vestibular rehab in short

8/6/2019 Vestibular Rehab in Short

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Vestibular

RehabilitationT H I R D E D I T I O N


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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.


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Vestibular

RehabilitationT H I R D E D I T I O N

Susan J. Herdman, PT, PhD, FAPTAProfessor, Departments of Rehabilitatio

Medicine and Otolaryngology Head and Neck Surger

Director, Division of Physical Therap

Emory Universi

Atlanta, Georg


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F. A. Davis Company

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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.

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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

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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: 0-8036-1376-81. Vestibular apparatusDiseasesPatientsRehabilitation. I. Herdman, Susan.

[DNLM: 1. Vestibular Diseasesrehabilitation. WV 255 V5836 2007]

RF260.V4725 2007

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is granted by F. A. Davis Company for users registered with the Copyright Clearance Center (CCC)

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5/43

v

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 par-

ticipating 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 cir-

cumstances far more surreal than circumstantial, I was

interviewed by Weekend America, a National PublicRadio show the day after the Red Sox miraculous come-

back against the New York Yankees to win the American

League title in 2004. The interview was taped on Thurs-

day, 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 immedi-

ately 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 play-

ers 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 cli-

nicians 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 prin

ciples of the Contemporary Perspectives in Rehabilita

tion Series by assuring that each contributor has update

references and has, when appropriate, challenged th

readers critical thinking skills. The text is written fo

any specialist in vestibular rehabilitation or any studen

or clinician aspiring to become one. While already estab

lished as the gold standard for the assessment and man

agement of patients with vestibular disorders, this thiredition takes off from where the second edition has lef

There are four new chapters and several others have bee

revamped considerably. The four new additions to th

already comprehensive text include: a chapter (12) b

Ronald Tusa on Migraine, Mnires Disease and Motio

Sickness that represents a considerable expansion from

his chapter on migraine in the second edition and distin

guishes these three problem areas and their medical man

agement; a chapter (13) by Timothy Hain and Jane

Helminski on Mal de Dbarquement Disorder, a problem

that has received increasing attention since the secon

edition of this book and now includes guidelines fo

treatment and indications that physical therapy may b

inappropriate in the treatment of this disorder; a chapte

(18) on Compensatory Strategies for the Treatment o

Vestibulo-Ocular Hypofunction by Michael Schubert tha

offers new information on compensatory mechanism

used by patients undergoing vestibular rehabilitation; an

a chapter (26) by Ronald Tusa on Non-vestibular Dizz

ness and Imbalance that uniquely addresses lesions no

directly implicated in the central vestibular pathway

including disuse disequilibrium, spino-cerebellar ataxi

leukoaraiosis, and normal pressure hydrocephalus. In fac

the last 5 chapters of the third edition are grouped t

emphasize assessment and management of disorder

either within or external to the central vestibular path

ways or in the treatment of non-vestibular dizziness.

Moreover in addition to adding several new contrib

utors including Janet Helminski, Sharon Polensek

Michael Schubert, Greg Marchetti, and Robert Lande

many chapters have undergone substantial revision

Ronald Tusa has converted what had been one presenta

Foreword


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tion on quantification of vestibular function tests and

clinical examination into two exciting chapters presented

from the physicians perspective on History and Clini-

cal 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 con-

tributions 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 hav

easily been extracted from dialogue amongst these inte

disciplinary specialists at a symposium or workshop

While students new to this topic might not appreciate th

value of such a constellation of knowledgeable profe

sionals, those clinicians familiar with many of thes

authors and their contributions to vestibular rehabilitatio

will recognize that within these hard covers lie conten

the sum of whose parts far exceeds the whole.

Steven L. Wolf, Ph.D., PT, FAPTA, FAHASeries Editor

viii FOREWORD


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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 exam-ples 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 won-

derful 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 present-

ed to include several new chapters and have augmented

the material presented in all the chapters to reflect

changes in our understanding of management of vestibu-

lar disorders. The new chapters include management of

persons with mal de dbarquement syndrome, and per-

sons with dizziness that is unrelated to the vestibular sys-

tem such as disuse disequilibrium and central disorder

The third new chapter presents new information abou

the mechanisms that underlie compensation for vestibu

lar hypofunction. In addition to these new chapters, ther

are a number of new topics presented within differen

chapters such as differential diagnosis in BPPV to ident

fy disorders that mimic BPPV, differentiation amon

Mnires, migraine, and motion sensitivity, and the rol

of chemical labyrinthectomy in the management oepisodic vertigo.

