 48–9 Screening and Opioid Assessment for Patients with Pain (SOAPP) 220 selective nerve root blocks (SNRB) 207–8 selective serotonin reputake inhibitors (SSRIs) 219, 226, 223, 325 Semmes-Weinstein monofilament test 100 senna (Senokot) 316 sensory complaints by level of lumbar involvement 54 sensory factors and stroke 331 sensory nerve action potentials (SNAP) 187 sensory nerve studies 186–7 septic (non-gonococcal) arthritis 270 serotonin: decreased 166 syndrome 226 see also selective serotonin reuptake inhibitors Sever’s disease 152 sexual activity and the disabled 396–7

INDEX sexual activity and exercise 349–50 short-wave diathermy 213 shoulder: bursitis 72–3 impingement syndrome 76–81 tendonitis 74–5 sildenafil (Viagra) 396 single axis prosthesis 284 sitting position, correct 428 skin and immobility syndrome 400 skin management (decubiti prevention) 314–15 sleep agents 325 Social Security Administration (SSA) 10–4 Social Security disability insurance (SSDI) 10–4 socket prosthesis 281, 284 socks (prosthesis) 285 spasticity 374–7 management 315 medications 316 see also cerebral palsy speech problems 413 Speed’s maneuver 75 sphincter electromyography (EMG) 371 spina bifida 360–2 occulta 360, 361, 360 spinal cord injury 305–19, 364 ASIA standard neurological classification 308–9 autonomic management 315 bladder management 314 bowel management 314 clinical assessment 307 common medications and their uses 316 complications 318–19 contracture prevention 315 deep vein thrombosis (DVT) prophylaxis 315 demographics 306 diagnostic testing 307 epidemiology 306 general description 306 partial spinal cord lesions 307 skin management (decubiti prevention) 314–15 spasticity management 315 see also function by level spinal cord lesions 23, 369

spinal cord stimulators (SCS) 178, 209–10 spinal cord transection 23 spinal traction 214 spine 33–70 compression fractures 34–5 see also osteoporosis; scoliosis; spinal cord spondyloarthropathies 254, 264 spondylolisthesis 64–6 spondylolysis 68–70 spray-and-stretch technique 173 springing technique 422 squeeze test 155 stance phase 424 STAR mnemonic 421 Stener lesions 116–17 step length 424 steroids 173 Steven-Johnson syndrome 226 still technique 422 stress fractures 161 stride length 424 stroke 327–42, 365 hemorrhagic 337–9 rehabilitation 340–2 subarachnoid hemorrhage 339–40 see also ischemic stroke subacromial space 199, 200 subarachnoid hemorrhage 339–40 substance P, increased 167 sulindac 218 superior labral tears (SLAP) and rehabilitation 88–9 supinator syndrome 96–7 supplemental security income (SSI) 10–14 suprapontine lesion 369 suspension prosthesis 284, 286 swallowing disorders 388–95 assessment results 394–5 bedside evaluation 391–3 fiber-optic endoscopic evaluation 393–4 modified barium swallow (MBS) 393 normal swallowing 388–9 signs and symptoms at esophageal stage 390–1 signs and symptoms at oral stage 389

signs and symptoms at pharyngeal stage 389–90 swan-neck deformity 258, 259–76 swing phase 424 sympathectomy 178 sympathetic blockade 178 syndesmosis/anterior ankle sprain 159 systemic hypoperfusion 329 systems review 4

T T11 48 T12 48 tadalafil (Cialis) 396 talar tilt test 154 tamsulosin (Flomax) 316, 372 tarsal tunnel syndrome 161 Taylor brace (TaylorKnight) 301 team approach to rehabilitation 6 telterodine (Detrol) 372 temporal lobe 412 tendonitis 153–4 ’tennis elbow’ 86–7 teriparatide (Forteo) 40 terminal stance 424 testosterone 396 tetraplegia see function by level and spinal cord injury 310–3 therapeutic exercise and prematurity 352–3 thoracic intervertebral disc herniations 48–9 thoracic paraplegia (T1-T12) 311, 312–13 thoracic radiculopathy 48–9 thoracolumbosacral (TLS) orthoses 300–1 thrombosis 328 thumb ligament injuries 116–17 Tinel sign/test 105, 95, 100, 111 tizanidine (Zanaflex) 224, 316, 358, 376 toileting and toilet transfers 436 topiramate 224 tramadol 219, 226 transcutaneous electrical nerve stimulation (TENS) 214 transfemoral prosthesis (above-knee) 285–6

