1. Copyright 2007 by F. A. Davis.

2. VestibularRehabilitationT H I R D E D I T I O NCopyright 2007 by F. A. Davis. 3. Copyright 2007 by F. A. Davis.Steven L. Wolf, PT, PhD, FAPTA, Editor-in-ChiefVestibular Rehabilitation, 3rd EditionSusan J. Herdman, PT, PhD, FAPTAPharmacology in Rehabilitation, 4th EditionCharles D. Ciccone, PT, PhDModalities for Therapeutic Intervention, 4th EditionSusan L. Michlovitz, PT, PhD, CHT and Thomas P. Nolan, Jr., PT, MS, OCSFundamentals of Musculoskeletal Imaging, 2nd EditionLynn N. McKinnis, PT, OCSWound Healing: Alternatives in Management, 3rd EditionLuther C. Kloth, PT, MS, CWS, FAPTA, andJoseph M. McCulloch, PT, PhD, CWS, FAPTAEvaluation and Treatment of the Shoulder:An Integration of the Guide to Physical Therapist PracticeBrian J. Tovin, PT, MMSc, SCS, ATC, FAAOMPT andBruce H. Greenfield, PT, PhD, OCSCardiopulmonary Rehabilitation: Basic Theory and Application, 3rd EditionFrances J. Brannon, PhD, Margaret W. Foley, RN, MN,Julie Ann Starr, PT, MS, CCS, and Lauren M. Saul, MSN, CCRNFor more information on each titlein the Contemporary Perspectives in Rehabilitation series, go towww.fadavis.com. 4. VestibularRehabilitationT H I R D E D I T I O NSusan J. Herdman, PT, PhD, FAPTAProfessor, Departments of RehabilitationMedicine and Otolaryngology Head and Neck SurgeryDirector, Division of Physical TherapyEmory UniversityAtlanta, GeorgiaCopyright 2007 by F. A. Davis. 5. Copyright 2007 by F. A. Davis.F. A. Davis Company1915 Arch StreetPhiladelphia, PA 19103www.fadavis.comCopyright 2007 by F. A. Davis CompanyCopyright 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 AmericaLast digit indicates print number: 10 9 8 7 6 5 4 3 2 1Publisher: Margaret M. BiblisManager, Content Development: Deborah J. ThorpDevelopmental Editor: Jennifer A. PineArt and Design Manager: Carolyn OBrienAs new scientific information becomes available through basic and clinical research, recommended treatmentsand drug threrapies undergo changes. The author and publisher have done everything possible to make thisbook 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, andmake no warranty, expressed or implied, in regard to the contents of the book. Any practice described in thisbook should be applied by the reader in accordance with professional standards of care used in regard to theunique circumstances that may apply in each situation. The reader is advised always to check productinformation (package inserts) for changes and new information regarding dose and contraindications beforeadministering any drug. Caution is especially urged when using new or infrequently ordered drugs.Library of Congress Cataloging-in-Publication DataVestibular rehabilitation / [edited by] Susan J. Herdman. 3rd ed.p. ; cm. (Contemporary perspectives in rehabilitation)Includes bibliographical references and index.ISBN-13: 978-0-8036-1376-8ISBN-10: 0-8036-1376-81. Vestibular apparatusDiseasesPatientsRehabilitation. I. Herdman, Susan.[DNLM: 1. Vestibular Diseasesrehabilitation. WV 255 V5836 2007]RF260.V4725 2007617.882dc22 2007007436Authorization 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 RosewoodDrive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, aseparate system of payment has been arranged. The fee code for users of the Transactional Reporting Serviceis: 8036-1376/07 0 + $.10 6. DedicationI would like to dedicate this edition ofVestibular Rehabilitation to my family.I love you all very much.Copyright 2007 by F. A. Davis. 7. viiForewordBaseball has always been my passion. I played the sportfrom the time I could walk all the way through college. Ialways thought one could learn a lot about life from par-ticipatingand from observing the game.teamwork,responsibility, strategy and so on. In that context and forreasons far transcending the purpose of this book, Iadopted the Boston Red Sox as my team. Through cir-cumstancesfar more surreal than circumstantial, I wasinterviewed by Weekend America, a National PublicRadio show the day after the Red Sox miraculous come-backagainst the New York Yankees to win the AmericanLeague title in 2004. The interview was taped on Thurs-day,October 21 two days before the first game of theWorld Series in which my team defeated the St. LouisCardinals in four consecutive games, and aired immedi-atelybefore the first game. During the interview, BillRadke asked if the Red Sox could win the Series (athought that any self-respecting Sox fan would nevercontemplate after 86 barren years filled with countlessfrustrations) and win or lose, if I thought the team play-erswould all be back the following year to start their owndynasty. To the latter question I responded that I doubtedthe possibility since in contemporary sports the notion ofteam loyalties and perpetuation of excellence amongst acohesive unit was easily supplicated by the lure of morelucrative promises from rival baseball clubs.So what does this stream of consciousness have todo with the third edition of Vestibular Rehabilitation?These thoughts about this radio interview crept into mymind as I was reviewing Susan Herdmans third edition.Here is a text already filled with contributions from cli-niciansand researchers acknowledged as superstars inthis field. Each of these individuals is already quite busyand well in demand for other academic and intellectualopportunities. Yet rather than abandoning the team, Dr.Herdman has strengthened it further and moreover hasrevised the line up to field an even stronger team thatwill have even greater appeal to the fans. Hence at atime when star quality seeks autonomy at the sacrifice ofteam congruity, the exact opposite has occurred forVestibular Rehabilitation, Third Edition.Dr. Herdman has painstakingly adhered to the prin-ciplesof the Contemporary Perspectives in Rehabilita-tionSeries by assuring that each contributor has updatedreferences and has, when appropriate, challenged thereaders critical thinking skills. The text is written forany specialist in vestibular rehabilitation or any studentor clinician aspiring to become one. While already estab-lishedas the gold standard for the assessment and man-agementof patients with vestibular disorders, this thirdedition takes off from where the second edition has left.There are four new chapters and several others have beenrevamped considerably. The four new additions to thisalready comprehensive text include: a chapter (12) byRonald Tusa on Migraine, Mnires Disease and MotionSickness that represents a considerable expansion fromhis chapter on migraine in the second edition and distin-guishesthese three problem areas and their medical man-agement;a chapter (13) by Timothy Hain and JanetHelminski on Mal de Dbarquement Disorder, a problemthat has received increasing attention since the secondedition of this book and now includes guidelines fortreatment and indications that physical therapy may beinappropriate in the treatment of this disorder; a chapter(18) on Compensatory Strategies for the Treatment ofVestibulo-Ocular Hypofunction by Michael Schubert thatoffers new information on compensatory mechanismsused by patients undergoing vestibular rehabilitation; anda chapter (26) by Ronald Tusa on Non-vestibular Dizzi-nessand Imbalance that uniquely addresses lesions notdirectly implicated in the central vestibular pathways,including disuse disequilibrium, spino-cerebellar ataxia,leukoaraiosis, and normal pressure hydrocephalus. In factthe last 5 chapters of the third edition are grouped toemphasize assessment and management of disorderseither within or external to the central vestibular path-waysor in the treatment of non-vestibular dizziness.Moreover in addition to adding several new contrib-utorsincluding 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 presenta-Copyright 2007 by F. A. Davis. 8. Copyright 2007 by F. A. Davis.tion on quantification of vestibular function tests andclinical examination into two exciting chapters presentedfrom the physicians perspective on History and Clini-calExamination (7) and Vestibular Function Tests (8).The chapter (24) by Helen Cohen on disability nowapproaches the concept in a diagnosis specific manner.Perhaps the most dominating impression createdfrom this unique team is deriving a realization that con-tributionsfrom vestibular neurorehabilitation therapistsand specialty physicians blend almost seamlessly into acontinuum of fact pointed toward a comprehensiveunderstanding of the assessment and management ofpatients with vestibular disorders. In fact, one gets theimpression that the content of this book could haveeasily been extracted from dialogue amongst these inter-disciplinaryspecialists at a symposium or workshop.While students new to this topic might not appreciate thevalue of such a constellation of knowledgeable profes-sionals,those clinicians familiar with many of theseauthors and their contributions to vestibular rehabilitationwill recognize that within these hard covers lie contentthe sum of whose parts far exceeds the whole.Steven L. Wolf, Ph.D., PT, FAPTA, FAHASeries Editorviii FOREWORD 9. ixCopyright 2007 by F. A. Davis.The 3rd edition of Vestibular Rehabilitation! I neverexpected that the little black book published in 1994would have multiple editions, much less that we would(or even could) provide a CD with the book to augmentthe written word with videos of patients. These videoshave been chosen to provide the reader with examples ofboth normal and abnormal clinical tests, with visualexamples of some of the exercises used in the treatmentof BPPV and of vestibular hypofunction, and with exam-plesof non-vestibular oculomotor and gait signs thatshould help with differential diagnosis. As I reviewed amultitude of video clips of patients we made over the past20 years, I found that I remembered these people andtheir individual personalities and problems. What a won-derfulexperience this has been and how thankful I am foreverything they taught me. If I had only one person tothank, it would be the accumulation of all these people.Once again, we have extended the material present-edto include several new chapters and have augmentedthe material presented in all the chapters to reflectchanges in our understanding of management of vestibu-lardisorders. The new chapters include management ofpersons with mal de dbarquement syndrome, and per-sonswith dizziness that is unrelated to the vestibular sys-temPrefacesuch as disuse disequilibrium and central disorders.The third new chapter presents new information aboutthe mechanisms that underlie compensation for vestibu-larhypofunction. In addition to these new chapters, thereare a number of new topics presented within differentchapters such as differential diagnosis in BPPV to identi-fydisorders that mimic BPPV, differentiation amongMnires, migraine, and motion sensitivity, and the roleof chemical labyrinthectomy in the management ofepisodic vertigo.Another shift you will find in the book, as well as inmany clinical studies, is an increasing use of functionalmeasures, rather than impairment measures, to assessoutcome of rehabilitation. Of great value is the