Vestibular Rehabilitation

THIRD EDITION

Steven L. Wolf, PT, PhD, FAPTA, Editor-in-Chief

Vestibular Rehabilitation, 3rd Edition Susan J. Herdman, PT, PhD, FAPTA Pharmacology in Rehabilitation, 4th Edition Charles D. Ciccone, PT, PhD Modalities for Therapeutic Intervention, 4th Edition Susan L. Michlovitz, PT, PhD, CHT and Thomas P. Nolan, Jr., PT, MS, OCS Fundamentals of Musculoskeletal Imaging, 2nd Edition Lynn N. McKinnis, PT, OCS Wound Healing: Alternatives in Management, 3rd Edition Luther C. Kloth, PT, MS, CWS, FAPTA, and Joseph M. McCulloch, PT, PhD, CWS, FAPTA Evaluation and Treatment of the Shoulder: An Integration of the Guide to Physical Therapist Practice Brian J. Tovin, PT, MMSc, SCS, ATC, FAAOMPT and Bruce H. Greenfield, PT, PhD, OCS Cardiopulmonary Rehabilitation: Basic Theory and Application, 3rd Edition Frances J. Brannon, PhD, Margaret W. Foley, RN, MN, Julie Ann Starr, PT, MS, CCS, and Lauren M. Saul, MSN, CCRN

For more information on each title in the Contemporary Perspectives in Rehabilitation series, go to www.fadavis.com.

Vestibular Rehabilitation
THIRD EDITION
Susan J. Herdman, PT, PhD, FAPTA
Professor, Departments of Rehabilitation Medicine and Otolaryngology Head and Neck Surgery Director, Division of Physical Therapy Emory University Atlanta, Georgia

F. A. Davis Company 1915 Arch Street Philadelphia, PA 19103 www.fadavis.com Copyright 2007 by F. A. Davis Company Copyright 2000 and 1994 by F. A. Davis Company. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any from or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America Last digit indicates print number: 10 9 8 7 6 5 4 3 2 1 Publisher: Margaret M. Biblis Manager, Content Development: Deborah J. Thorp Developmental Editor: Jennifer A. Pine Art and Design Manager: Carolyn OBrien

As new scientific information becomes available through basic and clinical research, recommended treatments and drug threrapies undergo changes. The author and publisher have done everything possible to make this book accurate, up to date, and in accord with accepted standards at the time of publication. The author, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of the book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised always to check product information (package inserts) for changes and new information regarding dose and contraindications before administering any drug. Caution is especially urged when using new or infrequently ordered drugs. Library of Congress Cataloging-in-Publication Data Vestibular rehabilitation / [edited by] Susan J. Herdman. 3rd ed. p. ; cm. (Contemporary perspectives in rehabilitation) Includes bibliographical references and index. ISBN-13: 978-0-8036-1376-8 ISBN-10: 0-8036-1376-8 1. Vestibular apparatusDiseasesPatientsRehabilitation. I. Herdman, Susan. [DNLM: 1. Vestibular Diseasesrehabilitation. WV 255 V5836 2007] RF260.V4725 2007 617.882dc22

2007007436

Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by F. A. Davis Company for users registered with the Copyright Clearance Center (CCC) Transactional Reporting Service, provided that the fee of $.10 per copy is paid directly to CCC, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payment has been arranged. The fee code for users of the Transactional Reporting Service is: 8036-1376/07 0 + $.10

Foreword
Baseball has always been my passion. I played the sport from the time I could walk all the way through college. I always thought one could learn a lot about life from participating and from observing the game.teamwork, responsibility, strategy and so on. In that context and for reasons far transcending the purpose of this book, I adopted the Boston Red Sox as my team. Through circumstances far more surreal than circumstantial, I was interviewed by Weekend America, a National Public Radio show the day after the Red Sox miraculous comeback against the New York Yankees to win the American League title in 2004. The interview was taped on Thursday, October 21 two days before the first game of the World Series in which my team defeated the St. Louis Cardinals in four consecutive games, and aired immediately before the first game. During the interview, Bill Radke asked if the Red Sox could win the Series (a thought that any self-respecting Sox fan would never contemplate after 86 barren years filled with countless frustrations) and win or lose, if I thought the team players would all be back the following year to start their own dynasty. To the latter question I responded that I doubted the possibility since in contemporary sports the notion of team loyalties and perpetuation of excellence amongst a cohesive unit was easily supplicated by the lure of more lucrative promises from rival baseball clubs. So what does this stream of consciousness have to do with the third edition of Vestibular Rehabilitation? These thoughts about this radio interview crept into my mind as I was reviewing Susan Herdmans third edition. Here is a text already filled with contributions from clinicians and researchers acknowledged as superstars in this field. Each of these individuals is already quite busy and well in demand for other academic and intellectual opportunities. Yet rather than abandoning the team, Dr. Herdman has strengthened it further and moreover has revised the line up to field an even stronger team that will have even greater appeal to the fans. Hence at a time when star quality seeks autonomy at the sacrifice of team congruity, the exact opposite has occurred for Vestibular Rehabilitation, Third Edition. Dr. Herdman has painstakingly adhered to the principles of the Contemporary Perspectives in Rehabilitation Series by assuring that each contributor has updated references and has, when appropriate, challenged the readers critical thinking skills. The text is written for any specialist in vestibular rehabilitation or any student or clinician aspiring to become one. While already established as the gold standard for the assessment and management of patients with vestibular disorders, this third edition takes off from where the second edition has left. There are four new chapters and several others have been revamped considerably. The four new additions to this already comprehensive text include: a chapter (12) by Ronald Tusa on Migraine, Mnires Disease and Motion Sickness that represents a considerable expansion from his chapter on migraine in the second edition and distinguishes these three problem areas and their medical management; a chapter (13) by Timothy Hain and Janet Helminski on Mal de Dbarquement Disorder, a problem that has received increasing attention since the second edition of this book and now includes guidelines for treatment and indications that physical therapy may be inappropriate in the treatment of this disorder; a chapter (18) on Compensatory Strategies for the Treatment of Vestibulo-Ocular Hypofunction by Michael Schubert that offers new information on compensatory mechanisms used by patients undergoing vestibular rehabilitation; and a chapter (26) by Ronald Tusa on Non-vestibular Dizziness and Imbalance that uniquely addresses lesions not directly implicated in the central vestibular pathways, including disuse disequilibrium, spino-cerebellar ataxia, leukoaraiosis, and normal pressure hydrocephalus. In fact the last 5 chapters of the third edition are grouped to emphasize assessment and management of disorders either within or external to the central vestibular pathways or in the treatment of non-vestibular dizziness. Moreover in addition to adding several new contributors including Janet Helminski, Sharon Polensek, Michael Schubert, Greg Marchetti, and Robert Landel, many chapters have undergone substantial revision. Ronald Tusa has converted what had been one presentavii

viii

FOREWORD

tion on quantification of vestibular function tests and clinical examination into two exciting chapters presented from the physicians perspective on History and Clinical Examination (7) and Vestibular Function Tests (8). The chapter (24) by Helen Cohen on disability now approaches the concept in a diagnosis specific manner. Perhaps the most dominating impression created from this unique team is deriving a realization that contributions from vestibular neurorehabilitation therapists and specialty physicians blend almost seamlessly into a continuum of fact pointed toward a comprehensive understanding of the assessment and management of patients with vestibular disorders. In fact, one gets the

impression that the content of this book could have easily been extracted from dialogue amongst these interdisciplinary specialists at a symposium or workshop. While students new to this topic might not appreciate the value of such a constellation of knowledgeable professionals, those clinicians familiar with many of these authors and their contributions to vestibular rehabilitation will recognize that within these hard covers lie content the sum of whose parts far exceeds the whole.

Steven L. Wolf, Ph.D., PT, FAPTA, FAHA

Series Editor

Preface
The 3rd edition of Vestibular Rehabilitation! I never expected that the little black book published in 1994 would have multiple editions, much less that we would (or even could) provide a CD with the book to augment the written word with videos of patients. These videos have been chosen to provide the reader with examples of both normal and abnormal clinical tests, with visual examples of some of the exercises used in the treatment of BPPV and of vestibular hypofunction, and with examples of non-vestibular oculomotor and gait signs that should help with differential diagnosis. As I reviewed a multitude of video clips of patients we made over the past 20 years, I found that I remembered these people and their individual personalities and problems. What a wonderful experience this has been and how thankful I am for everything they taught me. If I had only one person to thank, it would be the accumulation of all these people. Once again, we have extended the material presented to include several new chapters and have augmented the material presented in all the chapters to reflect changes in our understanding of management of vestibular disorders. The new chapters include management of persons with mal de dbarquement syndrome, and persons with dizziness that is unrelated to the vestibular system such as disuse disequilibrium and central disorders. The third new chapter presents new information about the mechanisms that underlie compensation for vestibular hypofunction. In addition to these new chapters, there are a number of new topics presented within different chapters such as differential diagnosis in BPPV to identify disorders that mimic BPPV, differentiation among Mnires, migraine, and motion sensitivity, and the role of chemical labyrinthectomy in the management of episodic vertigo. Another shift you will find in the book, as well as in many clinical studies, is an increasing use of functional measures, rather than impairment measures, to assess outcome of rehabilitation. Of great value is the International Classification of Functioning, Disability and Health (ICF) scheme (World Health Organization 2001. http://www.cdc.gov.hchs/about/otheract/ic99/icfhome. htm). The ICF provides a framework for the description of health-related states and includes both positive experiences and negative consequences of disease. It consists of three domains that can be used to describe the effect of different disorders or diseases on a persons health, with a number of environmental and personal contextual factors that may affect each of those domains (Table below).

HEALTH CONDITION DISORDER OR DISEASE

Activities Versus Limitations (individual level) Participation Versus Restriction (societal level)

Normal Function and Structure Versus Impairment (body level)

Contextual Factors e.g. Environmental Factors Natural environment Support and relationships Attitude of family Attitude of society Services, systems, policies Products and technology e.g. Personal Factors Gender, age Co-morbidities Social background Education and profession Past experience Coping style
ix

PREFACE

Because it provides a more comprehensive depiction of the health of an individual, the ICF model shifts the emphasis away from impairment and disability to a more balanced perspective. Finally, we have tried, as in the other editions of Vestibular Rehabilitation, to provide you with an update on evidence that supports our practice. There is an increasing body of research that support different exercise approaches as appropriate and successful tools in the management of patients with vestibular dysfunction. The number of blinded, randomized clinical trials is growing and they provide compelling evidence that we are effectively improving outcome in these patients. Some studies offer guidance in how certain treatment can be modified to simplify treatment for the patient. Still other studies

explore the extent of recovery that can be achieved. Some studies offer insight into new methods for identifying the nature of the vestibular dysfunction such as involvement of the utricle and saccule. I expect that in the next 5 to 10 years there will be another great leap in our knowledge and we will have several additional rehabilitation approaches. Researchers are exploring the use of techniques such as virtual reality, sensory substitution devices, vestibular implants, and methods to induce hair cells regeneration. These techniques are not ready yet but the next edition of this book may be filled with wonderful new ways to help people with vestibular disorders.