Another shift you will find in the book, as well as i

many clinical studies, is an increasing use of function

measures, rather than impairment measures, to asses

outcome of rehabilitation. Of great value is the Interna

tional Classification of Functioning, Disability an

Health (ICF) scheme (World Health Organization 200

http://www.cdc.gov.hchs/about/otheract/ic99/icfhom

htm). The ICF provides a framework for the descriptio

of health-related states and includes both positive expe

riences and negative consequences of disease. It consis

of three domains that can be used to describe the effect odifferent disorders or diseases on a persons health, wit

a number of environmental and personal contextual fac

tors that may affect each of those domains (Table below

Preface

Normal Function and Structure Activities ParticipationVersus Versus Versus

Impairment (body level) Limitations (individual level) Restriction (societal level

Contextual Factors

Environmental Factors Personal Factors

e.g. Natural environment e.g. Gender, age

Support and relationships Co-morbidities

Attitude of family Social background

Attitude of society Education and profession

Services, systems, policies Past experience

Products and technology Coping style

HEALTH CONDITION DISORDER OR DISEASE


8/43

Because it provides a more comprehensive depic-

tion 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 exer-

cise 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 effec-

tively 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. Som

studies offer insight into new methods for identifying th

nature of the vestibular dysfunction such as involvemen

of the utricle and saccule. I expect that in the next 5 to 1

years there will be another great leap in our knowledg

and we will have several additional rehabilitatio

approaches. Researchers are exploring the use of tech

niques such as virtual reality, sensory substitutio

devices, vestibular implants, and methods to induce ha

cells regeneration. These techniques are not ready yet bu

the next edition of this book may be filled with wonder

ful new ways to help people with vestibular disorders.

Susan J. Herdman, PT, PhD, FAPTAEditor

x PREFACE


9/43

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, FRCPDepartment 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, MDDepartment 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 SciencesNorthwestern 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


Case Western Reserve University

Director

Ocular Motility Laboratory

Cleveland VA Medical Center

Cleveland, Ohio

Gregory F. Marchetti, PT, PhD

Assistant Professor


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



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 Otolaryngology-

Head and Neck Surgery

Johns Hopkins School of Medicine

Baltimore, Maryland

Contributors


10/43

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



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


Johns Hopkins University

Baltimore, Maryland

**Series Editor**

Steven L. Wolf, PhD, PT, FAPTA,

FAHA

Professor, Medicine

Professor, Rehabilitation Medicine



Atlanta, Georgia

xii CONTRIBUTORS


11/43

x

Cheryl D. Ford-Smith, MS, PT, NCS

Assistant Professor


Virginia Commonwealth University

Richmond, Virginia

James Megna, PT, NCS

Coordinator

Balance and Vestibular Rehabilitation ClinicSouthside 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 DirectorPhysical Therapy Department

Temple University

Philadelphia, Pennsylvania

Reviewers


12/43

x

I would like to express my gratitude to the wonderful co

leagues I have worked with in the clinic. Over my year

as a physical therapist, they have honed my skills, cha

lenged my assumptions, contributed to my researc

and made me a better clinician. So my thanks go to Ro

Tusa, Courtney Hall, Lisa Gillig, Tim Hain, John Leigh

David Zee, Doug Mattox, Rick Clendaniel, and Michae

Schubert.

I also want to thank the authors of this edition oVestibular Rehabilitation. They have contributed the

considerable knowledge and perspectives so we can a

learn how best to help the dizzy patient. As a resul

many more clinicians will become familiar with the prob

lems and management of vestibular disorders and many

many more patients will receive appropriate treatment.

Acknowledgments


13/43

xvi

SECTION ONE

Fundamentals 1

CHAPTER 1 Anatomy and Physiology of the NormalVestibular System 2

Timothy C. Hain, MD


CHAPTER 2 Vestibular Adaptation 19

David S. Zee, MD

CHAPTER 3 Role of the Vestibular System inPostural Control 32


CHAPTER 4 Postural Abnormalities inVestibular Disorders 54


CHAPTER 5 Vestibular Compensation: ClinicalChanges in Vestibular Functionwith Time after UnilateralVestibular Loss 76

Ian S. Curthoys, PhD and


CHAPTER 6 Vestibular System Disorders 98

Michael Fetter, MD

SECTION TWO

Medical Assessment andVestibular Function Tests 107

CHAPTER 7 History and ClinicalExamination 108

Ronald J. Tusa, MD, PhD

CHAPTER 8 Vestibular Function Tests 125


CHAPTER 9 Otolith Function Tests 144

G. Michael Halmagyi, MD and


CHAPTER 10 Auditory Examination 162


SECTION THREE

Medical and SurgicalManagement 177

CHAPTER 11 Pharmacological and OpticalMethods of Treatment for VestibularDisorders and Nystagmus 178