Interna-tionalClassification of Functioning, Disability andHealth (ICF) scheme (World Health Organization 2001.http://www.cdc.gov.hchs/about/otheract/ic99/icfhome.htm). The ICF provides a framework for the descriptionof health-related states and includes both positive expe-riencesand negative consequences of disease. It consistsof three domains that can be used to describe the effect ofdifferent disorders or diseases on a persons health, witha number of environmental and personal contextual fac-torsthat may affect each of those domains (Table below). HEALTH CONDITION DISORDER OR DISEASENormal Function and Structure Activities ParticipationVersus Versus VersusImpairment (body level) Limitations (individual level) Restriction (societal level)Contextual FactorsEnvironmental Factors Personal Factorse.g. Natural environment e.g. Gender, ageSupport and relationships Co-morbiditiesAttitude of family Social backgroundAttitude of society Education and professionServices, systems, policies Past experienceProducts and technology Coping style 10. Copyright 2007 by F. A. Davis.Because it provides a more comprehensive depic-tionof the health of an individual, the ICF model shiftsthe emphasis away from impairment and disability to amore balanced perspective.Finally, we have tried, as in the other editions ofVestibular Rehabilitation, to provide you with an updateon evidence that supports our practice. There is anincreasing body of research that support different exer-ciseapproaches as appropriate and successful tools in themanagement of patients with vestibular dysfunction. Thenumber of blinded, randomized clinical trials is growingand they provide compelling evidence that we are effec-tivelyimproving outcome in these patients. Some studiesoffer guidance in how certain treatment can be modifiedto simplify treatment for the patient. Still other studiesexplore the extent of recovery that can be achieved. Somestudies offer insight into new methods for identifying thenature of the vestibular dysfunction such as involvementof the utricle and saccule. I expect that in the next 5 to 10years there will be another great leap in our knowledgeand we will have several additional rehabilitationapproaches. Researchers are exploring the use of tech-niquessuch as virtual reality, sensory substitutiondevices, vestibular implants, and methods to induce haircells regeneration. These techniques are not ready yet butthe next edition of this book may be filled with wonder-fulnew ways to help people with vestibular disorders.Susan J. Herdman, PT, PhD, FAPTAEditorx PREFACE 11. xiAnnamarie Asher, PTClinical Education CoordinatorPhysical Therapy DivisionPhysical Medicine and RehabilitationDepartmentUniversity of Michigan Health SystemAnn Arbor, MichiganThomas Brandt, MD, FRCPDepartment of NeurologyKlinikum GrosshadernUniversity of MunichMunich, GermanyRichard A. Clendaniel, PT, PhDAssistant ProfessorDoctor of Physical Therapy ProgramDepartment of Community and FamilyMedicineDuke University Medical CenterDurham, North CarolinaHelen Cohen, EdD, OTA, FAOTAAssociate ProfessorDepartment of OtorhinolaryngologyBaylor College of MedicineHouston, TexasIan S. Curthoys, PhDProfessor of Vestibular FunctionSchool of PsychologyUniversity of SydneySydney, AustraliaMarianne Dieterich, MDDepartment of NeurologyJohannes Gutenberg University ofMainzMainz, GermanyContributorsMichael Fetter, MDDepartment of Neurology IIKlinikum Karlsbad-LangensteinbachKarlsbad, GermanyTimothy C. Hain, MDAssociate ProfessorDepartment of Physical Therapy andMovement SciencesNorthwestern UniversityChicago, IllinoisG. Michael Halmagyi, MDDepartment of NeurologyRoyal Prince Alfred HospitalCamperdown, AustraliaJanet O. Helminski, PT, PhDAssociate ProfessorPhysical Therapy ProgramMidwestern UniversityDowners Grove, IllinoisFay B. Horak, PT, PhDSenior Scientist and Research FacultyNeuroscience Graduate ProgramR.S. Dow Neurological Sciences InstituteOregon Health and Science UniversityPortland, OregonEmily A. Keshner, PT, EdDProfessor and ChairDepartment of Physical TherapyTemple UniversityPhiladelphia, PennsylvaniaRobert Landel, PT, DPT, OCSAssociate ProfessorDepartment of Biokinesiology andPhysical TherapyUniversity Southern CaliforniaLos Angeles, CaliforniaR. John Leigh, MDProfessorDepartment of NeurologyCase Western Reserve UniversityDirectorOcular Motility LaboratoryCleveland VA Medical CenterCleveland, OhioGregory F. Marchetti, PT, PhDAssistant ProfessorDepartment of Physical TherapyDuquesne UniversityPittsburgh, PennsylvaniaDouglas E. Mattox, MDProfessor and ChairDepartment of Otolaryngology-HeadNeck SurgeryEmory University School of MedicineAtlanta, GeorgiaSharon Polensek, MD, PhDAssistant ProfessorDepartment of NeurologyEmory University School of MedicineNeurologistDizziness and Balance CenterCenter for Rehabilitation MedicineAtlanta, GeorgiaRose Marie Rine, PT, PhDAssociate ProfessorUniversity of North FloridaJacksonville, FloridaMichael C. Schubert, PT, PhDAssistant ProfessorDepartment of Otolaryngology-Head and Neck SurgeryJohns Hopkins School of MedicineBaltimore, MarylandCopyright 2007 by F. A. Davis. 12. Copyright 2007 by F. A. Davis.Neil T. Shepard, PhDProfessor of AudiologyDepartment of Special Education andCommunications DisordersUniversity of Nebraska LincolnLincoln, NebraskaAnne Shumway-Cook, PT, PhD,FAPTAProfessorDivision of Physical TherapyDepartment of Rehabilitation MedicineUniversity of WashingtonPhysical TherapistSeattle, WashingtonRonald J. Tusa, MD, PhD, NCS, ATCProfessorDepartments of Neurology andOtolaryngology Head and NeckSurgeryDirectorDizziness and Balance CenterCenter for Rehabilitation MedicineEmory University School of MedicineAtlanta, GeorgiaSusan L. Whitney, PT, PhD, NCS, ATCAssociate ProfessorDepartments of Physical Therapy andOtolaryngologyUniversity of PittsburghPittsburgh, PennsylvaniaDavid S. Zee, MDProfessorDepartment of NeurologyJohns Hopkins UniversityBaltimore, Maryland**Series Editor**Steven L. Wolf, PhD, PT, FAPTA,FAHAProfessor, MedicineProfessor, Rehabilitation MedicineEmory University School of MedicineCenter for Rehabilitation MedicineAtlanta, Georgiaxii CONTRIBUTORS 13. xiiiCheryl D. Ford-Smith, MS, PT, NCSAssistant ProfessorDepartment of Physical TherapyVirginia Commonwealth UniversityRichmond, VirginiaJames Megna, PT, NCSCoordinatorBalance and Vestibular Rehabilitation ClinicSouthside HospitalBay Shore, New YorkReviewersGail F. Metzger, BS, MS, OTR/LSenior Occupational Therapist &Assistant ProfessorDepartment of Occupational TherapyAlvernia CollegeReading, PennsylvaniaRoberta A. Newton, PT, PhDProfessor & Associate DirectorPhysical Therapy DepartmentTemple UniversityPhiladelphia, PennsylvaniaCopyright 2007 by F. A. Davis. 14. AcknowledgmentsI would like to express my gratitude to the wonderful col-leaguesI have worked with in the clinic. Over my yearsas a physical therapist, they have honed my skills, chal-lengedmy assumptions, contributed to my researchand made me a better clinician. So my thanks go to RonTusa, Courtney Hall, Lisa Gillig, Tim Hain, John Leigh,David Zee, Doug Mattox, Rick Clendaniel, and MichaelSchubert.I also want to thank the authors of this edition ofVestibular Rehabilitation. They have contributed theirconsiderable knowledge and perspectives so we can alllearn how best to help the dizzy patient. As a result,many more clinicians will become familiar with the prob-lemsand management of vestibular disorders and many,xvmany more patients will receive appropriate treatment.Copyright 2007 by F. A. Davis. 15. Contents in BriefSECTION ONEFundamentals 1CHAPTER 1 Anatomy and Physiology of the NormalxviVestibular System 2Timothy C. Hain, MDJanet O. Helminski, PT, PhDCHAPTER 2 Vestibular Adaptation 19David S. Zee, MDCHAPTER 3 Role of the Vestibular System inPostural Control 32Fay B. Horak, PT, PhDCHAPTER 4 Postural Abnormalities inVestibular Disorders 54Emily A. Keshner, PT, EdDCHAPTER 5 Vestibular Compensation: ClinicalChanges in Vestibular Functionwith Time after UnilateralVestibular Loss 76Ian S. Curthoys, PhD andG. Michael Halmagyi, MDCHAPTER 6 Vestibular System Disorders 98Michael Fetter, MDSECTION TWOMedical Assessment andVestibular Function Tests 107CHAPTER 7 History and ClinicalExamination 108Ronald J. Tusa, MD, PhDCHAPTER 8 Vestibular Function Tests 125Ronald J. Tusa, MD, PhDCHAPTER 9 Otolith Function Tests 144G. Michael Halmagyi, MD andIan S. Curthoys, PhDCHAPTER 10 Auditory Examination 162Sharon Polensek, MD, PhDSECTION THREEMedical and SurgicalManagement 177CHAPTER 11 Pharmacological and OpticalMethods of Treatment for VestibularDisorders and Nystagmus 178R. John Leigh, MDCHAPTER 12 Migraine, Mnires and MotionSensitivity 188Ronald J. Tusa, MD, PhDCHAPTER 13 Therapy for Mal deDbarquement Syndrome 202Timothy C. Hain, MDJanet O. Helminski, PT, PhDCHAPTER 14 Surgical Management of VestibularDisorders 205Douglas E. Mattox, MDCHAPTER 15 Psychological Problems andthe Dizzy Patient 214Ronald J. Tusa, MD, PhDCopyright 2007 by F. A. Davis. 16. CONTENTS IN BRIEF xviiSECTION FOURRehabilitation Assessment andManagement 227CHAPTER 16 Physical Therapy Diagnosis forVestibular Disorders 228Susan J. Herdman, PT, PhD, FAPTACHAPTER 17 Physical Therapy Management ofBenign Positional Vertigo 233Susan J. Herdman, PT, PhD, FAPTARonald J. Tusa, MD, PhDAppendix 17A-DifferentialDiagnosis: Mimicking BPPV 261Ronald J. Tusa, MD, PhDCHAPTER 18 Compensatory Strategiesfor Vestibulo-OcularHypofunction 265Michael C. Schubert, PT, PhDCHAPTER 19 Physical Therapy Assessment ofVestibular Hypofunction 272Susan L. Whitney, PT, PhD, NCS, ATCSusan J. Herdman, PT, PhD, FAPTAAppendix 19A EvaluationForm 300Appendix 19B Dizziness HandicapInventory 307CHAPTER 20 Interventions for the Patientwith Vestibular Hypofunction 309Susan J. Herdman, PT, PhD, FAPTASusan L. Whitney, PT, PhD, NCS, ATCCHAPTER 21 Assessment and Interventionsfor the Patient with CompleteVestibular Loss 338Susan J. Herdman, PT, PhD, FAPTARichard A. Clendaniel, PT, PhDCHAPTER 22 Management of the Pediatric Patientwith Vestibular Hypofunction 360Rose Marie Rine, PT, PhDCHAPTER 23 Management of the Elderly Personwith Vestibular Hypofunction 376Susan L. Whitney, PT, PhD, NCS, ATCGregory F. Marchetti, PT, PhDCHAPTER 24 Disability in VestibularDisorders 398Helen S. Cohen, OTR, EdD, FAOTACHAPTER 25 Assessment and Managementof Disorders Affecting CentralVestibular Pathways 409Marianne Dieterich, MDThomas Brandt, MD, FRCPCHAPTER 26 Non-vestibular Dizziness andImbalance: From DisuseDisequilibrium to CentralDegenerative Disorders 433Ronald J. Tusa, MD, PhDCHAPTER 27 Assessment and Managementof the Patient with TraumaticBrain Injury and VestibularDysfunction 444Anne Shumway-Cook, PT, PhD, FAPTACHAPTER 28 Non-vestibular Dizziness andImbalance: Suggestions forPatients with Migraine andMal de Dbarquement 458Neil T. Shepard, PhDAnnamarie Asher, PTCHAPTER 29 Non-vestibular Diagnosisand Imbalance: CervicogenicDizziness 467Richard A. Clendaniel, PT, PhDRobert Landel, PT, DPT, OCSAppendix A Questionnaire forHistory and Examination 485Index 493Copyright 2007 by F. A. Davis. 