Susan J. Herdman, PT, PhD, FAPTA

Editor

Contributors
Annamarie Asher, PT Clinical Education Coordinator Physical Therapy Division Physical Medicine and Rehabilitation Department University of Michigan Health System Ann Arbor, Michigan Thomas Brandt, MD, FRCP Department of Neurology Klinikum Grosshadern University of Munich Munich, Germany Richard A. Clendaniel, PT, PhD Assistant Professor Doctor of Physical Therapy Program Department of Community and Family Medicine Duke University Medical Center Durham, North Carolina Helen Cohen, EdD, OTA, FAOTA Associate Professor Department of Otorhinolaryngology Baylor College of Medicine Houston, Texas Ian S. Curthoys, PhD Professor of Vestibular Function School of Psychology University of Sydney Sydney, Australia Marianne Dieterich, MD Department of Neurology Johannes Gutenberg University of Mainz Mainz, Germany Michael Fetter, MD Department of Neurology II Klinikum Karlsbad-Langensteinbach Karlsbad, Germany Timothy C. Hain, MD Associate Professor Department of Physical Therapy and Movement Sciences Northwestern University Chicago, Illinois G. Michael Halmagyi, MD Department of Neurology Royal Prince Alfred Hospital Camperdown, Australia Janet O. Helminski, PT, PhD Associate Professor Physical Therapy Program Midwestern University Downers Grove, Illinois Fay B. Horak, PT, PhD Senior Scientist and Research Faculty Neuroscience Graduate Program R.S. Dow Neurological Sciences Institute Oregon Health and Science University Portland, Oregon Emily A. Keshner, PT, EdD Professor and Chair Department of Physical Therapy Temple University Philadelphia, Pennsylvania Robert Landel, PT, DPT, OCS Associate Professor Department of Biokinesiology and Physical Therapy University Southern California Los Angeles, California R. John Leigh, MD Professor Department of Neurology Case Western Reserve University Director Ocular Motility Laboratory Cleveland VA Medical Center Cleveland, Ohio Gregory F. Marchetti, PT, PhD Assistant Professor Department of Physical Therapy Duquesne University Pittsburgh, Pennsylvania Douglas E. Mattox, MD Professor and Chair Department of Otolaryngology-Head Neck Surgery Emory University School of Medicine Atlanta, Georgia Sharon Polensek, MD, PhD Assistant Professor Department of Neurology Emory University School of Medicine Neurologist Dizziness and Balance Center Center for Rehabilitation Medicine Atlanta, Georgia Rose Marie Rine, PT, PhD Associate Professor University of North Florida Jacksonville, Florida Michael C. Schubert, PT, PhD Assistant Professor Department of OtolaryngologyHead and Neck Surgery Johns Hopkins School of Medicine Baltimore, Maryland

xi

xii

CONTRIBUTORS

Neil T. Shepard, PhD Professor of Audiology Department of Special Education and Communications Disorders University of Nebraska Lincoln Lincoln, Nebraska Anne Shumway-Cook, PT, PhD, FAPTA Professor Division of Physical Therapy Department of Rehabilitation Medicine University of Washington Physical Therapist Seattle, Washington

Ronald J. Tusa, MD, PhD, NCS, ATC Professor Departments of Neurology and Otolaryngology Head and Neck Surgery Director Dizziness and Balance Center Center for Rehabilitation Medicine Emory University School of Medicine Atlanta, Georgia Susan L. Whitney, PT, PhD, NCS, ATC Associate Professor Departments of Physical Therapy and Otolaryngology University of Pittsburgh Pittsburgh, Pennsylvania

David S. Zee, MD Professor Department of Neurology Johns Hopkins University Baltimore, Maryland **Series Editor** Steven L. Wolf, PhD, PT, FAPTA, FAHA Professor, Medicine Professor, Rehabilitation Medicine Emory University School of Medicine Center for Rehabilitation Medicine Atlanta, Georgia

Reviewers
Cheryl D. Ford-Smith, MS, PT, NCS Assistant Professor Department of Physical Therapy Virginia Commonwealth University Richmond, Virginia James Megna, PT, NCS Coordinator Balance and Vestibular Rehabilitation Clinic Southside Hospital Bay Shore, New York Gail F. Metzger, BS, MS, OTR/L Senior Occupational Therapist & Assistant Professor Department of Occupational Therapy Alvernia College Reading, Pennsylvania Roberta A. Newton, PT, PhD Professor & Associate Director Physical Therapy Department Temple University Philadelphia, Pennsylvania

xiii

Acknowledgments
I would like to express my gratitude to the wonderful colleagues I have worked with in the clinic. Over my years as a physical therapist, they have honed my skills, challenged my assumptions, contributed to my research and made me a better clinician. So my thanks go to Ron Tusa, Courtney Hall, Lisa Gillig, Tim Hain, John Leigh, David Zee, Doug Mattox, Rick Clendaniel, and Michael Schubert. I also want to thank the authors of this edition of Vestibular Rehabilitation. They have contributed their considerable knowledge and perspectives so we can all learn how best to help the dizzy patient. As a result, many more clinicians will become familiar with the problems and management of vestibular disorders and many, many more patients will receive appropriate treatment.

xv

Contents in Brief
SECTION ONE
CHAPTER

8 Vestibular Function Tests

Ronald J. Tusa, MD, PhD

125

Fundamentals
CHAPTER

1
CHAPTER

1 Anatomy and Physiology of the Normal Vestibular System 2

Timothy C. Hain, MD Janet O. Helminski, PT, PhD

9 Otolith Function Tests

G. Michael Halmagyi, MD and Ian S. Curthoys, PhD

144

CHAPTER

2 Vestibular Adaptation
David S. Zee, MD

19

CHAPTER

10 Auditory Examination
Sharon Polensek, MD, PhD

162

CHAPTER

3 Role of the Vestibular System in Postural Control 32

Fay B. Horak, PT, PhD

SECTION THREE

Medical and Surgical 177 Management

CHAPTER

CHAPTER

4 Postural Abnormalities in Vestibular Disorders 54

Emily A. Keshner, PT, EdD

11 Pharmacological and Optical Methods of Treatment for Vestibular Disorders and Nystagmus 178
R. John Leigh, MD

CHAPTER

5 Vestibular Compensation: Clinical Changes in Vestibular Function with Time after Unilateral Vestibular Loss 76
Ian S. Curthoys, PhD and G. Michael Halmagyi, MD

CHAPTER

12 Migraine, Mnires and Motion Sensitivity 188

Ronald J. Tusa, MD, PhD

CHAPTER

CHAPTER

6 Vestibular System Disorders

Michael Fetter, MD

98

13 Therapy for Mal de Dbarquement Syndrome

Timothy C. Hain, MD Janet O. Helminski, PT, PhD

202

SECTION TWO

CHAPTER

Medical Assessment and Vestibular Function Tests

CHAPTER

14 Surgical Management of Vestibular Disorders 205

Douglas E. Mattox, MD

107
CHAPTER

7 History and Clinical Examination 108

Ronald J. Tusa, MD, PhD

15 Psychological Problems and the Dizzy Patient 214

Ronald J. Tusa, MD, PhD

xvi

CONTENTS IN BRIEF

xvii

SECTION FOUR

CHAPTER

Rehabilitation Assessment and 227 Management

CHAPTER

23 Management of the Elderly Person with Vestibular Hypofunction 376

Susan L. Whitney, PT, PhD, NCS, ATC Gregory F. Marchetti, PT, PhD

16 Physical Therapy Diagnosis for Vestibular Disorders 228

Susan J. Herdman, PT, PhD, FAPTA

CHAPTER

24 Disability in Vestibular Disorders 398

Helen S. Cohen, OTR, EdD, FAOTA

CHAPTER

17 Physical Therapy Management of Benign Positional Vertigo 233

Susan J. Herdman, PT, PhD, FAPTA Ronald J. Tusa, MD, PhD

CHAPTER

25 Assessment and Management of Disorders Affecting Central Vestibular Pathways 409

Marianne Dieterich, MD Thomas Brandt, MD, FRCP

Appendix 17A-Differential Diagnosis: Mimicking BPPV

Ronald J. Tusa, MD, PhD
CHAPTER

261
CHAPTER

18 Compensatory Strategies for Vestibulo-Ocular Hypofunction 265

Michael C. Schubert, PT, PhD

26 Non-vestibular Dizziness and Imbalance: From Disuse Disequilibrium to Central Degenerative Disorders 433
Ronald J. Tusa, MD, PhD

CHAPTER

19 Physical Therapy Assessment of Vestibular Hypofunction 272

Susan L. Whitney, PT, PhD, NCS, ATC Susan J. Herdman, PT, PhD, FAPTA

CHAPTER

27 Assessment and Management of the Patient with Traumatic Brain Injury and Vestibular Dysfunction 444
Anne Shumway-Cook, PT, PhD, FAPTA

Appendix 19A Evaluation Form 300 Appendix 19B Dizziness Handicap Inventory 307
CHAPTER

CHAPTER

20 Interventions for the Patient with Vestibular Hypofunction

Susan J. Herdman, PT, PhD, FAPTA Susan L. Whitney, PT, PhD, NCS, ATC

28 Non-vestibular Dizziness and Imbalance: Suggestions for Patients with Migraine and Mal de Dbarquement 458
Neil T. Shepard, PhD Annamarie Asher, PT

309

CHAPTER CHAPTER

21 Assessment and Interventions for the Patient with Complete Vestibular Loss 338
Susan J. Herdman, PT, PhD, FAPTA Richard A. Clendaniel, PT, PhD

29 Non-vestibular Diagnosis and Imbalance: Cervicogenic Dizziness 467

Richard A. Clendaniel, PT, PhD Robert Landel, PT, DPT, OCS

CHAPTER

22 Management of the Pediatric Patient with Vestibular Hypofunction 360

Rose Marie Rine, PT, PhD

Appendix A Questionnaire for History and Examination 485 Index

493

Contents
SECTION ONE

Fundamentals
CHAPTER

1 Anatomy and Physiology of the Normal Vestibular System 2

Timothy C. Hain, MD Janet O. Helminski, PT, PhD

Purpose of the Vestibular System 2 The Peripheral Sensory Apparatus 3 Bony Labyrinth 3 Membranous Labyrinth 3 Hair Cells 4 Vascular Supply 4 Physiology of the Periphery 5 Semicircular Canals 6 Otoliths 7 The Vestibular Nerve 7 Central Processing of Vestibular Input 8 Vestibular Nucleus 9 Vascular Supply 9 Cerebellum 10 Neural Integrator 10 Motor Output of the Vestibular System Neurons 10 Output for the Vestibulo-ocular Reflex 10 Output for the Vestibulospinal Reflex 10 Vestibular Reflexes 11 The Vestibulo-ocular Reflex 11 The Vestibulospinal Reflex 12 The Vestibulocollic Reflex 12 Cervical Reflexes 12 The Cervico-ocular Reflex 12 The Cervicospinal Reflex 12 The Cervicocollic Reflex 12 Visual Reflexes 13 Somatosensory Reflexes 13 Neurophysiology of Benign Paroxysmal Positional Vertigo 13 Higher-Level Vestibular Processing 14
xviii

Velocity Storage 14 Estimation: Going Beyond Reflexes Higher-Level Problems of the Vestibular System 16 Compensation for Overload 16 Sensor Ambiguity 16 Motion Sickness 16 Repair 17 Summary 18
CHAPTER

15

2 Vestibular Adaptation
David S. Zee, MD

19

Recalibration, Substitution, and Alternative Strategies 19 Compensation after Unilateral Labyrinthectomy 20 Bilateral Vestibular Loss 23 Experimental Results in Nonhuman Primates 23 Studies of Vestibulo-ocular Reflex Adaptation in Normal Subjects 24 Imagination and Effort of Spatial 00 Localization in Vestibular Adaptation 25 Context Specificity 26 Neurophysiologic Substrate 26 of Vestibulo-ocular Reflex Adaptation Summary 27
CHAPTER

3 Role of the Vestibular System in Postural Control 32

Fay B. Horak, PT, PhD 33

Sensing and Perceiving Position and Motion Orienting the Body to Vertical 34 Postural Alignment 34 Weighting Sensory Information 36 Controlling Center of Body Mass 40 Role in Automatic Postural Responses 41 Stabilizing the Head and Trunk 46 Summary 47

CONTENTS
CHAPTER

xix

4 Postural Abnormalities in Vestibular Disorders 54

Emily A. Keshner, PT, EdD

Examining the Vestibulospinal System 55 Advantages and Limitations of Clinical Tests Dynamic Posturography 55 Tests of Quiet Stance 58 Stabilometry 58 Tiltboards 59 Stepping Tests 59 Virtual Reality Environments 59 Postural Reactions in Peripheral Vestibular Disorders 59 Deficient Labyrinthine Inputs 60 Indicators of Vestibulospinal Deficiency 61 Indications of Vestibulospinal Distortion 63 Postural Reactions in Central Vestibular Lesions 63 Postural Dysfunction with Disorder of Other Sensory-Motor Centers 64 Mechanisms for Recovery of Postural Stability Sensory Substitution 66 Compensatory Processes 67 Summary 70
CHAPTER

55

Angular versus Linear Acceleration 92 Cerebellum 92 Neural Network Models of Vestibular Function and Compensation 92 Summary 93 Acknowledgments 93
CHAPTER