R. John Leigh, MD

CHAPTER 12 Migraine, Mnires and MotionSensitivity 188


CHAPTER 13 Therapy for Mal deDbarquement Syndrome 202

Timothy C. Hain, MD


CHAPTER 14 Surgical Management of VestibularDisorders 205


CHAPTER 15 Psychological Problems andthe Dizzy Patient 214


Contents in Brief


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CONTENTS IN BRIEF xv

SECTION FOUR

Rehabilitation Assessment andManagement 227

CHAPTER 16 Physical Therapy Diagnosis forVestibular Disorders 228


CHAPTER 17 Physical Therapy Management ofBenign Positional Vertigo 233



Appendix 17A-DifferentialDiagnosis: Mimicking BPPV 261


CHAPTER 18 Compensatory Strategiesfor Vestibulo-OcularHypofunction 265


CHAPTER 19 Physical Therapy Assessment ofVestibular Hypofunction 272



Appendix 19A EvaluationForm 300

Appendix 19B Dizziness HandicapInventory 307

CHAPTER 20 Interventions for the Patientwith Vestibular Hypofunction 309



CHAPTER 21 Assessment and Interventionsfor the Patient with CompleteVestibular Loss 338

Susan J. Herdman, PT, PhD, FAPTARichard A. Clendaniel, PT, PhD

CHAPTER 22 Management of the Pediatric Patientwith Vestibular Hypofunction 360


CHAPTER 23 Management of the Elderly Personwith Vestibular Hypofunction 376



CHAPTER 24 Disability in Vestibular

Disorders 398

Helen S. Cohen, OTR, EdD, FAOTA

CHAPTER 25 Assessment and Managementof Disorders Affecting CentralVestibular Pathways 409

Marianne Dieterich, MD

Thomas Brandt, MD, FRCP

CHAPTER 26 Non-vestibular Dizziness and

Imbalance: From DisuseDisequilibrium to CentralDegenerative Disorders 433


CHAPTER 27 Assessment and Managementof the Patient with TraumaticBrain Injury and VestibularDysfunction 444

Anne Shumway-Cook, PT, PhD, FAPTA

CHAPTER 28 Non-vestibular Dizziness andImbalance: Suggestions forPatients with Migraine andMal de Dbarquement 458


Annamarie Asher, PT

CHAPTER 29 Non-vestibular Diagnosisand Imbalance: CervicogenicDizziness 467



Appendix A Questionnaire forHistory and Examination 485

Index 493


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xviii

SECTION ONE

Fundamentals 1

CHAPTER 1 Anatomy and Physiology of theNormal Vestibular System 2

Timothy C. Hain, MD


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

Velocity Storage 14

Estimation: Going Beyond Reflexes 15

Higher-Level Problems of the

Vestibular System 16

Compensation for Overload 16

Sensor Ambiguity 16

Motion Sickness 16

Repair 17

Summary 18

CHAPTER 2 Vestibular Adaptation 19

David S. Zee, MD

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 Adaptationin Normal Subjects 24

Imagination and Effort of Spatial 00

Localization in Vestibular Adaptation 25

Context Specificity 26

Neurophysiologic Substrate

of Vestibulo-ocular Reflex Adaptation 26

Summary 27

CHAPTER 3 Role of the Vestibular System inPostural Control 32


Sensing and Perceiving Position and Motion 33

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


16/43

CONTENTS x

CHAPTER 4 Postural Abnormalities inVestibular Disorders 54


Examining the Vestibulospinal System 55

Advantages and Limitations of Clinical Tests 55

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 66

Sensory Substitution 66

Compensatory Processes 67

Summary 70

CHAPTER 5 Vestibular Compensation: ClinicalChanges in Vestibular Functionwith Time after UnilateralVestibular Loss 76

Ian S. Curthoys, PhD and


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 84Decompensation 87

Psychological Factors 87

Medication 88

Plasticity of the Vestibulo-Ocular Reflex 89

Rehabilitation 89

Neural Evidence Concerning Recovery after Unilateral

Vestibular Deafferentation 89

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 98

Michael Fetter, MD

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

Medical Assessment andVestibular Function Tests 107

CHAPTER 7 History and ClinicalExamination 108


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 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


17/43

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 9 Otolith Function Tests 144

G. Michael Halmagyi, MD and


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


Peripheral Vestibular Lesions 147

Central Vestibular Lesions and Settings of the

Subjective Visual Vertical 149

Clinical Significance 149

Vestibular Evoked Myogenic Potential Testing of


Physiological Background 150

Method 151

Clinical Applications 152

Comment 159

Summary 159

Acknowledgments 159

CHAPTER 10 Auditory Examination 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 170Sudden 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


Other Causes of Hearing Loss 175

Summary 175

SECTION THREE

Medical and Surgical

Management 177

CHAPTER 11 Pharmacological and OpticalMethods of Treatment for VestibularDisorders and Nystagmus 178