17. SECTION ONEFundamentals 1CHAPTER 1 Anatomy and Physiology of thexviiiNormal Vestibular System 2Timothy C. Hain, MDJanet O. Helminski, PT, PhDPurpose of the Vestibular System 2The Peripheral Sensory Apparatus 3Bony Labyrinth 3Membranous Labyrinth 3Hair Cells 4Vascular Supply 4Physiology of the Periphery 5Semicircular Canals 6Otoliths 7The Vestibular Nerve 7Central Processing of Vestibular Input 8Vestibular Nucleus 9Vascular Supply 9Cerebellum 10Neural Integrator 10Motor Output of the VestibularSystem Neurons 10Output for the Vestibulo-ocular Reflex 10Output for the Vestibulospinal Reflex 10Vestibular Reflexes 11The Vestibulo-ocular Reflex 11The Vestibulospinal Reflex 12The Vestibulocollic Reflex 12Cervical Reflexes 12The Cervico-ocular Reflex 12The Cervicospinal Reflex 12The Cervicocollic Reflex 12Visual Reflexes 13Somatosensory Reflexes 13Neurophysiology of Benign Paroxysmal PositionalVertigo 13Higher-Level Vestibular Processing 14Velocity Storage 14Estimation: Going Beyond Reflexes 15Higher-Level Problems of theVestibular System 16Compensation for Overload 16Sensor Ambiguity 16Motion Sickness 16Repair 17Summary 18CHAPTER 2 Vestibular Adaptation 19David S. Zee, MDRecalibration, Substitution,and Alternative Strategies 19Compensation after UnilateralLabyrinthectomy 20Bilateral Vestibular Loss 23Experimental Results in NonhumanPrimates 23Studies of Vestibulo-ocular Reflex Adaptationin Normal Subjects 24Imagination and Effort of Spatial 00Localization in Vestibular Adaptation 25Context Specificity 26Neurophysiologic Substrateof Vestibulo-ocular Reflex Adaptation 26Summary 27CHAPTER 3 Role of the Vestibular System inPostural Control 32Fay B. Horak, PT, PhDSensing and Perceiving Position and Motion 33Orienting the Body to Vertical 34Postural Alignment 34Weighting Sensory Information 36Controlling Center of Body Mass 40Role in Automatic Postural Responses 41Stabilizing the Head and Trunk 46Summary 47ContentsCopyright 2007 by F. A. Davis. 18. CONTENTS xixCHAPTER 4 Postural Abnormalities inVestibular Disorders 54Emily A. Keshner, PT, EdDExamining the Vestibulospinal System 55Advantages and Limitations of Clinical Tests 55Dynamic Posturography 55Tests of Quiet Stance 58Stabilometry 58Tiltboards 59Stepping Tests 59Virtual Reality Environments 59Postural Reactions in Peripheral VestibularDisorders 59Deficient Labyrinthine Inputs 60Indicators of VestibulospinalDeficiency 61Indications of VestibulospinalDistortion 63Postural Reactions in Central VestibularLesions 63Postural Dysfunction with Disorder ofOther Sensory-Motor Centers 64Mechanisms for Recovery of Postural Stability 66Sensory Substitution 66Compensatory Processes 67Summary 70CHAPTER 5 Vestibular Compensation: ClinicalChanges in Vestibular Functionwith Time after UnilateralVestibular Loss 76Ian S. Curthoys, PhD andG. Michael Halmagyi, MDOverview 77Causes 77The uVD Syndrome 79Static Symptoms 79Dynamic Symptoms 81Sensory Components 84Clinical Evidence Concerning Factors Affectingthe uVD Syndrome and VestibularCompensation 84Decompensation 87Psychological Factors 87Medication 88Plasticity of the Vestibulo-Ocular Reflex 89Rehabilitation 89Neural Evidence Concerning Recovery after UnilateralVestibular Deafferentation 89Angular versus Linear Acceleration 92Cerebellum 92Neural Network Models of Vestibular Functionand Compensation 92Summary 93Acknowledgments 93CHAPTER 6 Vestibular System Disorders 98Michael Fetter, MDBenign Paroxysmal Positional Vertigo 98Vestibular Neuritis 98Mnires Disease and EndolymphaticHydrops 100Perilymphatic Fistula 102Vestibular Paroxysmia(Disabling Positional Vertigo) 103Bilateral Vestibular Disorders 103Summary 104SECTION TWOMedical Assessment andVestibular Function Tests 107CHAPTER 7 History and ClinicalExamination 108Ronald J. Tusa, MD, PhDHistory 108Elements that Help with the Diagnosis 108Elements that Lead to Goals for Management,Including Physical Therapy 112Physical Examination 113Spontaneous Nystagmus 113Skew Eye Deviation 116Vestibular-Ocular Reflex 116Maneuver-Induced Vertigo and EyeMovements 118Visual Tracking 120Stance and Gait 122CHAPTER 8 Vestibular Function Tests 125Ronald J. Tusa, MD, PhDTests that Specifically Assess Labyrinth orVestibular Nerve 125Caloric Test 125Rotary Chair Testing 127Quantified Dynamic Visual Acuity 131Strengths of Test 132Weaknesses of Test 132Copyright 2007 by F. A. Davis. 19. xx CONTENTSVestibular Evoked Myogenic Potential Test 132Subjective Visual Vertical Test 133Tests That Do Not Specifically Assess Labyrinth orVestibular Nerve 134Visual Tracking 134Computerized Dynamic Posturography 134Summary 142CHAPTER 9 Otolith Function Tests 144G. Michael Halmagyi, MD andIan S. Curthoys, PhDOtolith Structure 144Otolith Function 146Primary Otolithic Afferents 146Central Projections 146Function of Otolithic Input 147Subjective Visual Horizontal or Vertical Testing ofOtolith Function 147Peripheral Vestibular Lesions 147Central Vestibular Lesions and Settings of theSubjective Visual Vertical 149Clinical Significance 149Vestibular Evoked Myogenic Potential Testing ofOtolith Function 150Physiological Background 150Method 151Clinical Applications 152Comment 159Summary 159Acknowledgments 159CHAPTER 10 Auditory Examination 162Sharon Polensek, MD, PhDHistory and Physical Examination 162Audiological Evaluation and Management 163Evaluative Procedures 163Audiological Management 169Medical Testing in the Evaluation of HearingLoss 170Laboratory Testing 170Radiological Imaging 170Clinical Presentations of Auditory Impairment 170Sudden Sensorineural Hearing Loss 170Hearing Loss from Infectious Disease 171Pharmacological Toxicity 171Surgical Management of Hearing Loss 172Cochlear Implants 172Cerebellopontine Angle Tumors 174Superior Semicircular Canal Dehiscence 174Perilymphatic Fistula 174Other Causes of Hearing Loss 175Summary 175SECTION THREEMedical and SurgicalManagement 177CHAPTER 11 Pharmacological and OpticalMethods of Treatment for VestibularDisorders and Nystagmus 178R. John Leigh, MDVertigo 178Pathophysiology of Vertigo 178Neuropharmacology of Vertigo andNystagmus 180Treatment of Vertigo 180Oscillopsia 182Pathogenesis 182Treatment of Oscillopsia 183Nystagmus and its Visual Consequences 183Pathogenesis 183Treatments 183Summary 186Acknowledgments 186CHAPTER 12 Migraine, Mnires and MotionSensitivity 188Ronald J. Tusa, MD, PhDIncidence of Migraine 188Symptoms of Migraine 188Case Example 188Symptoms during Vestibular Migraine Aura 189Classification and Criteria for Diagnosis 189Migraine 189Disorders Associated with Migraine 192Pathophysiology of Migraine 192Dopamine D2 Receptor 192Calcium Channel Receptor (CACNA1A) 193Noradrenergic System 193Serotonin 5HT1 Receptor and the HeadachePhase 193Management 193Treatment of Vestibular Migraine 193Prophylactic Medical Therapy 194Abortive Medical Therapy 196Migraine versus Mnires Disease 197Summary 200Patient Information 200Copyright 2007 by F. A. Davis. 20. CONTENTS xxiCHAPTER 13 Therapy for Mal deDbarquement Syndrome 202Timothy C. Hain, MDJanet O. Helminski, PT, PhDCause of the Syndrome: Persistent Adaptation toSwaying Environments? 202Treatment 203Summary 204CHAPTER 14 Surgical Management of VestibularDisorders 205Douglas E. Mattox, MDAcoustic Neuromas(Vestibular Schwannomas) 205Surgical Approaches 206Middle Cranial Fossa 206Translabyrinthine Approach 206Suboccipital Craniectomy 207Complications 208Stereotactic Radiosurgery 208Mnires Disease 208Surgical Management of Mnires Disease 209Chemical Labyrinthectomy 209Post-Traumatic Vertigo 211Benign Paroxysmal Positional Vertigo 211Perilymphatic Fistula 211Vascular Loops 212Summary 213CHAPTER 15 Psychological Problems andthe Dizzy Patient 214Ronald J. Tusa, MD, PhDPsychological Disorders and TheirPrevalence 214Dizziness in Patients with PsychologicalDisorders 214Psychological Problems in Patients withDizziness 215Assessment 216Scales 216Clinical Examination 218Examination for Psychogenic Stance andGait Disorders 218Dynamic Posturography 219Psychological Disorders 219Anxiety 219Mood Disorders 219Somatoform Disorders 220Factitious and Malingering Disorders 221Management 221Medications 222Summary 226SECTION FOURRehabilitation Assessment andManagement 227CHAPTER 16 Physical Therapy Diagnosis forVestibular Disorders 228Susan J. Herdman, PT, PhD, FAPTAPhysical Therapy Diagnosis and the InternationalClassification of Functioning, Disability,and Health Model of Diasablement 228History 229Clinical Examination 229Diagnostic Flowchart 230Identification of Modifiers 231Summary 232CHAPTER 17 Physical Therapy Management ofBenign Positional Vertigo 233Susan J. Herdman, PT, PhD, FAPTARonald J. Tusa, MD, PhDCharacteristics and History 233Mechanism 233Semicircular Canal Involvement 234Diagnosis 235Dix-Hallpike Test 236Side-Lying Test 237Roll Test 237Test Series 237Treatment 238Treatment of the Most Common Form of BPPV:Posterior Canal Canalithiasis 238Treatment of Posterior Canal BPPV:Cupulolithiasis 245Variations in SCC Involvement 248Algorithm for Treatment of BPPV 251Evidence-Based Practice 251Quality of Available Evidence to Use RepositioningManeuvers to Treat BPPV 251Quality of Available Evidence to Usethe Liberatory Maneuver to Treat BPPV 252Quality of Available Evidence to UseBrandt-Daroff Habituation Exercisesto Treat BPPV 253Managing Persistent Imbalance in Patientswith BPPV 254Copyright 2007 by F. A. Davis. 21. xxii CONTENTSContraindications to the Assessment andTreatment of BPPV 255Unraveling Complicated Cases 256Summary 259APPENDIX 17A Differential Diagnosis:Mimicking BPPV 261Ronald J. Tusa, MD, PhDCentral Positional Vertigo with Nystagmus 261Episodic Signs and Symptoms (Benign) 261Persistent Signs and Symptoms(Pathological) 261Central Positional Nystagmus withoutVertigo 261CPN Present Only When Patient Is Supine(Benign) 261CPN Present When Patient Is Supine and WhenSitting (Pathological) 262Peripheral Positional Vertigo with Nystagmus OtherThan BPPV 262Pressure-Induced Disorders 262Positional Dizziness without Nystagmus 263Orthostatic Hypotension 263Head Extension Dizziness and Extreme RotationDizziness 263CHAPTER 18 Compensatory Strategiesfor Vestibulo-OcularHypofunction 265Michael C. Schubert, PT, PhDNormal Vestibulo-Ocular Reflex 265Abnormal Vestibulo-Ocular Reflex 265Compensatory Strategies 265Saccadic Modifications 267Cervico-Ocular Reflex 267Effects of Prediction 268Enhanced Smooth Pursuit 270Summary 270CHAPTER 19 Physical Therapy Assessment ofVestibular Hypofunction 272Susan L. Whitney, PT, PhD, NCS, ATCSusan J. Herdman, PT, PhD, FAPTANormal Structure and Function versusImpairment 272Vestibulo-Ocular Function and Dysfunction 272Perception of Head Movement and Position 274Postural Instability 274Cervical Range of Motion 274Physical Deconditioning 274Activities versus Limitation 274Participation versus Restriction 275Physical Therapy Evaluation 275History 276Clinical Examination 278Oculomotor and Vestibulo-Ocular Testing 278Balance Assessment 284Gait Evaluation 289Red Flags 293Transition from Assessment to Treatment 294Is There a Documented Vestibular Deficit? 294What Type of Vestibular Problem Does this PatientHave? 