6 Vestibular System Disorders

Michael Fetter, MD

98

Benign Paroxysmal Positional Vertigo 98 Vestibular Neuritis 98 Mnires Disease and Endolymphatic Hydrops 100 Perilymphatic Fistula 102 Vestibular Paroxysmia (Disabling Positional Vertigo) 103 Bilateral Vestibular Disorders 103 Summary 104

SECTION TWO

66

Medical Assessment and Vestibular Function Tests

CHAPTER

107

7 History and Clinical Examination 108

Ronald J. Tusa, MD, PhD

5 Vestibular Compensation: Clinical Changes in Vestibular Function with Time after Unilateral Vestibular Loss 76
Ian S. Curthoys, PhD and G. Michael Halmagyi, MD

Overview 77 Causes 77 The uVD Syndrome 79 Static Symptoms 79 Dynamic Symptoms 81 Sensory Components 84 Clinical Evidence Concerning Factors Affecting the uVD Syndrome and Vestibular Compensation 84 Decompensation 87 Psychological Factors 87 Medication 88 Plasticity of the Vestibulo-Ocular Reflex 89 Rehabilitation 89 Neural Evidence Concerning Recovery after Unilateral 89 Vestibular Deafferentation

History 108 Elements that Help with the Diagnosis 108 Elements that Lead to Goals for Management, Including Physical Therapy 112 Physical Examination 113 Spontaneous Nystagmus 113 Skew Eye Deviation 116 Vestibular-Ocular Reflex 116 Maneuver-Induced Vertigo and Eye Movements 118 Visual Tracking 120 Stance and Gait 122
CHAPTER

8 Vestibular Function Tests

Ronald J. Tusa, MD, PhD

125

Tests that Specifically Assess Labyrinth or Vestibular Nerve 125 Caloric Test 125 Rotary Chair Testing 127 Quantified Dynamic Visual Acuity 131 Strengths of Test 132 Weaknesses of Test 132

xx

CONTENTS

Vestibular Evoked Myogenic Potential Test 132 Subjective Visual Vertical Test 133 Tests That Do Not Specifically Assess Labyrinth or Vestibular Nerve 134 Visual Tracking 134 Computerized Dynamic Posturography 134 Summary 142
CHAPTER

Perilymphatic Fistula 174 Other Causes of Hearing Loss Summary 175

175

SECTION THREE

Medical and Surgical 177 Management

CHAPTER

9 Otolith Function Tests

G. Michael Halmagyi, MD and Ian S. Curthoys, PhD

144

11 Pharmacological and Optical Methods of Treatment for Vestibular Disorders and Nystagmus 178
R. John Leigh, MD

Otolith Structure 144 Otolith Function 146 Primary Otolithic Afferents 146 Central Projections 146 Function of Otolithic Input 147 Subjective Visual Horizontal or Vertical Testing of Otolith Function 147 Peripheral Vestibular Lesions 147 Central Vestibular Lesions and Settings of the Subjective Visual Vertical 149 Clinical Significance 149 Vestibular Evoked Myogenic Potential Testing of Otolith Function 150 Physiological Background 150 Method 151 Clinical Applications 152 Comment 159 Summary 159 Acknowledgments 159
CHAPTER

Vertigo 178 Pathophysiology of Vertigo 178 Neuropharmacology of Vertigo and Nystagmus 180 Treatment of Vertigo 180 Oscillopsia 182 Pathogenesis 182 Treatment of Oscillopsia 183 Nystagmus and its Visual Consequences Pathogenesis 183 Treatments 183 Summary 186 Acknowledgments 186
CHAPTER

183

12 Migraine, Mnires and Motion Sensitivity 188

Ronald J. Tusa, MD, PhD

10 Auditory Examination
Sharon Polensek, MD, PhD

162

History and Physical Examination 162 Audiological Evaluation and Management 163 Evaluative Procedures 163 Audiological Management 169 Medical Testing in the Evaluation of Hearing Loss 170 Laboratory Testing 170 Radiological Imaging 170 Clinical Presentations of Auditory Impairment 170 Sudden Sensorineural Hearing Loss 170 Hearing Loss from Infectious Disease 171 Pharmacological Toxicity 171 Surgical Management of Hearing Loss 172 Cochlear Implants 172 Cerebellopontine Angle Tumors 174 Superior Semicircular Canal Dehiscence 174

Incidence of Migraine 188 Symptoms of Migraine 188 Case Example 188 Symptoms during Vestibular Migraine Aura 189 Classification and Criteria for Diagnosis 189 Migraine 189 Disorders Associated with Migraine 192 Pathophysiology of Migraine 192 Dopamine D2 Receptor 192 Calcium Channel Receptor (CACNA1A) 193 Noradrenergic System 193 Serotonin 5HT1 Receptor and the Headache Phase 193 Management 193 Treatment of Vestibular Migraine 193 Prophylactic Medical Therapy 194 Abortive Medical Therapy 196 Migraine versus Mnires Disease 197 Summary 200 Patient Information 200

CONTENTS
CHAPTER

xxi

13 Therapy for Mal de Dbarquement Syndrome

Timothy C. Hain, MD Janet O. Helminski, PT, PhD

202

Management 221 Medications 222 Summary 226

SECTION FOUR

Cause of the Syndrome: Persistent Adaptation to Swaying Environments? 202 Treatment 203 Summary 204
CHAPTER

Rehabilitation Assessment and 227 Management

CHAPTER

14 Surgical Management of Vestibular Disorders 205

Douglas E. Mattox, MD

16 Physical Therapy Diagnosis for Vestibular Disorders 228

Susan J. Herdman, PT, PhD, FAPTA

Acoustic Neuromas (Vestibular Schwannomas) 205 Surgical Approaches 206 Middle Cranial Fossa 206 Translabyrinthine Approach 206 Suboccipital Craniectomy 207 Complications 208 Stereotactic Radiosurgery 208 Mnires Disease 208 Surgical Management of Mnires Disease Chemical Labyrinthectomy 209 Post-Traumatic Vertigo 211 Benign Paroxysmal Positional Vertigo 211 Perilymphatic Fistula 211 Vascular Loops 212 Summary 213
CHAPTER

Physical Therapy Diagnosis and the International Classification of Functioning, Disability, and Health Model of Diasablement 228 History 229 Clinical Examination 229 Diagnostic Flowchart 230 Identification of Modifiers 231 Summary 232
CHAPTER

209

17 Physical Therapy Management of Benign Positional Vertigo 233

Susan J. Herdman, PT, PhD, FAPTA Ronald J. Tusa, MD, PhD

15 Psychological Problems and the Dizzy Patient 214

Ronald J. Tusa, MD, PhD

Psychological Disorders and Their Prevalence 214 Dizziness in Patients with Psychological 214 Disorders Psychological Problems in Patients with Dizziness 215 Assessment 216 Scales 216 Clinical Examination 218 Examination for Psychogenic Stance and Gait Disorders 218 Dynamic Posturography 219 Psychological Disorders 219 Anxiety 219 Mood Disorders 219 Somatoform Disorders 220 Factitious and Malingering Disorders 221

Characteristics and History 233 Mechanism 233 Semicircular Canal Involvement 234 Diagnosis 235 Dix-Hallpike Test 236 Side-Lying Test 237 Roll Test 237 Test Series 237 Treatment 238 Treatment of the Most Common Form of BPPV: Posterior Canal Canalithiasis 238 Treatment of Posterior Canal BPPV: Cupulolithiasis 245 Variations in SCC Involvement 248 Algorithm for Treatment of BPPV 251 Evidence-Based Practice 251 Quality of Available Evidence to Use Repositioning Maneuvers to Treat BPPV 251 Quality of Available Evidence to Use the Liberatory Maneuver to Treat BPPV 252 Quality of Available Evidence to Use Brandt-Daroff Habituation Exercises to Treat BPPV 253 Managing Persistent Imbalance in Patients with BPPV 254

xxii

CONTENTS

Contraindications to the Assessment and Treatment of BPPV 255 Unraveling Complicated Cases 256 Summary 259
APPENDIX

17A Differential Diagnosis: Mimicking BPPV 261

Ronald J. Tusa, MD, PhD

Central Positional Vertigo with Nystagmus 261 Episodic Signs and Symptoms (Benign) 261 Persistent Signs and Symptoms (Pathological) 261 Central Positional Nystagmus without Vertigo 261 CPN Present Only When Patient Is Supine (Benign) 261 CPN Present When Patient Is Supine and When Sitting (Pathological) 262 Peripheral Positional Vertigo with Nystagmus Other Than BPPV 262 Pressure-Induced Disorders 262 Positional Dizziness without Nystagmus 263 Orthostatic Hypotension 263 Head Extension Dizziness and Extreme Rotation Dizziness 263
CHAPTER

Cervical Range of Motion 274 Physical Deconditioning 274 Activities versus Limitation 274 Participation versus Restriction 275 Physical Therapy Evaluation 275 History 276 Clinical Examination 278 Oculomotor and Vestibulo-Ocular Testing 278 Balance Assessment 284 Gait Evaluation 289 Red Flags 293 Transition from Assessment to Treatment 294 Is There a Documented Vestibular Deficit? 294 What Type of Vestibular Problem Does this Patient Have? 294 Not All Dizzy Patients Have a Vestibular Lesion 294 Assess and Reassess 295 Quantify the Assessment 295 Determining Whether There Has Been Improvement 295 Summary 295 Acknowledgments 295
APPENDIX

19A

Evaluation Form

300

APPENDIX

18 Compensatory Strategies for Vestibulo-Ocular Hypofunction 265

Michael C. Schubert, PT, PhD

19B Dizziness Handicap Inventory 307 20 Interventions for the Patient with Vestibular Hypofunction
Susan J. Herdman, PT, PhD, FAPTA Susan L. Whitney, PT, PhD, NCS, ATC

CHAPTER

309

Normal Vestibulo-Ocular Reflex 265 Abnormal Vestibulo-Ocular Reflex 265 Compensatory Strategies 265 Saccadic Modifications 267 Cervico-Ocular Reflex 267 Effects of Prediction 268 Enhanced Smooth Pursuit 270 Summary 270
CHAPTER

19 Physical Therapy Assessment of Vestibular Hypofunction 272

Susan L. Whitney, PT, PhD, NCS, ATC Susan J. Herdman, PT, PhD, FAPTA

Normal Structure and Function versus Impairment 272 Vestibulo-Ocular Function and Dysfunction Perception of Head Movement and Position Postural Instability 274

272 274

Mechanisms of Recovery 309 Cellular Recovery 309 Reestablishment of Tonic Firing Rate 309 Recovery of the Dynamic Component 310 Vestibular Adaptation 310 Substitution 311 Habituation 312 Evidence that Exercise Facilitates Recovery 312 Goals of Treatment 313 Treatment Approaches 313 Adaptation Exercises 314 Substitution Exercises 315 Expectations for Recovery 317 Factors Affecting Outcome 317 Treatment 320 General Considerations 320 Problem-Oriented Approach 321

CONTENTS

xxiii

Problem: Visual Blurring and Dizziness When Performing Tasks that Require Visual Tracking or Gaze Stabilization 321 Problem: Exacerbation of Symptoms 323 Problem: Static and Dynamic Postural Instability 323 Problem: Progression of Balance and Gait Exercises 326 Problem: Physical Deconditioning 326 Problem: Return to Driving 327 Summary 328 Acknowledgment 329
CHAPTER

CHAPTER

23 Management of the Elderly Person with Vestibular Hypofunction 376

Susan L. Whitney, PT, PhD, NCS, ATC Gregory F. Marchetti, PT, PhD

21 Assessment and Interventions for the Patient with Complete Vestibular Loss 338

Susan J. Herdman, PT, PhD, FAPTA Richard A. Clendaniel, PT, PhD Primary Complaints 338 Balance 338 Oscillopsia 339

Sense of Disequilibrium or Dizziness 339 Physical Deconditioning 339 Assessment 339 History 339 Mechanisms of Recovery 343 Gaze Stability 343 Postural Stability 344 Compensatory Strategies 345 Evidence that Exercise Facilitates Recovery 345 Treatment 346 Progression of Exercises 346 Guidelines to Treatment and Prognosis 347 Future Directions 351 Summary 358 Acknowledgment 358
CHAPTER