R. John Leigh, MD

Vertigo 178

Pathophysiology of Vertigo 178

Neuropharmacology of Vertigo and

Nystagmus 180

Treatment of Vertigo 180

Oscillopsia 182Pathogenesis 182

Treatment of Oscillopsia 183

Nystagmus and its Visual Consequences 183

Pathogenesis 183

Treatments 183

Summary 186

Acknowledgments 186

CHAPTER 12 Migraine, Mnires and MotionSensitivity 188


Incidence of Migraine 188Symptoms 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


18/43

CONTENTS x

CHAPTER 13 Therapy for Mal deDbarquement Syndrome 202

Timothy C. Hain, MD


Cause of the Syndrome: Persistent Adaptation to

Swaying Environments? 202

Treatment 203

Summary 204

CHAPTER 14 Surgical Management of VestibularDisorders 205


Acoustic Neuromas

(Vestibular Schwannomas) 205

Surgical Approaches 206

Middle Cranial Fossa 206

Translabyrinthine Approach 206

Suboccipital Craniectomy 207Complications 208

Stereotactic Radiosurgery 208

Mnires Disease 208

Surgical Management of Mnires Disease 209

Chemical Labyrinthectomy 209

Post-Traumatic Vertigo 211



Vascular Loops 212

Summary 213

CHAPTER 15 Psychological Problems andthe Dizzy Patient 214


Psychological Disorders and Their

Prevalence 214

Dizziness in Patients with Psychological

Disorders 214

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

Management 221

Medications 222

Summary 226

SECTION FOUR

Rehabilitation Assessment and

Management 227

CHAPTER 16 Physical Therapy Diagnosis forVestibular Disorders 228


Physical Therapy Diagnosis and the International

Classification of Functioning, Disability,

and Health Model of Diasablement 228

History 229


Diagnostic Flowchart 230

Identification of Modifiers 231Summary 232

CHAPTER 17 Physical Therapy Management ofBenign Positional Vertigo 233



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


19/43

xxii CONTENTS

Contraindications to the Assessment and

Treatment of BPPV 255

Unraveling Complicated Cases 256

Summary 259

APPENDIX 17A Differential Diagnosis:

Mimicking BPPV261


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 18 Compensatory Strategiesfor Vestibulo-OcularHypofunction 265


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 272Susan L. Whitney, PT, PhD, NCS, ATC


Normal Structure and Function versus

Impairment 272

Vestibulo-Ocular Function and Dysfunction 272

Perception of Head Movement and Position 274

Postural Instability 274

Cervical Range of Motion 274

Physical Deconditioning 274

Activities versus Limitation 274

Participation versus Restriction 275

Physical Therapy Evaluation 275

History 276


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 19B Dizziness HandicapInventory 307

CHAPTER 20 Interventions for the Patient

with Vestibular Hypofunction 309Susan J. Herdman, PT, PhD, FAPTA


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 313Treatment 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


20/43

CONTENTS xx

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 21 Assessment and Interventionsfor the Patient with CompleteVestibular Loss 338



Primary Complaints 338Balance 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 346Progression of Exercises 346

Guidelines to Treatment and Prognosis 347

Future Directions 351

Summary 358

Acknowledgment 358

CHAPTER 22 Management of the Pediatric Patientwith Vestibular Hypofunction 360


Incidence of Vestibular Deficits in Children 360

Development of Postural and OculomotorControl 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

CHAPTER 23 Management of the Elderly Personwith Vestibular Hypofunction 376



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 VestibularDisorders 398

Helen S. Cohen, OTR, EdD, FAOTA

Evaluating Disablement 398


Chronic Vestibulopathy 400

Bilateral Vestibular Impairment 400

Acoustic Neuroma 402

Mnires Disease 404

Acknowledgments 406

CHAPTER 25 Assessment and Managementof Disorders Affecting CentralVestibular 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


21/43

xxiv CONTENTS

Thalamic and Cortical Astasia Associated

with Subjective Visual Vertical Tilts 417

Torsional Nystagmus 417

Vestibular Disorders in (Sagittal) Pitch Plane 417

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 26 Non-vestibular Dizziness andImbalance: From DisuseDisequilibrium to CentralDegenerative Disorders 433


Disuse Disequilibrium and Fear of Fall 433

Description 433

Useful Outcome Tests 434

Management 434

Leukoaraiosis and Normal-PressureHydrocephalus 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 27 Assessment and Managementof the Patient with TraumaticBrain Injury and VestibularDysfunction 444

Anne Shumway-Cook, PT, PhD, FAPTA

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 andImbalance: Suggestions forPatients with Migraine andMal de Dbarquement 458


Annamarie Asher, PT

Definition of Non-vestibular Dizziness 458

Mal de Dbarquement 459

Migraine-Associated Dizziness 460

Primary Anxiety and Panic 462

Methodological Considerations for

Assessment and Treatment

Development 464

CHAPTER 29 Non-vestibular Diagnosisand Imbalance:Cervicogenic Dizziness 467



Proposed Etiologies 468

Posterior Cervical Sympathetic

Syndrome 468

Vertebrobasilar Insufficiency 468

Altered Proprioceptive Signals 468

Examination 475

Management 476

Summary 477

Appendix A Questionnaire for Historyand Examination 485

Index 493


22/43

Patients with unilateral and bilateral vestibular hypofunc-

tion (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 lossof 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 fol-

lows:

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 rehabilita-

tion process, including the observation that not

all patients experience improvement.