449

450

INDEX transtibial (BKA) prosthesis components 284–5 traumatic brain injury 321–6, 365 causes 322 classification based on Glasgow coma Scale 322 complications 324 definition 322 Galveston Orientation and Amnesia Test (GOAT) 324 medications 325 post-traumatic amnesia 324 principles of treatment 324 prognosis 325–6 Ranchos Los Amigos Scale 323–4 symptoms 323 trazodone 223 treatment plan 5 tremor 228 Trendelburg gait 426 tricyclic antidepressants 181, 223, 243, 325, 372 trigger finger 118–20 trigger point injection 173, 192 triptans 225 trochanteric bursitis/ greater trochanter pain syndrome 126–7 truncal and cervical orthoses 300–3 T-strap 295 two-point discrimination 100 Tysabri (natalizumab) 232

U ulnar nerve 110 ulnar neuropathy at the elbow (UNE) 94–5, 189 ulnar sensory nerve action potential 95 ultrasound 213 upper extremity 71–120 adhesive capsulitis 86–7 bicipital tendonitis 92–3 carpal tunnel syndrome (CTS) 100–2 De Quervain’s tenosynovitis 106 epicondylitis 86–7 ganglion cyst 108 hand 110–1

mallet finger 112–13 olecranon bursitis 98 phalanx dislocations 114–15 radial tunnel syndrome and supinator syndrome 96–7 rotator cuff surgery and rehabilitation 82–4 shoulder bursitis 72–3 shoulder impingement syndrome 76–81 shoulder tendonitis 74–5 spasticity 374 superior labral tears (SLAP) and rehabilitation 88–9 thumb ligament injuries 116–17 trigger finger 118–20 ulnar neuropathy at the elbow (UNE) and cubital tunnel syndrome 94–5 wrist pain 104–5 upper limb prosthetics (transradial, transhumeral) 288–92 adaptive prosthesis 289 cable-operated prosthesis 288 elbows 291–2 general description 288 hands 289–90 myoelectric 289 passive prosthesis 288 wrists 290–1 upper lumbar paraplegia 311, 313 uricosuric agents 226, 271 urinary flow rate 370 urinary incontinence see bladder dysfunction urine cystoscopy 370 urodynamic testing 370

V vacuum-assisted devices 396 vaginal lubricants 396 valgus and varus testing 144 Valium (diazepam) 225, 316, 358, 376 valproic acid 224 vardenafil (Levitra) 396 varicella-zoster (VZV) 180 vascular assessment of hand 110 vascular claudication 58 vasospasm 340

vecuronium 252 venous thromboembolism 382–7 complications of deep vein thrombosis 385–6 diagnosis 383 diagnostic tests 384–5 and immobility syndrome 400 risk factors 382–3 tests 383–5 treatment of deep vein thrombosis and pulmonary embolism 386–7 ventral cord syndrome 23 verbal response 323 vertebroplasty 35, 209 vesicare 372 Viagra (sildenafil) 396 visceral manipulation (VIS) 422 visual field 331 vitamin c 316 vitamin E 251 voiding cystometogram (CMG) 371 volar plate injury 114

W walkers 432 Wallenberg syndrome 332 Weber syndrome 330 Wechsler Adult Intelligence Scale 417, 418 wheelchair prescriptions 428–31 whiplash 26–7 William brace 302 Wilmington brace 302 World Health Organization (WHO) 10–4, 11, 12, 13, 13–14, 216 ladder of pain 217–26 wrist pain 104–5 wrist prostheses 290–1

Y Yergason’s maneuver/ test 75, 92 Yocum’s test 78

Z Zanaflex (tizanidine) 224, 316, 358, 376 zonisamide 224 zostavax 181

Glasgow coma scale (GCS)* Score

Eye opening

Motor response

Verbal response

1

None

None

None

2

To pain

Extension

Sounds

3

To speech

Abnormal flexion

Words

4

Spontaneously

Flexion

Confused speech

5

Localizes

Orientated

6

Obeys commands

* Score is sum of highest in each category. Note that the minimum GCS score is 3.