294Not All Dizzy Patients Have a VestibularLesion 294Assess and Reassess 295Quantify the Assessment 295Determining Whether There Has BeenImprovement 295Summary 295Acknowledgments 295APPENDIX 19A Evaluation Form 300APPENDIX 19B Dizziness HandicapInventory 307CHAPTER 20 Interventions for the Patientwith Vestibular Hypofunction 309Susan J. Herdman, PT, PhD, FAPTASusan L. Whitney, PT, PhD, NCS, ATCMechanisms of Recovery 309Cellular Recovery 309Reestablishment of Tonic Firing Rate 309Recovery of the Dynamic Component 310Vestibular Adaptation 310Substitution 311Habituation 312Evidence that Exercise Facilitates Recovery 312Goals of Treatment 313Treatment Approaches 313Adaptation Exercises 314Substitution Exercises 315Expectations for Recovery 317Factors Affecting Outcome 317Treatment 320General Considerations 320Problem-Oriented Approach 321Copyright 2007 by F. A. Davis. 22. CONTENTS xxiiiProblem: Visual Blurring and Dizziness WhenPerforming Tasks that Require Visual Trackingor Gaze Stabilization 321Problem: Exacerbation of Symptoms 323Problem: Static and Dynamic PosturalInstability 323Problem: Progression of Balance andGait Exercises 326Problem: Physical Deconditioning 326Problem: Return to Driving 327Summary 328Acknowledgment 329CHAPTER 21 Assessment and Interventionsfor the Patient with CompleteVestibular Loss 338Susan J. Herdman, PT, PhD, FAPTARichard A. Clendaniel, PT, PhDPrimary Complaints 338Balance 338Oscillopsia 339Sense of Disequilibrium or Dizziness 339Physical Deconditioning 339Assessment 339History 339Mechanisms of Recovery 343Gaze Stability 343Postural Stability 344Compensatory Strategies 345Evidence that Exercise Facilitates Recovery 345Treatment 346Progression of Exercises 346Guidelines to Treatment and Prognosis 347Future Directions 351Summary 358Acknowledgment 358CHAPTER 22 Management of the Pediatric Patientwith Vestibular Hypofunction 360Rose Marie Rine, PT, PhDIncidence of Vestibular Deficits in Children 360Development of Postural and OculomotorControl as Related to Vestibular SystemFunction 363Evaluation of Children withVestibular System Dysfunction 365Treatment of Vestibular Dysfunction 370Peripheral Disorders 370Central Vestibular and PosturalControl Deficits 370CHAPTER 23 Management of the Elderly Personwith Vestibular Hypofunction 376Susan L. Whitney, PT, PhD, NCS, ATCGregory F. Marchetti, PT, PhDNormal Changes of Aging 376Vestibular Function 376Visual Deficits 378Somatosensory Changes 378Musculoskeletal Deficits 381Postural Hypotension 382Cerebellar Atrophy 382Fear of Falling 382Attention 382Depression 382Risk of Falling in Older Adults with VestibularDisorders 383Questionnaires for BalanceAssessment 383Dizziness Assessment 387Typical Balance Tests 390Home Assessment 390Duration of Treatment 390What to Do Once the Risk FactorHas Been Identified 390Summary 394CHAPTER 24 Disability in VestibularDisorders 398Helen S. Cohen, OTR, EdD, FAOTAEvaluating Disablement 398Benign Paroxysmal Positional Vertigo 399Chronic Vestibulopathy 400Bilateral Vestibular Impairment 400Acoustic Neuroma 402Mnires Disease 404Acknowledgments 406CHAPTER 25 Assessment and Managementof Disorders Affecting CentralVestibular Pathways 409Marianne Dieterich, MDThomas Brandt, MD, FRCPClinical Classification of CentralVestibular Disorders 409Vestibular Disorders in (Frontal)Roll Plane 410Etiology 415Natural Course and Management 415Copyright 2007 by F. A. Davis. 23. xxiv CONTENTSThalamic and Cortical Astasia Associatedwith Subjective Visual Vertical Tilts 417Torsional Nystagmus 417Vestibular Disorders in (Sagittal) Pitch Plane 417Downbeat Nystagmus 418Upbeat Nystagmus(Upbeat Nystagmus Syndrome) 419Summary 423Vestibular Disorders in (Horizontal)Yaw Plane 423Vestibular Cortex: Locations, Functions,and Disorders 424Multimodal Sensorimotor Vestibular CortexFunction and Dysfunction 424Spatial Hemineglect: a CorticalVestibular Syndrome? 426Vestibular Epilepsy 426Paroxysmal Central Vertigo 427Summary 428Acknowledgment 428CHAPTER 26 Non-vestibular Dizziness andImbalance: From DisuseDisequilibrium to CentralDegenerative Disorders 433Ronald J. Tusa, MD, PhDDisuse Disequilibrium and Fear of Fall 433Description 433Useful Outcome Tests 434Management 434Leukoaraiosis and Normal-PressureHydrocephalus 434Description 434Useful Outcome Scores 436Management 436Progressive Supranuclear Palsy,Parkinsons Disease, Large-Fiber PeripheralNeuropathy, and SpinocerebellarAtaxia 437Description 437Useful Outcome Scores 438Management 438CHAPTER 27 Assessment and Managementof the Patient with TraumaticBrain Injury and VestibularDysfunction 444Anne Shumway-Cook, PT, PhD, FAPTAVestibular Pathology 444Concussion 445Fractures 446Central Vestibular Lesions 446Vestibular Rehabilitation 446Vertigo 447Eye-Head Coordination 447Postural Control UnderlyingStability 448Assessment 448Impairments Limiting PosturalStability 452Time Course for Recovery 453Summary 456CHAPTER 28 Non-vestibular Dizziness andImbalance: Suggestions forPatients with Migraine andMal de Dbarquement 458Neil T. Shepard, PhDAnnamarie Asher, PTDefinition of Non-vestibular Dizziness 458Mal de Dbarquement 459Migraine-Associated Dizziness 460Primary Anxiety and Panic 462Methodological Considerations forAssessment and TreatmentDevelopment 464CHAPTER 29 Non-vestibular Diagnosisand Imbalance:Cervicogenic Dizziness 467Richard A. Clendaniel, PT, PhDRobert Landel, PT, DPT, OCSProposed Etiologies 468Posterior Cervical SympatheticSyndrome 468Vertebrobasilar Insufficiency 468Altered Proprioceptive Signals 468Examination 475Management 476Summary 477Appendix A Questionnaire for Historyand Examination 485Index 493Copyright 2007 by F. A. Davis. 24. ONEFundamentalsCopyright 2007 by F. A. Davis. 25. CHAPTER 12Anatomy and Physiologyof the Normal VestibularSystemTimothy C. Hain, MD Janet O. Helminski, PT, PhDPurpose of the Vestibular SystemThe human vestibular system is made up of three compo-nents:a peripheral sensory apparatus, a central processor,and a mechanism for motor output (Fig. 1.1). The periph-eralapparatus consists of a set of motion sensors that sendinformation to the central nervous systemspecifically,the vestibular nucleus complex and the cerebellumabout head angular velocity and linear acceleration. Thecentral nervous system processes these signals and com-binesthem with other sensory information to estimatehead and body orientation. The output of the centralvestibular system goes to the ocular muscles and spinalcord to serve three important reflexes, the vestibulo-ocularreflex (VOR), the vestibulocollic reflex (VCR),and the vestibulospinal reflex (VSR). The VOR generateseye movements that enable clear vision while the head isin motion. The VCR acts on the neck musculature tostabilize the head. The VSR generates compensatorybody movement in order to maintain head and posturalstability and thereby prevent falls. The performance of theVOR, VCR and VSR is monitored by the central nervousFigure 1.1 Block diagram illustrating the organization of the vestibular system.Copyright 2007 by F. A. Davis. 26. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 3Copyright 2007 by F. A. Davis.system, is readjusted as necessary by the cerebellum, andis supplemented by slower but more capable higher corti-calprocesses.From a rehabilitation perspective, it is crucial to real-izethat because orientation in space is a critical function,multiple fail-safe mechanisms are closely integrated intovestibular responses. The capability for repair and adap-tationis remarkable! Two years after removal of half ofthe peripheral vestibular system, such as by a unilateralvestibular nerve section, finding clinical evidence ofvestibular dysfunction is often quite difficult. The abilityof central mechanisms to use vision, proprioception, audi-toryinput, tactile input, or knowledge about an impend-ingmovement allows vestibular responses to be based ona richly textured, multimodal sensory array.With these general philosophical considerationskept in mind, the purpose of this chapter is to describe theanatomy and the physiologic responses of the vestibularsystem, with particular attention to aspects relevant torehabilitation. We proceed from the peripheral structuresto central structures and conclude with a discussion ofhigher-level problems in vestibular physiology that arerelevant to rehabilitation.The Peripheral Sensory ApparatusFigure 1.2 illustrates the peripheral vestibular systemin relation to the ear. The peripheral vestibular systemconsists of the membranous and bony labyrinths aswell as the motion sensors of the vestibular system,the hair cells. The peripheral vestibular system lies with-inthe inner ear. Bordered laterally by the air-filled mid-dleear and medially by temporal bone, it is posterior tothe cochlea.1Bony LabyrinthThe bony labyrinth consists of three semicircularcanals (SCCs), the cochlea, and a central chamber calledthe vestibule (Fig. 1.3). The bony labyrinth is filledwith perilymphatic fluid, which has a chemistrysimilar to that of cerebrospinal fluid (high Na:K ratio).Perilymphatic fluid communicates via the cochlearaqueduct with cerebrospinal fluid. Because of thiscommunication, disorders that affect spinal fluid pres-sure(such as lumbar puncture) can also affect innerear function. [2]Membranous LabyrinthThe membranous labyrinth is suspended within the bonylabyrinth by perilymphatic fluid and supportive connec-tivetissue. It contains five sensory organs: the membra-nousportions of the three SCCs and the two otolithorgans, the utricle and saccule. Note that one end of eachSCC is widened in diameter to form an ampulla. ThisFigure 1.2 Anatomy of the peripheralvestibular system in relation to the ear.(Illustration adapted from http://www.dizziness-and-balance.com/disorders/hearing/sensorineural.htm, with permission.) 27. MembraneCopyright 2007 by F. A. Davis.widening is relevant to the understanding of a commonvestibular condition, benign paroxysmal positional verti-go(see later).The membranous labyrinth is filled with endolym-phaticfluid (see Fig. 1.3). In contrast to perilymph, theendolymph resembles intracellular fluid in electrolytecomposition (high K:Na ratio). Under normal circum-stances,there is no direct communication between theendolymph and perilymph compartments.Hair CellsSpecialized hair cells contained in each ampulla andotolith organ are biological sensors that convert displace-mentdue to head motion into neural firing (Fig. 1.4). Thehair cells of the ampullae rest on a tuft of blood vessels,nerve fibers, and supporting tissue called the cristaampullaris. The hair cells of the saccule and utricle, themaculae, are located on the medial wall of the sacculeand the floor of the utricle. Each hair cell is innervatedby an afferent neuron located in the vestibular (Scarpas)ganglion, which is located close to the ampulla. Whenhairs are bent toward or away from the longest processof the hair cell, firing rate increases or decreases inthe vestibular nerve (see Fig. 1.4A). A flexible, diaphrag-maticmembrane called the cupula overlies each cristaand completely seals the ampulla from the adjacent ves-tibule.Associated with angular head motion, endolym-phaticpressure differentials across the cupula cause thecupula to bend back and forth, stimulating the hair cells(Fig. 1.4B). 