5. The necessity for patients with BVH to continu

with exercises or with activities that challenge

balance in order to sustain their improvement.

In addition, several case studies are used to illustrat

different points.

Primary Complaints

Balance

Patients with BVL are primarily concerned with the

balance and gait problems. During the acute stage of the

disease, they may feel off balance even when lying or si

ting down. More typically, however, their balance prob

lems are obvious only when they are standing or walking

Patients in whom BVL develops after the use of an oto

toxic medicationthe most common cause of BVL

often do not know they have a balance problem until the

get out of bed. Typically, these patients have been treate

with the ototoxic medication because of a serious infec

tion. They are often debilitated, and their balance prob

lems are initially attributed to weakness.

Even with full compensation, balance problem

persist. Although the other sensory and motor systems d

help compensate for the vestibular loss, these system

cannot substitute completely for the loss of vestibula

function (see Chapter 20, Figs. 20.2 and 20.3). Norm

postural stability while walking requires the combine

use of at least two of three sensory cues: visual, vestibu

338

CHAPTER 21Assessment andInterventions for thePatient with CompleteVestibular Loss

Susan J. Herdman, PT, PhD, FAPTA Richard A. Clendaniel, PT, PhD


23/43

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 pre-

vent falls even though they may sidestep or stagger occa-

sionally.

Oscillopsia

Another problem for patients with BVL is the visual blur-

ring 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 sup-

ported.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 aswould 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 pos-

tural stability because decreased visual acuity affects the

persons ability to use visual cues for stability.6

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 disap-pears 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 medica-

tions, who are already debilitated because of severe

infection. Many patients undergoing peritoneal dialysis,

for example, develop infections that are treated with gen-

tamicin, a vestibulotoxic aminoglycoside.

Assessment

The assessment of patients with BVL is similar to th

for patients with unilateral vestibular deficits; therefore

only certain aspects of the assessment are described here

Physical therapy assessment of patients with BVL mu

address the intensity of their subjective complaints, pos

tural instability, and oscillopsia, overall physical condition, and their ability to perform activities of dail

living (ADLs). This assessment must also identify othe

factors that might affect recovery, especially visual an

somatosensory deficits. A summary of the assessmen

and the usual findings for patients with BVL is presente

in Box 21-1.

History

Etiology

Bilateral loss of vestibular function can occur for severa

reasons (see Chapter 6). Most common is the effect o

an ototoxic medication such as gentamicin. Bilater

vestibular loss was once considered to be an idiosyn

cratic response to gentamicin; initial studies indicate

that less than 3% of people who received gentamici

have a vestibular deficit.7 Subsequent studies, howeve

showed that the incidence of aminoglycoside ototoxicit

ranges from 9% to 15%.810 These are most likely con

servative estimates based on relatively small studie

(fewer than 150 participants in each study) and the fac

that vestibular loss was assessed with electronystagmog

raphy. The prevalence is between 10% and 20%. I

patients who have renal impairment, are older than 6

years, are taking loop diuretics, or have previous vestibu

lar loss, it rises to 20% if they undergo renal dialysis an

receive gentamicin.

The significance of knowing the underlying etiolo

gy of the BVL lies in the accompanying problem

that the patient may have. The patient who has a sponta

neous or sequential BVL is less likely to have othe

health problems that will affect recovery than the patien

who had a severe infection and was treated with a

ototoxic medication. Furthermore, the patient who ha

a loss of vestibular function, with its resultant balanc

and visual problems, secondary to ototoxic medica

tion may also have to deal with significant anger an

depression.

Fall History

Patients with BVH are more likely to fall than norma

subjects in their age range and than patients with unila

eral vestibular hypofunction.11 It is imperative that info

Chapter 21 ASSESSMENT AND INTERVENTIONS FOR THE PATIENT WITH COMPLETE VESTIBULAR LOSS 33


24/43

340 Section FOUR REHABILITATION ASSESSMENT AND MANAGEMENT

TEST RESULTS IN PATIENTS WITH BILATERAL VESTIBULAR LOSS (BVL)

Box 21-1

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 toi-

let, preparing a simple meal, and light housekeep-

ing. 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 confi-

dence 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 com-

puterized system, remains abnormal during active

head movements in at least 25% of patients (seeChapter 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 beattempted in many patients.