Normal Changes of Aging 376 Vestibular Function 376 Visual Deficits 378 Somatosensory Changes 378 Musculoskeletal Deficits 381 Postural Hypotension 382 Cerebellar Atrophy 382 Fear of Falling 382 Attention 382 Depression 382 Risk of Falling in Older Adults with Vestibular Disorders 383 Questionnaires for Balance Assessment 383 Dizziness Assessment 387 Typical Balance Tests 390 Home Assessment 390 Duration of Treatment 390 What to Do Once the Risk Factor Has Been Identified 390 Summary 394
CHAPTER

24 Disability in Vestibular Disorders 398

Helen S. Cohen, OTR, EdD, FAOTA

22 Management of the Pediatric Patient with Vestibular Hypofunction 360

Rose Marie Rine, PT, PhD 360

Evaluating Disablement 398 Benign Paroxysmal Positional Vertigo Chronic Vestibulopathy 400 Bilateral Vestibular Impairment 400 Acoustic Neuroma 402 Mnires Disease 404 Acknowledgments 406
CHAPTER

399

Incidence of Vestibular Deficits in Children Development of Postural and Oculomotor Control as Related to Vestibular System Function 363 Evaluation of Children with Vestibular System Dysfunction 365 Treatment of Vestibular Dysfunction 370 Peripheral Disorders 370 Central Vestibular and Postural Control Deficits 370

25 Assessment and Management of Disorders Affecting Central Vestibular Pathways 409

Marianne Dieterich, MD Thomas Brandt, MD, FRCP

Clinical Classification of Central Vestibular Disorders 409 Vestibular Disorders in (Frontal) Roll Plane 410 Etiology 415 Natural Course and Management

415

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CONTENTS

Thalamic and Cortical Astasia Associated with Subjective Visual Vertical Tilts 417 Torsional Nystagmus 417 Vestibular Disorders in (Sagittal) Pitch Plane Downbeat Nystagmus 418 Upbeat Nystagmus (Upbeat Nystagmus Syndrome) 419 Summary 423 Vestibular Disorders in (Horizontal) Yaw Plane 423 Vestibular Cortex: Locations, Functions, and Disorders 424 Multimodal Sensorimotor Vestibular Cortex Function and Dysfunction 424 Spatial Hemineglect: a Cortical Vestibular Syndrome? 426 Vestibular Epilepsy 426 Paroxysmal Central Vertigo 427 Summary 428 Acknowledgment 428
CHAPTER

417

Vestibular Pathology 444 Concussion 445 Fractures 446 Central Vestibular Lesions 446 Vestibular Rehabilitation 446 Vertigo 447 Eye-Head Coordination 447 Postural Control Underlying Stability 448 Assessment 448 Impairments Limiting Postural Stability 452 Time Course for Recovery 453 Summary 456
CHAPTER

28 Non-vestibular Dizziness and Imbalance: Suggestions for Patients with Migraine and Mal de Dbarquement 458
Neil T. Shepard, PhD Annamarie Asher, PT

26 Non-vestibular Dizziness and Imbalance: From Disuse Disequilibrium to Central Degenerative Disorders 433
Ronald J. Tusa, MD, PhD

Disuse Disequilibrium and Fear of Fall 433 Description 433 Useful Outcome Tests 434 Management 434 Leukoaraiosis and Normal-Pressure Hydrocephalus 434 Description 434 Useful Outcome Scores 436 Management 436 Progressive Supranuclear Palsy, Parkinsons Disease, Large-Fiber Peripheral Neuropathy, and Spinocerebellar Ataxia 437 Description 437 Useful Outcome Scores 438 Management 438
CHAPTER

Definition of Non-vestibular Dizziness Mal de Dbarquement 459 Migraine-Associated Dizziness 460 Primary Anxiety and Panic 462 Methodological Considerations for Assessment and Treatment Development 464
CHAPTER

458

29 Non-vestibular Diagnosis and Imbalance: Cervicogenic Dizziness

Richard A. Clendaniel, PT, PhD Robert Landel, PT, DPT, OCS

467

27 Assessment and Management of the Patient with Traumatic Brain Injury and Vestibular Dysfunction 444
Anne Shumway-Cook, PT, PhD, FAPTA

Proposed Etiologies 468 Posterior Cervical Sympathetic Syndrome 468 Vertebrobasilar Insufficiency Altered Proprioceptive Signals Examination 475 Management 476 Summary 477

468 468

Appendix A Questionnaire for History and Examination 485 Index

493

CHAPTER

21
Assessment and Interventions for the Patient with Complete Vestibular Loss
Susan J. Herdman, PT, PhD, FAPTA Richard A. Clendaniel, PT, PhD

Patients with unilateral and bilateral vestibular hypofunction (BVH) typically have subjective complaints of imbalance, and they frequently complain of oscillopsia a visual blurring or jumping of the environment during head movement. These are all serious problems, resulting in decreased activity level, avoidance or modification of driving with resultant diminished independence, limited social interactions, and poor quality of life. Bilateral loss of vestibular function potentially has a more profound effect on a persons ability to participate in the normal activities of daily living than would a unilateral loss of vestibular function, and patients with bilateral vestibular loss (BVL) often restrict their activities and can become isolated. The main points this chapter addresses are as follows: 1. The assessment and physical therapy treatment appropriate for people with bilateral vestibular hypofunction (BVH) or loss (BVL). 2. The evidence that vestibular rehabilitation can improve postural stability and decrease the sense of disequilibrium in many patients, enabling them to resume a more normal life.14 3. Preliminary evidence that visual acuity during head movement also improves. 4. Expectations for the outcome of the rehabilitation process, including the observation that not all patients experience improvement.
338

5. The necessity for patients with BVH to continue with exercises or with activities that challenge balance in order to sustain their improvement. In addition, several case studies are used to illustrate different points.

Primary Complaints
Balance
Patients with BVL are primarily concerned with their balance and gait problems. During the acute stage of their disease, they may feel off balance even when lying or sitting down. More typically, however, their balance problems are obvious only when they are standing or walking. Patients in whom BVL develops after the use of an ototoxic medicationthe most common cause of BVL often do not know they have a balance problem until they get out of bed. Typically, these patients have been treated with the ototoxic medication because of a serious infection. They are often debilitated, and their balance problems are initially attributed to weakness. Even with full compensation, balance problems persist. Although the other sensory and motor systems do help compensate for the vestibular loss, these systems cannot substitute completely for the loss of vestibular function (see Chapter 20, Figs. 20.2 and 20.3). Normal postural stability while walking requires the combined use of at least two of three sensory cues: visual, vestibu-

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lar, and somatosensory. Patients who have no vestibular function, therefore, have difficulty when either visual or somatosensory cues are also significantly decreased (e.g., walking in the dark). Although balance may be poor, it is not known what the actual frequency of falling is for patients with BVL. Most patients are able to prevent falls even though they may sidestep or stagger occasionally.

Assessment
The assessment of patients with BVL is similar to that for patients with unilateral vestibular deficits; therefore, only certain aspects of the assessment are described here. Physical therapy assessment of patients with BVL must address the intensity of their subjective complaints, postural instability, and oscillopsia, overall physical condition, and their ability to perform activities of daily living (ADLs). This assessment must also identify other factors that might affect recovery, especially visual and somatosensory deficits. A summary of the assessment and the usual findings for patients with BVL is presented in Box 21-1.

Oscillopsia
Another problem for patients with BVL is the visual blurring that occurs during head movements. Initially, loss of vestibular function results in a decrement in visual acuity even when the patient is stationary, if the head is not supported.5 Even after the best compensation, patients say that objects that are far away appear to be jumping or bouncing. This visual blurring or oscillopsia increases with irregular or unpredictable head movements such as would occur while walking. As a result, patients may not be able to read street signs or identify peoples faces as they walk, or they may have difficulty seeing clearly while in a moving car. Severe oscillopsia also affects postural stability because decreased visual acuity affects the persons ability to use visual cues for stability.6

History Etiology
Bilateral loss of vestibular function can occur for several reasons (see Chapter 6). Most common is the effect of an ototoxic medication such as gentamicin. Bilateral vestibular loss was once considered to be an idiosyncratic response to gentamicin; initial studies indicated that less than 3% of people who received gentamicin have a vestibular deficit.7 Subsequent studies, however, showed that the incidence of aminoglycoside ototoxicity ranges from 9% to 15%.810 These are most likely conservative estimates based on relatively small studies (fewer than 150 participants in each study) and the fact that vestibular loss was assessed with electronystagmography. The prevalence is between 10% and 20%. In patients who have renal impairment, are older than 65 years, are taking loop diuretics, or have previous vestibular loss, it rises to 20% if they undergo renal dialysis and receive gentamicin. The significance of knowing the underlying etiology of the BVL lies in the accompanying problems that the patient may have. The patient who has a spontaneous or sequential BVL is less likely to have other health problems that will affect recovery than the patient who had a severe infection and was treated with an ototoxic medication. Furthermore, the patient who has a loss of vestibular function, with its resultant balance and visual problems, secondary to ototoxic medication may also have to deal with significant anger and depression.

Sense of Disequilibrium or Dizziness

Patients often complain of dizziness, heaviness, or a sense of being off-balance that is separate from their actual postural instability. This feeling lessens or disappears when the person is lying down or sitting with the head supported. It increases dramatically when the person is moving. This dizziness or disequilibrium may diminish as a result of compensation, but for many patients, it remains a serious and debilitating problem that can lead to decreased physical activity, social isolation, and depression.

Physical Deconditioning
Poor physical condition can be a significant problem for patients with BVL. It can be caused directly by a decreased activity level because of either the patients fear of falling or by the increased dizziness that occurs with movement. It is especially a problem for patients whose vestibular loss is secondary to ototoxic medications, who are already debilitated because of severe infection. Many patients undergoing peritoneal dialysis, for example, develop infections that are treated with gentamicin, a vestibulotoxic aminoglycoside.

Fall History
Patients with BVH are more likely to fall than normal subjects in their age range and than patients with unilateral vestibular hypofunction.11 It is imperative that infor-

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Box 21-1

TEST RESULTS IN PATIENTS WITH BILATERAL VESTIBULAR LOSS (BVL)

Subjective Complaints Disability score: Continues to be abnormal with symptoms typically interfering with both work and leisure activities. Activities of daily living (ADLs): Most people with BVL will be independent in their basic ADLs, such as dressing, bathing, getting on and off a toilet, preparing a simple meal, and light housekeeping. Bathing often is modified, however, because of the difficulty getting into and out of a bathtub and/or maintaining balance in a shower when the person closes the eyes. Balance confidence: Patient may or may not achieve a criteria improvement to an average confidence in balance 80% across activities. Oculomotor Examination Abnormal findings in room light, including poor vestibulo-ocular reflex (VOR) to slow and rapid head thrusts; visual acuity with head stationary is usually normal, but during gentle oscillation of the head, acuity could change to 20/100 or worse. With Frenzel lenses: No spontaneous, gaze-evoked, head shakinginduced, tragal pressureinduced, hyperventilation-induced, or positional nystagmus. Dynamic visual acuity, as measured with the computerized system, remains abnormal during active head movements in at least 25% of patients (see Chapter 8). Sensation Somatosensory and visual information is critical to functional recovery and must be carefully evaluated. Coordination Should be normal. Range of Motion Should be normal, but patients may voluntarily restrict head movement because it makes them less stable and also results in poor vision. Strength (Gross) Should be normal unless patient has become inactive. Postural Deviations Should be normal. Positional and Movements Testing Should not result in vertigo. Sitting Balance Patients may have difficulty maintaining their balance during weight-shifting while sitting during the acute stage but should not during the compensated stage. Static Balance Romberg test: Abnormal result during acute stage in many patients. Sharpened Romberg test: Patients with complete or severe bilateral loss will not be able to perform this with eyes closed. Single-leg stance: Difficult to perform even during compensated stage, with eyes open. Standing on rail: Usually not tested. Standing on foam surface: Difficult to perform with decreasing base of support. Should not be attempted in many patients. Force platform: During compensated stage, anterior-posterior sway should be normal or close to normal with eyes open and closed on stable surface. Balance with Altered Sensory Cues Increased sway when visual or somatosensory cues are altered; loss of balance when both visual and somatosensory cues are altered. Dynamic Balance (Self-Initiated Movements) Fukudas stepping test: Normal result with eyes open during compensated stage; patient cannot perform with eyes closed (rapid loss of balance). Functional Reach May be decreased with eyes closed. Ambulation The patients gait is usually at least slightly widebased during compensated stage. There is a tendency to use visual fixation while walking and to turn en bloc. Tandem walking cannot be performed with eyes closed. Gait speed: Preferred gait speed remains slower than normal for age in at least 30% of patients with BVL Walk while turning head: Gait slows and becomes ataxic. Singleton test: Loss of balance is expected. Uneven surfaces or poor light will result in increased ataxia and, possibly, loss of balance. Fall risk: There can be clinically important improvement in scores, but the majority of patients (73%) remain at risk for falling on the basis of Dynamic Gait Index scores.3