3The otolithic membranes are structures that aresimilar to the cupulae but they are also weighted. Theycontain calcium carbonate (limestone) crystals calledotoconia and have substantially more mass than thecupulae (Fig. 1.5). The mass of the otolithic membranecauses the maculae to be sensitive to gravity and linearacceleration. In contrast, the cupulae normally have thesame density as the surrounding endolymphatic fluid andare insensitive to gravity. 4Vascular SupplyThe labyrinthine artery supplies the peripheral vestibu-larsystem (Fig. 1.6; see also Fig. 1.11). The labyrinthineartery has a variable origin. Most often it is a branchof the anterior-inferior cerebellar artery (AICA), butoccasionally it is a direct branch of the basilar artery.Upon entering the inner ear, the labyrinthine arterydivides into the anterior vestibular artery and the com-4 Section ONE FUNDAMENTALSCochleaVestibuleCupulaAmpullaBoneFigure 1.3 The membranous and bony labyrinths. The inset illustrates the perilymphatic andendolymphatic fluid compartments. (Adapted from an illustration by Mary Dersch; originally adaptedfrom Pender, 1992.2) 28. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 5Copyright 2007 by F. A. Davis.mon cochlear artery. The anterior vestibular artery sup-pliesthe vestibular nerve, most of the utricle, and theampullae of the lateral and anterior SCCs. The commoncochlear artery divides into a main branch, the maincochlear artery, and the vestibulocochlear artery. Themain cochlear artery supplies the cochlea. The vestibulo-cochlearartery supplies part of the cochlea, the ampullaof the posterior semicircular canal, and the inferior partof the saccule.5The labyrinth has no collateral anastomotic networkand is highly susceptible to ischemia. Only 15 seconds ofselective blood flow cessation is needed to abolish audi-torynerve excitability.6Physiology of the PeripheryThe hair cells of the canals and otoliths convert themechanical energy generated by head motion into neuraldischarges directed to specific areas of the brainstem andthe cerebellum. By virtue of their orientation, the canalsand otolith organs are able to respond selectively to headmotion in particular directions. By virtue of differencesin their fluid mechanics, the canals respond to angularvelocity, and the otoliths to linear acceleration.Semicircular CanalsThe SCCs provide sensory input about head velocity,which enables the VOR to generate an eye movement thatmatches the velocity of the head movement. The desiredresult is that the eye remains still in space during headmotion, enabling clear vision. Neural firing in thevestibular nerve is proportional to head velocity overthe range of frequencies in which the head commonlymoves (0.57 Hz). In engineering terms, the canals arerate sensors.A second important dynamic characteristic of thecanals has to do with their response to prolonged rotationat constant velocity. Instead of producing a signal pro-portionalto velocity, as a perfect rate sensor should, thecanals respond reasonably well only in the first second orso, because output decays exponentially with a time con-stantof about 7 seconds. This behavior is due to a spring-likeaction of the cupula that tends to restore it to itsresting position.7Figure 1.4 Effects of head rotationon the canals. (A) The direction fromwhich hair cells are deflected determineswhether or not hair-cell discharge frequ-encyincreases or decreases. (B) Crosssection of the membranous labyrinthillustrating endolymphatic flow and cupu-lardeflection in response to headmotion. (From Bach-Y-Rita et al, 1971.3)Figure 1.5 The otolithic macula and its overlying membrane.(From Baloh et al, 1990.4) 29. Three important spatial arrangements characterizethe alignment of the SCCs loops. First, each canal planewithin each labyrinth is perpendicular to the other canalplanes, analogous to the spatial relationship between twowalls and the floor of a rectangular room (Fig. 1.7).Second, paired planes of the SCCs between the labyrinthsconform very closely to each other. The six individualSCCs become the following three coplanar pairs: (1) rightand left lateral, (2) left anterior and right posterior, and(3) left posterior and right anterior. Third, the planes ofthe canals are close to the planes of the extraocular mus-cles,thus allowing relatively simple connections betweensensory neurons (related to individual canals), and motoroutput neurons (related to individual ocular muscles).The coplanar pairing of canals is associated with apush-pull change in the quantity of SCC output. Whenangular head motion occurs within their shared plane, theendolymph of the coplanar pair is displaced in oppositedirections with respect to their ampullae, and neuralfiring increases in one vestibular nerve and decreaseson the other side. For the lateral canals, displacement ofthe cupula towards the ampulla (ampullopetal flow) isexcitatory.There are three advantages to the push-pull arrange-mentof coplanar pairing. First, pairing provides sensoryredundancy. If disease or surgical intervention affectsthe SCC input from one member of a pair (e.g., as investibular neuritis, or canal plugging for benign paroxys-malpositional vertigo), the central nervous system willstill receive vestibular information about head velocitywithin that plane from the contralateral member of thecoplanar pair.Second, such a pairing allows the brain to ignorechanges in neural firing that occur on both sides simulta-neously,such as might occur due to changes in body tem-peratureor chemistry. These changes are not related to6 Section ONE FUNDAMENTALSArteries ofthe CanalsAnteriorVestibularArteryBasilarArteryAnterior InferiorCerebellar ArteryLabyrinthine ArteryCommonCochlearArteryMainCochlearArteryCochlear Ramus Vestibulocochlear Artery Posterior Vestibular ArteryFigure 1.6 The arterial supply of thelabyrinth. (Redrawn from Schuknecht,1993.5)Figure 1.7 The spatial arrangement of the semicircularcanals. The canals on each side are mutually perpendicular, arepaired with conjugate canals on the opposite side of the head,and also are closely aligned with the optimal pulling directionsof the extraocular muscles.Copyright 2007 by F. A. Davis. 30. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 7Copyright 2007 by F. A. Davis.head motion and are common-mode noise. The engi-neeringterm for this desirable characteristic is common-moderejection. Third, as discussed in a later section, apush-pull configuration assists in compensation for sen-soryoverload.OtolithsThe otoliths register forces related to linear acceleration(Fig. 1.8). They respond to both linear head motion andstatic tilt with respect to the gravitational axis. The func-tionof the otoliths is illustrated by the situation of a pas-sengerin a commercial jet. During flight at a constantvelocity, he has no sense that he is traveling at 300 milesper hour. However, in the process of taking off and ascend-ingto cruising altitude, he senses the change in velocity(acceleration) as well as the tilt of the plane on ascent. Theotoliths therefore differ from the SCCs in two basic ways:They respond to linear motion instead of angular motion,and to acceleration rather than to velocity.7The otoliths have a simpler task to perform than thecanals. Unlike the canals, which must convert head veloc-ityinto displacement to properly activate the hair cells ofthe cristae, the otoliths need no special hydrodynamicsystem. Exquisite sensitivity to gravity and linear accel-erationis obtained by incorporation of the mass of theotoconia into the otolithic membrane (see Fig. 1.5). Forceis equal to mass multiplied by acceleration, so with incor-porationof a large mass, a given acceleration producesenough shearing force to make the otoliths extremely sen-sitive(shearing force refers to force that is directed per-pendicularlyto the processes of the hair cells).Like the canals, the otoliths are arranged to enablethem to respond to motion in all three dimensions(Fig. 1.9). However, unlike the canals, which have onesensory organ per axis of angular motion, the otolithshave only two sensory organs for three axes of linearmotion. In an upright individual, the saccule is vertical(parasagittal), whereas the utricle is horizontally oriented(near the plane of the lateral SCCs). In this posture, thesaccule can sense linear acceleration in its plane, whichincludes the acceleration oriented along the occipitocau-dalaxis as well as linear motion along the anterior-poste-rioraxis. The utricle senses acceleration in its plane,which includes lateral accelerations along the interauralaxis as well as anterior-posterior motion.8The earths gravitational field is a linear accelerationfield, so in a person on the earth, the otoliths register tilt.For example, as the head is tilted laterally (which is alsocalled roll; see Fig. 1.8), shear force is exerted upon theutricle, causing excitation, but shear force is lessenedupon the saccule. Similar changes occur when the head istilted forwards or backwards (called pitch). Because lin-earacceleration can come from two sourcesearthsgravitational field as well as linear motionthere is asensor ambiguity problem. We discuss strategies that thecentral nervous system might use to solve this problemlater, in the section on higher-level vestibular processing.In the otoliths, as in the canals, there is redundancy,with similar sensors on both sides of the head. Push-pullprocessing for the otoliths is also incorporated into thegeometry of each of the otolithic membranes. Withineach otolithic macula, a curving zone, the striola, sepa-ratesthe direction of hair-cell polarization on each side.Consequently, head tilt increases afferent discharge fromone part of a macula while reducing the afferent dis-chargefrom another portion of the same macula. Thisextra level of redundancy in comparison with the SCCsprobably makes the otoliths less vulnerable to unilateralvestibular lesions.The Vestibular NerveVestibular nerve fibers are the afferent projections fromthe bipolar neurons of Scarpas (vestibular) ganglion. TheFigure 1.8 The otoliths register linear acceleration andstatic tilt. 31. vestibular nerve transmits afferent signals from thelabyrinths along its course through the internal auditorycanal (IAC). In addition to the vestibular nerve, the IACcontains the cochlear nerve (hearing), the facial nerve,the nervus intermedius (a branch of the facial nerve,which carries sensation), and the labyrinthine artery. TheIAC travels through the petrous portion of the temporalbone to open into the posterior fossa at the level of thepons. The vestibular nerve enters the brainstem at thepontomedullary junction. Because the vestibular nerve isinterposed between the labyrinth and the brainstem, someauthorities consider this nerve a peripheral structure,whereas others consider it a central structure. We con-siderit a peripheral structure.There are two patterns of firing in vestibular afferentneurons. Regular afferents usually have a