Force platform: During compensated stage, anteri-

or-posterior sway should be normal or close to nor-

mal 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 per-

form with eyes closed (rapid loss of balance).

Functional Reach

May be decreased with eyes closed.

Ambulation

The patients gait is usually at least slightly wide-

based during compensated stage. There is a tenden-

cy 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


25/43

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.

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.

Subjective ComplaintsThe patients complaints of disequilibrium and oscillop-

sia 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 dis-

ability or handicap as well as the patients functional abil-

ities and problems.

Vestibular Function

One important consideration in designing a treatment

program is the presence or absence of remaining vestibu-

lar 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 amino-

glycoside antibiotics are selectively taken up by vestibu-

lar hair cells, leading to a gradual loss of vestibular

function. Typically, loss of vestibular function continue

even after the medication is stopped. Some improvemen

in vestibular function may occur if some hair cells wer

affected by the ototoxic drug but not killed. Potentially, a

increase in gain may also occur with the use of vestibula

adaptation exercises. This has been demonstrated i

patients with unilateral vestibular loss but not in patien

with BVL.16

Visual System

Assessment of visual function should include at least

gross test of visual field and a measure of visual acuity

because both can affect postural stability.6 Measurin

visual acuity during head movement is particularly impo

tant. The vestibulo-ocular system normally stabilizes th

eyes during head movements; when there is no vestibulo

ocular reflex (VOR) to stabilize the eyes during hea

movement, small amounts of retinal slip (movement o

image across the retina) will degrade vision. For instanc

a retinal slip of 3 degrees per second (deg/sec) woul

cause visual acuity to change from 20/20 to 20/200.17 A

such, in patients with no vestibular function, the hea

movement that occurs in a moving car can cause a degra

dation of visual acuity that would make driving unsafe.

Dynamic Visual Acuity

Assessment of visual acuity during head movemen

(dynamic visual acuity [DVA]) can be performed eithe

clinically or with a computerized system. The advantag

of the computerized system is that the test and result ar

standardized and more reliable.18 Clear differences i

DVA scores occur among normal subjects, those wit

dizziness from non-vestibular causes, and patients wit

known vestibular loss (Table 21-1). The results of th

computerized DVA test are both sensitive (90% for thos

older than 65 years and 97% for those younger than 6

years) and specific (94%) for vestibular loss. The clinic

DVA, however, is easy to perform and is sufficiently rel

able to be useful as a guide to treatment and its efficac

(Fig. 21.1).19

Somatosensory System

Particular attention should be paid to assessment o

vibration, proprioception, and kinesthesia in the fee

Although mild deficits in sensation in the feet ma

have no effect on postural stability in otherwise norma

individuals, but in patients with vestibular loss, somato

sensory deficits may have profound effects on balanc

and on the potential for functional recovery. As with visu

al system disorders, being aware of potentially progre



26/43

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 te

results. In the compensated stage, the Romberg result i

usually normal. Although some patients are able to per

form the Sharpened Romberg test with eyes open, thecannot do so with eyes closed. Patients with bilatera

vestibular deficits also have difficulty performing tests i

which both visual and somatosensory cues are altered

An example would be Fukudas stepping test, in whic


Table 21-1 DISTRIBUTION OF NORMAL AND ABNORMALDVA SCORES BASED ON A COMPUTERIZED SYSTEM

DVA Normal DVA Abnormal DVAType of Subject (LogMAR) Score (%) Score (%)

Normal (n 51) 0.040 0.045 96.1 3.9

Dizzy, non-vestibular (n 16) 0.097 0.099 87.5 12.5

Unilateral vestibular loss (n 53) 0.282 0.140 11.3 88.7

Bilateral vestibular loss (n 34) 0.405 0.134 0 100

DVA Dynamic Visual Acuity; LogMAR logarithm of the mminimum angle of resolution.

cDVAL(LogMAR)

cDVA Scores of Patients with Dizziness or Imbalance

BVL UVL No Vestibular Loss

1.20

1.00

0.80

0.60

0.40

0.20

0.00

Figure 21.1 Distribution of dynamic visual acuity scores (shown as the logarithm of the minimumangle 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)


27/43

the eyes are closed and the patient is marching in place.

Patients may have normal responses with eyes open dur-

ing 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 rec-

ognize 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 sta-

bility by avoiding head movements. Arm swing is simi-

larly decreased. Many patients use excessive visual fixa

tion and therefore have increased difficulty if asked t

look up while walking. Patients typically turn en bloc

and may even stop before they turn. Asking patients t

turn their heads while walking results in increased ataxi

and, often, loss of balance.