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341

mation about frequency of falls, when the most recent fall occurred, conditions under which the fall occurred, and whether or not an injury was sustained be obtained from the patient. It is also important to identify whether or not the patient has had any near falls, times when falling to the ground was prevented because they grabbed onto an object or a person or because someone caught them.

function. Typically, loss of vestibular function continues even after the medication is stopped. Some improvement in vestibular function may occur if some hair cells were affected by the ototoxic drug but not killed. Potentially, an increase in gain may also occur with the use of vestibular adaptation exercises. This has been demonstrated in patients with unilateral vestibular loss but not in patients with BVL.16

Comorbidities
While taking the patients history, the clinician should identify the presence of progressive disorders, especially those affecting vision such as macular degeneration and cataracts, and those affecting sensation in the feet, such as diabetes. These disorders lead to a gradual decrease in available sensory cues and will have an adverse effect on balance in the future.

Visual System
Assessment of visual function should include at least a gross test of visual field and a measure of visual acuity, because both can affect postural stability.6 Measuring visual acuity during head movement is particularly important. The vestibulo-ocular system normally stabilizes the eyes during head movements; when there is no vestibuloocular reflex (VOR) to stabilize the eyes during head movement, small amounts of retinal slip (movement of image across the retina) will degrade vision. For instance, a retinal slip of 3 degrees per second (deg/sec) would cause visual acuity to change from 20/20 to 20/200.17 As such, in patients with no vestibular function, the head movement that occurs in a moving car can cause a degradation of visual acuity that would make driving unsafe.

Subjective Complaints
The patients complaints of disequilibrium and oscillopsia can be assessed using a visual analog scale (VAS). The Dizziness Handicap Inventory12 and the Activities of Daily Living Assessment for Vestibular Patients13 are useful tools for assessing the patients perception of disability or handicap as well as the patients functional abilities and problems.

Dynamic Visual Acuity

Assessment of visual acuity during head movement (dynamic visual acuity [DVA]) can be performed either clinically or with a computerized system. The advantage of the computerized system is that the test and result are standardized and more reliable.18 Clear differences in DVA scores occur among normal subjects, those with dizziness from non-vestibular causes, and patients with known vestibular loss (Table 21-1). The results of the computerized DVA test are both sensitive (90% for those older than 65 years and 97% for those younger than 65 years) and specific (94%) for vestibular loss. The clinical DVA, however, is easy to perform and is sufficiently reliable to be useful as a guide to treatment and its efficacy (Fig. 21.1).19

Vestibular Function
One important consideration in designing a treatment program is the presence or absence of remaining vestibular function. Vestibular function can be documented with tests such as the rotational chair and caloric tests. This information is then used to determine which exercises to give the patient. If no vestibular function remains, the exercises must be directed at the substitution of visual and somatosensory cues to improve gaze and postural stability. The presence of remaining vestibular function can be used as a guide to predict the final level of recovery for patients.2,3 Patients with incomplete BVL are often able to return to activities such as driving at night and to some sports. Patients with severe bilateral loss may not be able to drive at night, and some patients cannot drive at all because of the gaze instability. Activities such as sports and dancing may be limited by the visual and the balance problems. Vestibular function tests can also be used to follow the course of the vestibular loss and of any recovery of vestibular function that might occur.14, 15 Certain aminoglycoside antibiotics are selectively taken up by vestibular hair cells, leading to a gradual loss of vestibular

Somatosensory System
Particular attention should be paid to assessment of vibration, proprioception, and kinesthesia in the feet. Although mild deficits in sensation in the feet may have no effect on postural stability in otherwise normal individuals, but in patients with vestibular loss, somatosensory deficits may have profound effects on balance and on the potential for functional recovery. As with visual system disorders, being aware of potentially progres-

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Table 21-1 DISTRIBUTION OF NORMAL AND ABNORMAL DVA SCORES BASED ON A COMPUTERIZED SYSTEM
Type of Subject DVA (LogMAR) Normal DVA Score (%) Abnormal DVA Score (%)

Normal (n

51) 16) 53) 34)

0.040 0.097 0.282 0.405

0.045 0.099 0.140 0.134

96.1 87.5 11.3 0

3.9 12.5 88.7 100

Dizzy, non-vestibular (n

Unilateral vestibular loss (n Bilateral vestibular loss (n

DVA

Dynamic Visual Acuity; LogMAR

logarithm of the mminimum angle of resolution.

sive disorders affecting somatosensory information is important.

Balance and Gait

Patients with BVL must be given a detailed assessment of balance and gait. Obviously, static balance should be assessed first. In the acute stage, patients with bilateral

vestibular deficits may have positive Romberg test results. In the compensated stage, the Romberg result is usually normal. Although some patients are able to perform the Sharpened Romberg test with eyes open, they cannot do so with eyes closed. Patients with bilateral vestibular deficits also have difficulty performing tests in which both visual and somatosensory cues are altered. An example would be Fukudas stepping test, in which

cDVA Scores of Patients with Dizziness or Imbalance

1.20

1.00

cDVAL (LogMAR)

0.80

0.60

0.40

0.20

0.00

BVL

UVL

No Vestibular Loss

Figure 21.1 Distribution of dynamic visual acuity scores (shown as the logarithm of the minimum angle of resolution [LogMAR]) obtained with the clinical test in patients with unilateral vestibular loss (UVL) and bilateral vestibular loss (BVL) and in normal subjects. (From Venuto, et al, 1998.19)

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the eyes are closed and the patient is marching in place. Patients may have normal responses with eyes open during this test but will fall with eyes closed. Determining how well patients use different sensory cues to maintain balance and whether they depend on particular sensory cues is critical. It is important to recognize that these features may vary considerably from patient to patient and can change over the course of recovery. Bles and colleagues20 have shown that patients with BVL are initially more dependent on visual cues than on somatosensory cues for balance. With time, their ability to use somatosensory cues improves. This improvement varies from patient to patient, however, and must be carefully assessed (Fig. 21.2). The gait of patients with bilateral vestibular deficits is often wide-based, slow, and ataxic. Patients decrease their trunk and neck rotation in an effort to improve stability by avoiding head movements. Arm swing is simi-

larly decreased. Many patients use excessive visual fixation and therefore have increased difficulty if asked to look up while walking. Patients typically turn en bloc and may even stop before they turn. Asking patients to turn their heads while walking results in increased ataxia and, often, loss of balance.

Mechanisms of Recovery
The mechanisms used to stabilize gaze in the absence of vestibular inputs have been well studied (Box 21-2). The mechanisms involved in maintaining postural stability are still somewhat less well understood, although research is being done in this area.

Gaze Stability
Subjects without vestibular function must develop different mechanisms to keep the image of the target on the

Figure 21.2 Posturography test results from patients with bilateral vestibular loss demonstrating the differences in ability to maintain postural stability when different sensory cues are altered or removed. Patients are tested using the following six different conditions: Available cues: Unavailable or altered cues: Test condition 1 Vision, vestibular, somatosensory Test condition 2 Vestibular, somatosensory Vision absent Test condition 3 Vestibular, somatosensory Vision altered Test condition 4 Vision, vestibular Somatosensory altered Test condition 5 Vestibular Vision absent, somatosensory altered Test condition 6 Vestibular Vision altered, somatosensory altered Results show patients who have difficulty when both visual and somatosensory cues are altered (A), when somatosensory cues only are altered (B), when visual cues only are altered (C), and when either visual or somatosensory cues are altered (D).

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Box 21-2

MECHANISMS USED TO STABILIZE GAZE

Change in amplitude of saccades Use of corrective saccades Modification of pursuit eye movements Central preprogramming of eye movements

fovea during head movements (see Box 21-2). Central preprogramming of movements is probably the primary mechanism by which gaze stability is improved in patients with BVL. The contribution of central preprogramming has been assessed by comparing the gain of compensatory eye movements21,22 or by comparing visual acuity during predictable and unpredictable head movements.23 The difficulty with central preprogramming as a substitute for the loss of vestibular function is that it would not be effective in situations in which head movements are unpredictable, such as walking. Other mechanisms used to improve gaze stability are modifications in saccadic and pursuit eye movements.21,24 Patients with complete BVL may make hypometric saccades toward a visual target. Then, as the head moves toward the target, the eyes would be moved passively into alignment with the target. They may also make accurate saccadic eye movements during combined eye and head movements toward a target, and then make corrective saccades back to the target as the head movement pulls the eyes off the target. These strategies enable the patient to recapture a visual target after a head movement.21 Pursuit eye movements can be used during lowfrequency (and low-velocity) head movements to stabilize the eyes. The limits of smooth-pursuit eye movements depend on the nature of the stimulus (predictable vs. unpredictable; sinusoidal vs. constant-velocity). In general, for sinusoidal stimuli, smooth pursuit works well at frequencies of up to 1 Hz. For constantvelocity stimuli, smooth pursuit can work well up to target velocities of 100 deg/sec. Later evidence demonstrates that patients with bilateral vestibular deficits have higher smoothpursuit gains than normal controls, although the patients performance is still within the normal range.24 At one time, potentiation of the cervico-ocular reflex (COR) was thought to contribute to the recovery of gaze stability in patients with BVL.21,25,26 In the COR, sensory inputs from neck muscles and facet joints act to produce

a slow-phase eye movement that is opposite to the direction of the head movement during low-frequency, brief head movements. The COR, therefore, complements the VOR, although in normal subjects it is often absent and, when present, contributes at most 15% of the compensatory eye movement. In patients with complete BVL, the COR operates at head movement frequencies up to 0.3 Hz, well below the frequency range of head movements during normal activities. Therefore, although the COR is increased in patients with BVL, it does not actually operate at frequencies that would contribute significantly to gaze stability during the head movements that would occur during most activities. Kasai and Zee21 found that different patients with complete BVL use different sets of strategies to compensate for the loss of VOR. Therefore, exercises to improve gaze stability should not be designed to emphasize any particular strategy but, instead, should provide situations in which patients can develop their own strategies to maintain gaze stability (see Box 21-2). No mechanism to improve gaze stability fully compensates for the loss of the VOR, however, and patients continue to have difficulty seeing during rapid head movements.