tonic rate andlittle variability in interspike intervals. Irregular afferentsoften show no firing at rest and, when stimulated by headmotion, develop highly variable interspike intervals.9Regular afferents appear to be the most important typefor the VOR, because in experimental animals irregularafferents can be ablated without much change in theVOR. However, irregular afferents may be important forthe VSR and in coordinating responses between theotoliths and canals.Regular afferents of the monkey have tonic firingrates of about 90 spikes per second and a sensitivityto head velocity of about 0.5 spike per degree persecond.10,11We can speculate about what happens imme-diatelyafter a sudden change in head velocity. Humanscan easily move their heads at velocities exceeding 300degrees per second (deg/sec). As noted previously, theSCCS are connected in a push-pull arrangement, so thatone side is always being inhibited while the other is beingexcited. Given the sensitivity and tonic rate noted previ-ously,the vestibular nerve, which is being inhibited,should be driven to a firing rate of 0 spikes per second,for head velocities of only 180 deg/sec! In other words,head velocities greater than 180 deg/sec may be unquan-tifiableby half of the vestibular system. This cutoffbehavior has been advanced as the explanation forEwalds second law, which says that responses to rota-tionsthat excite a canal are greater than those to rotationsthat inhibit a canal.12,13 Cutoff behavior explains why apatient with unilateral vestibular loss avoids head motiontoward the side of the lesion. More is said about this issuein the later discussion of how the central nervous systemmay compensate for overload.Central Processingof Vestibular InputThere are two main targets for vestibular input from pri-maryafferents: the vestibular nuclear complex and thecerebellum (see Fig. 1.1). The vestibular nuclear complexis the primary processor of vestibular input and imple-mentsdirect, fast connections between incoming afferentinformation and motor output neurons. The cerebellum isthe adaptive processor; it monitors vestibular perform-anceand readjusts central vestibular processing if neces-sary.At both locations, vestibular sensory input isprocessed in association with somatosensory and visualsensory input.8 Section ONE FUNDAMENTALSFigure 1.9 Geometry of the otoliths. (FromBarber and Stockwell, 1976.) [8]Copyright 2007 by F. A. Davis. 32. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 9Vestibular NucleusThe vestibular nuclear complex consists of four majornuclei (superior, medial, lateral, and descending) and atleast seven minor nuclei (Fig. 1.10). This large struc-ture,located primarily within the pons, also extends cau-dallyinto the medulla. The superior and medialvestibular nuclei are relays for the VOR. The medialvestibular nucleus is also involved in VSRs and coordi-nateshead and eye movements that occur together. Thelateral vestibular nucleus is the principal nucleus forthe VSR. The descending nucleus is connected to all ofthe other nuclei and the cerebellum but has no primaryoutflow of its own. The vestibular nuclei between the twosides of the brainstem are laced together via a system ofcommissures that are mutually inhibitory. The commis-suresallow information to be shared between the twosides of the brainstem and implement the push-pull pair-ingof canals discussed earlier.14In the vestibular nuclear complex, processing of thevestibular sensory input occurs concurrently with theprocessing of extravestibular sensory information (pro-prioceptive,visual, tactile, and auditory). Extensive con-nectionsbetween the vestibular nuclear complex,cerebellum, ocular motor nuclei, and brainstem reticularactivating systems are required to formulate appropriateefferent signals to the VOR and VSR effector organs, theextraocular and skeletal muscles.Vascular SupplyThe vertebral-basilar arterial system supplies blood to theperipheral and central vestibular system (Fig. 1.11). TheFigure 1.10 The vestibular nuclear complex. This sectionshows the brainstem with the cerebellum removed. DVN descending vestibular nucleus; LVNlateral vestibular nucle-us;NPHnucleus prepositus hypoglossi; IIIoculomotornucleus (inferior oblique muscle and medial, superior, and infe-riorrectus muscles); IVtrochlear nucleus (superior obliquemuscle); VIabducens nucleus (lateral rectus muscle). Themedial vestibular nucleus (not labeled) lies between the NPHand the DVN. (From Brodal, 1981.14)BRAINSTEMPCASCA SCAAICAPICAPICAVertebral Arteries114 3 36781012495Figure 1.11 The vertebral-basilar system. AICAanteriorinferior cerebellar artery; PCAposterior cerebellar artery;PICAposterior inferior cerebellar artery; SCAsuperiorcerebellar artery. Numerals indicate individual cranial nerve roots(all nerves are paired, but for clarity, both sides are not alwayslabeled here). ( Northwestern University, with permission.)Copyright 2007 by F. A. Davis. 33. Copyright 2007 by F. A. Davis.posterior-inferior cerebellar arteries (PICAs) branch offthe vertebral arteries. The two PICAs are the most impor-tantarteries for the central vestibular system. They sup-plythe surface of the inferior portions of the cerebellarhemispheres as well as the dorsolateral medulla, whichincludes the inferior aspects of the vestibular nuclearcomplex. The basilar artery is the principal artery of thepons. The basilar artery supplies central vestibular struc-turesvia perforator branches, which penetrate the medialpons, short circumferential branches, which supply theanterolateral aspect of the pons, and long circumferentialbranches, which supply the dorsolateral pons. The AICAis an important branch of the basilar artery because it isthe sole blood supply for the peripheral vestibular systemvia the labyrinthine artery. The AICA also supplies bloodto the ventrolateral cerebellum and the lateral tegmentumof the lower two-thirds of the pons. Recognizable clinicalsyndromes with vestibular components may appear afterocclusions of the basilar artery, labyrinthine artery,AICA, and PICA.CerebellumThe cerebellum, a major recipient of outflow from thevestibular nucleus complex, is also a major source ofinput itself. Although the cerebellum is not required forvestibular reflexes, vestibular reflexes become uncali-bratedand ineffective when this structure is removed.Originally, the vestibulocerebellum was defined as theportions of the cerebellum receiving direct input from theprimary vestibular afferents. We now understand thatmost parts of the cerebellar vermis (midline) respond tovestibular stimulation. The cerebellar projections to thevestibular nuclear complex have an inhibitory influenceon the vestibular nuclear complex.The cerebellar flocculus adjusts and maintains thegain of the VOR.15 Lesions of the flocculus reduce theability of experimental animals to adapt to disorders thatreduce or increase the gain of the VOR. Patients withcerebellar degenerations or the Arnold-Chiari malforma-tiontypically have floccular disorders.The cerebellar nodulus adjusts the duration of VORresponses and is also involved with processing of otolithinput. Patients with lesions of the cerebellar nodulus,such as those with medulloblastoma, show gait ataxia andoften have nystagmus, which is strongly affected by theposition of the head with respect to the gravitational axis.Lesions of the anterior-superior vermis of the cere-bellumaffect the VSR and cause a profound gait ataxiawith truncal instability. Patients with such lesions areunable to use sensory input from their lower extremitiesto stabilize their posture. The lesions are commonly relat-edto excessive alcohol intake and thiamine deficiency.Neural IntegratorThus far we have discussed processing of velocity signalsfrom the canals and acceleration signals from theotoliths. These signals are not suitable for driving theocular motor neurons, which need a neural signal encod-ingeye position. The transformation of velocity to posi-tionis accomplished by a brainstem structure called theneural integrator. The nucleus prepositus hypoglossi,located just below the medial vestibular nucleus, appearsto provide this function for the horizontal oculomotorsystem.15 Although a similar structure must exist for thevestibulospinal system, the location of the VSR neuralintegrator is currently unknown. Clinically, poor functionof the oculomotor neural integrator causes gaze-evokednystagmus.Motor Output of theVestibular System NeuronsOutput for the Vestibulo-ocular ReflexThe output neurons of the VOR are the motor neurons ofthe ocular motor nuclei, which drive the extraocular mus-cles.The extraocular muscles are arranged in pairs, whichare oriented in planes very close to those of the canals.This geometrical arrangement enables a single pair ofcanals to be connected predominantly to a single pair ofextraocular muscles. The result is conjugate movementsof the eyes in the same plane as head motion.Two white matter tracts carry output from thevestibular nuclear complex to the ocular motor nuclei.The ascending tract of Deiters carries output from thevestibular nucleus to the ipsilateral abducens nucleus(lateral rectus) during the horizontal VOR. All otherVOR-related output to the ocular motor nuclei is trans-mittedby the medial longitudinal fasciculus (MLF) (Fig.1.12). Because the median longitudinal fasciculus isoften injured in multiple sclerosis, this connection mayaccount for central vestibular symptoms in patients withthis disorder.14Output for the Vestibulospinal ReflexThe output neurons of the VSR are the anterior horn cellsof the spinal cord gray matter, which drive skeletal mus-cle.However, the connection between the vestibularnuclear complex and the motor neurons is more compli-10 Section ONE FUNDAMENTALS 34. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 11Copyright 2007 by F. A. Davis.cated than that for the VOR. The VSR has a much moredifficult task than the VOR, because multiple strategiesinvolving entirely different motor synergies can be usedto prevent falls. For example, when one is shoved frombehind, ones center of gravity might become displacedanteriorly. In order to restore balance, one might (1)plantar-flex at the ankles, (2) take a step, (3) grab forsupport, or (4) use some combination of all three activi-ties.The VSR also has to adjust limb motion appropri-atelyfor the position of the head on the body (see theframe of reference problem discussed later in the sectionon higher-level problems in vestibular processing).The VSR must also use otolith input, reflecting lin-earmotion, to a greater extent than the VOR. Although theeyes can only rotate and thus can do little to compensatefor linear motion, the body can both rotate and translate.Three major white matter pathways connect thevestibular nucleus to the anterior horn cells of the spinalcord. The lateral vestibulospinal tract originates from theipsilateral lateral vestibular nucleus, which receives themajority of its input from the otoliths and the cerebellum(see Fig. 1.12). This pathway generates antigravity pos-turalmotor activity or protective extension, primarily inthe lower extremities, in response to the head positionchanges that occur with respect to gravity. The medialvestibulospinal tract originates from the contralateralmedial, superior, and descending vestibular nuclei (seeFig. 