Mechanisms of RecoveryThe mechanisms used to stabilize gaze in the absence o

vestibular inputs have been well studied (Box 21-2). Th

mechanisms involved in maintaining postural stabilit

are still somewhat less well understood, althoug

research is being done in this area.

Gaze Stability

Subjects without vestibular function must develop diffe

ent mechanisms to keep the image of the target on th


Figure 21.2 Posturography test results from patients with bilateral vestibular loss demonstratingthe 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 absentTest condition 3 Vestibular, somatosensory Vision alteredTest condition 4 Vision, vestibular Somatosensory alteredTest condition 5 Vestibular Vision absent, somatosensory alteredTest condition 6 Vestibular Vision altered, somatosensory alteredResults 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 wheneither visual or somatosensory cues are altered (D).


28/43

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 prepro-

gramming has been assessed by comparing the gain of

compensatory eye movements21,22 or by comparing visu-

al acuity during predictable and unpredictable head

movements.23 The difficulty with central preprogram-

ming 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 move-

ments.21,24 Patients with complete BVL may make hypo-

metric saccades toward a visual target. Then, as the head

moves toward the target, the eyes would be moved pas-

sively 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 move-

ment pulls the eyes off the target. These strategies enable

the patient to recapture a visual target after a head move-

ment.21 Pursuit eye movements can be used during low-

frequency (and low-velocity) head movements to

stabilize the eyes. The limits of smooth-pursuit eye

movements depend on the nature of the stimulus (pre-

dictable vs. unpredictable; sinusoidal vs. constant-veloc-

ity). In general, for sinusoidal stimuli, smooth pursuit

works well at frequencies of up to 1 Hz. For constant-

velocity stimuli, smooth pursuit can work well up to

target velocities of 100 deg/sec. Later evidence demon-

strates that patients with bilateral vestibular deficits have

higher smoothpursuit gains than normal controls,

although the patients performance is still within the nor-

mal 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 direc

tion of the head movement during low-frequency, brie

head movements. The COR, therefore, complements th

VOR, although in normal subjects it is often absent and

when present, contributes at most 15% of the compensa

tory eye movement. In patients with complete BVL, th

COR operates at head movement frequencies up to 0.

Hz, well below the frequency range of head movemen

during normal activities. Therefore, although the COR

increased in patients with BVL, it does not actually oper

ate at frequencies that would contribute significantly t

gaze stability during the head movements that woul

occur during most activities.

Kasai and Zee21 found that different patients wit

complete BVL use different sets of strategies to compen

sate for the loss of VOR. Therefore, exercises to improv

gaze stability should not be designed to emphasize an

particular strategy but, instead, should provide situation

in which patients can develop their own strategies t

maintain gaze stability (see Box 21-2). No mechanism t

improve gaze stability fully compensates for the loss o

the VOR, however, and patients continue to have diff

culty seeing during rapid head movements.

Postural Stability

A study on the course of recovery of patients with com

plete bilateral vestibular deficits over a 2-year period ha

shown that patients switch the sensory cues upon whic

they rely.20 Initially they rely on visual cues as a subst

tute for the loss of vestibular cues, but over time, the

become more reliant on somatosensory cues to maintai

balance. In this study, patients were required to maintai

balance when facing a moving visual surround. Over th

2-year study, the subjects recovered the ability to main

tain balance to within normal limits in the testing para

digm except at high frequencies. The vestibular system

functions at higher frequencies than the visual o

somatosensory systems, a difference that would explai

why neither visual nor somatosensory cues can substitut

completely for loss of vestibular cues.

The contribution of somatosensory inputs from th

cervical region to postural stability in patients with com

plete BVL is not clearly understood. Bles and co

leagues27 found that changes in neck position did no

affect postural stability in patients with complete BVL

They concluded that somatosensory signals from the nec

do not contribute to postural stability. We do not know

however, whether kinesthetic signals from the neck

which would occur during head movement, affect postu

al stability. Certainly patients with bilateral vestibula


MECHANISMS USED TO

STABILIZE GAZE Change in amplitude of saccades

Use of corrective saccades

Modification of pursuit eye movements Central preprogramming of eye movements

Box 21-2


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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 dynam-

ic postural stability. Another interpretation is that such

patients rely more on visual cues to maintain postural sta-

bility, 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 pos-

tural stability in patients with BVL is also not well under-

stood. Certainly some patients depend on somatosensory

cues rather than on visual cues. Perhaps more important-

ly, 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 environ-

ments, 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 shop-

ping 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 ExerciseFacilitates Recovery