Postural Stability
A study on the course of recovery of patients with complete bilateral vestibular deficits over a 2-year period has shown that patients switch the sensory cues upon which they rely.20 Initially they rely on visual cues as a substitute for the loss of vestibular cues, but over time, they become more reliant on somatosensory cues to maintain balance. In this study, patients were required to maintain balance when facing a moving visual surround. Over the 2-year study, the subjects recovered the ability to maintain balance to within normal limits in the testing paradigm except at high frequencies. The vestibular system functions at higher frequencies than the visual or somatosensory systems, a difference that would explain why neither visual nor somatosensory cues can substitute completely for loss of vestibular cues. The contribution of somatosensory inputs from the cervical region to postural stability in patients with complete BVL is not clearly understood. Bles and colleagues27 found that changes in neck position did not affect postural stability in patients with complete BVL. They concluded that somatosensory signals from the neck do not contribute to postural stability. We do not know, however, whether kinesthetic signals from the neck, which would occur during head movement, affect postural stability. Certainly patients with bilateral vestibular

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dysfunction become less stable when asked to turn their heads while walking. This observation may indicate that kinesthetic cues do not contribute significantly to dynamic postural stability. Another interpretation is that such patients rely more on visual cues to maintain postural stability, and thus, when the head moves and visual cues are degraded, their balance becomes worse. The contribution of somatosensory cues from the lower extremities to postural stability in patients with BVL is also not well understood. Certainly some patients depend on somatosensory cues rather than on visual cues. Perhaps more importantly, we do not yet know how the degree of somatosensory loss affects postural stability in these patients. The loss of either visual or somatosensory cues in addition to vestibular cues has a devastating effect on postural control. Paulus and associates28 reported a case in which the patient had a complete BVL plus a loss of lower extremity proprioception. This patient relied on visual cues to maintain his balance. When the effectiveness of the visual cues was degraded (i.e., by fixation on a visual target more than 1 m away), his postural stability deteriorated significantly. Again, visual and somatosensory cues do not substitute fully for the lost vestibular contribution to postural stability (see Chapter 20).2931

Compensatory Strategies
Patients can be taught, and often develop on their own, strategies to use when in situations in which their balance will be stressed. For example, they learn to turn on lights at night if they have to get out of bed. They may also wait, sitting at the edge of the bed, before getting up in the dark to allow themselves to awaken more fully and for their eyes to adjust to the darkened room. They should be advised to use lights that come on automatically and to have emergency lighting inside and outside the house in case of a power failure. Patients may need to learn how to plan to move around places with busy visual environments, such as shopping malls and grocery stores. For some patients, moving in busy environments may require the use of some type of assistive device, such as a shopping cart or a cane, but for many patients with BVL, no assistive devices are needed after the patients become comfortable walking in the environment.

Evidence that Exercise Facilitates Recovery

There is some evidence that experience facilitates recovery after bilateral ablation of the labyrinth. Igarashi and

coworkers32 trained monkeys to run along a straight platform. Performance was scored by counting the number of times the monkeys moved off the straight line. A twostage ablation of the labyrinth was then performed. After the unilateral ablation, animals given specific exercises recovered faster than nonexercised animals, but all animals eventually achieved preoperative functional levels. After ablation of the second labyrinth, all monkeys had difficulty with the platform run task. The control group reached preoperative balance performance levels in 81 days, whereas the exercise group did so in 62 days. This result was not significantly different owing to the large variation in individual animals. These researchers also measured how long the animals took to reach 8 consecutive trial days in which they could keep their balance at preoperative levels. The exercise group achieved this criterion in 118 days. The control group took longer. One animal took 126 days, another took 168 days, and one animal had not achieved that criterion at 300 days. The conclusions from this study are that (1) recovery from bilateral deficits occurs more slowly than recovery from unilateral lesions, (2) exercise affects that rate of recovery in bilateral and unilateral lesions, and (3) the final level of function may be improved if exercises are given after bilateral lesions. Several studies have studied the effectiveness of vestibular exercises on postural stability during functional activities for patients with chronic bilateral vestibular deficits. Krebs and colleagues,1 in a double-blinded, placebo-controlled trial, found that the patients performing customized vestibular and balance exercises had better stability while walking and during stair climbing than patients performing isometric and conditioning exercises, such as using an exercise bicycle. Furthermore, the patients who had vestibular rehabilitation were able to walk faster. They used vestibular adaptation and eye-head exercises as well as balance and gait training. In a continuation of this study, Krebs and colleagues4 again demonstrated that as a group, those individuals performing the vestibular rehabilitation exercises had increased gait velocity, improved stability while walking, and decreased vertical excursion of the center of mass while walking. They noted a moderate correlation between improved gait measures at 1 year and the frequency of performing the home exercise program over the preceding year. When results for the patients with BVL (n 51) were combined with those for patients with UVL (n 33), 61% of the patients demonstrated significant improvements in gait. In a retrospective chart review of 13 patients with BVL, Brown and associates3 noted that as a group, the

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patients had significant improvements in various measures (Dizziness Handicap Inventory, Activities-specific Balance Confidence Scale, Dynamic Gait Index, Timed Up and Go test, and Sensory Organization Test component of dynamic posturography). Again, not all patients benefited to the same extent. These investigators noted that 33% to 55% of the patients demonstrated what were considered clinically significant changes on the different measures. In another retrospective study, Gillespie and Minor2 found that 63% of the patients with BVL who received vestibular rehabilitation demonstrated improvements (defined as reported increased activity levels, reduced symptoms, and demonstrated normal gait velocity, normal Romberg test result, or normal DVA score).

Expectations of Level of Recovery

Several studies of patients with vestibular hypofunction clearly state that some patients do not improve.3,4,3336 In patients with UVH, depending on what outcome measure is used, between 10% and 30% of subjects do not improve.34,35 In patients with BVH, outcome is worse, with between 25% and 66% failing to show improvement3 (Herdman preliminary data). These findings are extremely important, because as clinicians, we deal with individuals, not groups.

Treatment Approach
Not all exercise approaches are appropriate for patients with BVL, however. Telian and coworkers37 studied the effectiveness of a combination of balance exercises, vestibular habituation exercises, and general conditioning exercises for patients with bilateral vestibular deficits. They were unable to demonstrate a significant change in functional activity in these subjects after treatment. Thus, vestibular habituation exercises do not appear to be appropriate for these patients. This makes sense, because habituation exercises are designed to decrease unwanted responses to vestibular signals rather than to improve gaze or postural stability.

remaining vestibular function may benefit from vestibular adaptation exercises to enhance remaining vestibular function (Fig. 21.3, page 347). For both groups, postural stability can be improved by fostering the use of visual and somatosensory cues. This approach is also used in the treatment of patients unilateral with vestibular hypofunction (see Box 21-4). Once the patients specific problems have been identified, the exercise program can be established. During the initial sessions, particular attention should be paid to the extent to which the exercises increase the patients complaints of dizziness. The patients perception of dizziness can be the major deterrent (limiting factor) to his or her eventual return to normal activities. Head movement, a component of all exercises, increases that dizziness. Also, the home exercise program typically requires that the patient perform exercises many times daily. Patients may find that they become increasingly dizzy with each performance of the exercises; the Head Movement VAS can be used to quantify this problem. Additionally, inability of the patient to sustain head movement for 1 minute helps define the initial exercise program. It is important to explain to the patient that some increase in dizziness is expected at the beginning of the exercise program and with any increase in the intensity of the exercises. Only one exercise involving head movement should be prescribed initially. Other exercises can be added and the frequency and duration of the exercises can be increased as the patient improves. The patient should perform at least one set of all the exercises at the time of the clinic visit. Patients should also be taught how to modify the exercises if the dizziness becomes overwhelming (Box 21-5, page 347). They should be strongly encouraged to contact the therapist if they are having difficulty. In patients for whom dizziness continues to be a problem, we suggest meditation and relaxation techniques to try to reduce the effect of the dizziness on the patients life.

Progression of Exercises
The reported number and frequency of patient visits to the clinic varies tremendously from study to study. Improvement in patients undergoing vestibular rehabilitation has been reported when patients were seen once a day for 3 days38, two or three times a week for months, once a week for 4 or 5 weeks,34,35,38, once a month,3,39-41 or even once in several months.42,43 It is difficult to determine appropriate practice patterns by comparing these studies, however, because different exercise approaches,

Treatment
The treatment approach for patients with complete loss of vestibular function involves the use of exercises that foster (1) the substitution of visual and somatosensory information to improve gaze and postural stability and (2) the development of compensatory strategies that can be used in situations in which balance is maximally stressed (Boxes 21-3 and 21-4). Patients with some

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Box 21-3

PATIENT INSTRUCTIONS FOR EXERCISES TO IMPROVE GAZE STABILITY

1. To improve remaining vestibular function and central preprogramming: Tape a business card on the wall in front of you so that you can read it. Move your head back and forth sideways, keep the words in focus. Move your head faster but keep the words in focus. Continue to do this for 1 to 2 minutes without stopping. Repeat the exercise moving your head up and down. Repeat the exercises using a large pattern such as a checkerboard (full-field stimulus). Note: When training the patient to perform this exercise, the physical therapist should watch the patients eyes closely. If the patient is making corrective saccades, he or she should slow the head movement down. 2. Active eye-head movements between two horizontal targets to foster the use of saccadic or pursuit strategies and central preprogramming: Look directly at one target, being sure that your head is also lined up with the target. Look at the other target with your eyes and then turn your head to the target (saccade should precede head movement). Be sure to keep the target in focus during the head movement. Repeat in the opposite direction. Vary the speed of the head movement, but always keep the targets in focus. Note: Place the two targets close enough together that when you are looking directly at one, you can see the other with your peripheral vision. Practice for 23 minutes, resting if necessary. This exercise can also be performed with two vertically placed targets. 3. Visualization of remembered targets to foster central preprogramming: Look at a target directly in front of you. Close your eyes and turn your head slightly, imagining that you are still looking directly at the target. Open your eyes and check to see whether you have been able to keep your eyes on the target. Repeat in the opposite direction. Be as accurate as possible. Vary the speed on the head movement. Practice for up to 25 minutes, resting if necessary during the exercise.

different outcome measures, and different patient populations were used. However, two randomized clinical trials demonstrated significant benefits in function in patients with BVH who were supervised in the clinic only one visit per week and performed an extensive home exercise program for 8 weeks.1,4 Changing the duration of any given exercise, the frequency of performance, and how many different exercises are given (Table 21-2 page 348) can modify the intensity of the exercise program to improve gaze stability. Patients find the exercises more challenging if they have to perform them while standing as opposed to sitting. Exactly which exercises are given initially and the progression itself depend on the individual patient. Concurrent with the exercises to improve gaze stability, of course, the patient should be instructed in exercises to improve postural stability. As with other types of exercises, the initial program and the rate of progression should be customized for each patient.

Guidelines to Treatment and Prognosis

The physical therapist should keep the following factors in mind when working with the patient with a bilateral vestibular deficit: 1. The patients perception of dizziness can be the major deterrent to his or her return to normal activities. 2. Recovery after bilateral deficits is slower than after unilateral lesions and can continue for as long as 2 years. This is not to suggest that the patient should be actively engaged in rehabilitation for the entire 2 years but, rather, that imparting this knowledge should help the patient with BVH understand that improvement will most likely be a slow process. 3. Recovery is easily upset by other medical problems, such as having a cold or receiving chemotherapy.

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Box 21-4

PATIENT INSTRUCTIONS FOR EXERCISES TO IMPROVE POSTURAL STABILITY*

The purpose of these exercises is to force you to develop strategies for performing daily activities even when deprived of vision, proprioception, or normal vestibular inputs. The activities are supposed to help you develop confidence and establish your functional limits. For all of these exercises, you should take extra precautions so you do not fall. 1. Stand with your feet as close together as possible with both hands helping you maintain your balance by touching a wall. Take your hand or hands off the wall for longer and longer periods of time while maintaining your balance. Try moving your feet even closer together. Repeat this for minutes twice each day. Repeat exercise #1 with eyes closed, at first intermittently and then continuously, all the while making a special effort to mentally visualize your surroundings. 2. Stand with your feet shoulder-width apart with eyes open, looking straight ahead at a target on the wall. Progressively narrow your base of support from: feet apart to feet together to a semiheel-to-toe position to heel almost directly in front of the toes. Note: Change your foot position 1 inch at a time. Do the exercise first: with arms outstretched and then with arms close to your body and then with arms folded across your chest. 6. Hold each position for 15 seconds and then move on to the next most difficult exercise. Repeat exercise #2 with eyes closed, at first intermittently and then continuously, all the while making a special effort to mentally visualize your surroundings. Repeat # above but while standing on a foam pillow. (Note: Unusual for patients with bilateral vestibular loss to do this exercise.) Walk close to a wall with your hand braced available for balancing. Walk with a narrower base of support. Finally, walk heel-to-toe. Do this with eyes (open/closed). Practice for minutes. Walk close to a wall and turn your head to the right and to the left as you walk. Try to focus on different objects as you walk. Gradually turn your head more often and faster. Practice for minutes. Walk and turn your head to the right and to the left as you walk while you count backwards out loud from 100 by 3s. Try to focus on different objects as you walk. Gradually turn your head faster. Practice for minutes. Practice turning around while you walk. At first, turn in a large circle, but gradually make smaller and smaller turns. Be sure to turn in both directions.