ROOTS: from C4 TRUNKS: upper

suprascapular nerve

C5 nerve to rhomboids C6

lateral pectoral nerve

nerve to subclavius middle

CORDS:

C7

lateral NERVES: axillary

lower

C8

post

musculocutaneous

T1

radial

medial medial pectoral nerve

median ulnar

medial cutaneous of arm and forearm

nerves to subscapularis and latissimus dorsi

The Brachial Plexus

long thoracic nerve (to serratus anterior)

C2 C2 C3 C4 C5

C3 C4 C5 T2 T5 T4 T5 T6 T7 T8 T9

T1 C6 C7 C8 T5 T7 T9 T1 L1 L3

T10 T11

C6 C7 C8

L5

T12 L1

S1 S2 S3 S4 S5

L2

L3

L4

S1 S2

S1 L5 L4 S1 L5 L4

Dermatomes

T2 T4 T6 T8 T10 T12 L2 L4

C6 C7

Muscles by root level C5–T1 and L2–S1 (although almost all muscles are innervated by multiple root levels, the primary roots are indicated here) Level

Muscle

Action

Nerve

C5

Biceps, brachialis

Elbow flexion

Musculocutaneous

C6

Extensor carpi radialis

Wrist extension

Radial

C7

Triceps

Elbow extension

Radial

C8

Flexor digitorum profundus

Finger flexion

Median

T1

Abductor digiti minimi

Fifth digit abduction

Ulnar

L2

Iliopsoas

Hip flexion

lLmbar plexus & femoral

L3

Quadriceps

Knee extension

Femoral

L4

Tibialis anterior

Ankle dorsiflexion

Peroneal

L5

Extensor hallucis longus

Great toe extension

Peroneal

S1

Gastrocnemius

Ankle plantarflexion

Tibial

Treatment Duration for DVT Patient factors

Duration

First episode DVT/PE with transient (reversible) risk factor* First episode of idiopathic DVT/PE DVT/PE in presence of cancer† First episode of DVT/PE with documented antiphospholipid antibodies or 2 or more thrombophilic conditions (e.g., combined factor V Leiden and prothrombin gene mutation) First episode of DVT/PE with documented deficiency of antithrombin, protein C or S, factor V Leiden, or prothrombin gene mutation, homocysteinemia, or high factor VIII levels 2 or more episodes of DVT/PE, 1 episode of life-threatening thrombosis, 1 episode of thrombosis in unusual site, other high-risk patients

3 months 6–12 months Indefinite‡ 12 months

6–12 months Indefinite

* Applies to proximal vein thrombosis and symptomatic DVT confined to calf veins. † Recommended first 3–6 months of long-term anticoagulation therapy with LMWH. ‡ Or until cancer resolves.

Medications for the treatment of spasticity Medication

Mechanism

Dosage

Indication

Baclofen

Not fully known, likely GABA agonist

Start 5 mg tid; titrate to max 20 mg qid

Spasticity due to Drowsiness, spinal etiology dizziness, N/V, CNS depression

Clonidine

Central alpha agonist

0.1–0.2 mg TTS

Spasticity due to Hypotension, spinal etiology fatigues, limb pain

Diazepam

Postsynaptic GABA facilitator

2–10 mg bid–qid

Spasticity due to Sedation, spinal etiology dizziness, ataxia, hypotension, confusion

Dantrolene

Reduces sarcoplasmic reticulum Ca release

Start 25 mg qd; titrate to max 400 mg/ day

Spasticity due to Elevated LFTs, brain etiology weakness

Tizanidine

Central alpha-2 Start 2 mg Spasticity due to Fatigue, agonist qhs; titrate to brain or spinal weakness, 4 mg tid etiology hypotension

Botulinum toxin

Blocks release Varies by of acetylcholine muscle and type used

To selectively decrease spasticity in targeted muscles

Adverse reactions

Weakness, flu-like symptoms, pain, antibodies to toxin

About the Oxford American Handbooks in Medicine The Oxford American Handbooks are flexi-covered pocket clinical books, providing practical guidance in quick reference, note form. Titles cover major medical specialties or cross-specialty topics and are aimed at students, residents, internists, family physicians, and practicing physicians within specific disciplines. Their reputation is built on including the best clinical information, complemented by hints, tips, and advice from the authors. Each one is carefully reviewed by senior subject experts, residents, and students to ensure that content reflects the reality of day-to-day medical practice.

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