There is some evidence that experience facilitates recov-

ery after bilateral ablation of the labyrinth. Igarashi and

coworkers32 trained monkeys to run along a straight pla

form. Performance was scored by counting the number o

times the monkeys moved off the straight line. A two

stage ablation of the labyrinth was then performed. Afte

the unilateral ablation, animals given specific exercise

recovered faster than nonexercised animals, but all an

mals eventually achieved preoperative functional level

After ablation of the second labyrinth, all monkeys ha

difficulty with the platform run task. The control grou

reached preoperative balance performance levels i

81 days, whereas the exercise group did so in 62 day

This result was not significantly different owing to th

large variation in individual animals. These researcher

also measured how long the animals took to reach 8 con

secutive trial days in which they could keep their balanc

at preoperative levels. The exercise group achieved thi

criterion in 118 days. The control group took longer. On

animal took 126 days, another took 168 days, and on

animal had not achieved that criterion at 300 days. Th

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 recov

ery in bilateral and unilateral lesions, and (3) the fina

level of function may be improved if exercises are give

after bilateral lesions.

Several studies have studied the effectiveness o

vestibular exercises on postural stability during function

al activities for patients with chronic bilateral vestibula

deficits. Krebs and colleagues,1 in a double-blinded

placebo-controlled trial, found that the patients perform

ing customized vestibular and balance exercises had be

ter stability while walking and during stair climbing tha

patients performing isometric and conditioning exercise

such as using an exercise bicycle. Furthermore, th

patients who had vestibular rehabilitation were able t

walk faster. They used vestibular adaptation and eye-hea

exercises as well as balance and gait training. In a con

tinuation of this study, Krebs and colleagues4 agai

demonstrated that as a group, those individuals perform

ing the vestibular rehabilitation exercises had increase

gait velocity, improved stability while walking, an

decreased vertical excursion of the center of mass whil

walking. They noted a moderate correlation betwee

improved gait measures at 1 year and the frequency o

performing the home exercise program over the preced

ing 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 significan

improvements in gait.

In a retrospective chart review of 13 patients wit

BVL, Brown and associates3 noted that as a group, th



30/43

patients had significant improvements in various meas-

ures (Dizziness Handicap Inventory, Activities-specific

Balance Confidence Scale, Dynamic Gait Index, Timed

Up and Go test, and Sensory Organization Test com-

ponent 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 dif-

ferent measures. In another retrospective study, Gillespie

and Minor2 found that 63% of the patients with BVL who

received vestibular rehabilitation demonstrated improve-

ments (defined as reported increased activity levels,

reduced symptoms, and demonstrated normal gait veloc-

ity, 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 improve-

ment3 (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.

TreatmentThe 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

remaining vestibular function may benefit from vestibu

lar adaptation exercises to enhance remaining vestibula

function (Fig. 21.3, page 347). For both groups, postura

stability can be improved by fostering the use of visua

and somatosensory cues. This approach is also used i

the treatment of patients unilateral with vestibular hypo

function (see Box 21-4).

Once the patients specific problems have bee

identified, the exercise program can be established

During the initial sessions, particular attention should b

paid to the extent to which the exercises increase th

patients complaints of dizziness. The patients percep

tion of dizziness can be the major deterrent (limiting fac

tor) to his or her eventual return to normal activitie

Head movement, a component of all exercises, increase

that dizziness. Also, the home exercise program typicall

requires that the patient perform exercises many time

daily. Patients may find that they become increasingl

dizzy with each performance of the exercises; the Hea

Movement VAS can be used to quantify this problem

Additionally, inability of the patient to sustain hea

movement for 1 minute helps define the initial exercis

program.

It is important to explain to the patient that som

increase in dizziness is expected at the beginning of th

exercise program and with any increase in the intensit

of the exercises. Only one exercise involving head move

ment should be prescribed initially. Other exercises ca

be added and the frequency and duration of the exercise

can be increased as the patient improves. The patien

should perform at least one set of all the exercises at th

time of the clinic visit. Patients should also be taught ho

to modify the exercises if the dizziness becomes over

whelming (Box 21-5, page 347). They should be strong

ly encouraged to contact the therapist if they are havin

difficulty. In patients for whom dizziness continues to b

a problem, we suggest meditation and relaxation tech

niques to try to reduce the effect of the dizziness on th

patients life.

Progression of Exercises

The reported number and frequency of patient visits t

the clinic varies tremendously from study to study

Improvement in patients undergoing vestibular rehabil

tation has been reported when patients were seen once

day for 3 days38, two or three times a week for month

once a week for 4 or 5 weeks,34,35,38, once a month,3,39-

or even once in several months.42,43 It is difficult to dete

mine appropriate practice patterns by comparing thes

studies, however, because different exercise approache



31/43


PATIENT INSTRUCTIONS FOR EXERCISES TO IMPROVE GAZE STABILITY

Box 21-3

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 cor-rective saccades, he or she should slow the head

movement down.

2. Active eye-head movements between two hori-

zontal targets to foster the use of saccadic or pur-

suit 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, butalways 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.

T

vestibular rehab in short

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