3.

4.

5.

7.

*Therapist uses the blanks to mark which exercises the patient should perform as well as to specify durations and variations.

4. To maintain recovered function, patients may always need to be doing some exercises, at least intermittently.4 5. The patients postural stability will never be completely normal. The patient may demonstrate a negative Romberg test result and may

be able to maintain the Sharpened Romberg position with eyes open, but will not be able to do so with eyes closed. 6. Initially, the patient may need to use a cane or a walker while ambulating. Some patients, especially older patients, need to use a cane at least

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Figure 21.3 Exercises that enhance the adaptation of the vestibular system should be used for any patient who has remaining vestibular function. These exercises should be performed many times a day and can be done while the patient is sitting and, eventually, standing. (Modified from Tusa and Herdman, 1993.46)

Box 21-5

ADJUSTMENTS MADE TO EXERCISES BECAUSE OF SEVERE DIZZINESS

Perform the exercises fewer times each day. Move the head more slowly. Perform each exercise for a shorter period. Rest longer after each exercise.

some of the time. Most patients, however, are eventually able to walk without any assistive devices. Ambulation during the acute stage is wide-based and ataxic with shortened stride length and sidestepping to the right and left. The patient will turn en bloc and turning the head will increase instability. Ambulation will improve, but it, too, will not be normal. 7. Patients will be at increased risk for falls.11 Patients will need to be careful when walking in low-vision situations, over uneven surfaces, or when they are fatigued.

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Table 21-2 SUGGESTED PROGRESSION FOR GAZE STABILITY EXERCISES

Exercise Duration Frequency Position

X1 viewing paradigm against plain stationary background; horizontal or horizontal-andvertical head movement X1 viewing paradigm against plain stationary background; horizontal or horizontal-andvertical head movement X1 viewing paradigm with target held in hand against a plain background; horizontal and then vertical head movements Add eye-head exercises, horizontal and vertical X1 viewing paradigm with target held in hand and also with target at distance Eye-head exercises, horizontal and vertical X1 viewing paradigm with target held in hand and also with target at distance Eye-head exercises, horizontal and vertical Add remembered target exercise X1 viewing paradigm with target held in hand and also with target at distance Eye-head exercises, horizontal and vertical Remembered target exercise Some patients may be able to progress to X2 viewing paradigm with target held in hand and also with target at distance Eye-head exercises, horizontal and vertical Remembered target exercise X1 with target held in hand and also with target at distance Eye-head exercises, horizontal and vertical Remembered target exercise

Maybe for 1 minute each time

2 or 3 times daily

Sitting until can perform the head movements easily and then standing Standing*

Increase to 1 minute each exercise 1 minute each exercise No specific duration 1 minute each exercise No specific duration 1 minute each exercise No specific duration No specific duration 1 minute each exercise No specific duration No specific duration 1 minute each exercise No specific duration No specific duration 1 minute each exercise No specific duration No specific duration

Increase to 5 times daily Up to 5 times daily 2 or 3 times daily 2 or 3 times daily 2 or 3 times daily 4 times daily 4 times daily 4 times daily 4 times daily 4 times daily 4 times daily 4 times daily

Standing*

Sitting at first and then standing Standing* Standing* if possible Standing* Standing* Sitting at first and then standing Standing* Standing* Standing* Standing*

4 times daily 4 times daily 4 times daily 4 times daily 4 times daily 2 times daily

Standing* Standing* Standing* Standing* Standing* Stand and step to touch number

Add finding numbers written randomly on large No specific duration (6 ft 5 ft) checkerboard pattern placed on wall
*

The exercise can be made more difficult by changing the base of support (e.g., from feet apart to feet together).

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Future Directions
Currently research is being conducted to determine whether individuals with BVL may benefit from some form of sensory stimulation to replace the absent vestibular signals. Although this work is in its infancy, the preliminary results are promising. Kentala and colleagues44 have used a rate gyroscope and linear accelerometer to encode an individuals anterior-posterior sway. This information is then fed back to the individual via a vibrotactile array. The amount of vibration and the location of the vibration is related to the degree and direction of sway. These investigators found that individuals with UVL and BVL demonstrated a marked reduction of anterior-posterior sway on the Sensory Organization Test component of the computerized dynamic posturography test when they were using the vibrotactile array.

Rather than a vibrotactile cue, Hegeman and colleagues45 used auditory feedback to indicate either the amount of sway or the sway velocity of patients with BVL. Anterior-posterior and side-to-side sway was measured and encoded in four different stance conditions: eyes openfirm surface, eyes closedfirm surface, eyes opencompliant surface, and eyes closedcompliant surface. These researchers reported improvements, to normal levels, in single-limb stance with eyes open on a firm surface when patients used the auditory feedback. They noted no improvements, however, when tests were conducted with eyes closed on a compliant surface. Although these initial results are encouraging, it remains to be seen how useful these devices will be and how the devices will affect the approach to rehabilitation.

CASE STUDY 1
A 64-year-old woman with a history of acute unsteadiness is referred for treatment. Six weeks prior to this clinic visit, she had a chronic bladder infection that had not responded to other antibiotics and was started on IV gentamicin at home q8hr for 10 days. She had no history of renal failure, nor was she taking other antibiotics or a loop diuretic at that time. She began to complain of imbalance 2 days after the last dose of gentamicin. She had no complaints of hearing loss, tinnitus, or vertigo. Her imbalance was severe, and she was using a walker. She was unable to walk independently. Standing, walking or moving her head exacerbated the balance problem. Comment This patients history suggests an ototoxic reaction to gentamicin. Fewer than 15% of all individuals treated with gentamicin experience BVL, and she had no known risk factors that would increase the likelihood of an ototoxic reaction, such as renal failure and taking a loop diuretic. Pertinent History The patient had been treated for depression and anxiety. Current medications were Zoloft, Valium, and Premarin. Neurological Examination Neurological findings were normal except for visual acuity of 20/20 3 OU with head stationary, which decreased to 20/80 4 during 2-Hz head oscillations (clinical DVA test). Patient made corrective saccades with slow and rapid head thrusts, worse to the right. She had a positive Romberg response. Gait was extremely slow and cautious without the walker. She stopped frequently and could not turn around without stopping. Patient also had a significant scoliosis.
Comment. The large decrease in visual acuity during

head movement ( 4 lines) is consistent with a severe vestibular deficit. The presence of corrective saccades with slow head rotations as well as with rapid head thrusts also suggests a profound deficit. Although gentamicin was given systemically, her vestibular loss appears to be asymmetrical. The loss does not apper to have been compensated at this time, on the basis of the positive Romberg result as well as the poor VOR during slow head rotations. Her gait pattern may reflect fear as well as the vestibular deficit. Her history of depression may be a factor in the final level of recovery. Caloric Test No response to either cool or warm irrigation of either ear. Iced-water irrigation of both the right and left ears resulted in nystagmus with peak slow-phase eye velocities of 8 deg/sec. The direction of the nystagmus reversed when the patient was moved from supine to prone position.
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C A S E S T U D Y 1 (continued)
Comment. Iced water is a stronger stimulus than either cool or warm water. The nystagmus generated by iced water irrigation may represent either a response of the peripheral vestibular system or an alerting response to the extreme cold. If the nystagmus were due to excitation of the hair cells in the inner ear, the direction of the nystagmus would reverse when the patient was moved from supine to prone because the direction of endolymph flow would reverse. If the nystagmus were due to an alerting response, it would not reverse when the patient was moved from supine to prone position. The test results for this patient suggest some residual function in each ear.

Quantitative Dynamic Visual Acuity The patients visual acuity during 120-deg/sec horizontal head movements was LogMAR .450 (approximately 20/50-3; normal LogMAR 0.000). Gait When asked to walk without the walker, her cadence was slow and she had a widened base of support. Her step length was decreased but symmetrical. Arm swing and head and trunk rotation were markedly decreased, especially when she turned. She could not walk a straight path but had no sidestepping or foot crossover. Her gait pattern was affected by her scoliosis (arm swing asymmetry). She was able to walk more rapidly without a significant change in base of support or gait pattern. When asked to try to turn her head horizontally while walking, her cadence slowed significantly and she sidestepped occasionally. Comment The patients Disability Scale and Dizziness Handicap Inventory scores both indicate a moderate perception of disability/handicap. Shepard and colleagues have demonstrated that patients who score a 5 on the Disability Scale are less likely to experience improvement with vestibular rehabilitation than those who score 3 or lower, as this patient did (see Chapter 19). Although she has been using a walker, she was able to ambulate safely without it. Head movements (turning her head or turning herself around) increased her instability. Her dynamic visual acuity was consistent with that of other patients with BVL. Goals The short-term goals for this patient were (1) to perform the vestibular adaptation exercises without a significant increase in symptoms, (2) to walk daily, and (3) to no longer use her walker at home. The long-term goals were (1) to return to all normal activities except possibly driving, (2) to improve visual acuity during head movements by two lines on the quantitative DVA test and to 20/50 on the clinical DVA test, and (3) to decrease symptoms by 50% during head movements.

Vestibular Rehabilitation The patient was seen 1 week later to institute a vestibular rehabilitation program. At that time she was still using a walker. She reported that her imbalance was induced by movement, occurred only while walking, and was worse in the dark. She denied having any falls but reported that she did stagger and sidestep while walking, and tended to drift to both the right and the left if she tried to walk without her walker. Social History The patient lived with her husband. Her home had no stairs. She did not smoke or use alcohol. Current Functional Level She was independent in self-care activities but was no longer driving. She had been inactive since the onset of this problem. Subjective Complaints She stated that her symptoms disrupted her performance of both her usual work and outside activities (rated a 3 on the Disability Scale). She scored a 56 on Jacobsons Dizziness Handicap Inventory, indicating that she would not go for a walk by herself, could not walk in the dark, and was limited in her ability to travel or participate in social activities. She also reported feeling frustrated, embarrassed in front of others, and handicapped. She rated her disequilibrium while walking as a 9.3 on an analog scale of 0 to 10 (10 worst). She rated her oscillopsia as a 5.7 on a similar scale.

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Plan The patient was started on a home exercise program, which included the X1 viewing paradigm to be performed with both horizontal and vertical head movements for 1 minute each four times a day. The target was to be placed against a plain wall. Initially, she was to perform this exercise seated and then was to perform the exercise standing with her feet apart. She was also instructed to practice walking in a hallway twice daily for 5 minutes each time, with rests, without touching the walls. Finally, she was told to walk for 20 minutes daily outside with her husband. She was given a calendar to fill in to ensure compliance. The total daily duration of her exercises at this point was 36 minutes. The program was limited until the patients response could be determined. The patient was seen at 1-week intervals. On the first follow-up, the patient was doing well with the exercises and was no longer using her walker at all. The exercise program was changed to include the eye-head exercises both vertically and horizontally, and the X1 paradigm using a near target held in the hand was added. She was to practice walking and turning her head horizontally for 5 minutes twice daily. She was also instructed in a static balance exercise, in which she would stand while gradually decreasing her base of support. This was to be performed with eyes open and then eyes closed. She was to continue walking for 20 minutes daily. Total exercise time was increased to 45 minutes. On next follow-up visit, the patient reported that she initially had difficulty with the exercises involving head movements, all of which increased her dizziness. However, she reported that after 2 days of performing the exercises, she was able to perform them without a significant increase in dizziness. Review of the exercises showed that she was performing them all correctly and was maintaining fixation on the X1 viewing paradigms, although her head movements were slow. The exercise program was modified to include performing the X1 paradigm using a target on a checkerboard, and the imaginary target exercise was added. For these exercises, she was instructed to attempt to move her head more rapidly while maintaining focus on the target. She was also instructed to add walking and moving her head vertically. The X1 viewing paradigm using a target

placed against the wall was discontinued. Eventually, the patient was instructed in the X2 viewing paradigm. One month after the initiation of her exercise program, the patient was walking with improved cadence and a narrower base of support. She still had difficulty walking a straight line, but she was able to turn her head while walking and turn around without stopping. She no longer used a walker at any time. Her rating of subjective complaints of disequilibrium was a 0.6 (down from 9.3) and of oscillopsia was a 1.5 (down from 5.7). Her quantitative DVA score was LogMAR 0.143 (initial DVA was LogMAR 0.450), a three-line improvement. The plan at that time was for the patient to continue with the rehabilitation process to further improve her gait and to enable her to return to more of her normal activities. On her next visit, 1 week later, the patient came in complaining of increased difficulty with her balance and greater dizziness. She reported that the exercises were okay but she was dizzy while walking and even when she rolled over in bed. Comment The patient was making good progress, and both her balance and dynamic visual acuity had improved considerably when she suddenly had greater difficulty walking and more complaints of dizziness. Her complaint that she has increased dizziness when she rolls over in bed sounds like benign paroxysmal positional vertigo (BPPV). Re-examination Eye movements were recorded while the patient was moved into the right and left Dix-Hallpike positions. She developed an upbeating nystagmus, concurrent with complaints of vertigo, when moved into the left Dix-Hallpike position. The latency and duration of the nystagmus and vertigo were consistent with posterior canal canalithiasis. These results indicated that although the patient had a bilateral vestibular deficit, there was remaining function in the left posterior canal. The caloric test had previously shown remaining function in the left horizontal canal. The patient was treated for left posterior canal BPPV using the canalith repositioning maneuver. After successful remission of her positional vertigo, she resumed her exercises for the bilateral vestibular deficit.