1.12) and mediates ongoing postural changes or headrighting in response to SCC sensory input (angular headmotion). The medial vestibulospinal tract descends onlythrough the cervical spinal cord in the medial longitudi-nalfasciculus and activates cervical axial musculature.The reticulospinal tract receives sensory input fromall of the vestibular nuclei as well as from all of the othersensory and motor systems involved with maintainingbalance. This projection has both crossed and uncrossedcomponents and is very highly collateralized. As a result,the reticulospinal tract through the entire extent of thespinal cord is poorly defined, but it is probably involvedin most balance reflex motor actions, including posturaladjustments made to extravestibular sensory input (audi-tory,visual, and tactile stimuli).Vestibular ReflexesThe sensory, central, and motor output components of thevestibular system have been described. We now discusstheir integration into the VOR, VSR, and VCR. Additio-nally,we include brief descriptions of cervical, visual,and somatosensory reflexes. Although not directly medi-atedby the vestibular apparatus, these reflexes have aclose interaction with vestibular reflexes.The Vestibulo-ocular ReflexThe VOR normally acts to maintain stable vision dur-inghead motion. This reflex has two components. Theangular VOR, mediated by the SCCs, compensates forrotation. The linear VOR, mediated by the otoliths, com-pensatesfor translation. The angular VOR is primarilyresponsible for gaze stabilization. The linear VOR ismost important when near targets are being viewed andthe head is being moved at relatively high frequencies.An example of how the horizontal canal VOR is orches-tratedfollows:1. When the head turns to the right, endolym-phaticflow deflects the cupulae to the left(see Fig. 1.4B).2. The discharge rate from hair cells in the rightcrista increases in proportion to the velocityFigure 1.12 The vestibulo-ocular reflex (VOR) and vestibu-lospinalreflex (VSR) arcs. S, L, M, and D indicate the superior,lateral, medial, and descending vestibular nuclei, respectively.The lateral vestibulospinal and medial vestibulospinal tracts areshown as heavy lines and light lines, beginning in the lateralvestibular nucleus and medial vestibular nucleus, respectively.(From Brodal, 1981.14) 35. Copyright 2007 by F. A. Davis.of the head motion, whereas the discharge ratefrom hair cells in the left lateral crista decreases(see Fig. 1.4A).3. These changes in firing rate are transmittedalong the vestibular nerve and influence thedischarge of the neurons of the medial andsuperior vestibular nuclei and cerebellum.4. Excitatory impulses are transmitted via whitematter tracts in the brainstem to the oculomotornuclei, which activate the right (ipsilateral)medial rectus and the left (contralateral) lateralrectus. Inhibitory impulses are also transmittedto their antagonists.5. Simultaneously, contraction of the left lateralrectus and right medial rectus muscles andrelaxation of the left medial rectus and right lat-eralrectus muscles occur, resulting in lateralcompensatory eye movements toward the left.6. If the eye velocity is not adequate for the givenhead velocity and retina image motion is morethan 2 deg/sec, the cerebellar projection to thevestibular nuclei will modify the firing rate ofthe neurons within the vestibular nuclei toreduce the error.The Vestibulospinal ReflexThe purpose of the VSR is to stabilize the body. The VSRactually consists of an assemblage of several reflexesnamed according to the timing (dynamic vs. static ortonic) and sensory input (canal vs. otolith); these reflex-esare discussed in more detail in Chapter 2. As an exam-pleof a VSR, let us examine the sequence of eventsinvolved in generating a labyrinthine reflex, as follows:1. When the head is tilted to one side, both thecanals and the otoliths are stimulated. Endolym-phaticflow deflects the cupula, and shear forcedeflects hair cells within the otoliths.2. The vestibular nerve and vestibular nucleus areactivated.3. Impulses are transmitted via the lateral andmedial vestibulospinal tracts to the spinal cord.4. Extensor activity is induced on the side towhich the head is inclined, and flexor activityis induced on the opposite side. The head move-mentopposes the movement sensed by themotion sensors.The Vestibulocollic ReflexThe VCR acts on the neck musculature to stabilize thehead. The reflex head movement produced counters themovement sensed by the otolithic or SCC organs. Theprecise pathways mediating this reflex have yet to bedetailed.Cervical ReflexesThe Cervico-ocular ReflexThe cervico-ocular reflex (COR) interacts with the VOR.The COR consists of eye movements driven by neck pro-prioceptorsthat can supplement the VOR under certaincircumstances. Normally, the gain of the COR is verylow.16 The COR is facilitated when the vestibular appara-tusis injured.17,18 It is rare, however, for the COR to haveany clinical significance.The Cervicospinal ReflexThe cervicospinal reflex (CSR) is defined as changes inlimb position driven by neck afferent activity. Analogousto the COR, which supplements the VOR under certaincircumstances, the CSR can supplement the VSR byaltering motor tone in the body. Like the VSR, the CSRconsists of an assemblage of several reflexes. Two path-waysare thought to mediate these reflex signals: an exci-tatorypathway from the lateral vestibular nucleus and aninhibitory pathway from the medial part of the medullaryreticular formation.When the body is rotated with head stable, neuronsof the excitatory vestibulospinal system increase theirrate of firing on the side to which the chin is pointed. Atthe same time, neurons thought to be in the inhibitoryreticulospinal system show a reduced rate of firing. Thisactivity leads to extension of the limb on the side towhich the chin is pointed and flexion of the limb on thecontralateral side. Vestibular receptors influence both ofthese systems by modulating the firing of medullary neu-ronsin a pattern opposite to that elicited by neck recep-tors.With their interaction, the effects on the body ofvestibular and neck inputs tend to cancel one anotherwhen the head moves freely on the body, so that postureremains stable.19The Cervicocollic ReflexThe cervicocollic reflex (CCR) is a cervical reflex that sta-bilizesthe head on the body. The afferent sensory changescaused by changes in neck position create opposition tothat stretch by way of reflexive contractions of appropri-ateneck muscles. The reflex is thought to be primarilya monosynaptic one.16 The extent to which the CCRcontributes to head stabilization in normal humans is cur-12 Section ONE FUNDAMENTALS 36. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 13Copyright 2007 by F. A. Davis.rently uncertain, but it seems likely that the CCR is usefulprimarily to stabilize head movement in the vertical plane,and it may also be facilitated after labyrinthine loss.Visual ReflexesThe visual system is a capable and sophisticated sensorysystem that influences vestibular central circuitry anddrives visual after-responses (i.e., smooth pursuit) andpostural reactions. Because of intrinsic delays in multisy-napticvisual mechanisms, visual responses occur at asubstantially longer latency and are much less suited totracking at frequencies above about 0.5 Hz than vestibu-larresponses. Visual tracking responses may be facilitat-edafter vestibular loss.Somatosensory ReflexesSomatosensory mechanisms appear to be involved inpostural stability as well. Bles and associates document-edsomatosensory-induced nystagmus (stepping-aroundnystagmus).20 Interestingly, the subjects in their studywith bilateral vestibular loss developed a more pro-nouncednystagmus than normal subjects. This findingimplies that subjects with bilateral vestibular loss usesomatosensory information to a greater extent than nor-malsubjects.Neurophysiology of BenignParoxysmal Positional VertigoAlthough most vestibular disorders can be described interms of imbalance between the ears or loss of function,benign paroxysmal positional vertigo (BPPV) has anentirely different mechanism. BPPV is caused by move-mentof detached otoconia within the inner ear (canalithi-asis)or otoconia adherent to the cupula (cupulolithiasis)(Fig. 1.13). Great progress has now been made in ourunderstanding of BPPV.Figure 1.14, from Squires and colleagues,21 illus-tratesthe fluid mechanics of BPPV. In this disorder, ver-tigoand nystagmus begin after a characteristic latency ofabout 5 seconds. The delay in onset of symptoms iscaused by movement of detached otoconia through theampulla, because pressure caused by moving otoconia isnegligible until otoconia enter the narrow duct of theSCC. Figure 1.14 also shows that particle-wall interac-tionscan account for variability in duration and latencyof BPPV.21Other results from fluid mechanics have direct bear-ingon our understanding of treatment maneuvers forBPPV. Under the influence of a full 1 g of gravity, typi-calotoconia move at a rate of 0.2 mm/sec, or only about1% of the circumference of the canal each second. It fol-lowsthat inertial effects of treatment maneuvers canDIRECTION OF VIEWSTRAIGHT LATERALPOSTERIORSEMI-CIRCULAR CANALDARK CELLSUTRICLESACCULECOCHLEACUPULADISPLACED OTOCONIAOTOCONIA Figure 1.13 Physiology of benignparoxysmal positional vertigo. Otoconiabecome displaced from the utricle andrelocate to the bottom of the posteriorsemicircular canal, which is the lowestpart of the inner ear. ( NorthwesternUniversity, with permission.) 