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CASE STUDY 2
A 34-year-old woman with a history of diabetes and renal failure had been undergoing peritoneal dialysis for 11/2 years. She had been treated with gentamicin 9 months and 6 months previously for peritonitis. She had no complaints of disequilibrium after either of those drug courses. Two months after her previous treatment with gentamicin, she again developed peritonitis and again received IV gentamicin. After a few days, she complained of vertigo and tinnitus, experienced disequilibrium, and could not walk unassisted. She also complained that she was not able to see clearly when her head was moving. She was admitted to the hospital for a work-up of the vertigo and disequilibrium. Clinical Examination Significant findings on clinical examination included a spontaneous nystagmus with fast component to the left, poor VOR to slow head movements, and large corrective saccades with rapid head movements bilaterally, worse with head movements to the right than to the left. The test for head-shaking nystagmus was not performed because the patient complained of severe nausea after even gentle head movements and vomited. She also had a positive Romberg test result. The Sharpened Romberg and Fukudas stepping tests were not performed. The patient could not ambulate without the assistance of two people. Comment This patients signs and symptoms (vertigo, disequilibrium, oscillopsia, spontaneous nystagmus, and poor VOR) certainly were suggestive of a vestibular disorder. Furthermore, her history included multiple treatments with gentamicin, an ototoxic medication. In bilateral dysfunction due to treatment with an ototoxic drug, the symptoms of oscillopsia and disequilibrium develop over time and may not appear until after the drug treatment is finished. Once the symptoms appear, they may continue to worsen for several weeks. Some patients have a partial reversal of symptoms with time. Often the vestibular symptoms are accompanied by hearing loss. Typically, however, the vestibular loss is symmetrical and patients do not have vertigo or spontaneous nystagmus, both of which are associated with either unilateral vestibular loss or asymmetrical bilateral vestibular deficits. Although gentamicin usually results in BVL, symptoms of asymmetrical effects on the vestibular and auditory systems have been reported.6 This patients poor VOR to slow head movements and the presence of corrective saccades during rapid head thrusts bilaterally suggested a bilateral vestibular deficit, which was confirmed by the rotational test results. This patients gait disturbance appeared to be unusually severe, and further testing showed a moderate loss of proprioceptive and kinesthetic perception in the feet, which would contribute significantly to the vestibular problem. This sensory loss was probably due to diabetes. This finding was particularly important in developing her exercise program and in predicting her final level of recovery. Both computed tomography and magnetic resonance imaging were normal. Audiogram showed an asymmetric sensorineural hearing loss, right worse than left (Fig. 21.4). Caloric tests showed a poor

Figure 21.4 Hearing test results from a patient with gentamicin ototoxicity. Circles and triangles indicate right ear, and Xs and squares indicate left ear. Note the asymmetry in hearing loss for this patient.

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response bilaterally to warm or cool water, although iced water in the left ear did result in a weak but appropriate response. There was a directional preponderance to the right. Rotational chair test showed a severe bilateral vestibular deficit (Fig. 21.5). There was little optokinetic after-nystagmus, and the VOR time constant (Tc) was 2.4 sec to 60-deg/sec step rotations. At 240-deg/sec step rotations, some vestibular response was evidentthe gain of the response was 0.15, and the Tc was 2.4 sec. Treatment At this point, the patient was started on a vestibular rehabilitation program. She performed the X1 viewing paradigm exercise (see Fig. 21.3) first with horizontal head movements for 1 minute, and then with vertical head movements for 1 minute. Because head movement exacerbated her nausea, she rested for 10 minutes or more after each of these exercises. Initially she performed these exercises while sitting, up to 5 times a day. She also practiced standing unsupported, first with her feet apart and her eyes open and then gradually moving her feet 240.0 Eye velocity

together and briefly closing her eyes. She was instructed on how to use a walker, and emphasis was placed on increasing her endurance. Initially, she needed contact guarding while using the walker and would occasionally lose her balance, especially when trying to turn or if she moved her head too quickly. After 4 days, she was able to walk independently with the walker and was discharged from the hospital. At that time, she no longer had nausea with gentle head movements. Comments Although this patient had a bilateral vestibular deficit, the caloric and rotary chair tests showed that she had remaining vestibular function (response to iced water caloric test on the left and the responses to 60- and 240-deg/sec step rotations). Her initial exercise program, therefore, consisted of vestibular adaptation exercises, because she had remaining vestibular function, and ambulation training. Her balance exercises were designed to gradually increase the difficulty of maintaining balance by slowly reducing her base of support, changing her arm positions (arms out, arms at sides, arms across the chest), and then altering her use of visual cues. Although she had decreased sensation in her feet, subtracting visual cues was used as a treatment approach in order to facilitate her ability to use the remaining somatosensory and vestibular cues. Follow-Up The patient continued to be followed up as an outpatient. Exercises designed to facilitate the substitution of alterative strategies to maintain gaze stability as well to improve her static and dynamic balance were added to her program. The patient no longer needed to use a walker but she had a wide-based gait and had to stop walking before turning around. Her Romberg test result was negative but she could not perform the Sharpened Romberg test. Although her vision improved and she could read if she was sitting quietly, she could not see clearly while in a car and had not resumed driving. Approximately 2 months later, the patient had a retinal hemorrhage in her left eye. She already had
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0.0

VOR 240

10

20

30

Time, sec
Figure 21.5 Plot of the decay in slow-phase eye velocity with time during VOR-after nystagmus. Patient is first rotated in a chair in complete darkness for 2 minutes, and then the chair is stopped. The slow-phase eye movements that occur are due to the discharge of the velocity storage system and represent the function of the vestibular system. The results here show the poor peak slow-phase eye velocity (35 deg/sec) and the short time constant ( 2 sec) in a patient with bilateral vestibular loss. A step rotation at 240 deg/sec was used. Eye movements were recorded with electro-oculography.

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C A S E S T U D Y 2 (continued)
retinal damage in the right eye from her diabetes, which essentially meant that she now had only partial visual, vestibular, and somatosensory cues for balance. As a result, she could no longer keep her balance even in well-lighted conditions. For 1 week she used either a wheelchair or, at home, a walker. Fortunately, her vision recovered and she was again able to walk independently. On her last visit she reported that she had returned to most activities except driving. Her base of support while walking was more narrow, and her stability while turning had improved. Her Romberg test result was clinically normal but she could not perform a Sharpened Romberg test with eyes open. She was seeking part-time employment and was waiting for a kidney transplant.

CASE STUDY 3
A 61-year-old man was referred by a neurologist for treatment of disequilibrium secondary to BVL. The patient had been hospitalized for a subarachnoid hemorrhage 18 months previously. During his hospitalization, he had several systemic complications, including renal failure, pulmonary infiltrates, and ventriculitis, and was treated with two courses of vancomycin, gentamicin, and ceftazidime. The neurologist saw him 7 months after this hospitalization because of the patients persistent disequilibrium. At that time, the patient complained that he stumbled occasionally and that he had increased difficulty walking on uneven surfaces, in the dark, or when he moved his head quickly. He denied having nausea, vertigo, or a rocking sensation, although he did state that he had a feeling of being tilted when he walked. He stated that the disequilibrium began after the hospitalization. He also had bilateral hearing loss but had no complaints of tinnitus, pressure, or fullness in the ears. The remainder of his history was noncontributory. The neurological findings were normal except for the following: (1) visual acuity, as assessed using a wall chart, decreased from 20/20 with the head stationary to 20/100 during 2-Hz oscillations of the head, (2) right Horners syndrome, (3) staircase saccades downward from the midposition, (4) decreased VOR gain based on visualization of the optic nerve head and on the presence of compensatory saccades during rapid head thrusts, (5) mild decrease in vibration sensation in his feet, right more than left, (6) inability to perform tandem walking, Sharpened Romberg test, or Fukudas stepping test, and (7) bilateral hearing loss. The caloric test showed a severe reduction in function bilaterally (Fig. 21.6). Quantitative rotary chair testing of the oculomotor system using step rotations showed low VOR gain (0.2 and 0.13 to the right and left, respectively) and short Tcs (2.2 sec bilaterally) to a 60-deg/sec step rotation and low gain (0.19 and 0.34) and Tcs (1.9 sec and 1.2 sec) to 240-deg/sec rotations. It was concluded that the patient had BVL, probably from the gentamicin, and he was referred for vestibular rehabilitation. Treatment Prior to establishment of an exercise program, additional testing was performed. Dynamic posturography showed inability to maintain balance when both visual and somatosensory cues were altered and a decreased ability to maintain balance when visual cues were inappropriate (Fig. 21.7). Quantitative DVA testing showed a change in acuity from 20/20 (static) to 20/40 during head movements. Quantitative vibration threshold confirmed the moderate loss of vibration perception in the patients feet. His gait was wide-based, and he frequently sidestepped while walking. He appeared to use excessive visual fixation to maintain balance during ambulation. The patient was started on a program of exercises designed to (1) enhance remaining vestibular function, (2) develop alternative mechanisms to improve gaze stability, (3) improve static balance in the absence of visual cues, and (4) improve balance while ambulating. Follow-Up Six weeks later, the patients Romberg test result was normal but he still could not perform a Sharpened Romberg test with eyes open, nor could he perform Fukudas stepping test with eyes closed. He continued to walk with a widened base of support. Quantitative testing of the oculomotor system showed no change

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Figure 21.6 Results from bithermal caloric irrigation of the external auditory canals in a patient with profound bilateral vestibular hypofunction. SCV Slow component velocity.

from the previous test. Quantitative DVA testing showed an acuity of 20/30, a marked improvement over the previous value. The patient wished to return to driving, and the physical therapist suggested that should he decide to drive, he should start first in local traffic and even in an empty parking lot on a weekend. He was advised that driving at night and high-speed driving would still be hazardous.

One month later the patient reported that he had returned to driving during the day and that he was working part-time. He still could not walk in the dark or with his eyes closed without assistance. Several suggestions were made to the patient concerning modifications in his home to ensure safety, including emergency lighting that would come on automatically if there were a power failure, railings for all stairways, and safety bars in the bathroom.

Figure 21.7 Results from posturography test in a patient with bilateral vestibular loss. Test conditions were those shown in Figure 21.2.

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Section FOUR REHABILITATION ASSESSMENT AND MANAGEMENT

Summary
Patients with bilateral vestibular problems can be expected to return to many activities but will continue to have difficulties with balance in situations in which visual cues are absent or diminished. The level of disability partly depends on the degree of the vestibular loss but also reflects involvement of the visual and somatosensory systems. Treatment approaches include increasing the function of the remaining vestibular system, inducing the substitution of alternative mechanisms to maintain gaze stability and postural stability during head movements, and modifications of the home and working environment for safety. Patients should be able to return to work, and most of them will be able to ambulate without the use of a cane or walker, at least when they are in well-lighted environments.

Acknowledgment
The work described here was supported by NIH grant DC 03196 (SJH).

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