37. Cupular Pressure0 5 10 15 20 25Cupular Volume Displacement0 5 10 15 20 250 5 10 15 20 25Copyright 2007 by F. A. Davis.cause negligible movement of otoconia and that, practi-cally,sudden jerks of the head or maneuvers that incor-porateeccentric moments (such as the Semont maneuver)are unlikely to have a substantial additional effect incomparison with maneuvers that rely on gravity toaccomplish canalith repositioning.22Higher-Level Vestibular ProcessingIn this section we identify some of the more sophisticat-edaspects of central vestibular processing, which are notreflexes but rather require much more processing, aregenerally much more accurate, and often are at least par-tiallyunder conscious control. Because these mecha-nismsare more modifiable than vestibular reflexes, theyare especially relevant to rehabilitation. Most of thesemechanisms process multiple sensory inputs.Velocity StorageHow good does the VOR have to be? In order to keep theeye still in space while the head is moving, the velocityof the eyes should be exactly opposite to that of headmovement. When this happens, the ratio of eye move-mentto head movement velocity, called the gain, equals1.0. In order to maintain normal vision, retinal imagemotion must be less than 2 deg/sec. In other words, for ahead velocity of 100 deg/sec, which is easily produced byan ordinary head movement, the gain of the VOR must be98% accurate, because any greater error would causevision to be obscured.The normal VOR can deliver this high standard ofperformance only for brief head movements. In otherwords, the VOR is compensatory for high-frequencyhead motion but not for low-frequency head motion.This fact can be most easily seen if one considers theresponse of the SCCs to a sustained head movement,which has a constant velocity. The canals respond by pro-ducingan exponentially decaying change in neural firingin the vestibular nerve. The time constant of the expo-nentialis about 7 seconds; in other words, the firing ratedecays to 32% of the initial amount in 7 seconds. Ideally,the time constant should be infinite, which would beassociated with no response decline. Apparently, a timeconstant of 7 seconds is not long enough, because thecentral nervous system goes to the trouble to perse-veratethe response, replacing the peripheral time con-stantof 7 seconds with a central time constant of about20 seconds.14 Section ONE FUNDAMENTALSa) b)A AAABBBBbcbdPcVc= 0.68 mm= 0.16 mm(mPa)(pL)(/sec)Time(s)10.50302010210CCCCNystagmusFigure 1.14 Fluid mechanics of benign paroxysmal positional vertigo. (A) Trajectories of threeotoconia after a sudden change of head position that makes the posterior canal vertical. Otoconiabegin close to the cupula, fall through the ampulla with radius bc, and then enter the duct with radiusbd. (B) Simulated pressure, displacement, and nystagmus due to otoconia falling with the trajectoriesof A. (From Squires et al, 2004.) 21 38. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 15Copyright 2007 by F. A. Davis.The perseveration is provided via a brainstem struc-turecalled the velocity storage mechanism.23The velocity storage mechanism is used as a reposi-toryfor information about head velocity derived fromseveral kinds of motion sensors. During rotation in thelight, the vestibular nucleus is supplied with retinal slipinformation. Retinal slip is the difference between eyevelocity and head velocity. Retinal slip can drive thevelocity storage mechanism and keep vestibular-relatedresponses going even after vestibular afferent informationdecays. The vestibular system also uses somatosensoryand otolithic information to drive the velocity storagemechanism.24 The example discussed here shows how thevestibular system resolves multiple, partially redundantsensory inputs.Estimation: Going Beyond ReflexesReflexes are by definition simple sensory processors thatrapidly convert sensory input into motor outflow. Whathappens when sensory input is not available (such aswhen the eyes are closed) or inaccurate (such as when aperson with positional vertigo tilts the head), or noisy(such as when a sensor has been damaged)? A mecha-nismthat combines sensory inputs, weights them accord-ingto their relevance and reliability, and provides areasonable estimate of orientation in space, even withoutany recent sensory input, is needed. In engineering terms,we are discussing an estimator.Navigating the space shuttle involves similar prob-lems.The shuttle has dozens of sensors and motors.Some sensors respond quickly, and some slowly. Theymay differ in accuracy, scaling, coordinate frame, timing,and noise characteristics. No single sensor can provide acomplete picture of the shuttles state. A mechanism isneeded to integrate sensor output and to develop an inter-nalestimate of the state of the system (i.e., position,velocity, acceleration) in order to keep the shuttle on thedesired course and heading.The engineering solution to this problem developedout of work performed by Kalman and is often called aKalman filter. It is also commonly called an optimalestimator or an internal model. The essentials of theKalman filter are shown in Figure 1.15. There is consid-erableevidence that mechanisms similar to Kalman fil-tersare used for human sensorimotor processing.25The Kalman filter is far more powerful than a simplereflex. Several key concepts must be considered beforeone can understand how it is superior. First, internal mod-elsof sensors and motor output are used to develop anestimate of the current sensory and motor state. Theseinternal models are adjusted according to experience andMotorCommandCurrent StateEstimatePredictedNext StateNext StateEstimateModel ofSensoryOutputPredictedSensoryFeedbackActual SensoryFeedbackStateCorrectionSensoryErrorKalman GainForward Modelof DynamicsTime(s)Feedforward pathFeedback path0 1 2Gain++- +Figure 1.15 Block diagram showing a Kalman filter such as may be used by the body for sensori-motorintegration. Sensory inflow and motor outflow are used to estimate the current state. (FromWolpert and Miall, 1997.) [25] 39. Copyright 2007 by F. A. Davis.must track changes in bodily function. It seems likely thatvestibular rehabilitation affects internal models.Second, sensory input is not used to directly com-putebody state, but rather, the difference between senso-ryinput and predicted sensory input is used to correct thecurrent estimate of body state. This design allows theKalman filter to easily combine multiple sensor inputsfrom eyes, ears, and somatosensors. The Kalman filtercontinues to work even in the absence of a sensory input,because it uses its estimate when the sensor is missing.Both of these highly desirable features make the Kalmanfilter far superior to a simple assemblage of reflexes.The Kalman gain weights the extent to which a sen-soryinput affects the ongoing state estimate. Thisweighting provides a method of adjusting for the salienceand reliability of sensory streams. It seems highly likelythat vestibular rehabilitation adjusts the Kalman gain.Overall, this sort of mechanism is clearly far supe-riorto vestibular reflexes: Although not as fast, it can befar more accurate, it functions even in the absence of sen-soryinput, and it is modifiable by experience and reha-bilitation.Higher-Level Problemsof the Vestibular SystemCompensation for OverloadHumans can easily move their heads at velocities exceed-ing300 deg/sec. Consider, for example, driving a car.When one hears a horn to the side, ones head may rapid-lyrotate to visualize the problem and, potentially, avoidan impending collision. Similarly, during certain sports(e.g., racquetball), head velocity and acceleration reachhigh levels. One must be able to see during these sorts ofactivities, but the vestibular nerve is not well suited totransmission of high-velocity signals. The reason is thecutoff behavior discussed in the earlier section on motoroutput of the vestibular system. High-velocity head move-mentmay cause the nerve on the inhibited side to be driv-ento a firing rate of 0.In this instance, the vestibular system must dependon the excited side, which is arranged in push-pull con-figurationwith the inhibited side. Whereas the inhibitedside can be driven only to 0 spikes per second, the sidebeing excited can be driven to much higher levels. Thus,the push-pull arrangement takes care of part of the over-loadproblem. Note, however, that in patients with unilat-eralvestibular loss, this mechanism is not available to dealwith the overload problem, and they are commonly dis-turbedby rapid head motion toward the side of the lesion.Sensor AmbiguitySensory input from the otoliths is intrinsically ambigu-ous,because the same pattern of otolith activation can beproduced by either a linear acceleration or a tilt. In otherwords, in the absence of other information, we have nomethod of deciding whether we are being whisked offalong an axis or whether the whole room just tilted.Canal information may not be that useful in resolving theambiguity, because one might be rotating and tilting atthe same time. These sorts of problems are graphicallydemonstrated in subway cars and airplanes, which canboth tilt and/or translate briskly.Outside of moving vehicles, vision and tactile sen-sationcan be used to decide what is happening, perhapsthrough the use of a Kalman filter as discussed previous-ly.As long as one does not have to make a quick decision,these senses may be perfectly adequate. However, visualinput takes 80 msec to get to the vestibular nucleus andtactile input must be considered in the context of jointposition and of the intrinsic neural transmission delaysbetween the point of contact and the vestibular nuclearcomplex.Another strategy that the brain can use to separatetilt from linear acceleration is filtering. In most instances,tilts are prolonged but linear accelerations are brief.Neural filters that pass low or high frequencies can beused to tell one from the other.Nevertheless, in humans, evolution apparently hasdecided that the ambiguity problem is not worth solving.Otolith-ocular reflexes appropriate to compensate for lin-earacceleration or tilt do exist in darkness but areextremely weak in normal humans.26 Stronger otolith-ocularreflexes are generally seen only in the light, whenvision is available to solve the ambiguity problem.Sensory ambiguity becomes most problematic forpatients who have multiple sensory deficits, because theycannot use other senses to formulate appropriate vestibu-lospinalresponses.Motion SicknessThe phenomenon of motion sickness illustrates how thebrain routinely processes multiple channels of sensoryinformation simultaneously. The motion sickness syn-dromeconsists of dizziness, nausea or emesis, andmalaise after motion. It is thought to be caused by a con-flictbetween movement information in related sensorychannels, such as visual-vestibular conflict or conflictbetween an actual and an anticipated sensory input. Forexample, motion sickness is often triggered by reading a16 Section ONE FUNDAMENTALS 40. Chapter 1 ANATOMY AND PHYSIOLOGY OF THE NORMAL VESTIBULAR SYSTEM 17book while riding in a car. In this instance, the vestibularand proprioceptive systems signal movement, but thevisual system signals relative stability.The vestibular apparatus provides partially redun-dantinformation, allowing for the possibility of intra-labyrinthineconflict. Space motion sickness is thought tobe caused by intralabyrinthine conflict. About 50% ofspace shuttle astronauts experience motion sickness dur-ingthe initial 24 to 72 hours of orbital flight. It is cur-rentlythought that space motion sickness is due to adisturbance in otolith-tilt translation.27 The otoliths nor-mallyfunction in the context of a gravitational field, sothat at any moment the total force acting on the otoliths isthe vector sum of the force due to gravity and that due tolinear acceleration of the head. The central nervous sys-temexpects linear acceleration to be mainly related to tilt,because linear acceleration due to gravity is usually muchgreater than that due to acceleration of the head. Whenone is outside earths gravitational field, like astronauts inouter space, the only source of otolith stimulation is linearacceleration of the head. In susceptible individuals, thecentral nervous system continues to interpret linear accel-erationas being primarily related to tilt, which is nowuntrue, causing the motion sick