Utilizing Vestibular Function Testing to Assess and Treat Vestibular ...
Utilizing Vestibular Function Testing to Assess and Treat Vestibular ...
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<strong>Utilizing</strong> <strong>Vestibular</strong> <strong>Function</strong><strong>Testing</strong> <strong>to</strong> <strong>Assess</strong> <strong>and</strong> <strong>Treat</strong><strong>Vestibular</strong> System DysfunctionCombined Sections Meeting 2013San Diego CA, January 24, 2013Pat Flemming PT DSc GCS; Sarah Grantham, Aud D,CCC-A; Cathey Nor<strong>to</strong>n, PT; Amy Pause PT, DPTV<strong>and</strong>erbilt Bill Wilkerson Center Nashville, Tennessee
Course Objectives for Participants• Discuss challenges faced in PT assessment <strong>and</strong>management of concomitant BPPV <strong>and</strong>peripheral hypofunction.• Identify the most common causes for bilateralvestibular hypofunction.• Discuss functional impairments <strong>and</strong> rationale fortreatment in patients with bilateral vestibularloss.• Identify central <strong>and</strong> peripheral causes ofvestibular dysfunction.
Course Objectives for Participants• Describe how vestibular rehabilitative therapygoals for treatment will vary based on thetype <strong>and</strong> degree of vestibular dysfunction.
V<strong>and</strong>erbilt Bill Wilkerson Center for O<strong>to</strong>laryngology<strong>and</strong> Communication Sciences• Department of Audiology (Balance <strong>Function</strong> <strong>Testing</strong>,Pediatric <strong>and</strong> Adult Hearing Clinics)• Pi Beta Phi Rehabilitation Institute (PT, OT, ST, MSW,Driving Program, Seating <strong>and</strong> Mobility, Neurological PTClinical Residency Program)• Department of O<strong>to</strong>laryngology (Neuro<strong>to</strong>logy, CochlearImplantation, Voice Center, Head <strong>and</strong> Neck Cancer,O<strong>to</strong>logy)• Department of Speech Language Pathology (Adult <strong>and</strong>Pediatric programs, Mama Lere School)• Graduate level teaching (MD, SLP, AuD, PT, OT)
COI Disclosure• We have NO financial relationships <strong>to</strong>disclose.
<strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong>Sarah L. Grantham, Au.D.
Department of <strong>Vestibular</strong> SciencesFaculty <strong>and</strong> StaffGary Jacobson, Ph.D. Devin McCaslin, Ph.D. Sarah Grantham, Au.D. Jill Gruenwald, Au.D.Lauren Tegel, Au.D.Lindsay Daniel, Au.D.
Balance Disorders Labora<strong>to</strong>riesRotary Chair VNG/ENG 1VNG/ENG 2 VNG/ENG 3 Posturography
Clinical Tests/Programs• Electro-Videonystagmography (ENG/VNG)• Rotational <strong>Testing</strong>• <strong>Vestibular</strong> Evoked Myogenic Potentials– Cervical (cVEMP)– Ocular (oVEMP)• Computerized Dynamic Posturography• Pediatric Balance <strong>Function</strong> <strong>Assess</strong>ment• Falls Risk <strong>Assess</strong>ment
The <strong>Vestibular</strong> System
Objectives• Present current <strong>Vestibular</strong> <strong>Function</strong> Test (VFT) battery– Review the neural pathways of:• The Vestibulo-Ocular Reflex (VOR)• The Vestibulo-Collic Reflex (VCR)– Review recording techniques <strong>and</strong> interpretation of VFTfindings.• Present patterns of abnormality commonly identified duringVFT.
ENG/VNG• Ocular Motility– Saccades, Smooth Pursuit,Op<strong>to</strong>kinetics, Spontaneous<strong>and</strong>/or Gaze-EvokedNystagmus• Positional/Positioning <strong>Testing</strong>– Benign Paroxysmal PositionalVertigo (BPPV)– Spontaneous & CentralPositional Nystagmus• Bithermal Caloric Test– “Gold St<strong>and</strong>ard” for identifyingperipheral vestibular systemimpairment affecting the lateralSCC <strong>and</strong>/or superior vestibularnerve.
Vestibulo-Ocular Reflex (VOR)• Stimulation of the IpsilateralHorizontal SemicircularCanal (hSCC)– Activates: Ipsi. MedialRectus, Contra. LateralRectus– Inhibits: Ipsi. LateralRectus, Contra. MedialRectus– Generates a horizontaleye movement with slowphase away fromstimulated ear
Benign Paroxysmal Positional Vertigo (BPPV)• Screening for BPPV• Dix-Hallpike <strong>Assess</strong>es:– Posterior SCC (pSCC)• Up-beatingNystagmus– Anterior SCC (aSCC)• Down-beatingNystagmus• Roll Tests <strong>Assess</strong>:– Horizontal SCC (hSCC)• Geotropic vs.Ageotropic Nystagmus
Pathophysiology of BPPV• Displaced o<strong>to</strong>conia act asmobile densities within thecanal.• Head movement causesmass of o<strong>to</strong>conia <strong>to</strong> shiftwithin the SCC.• Endolymphatic fluidbecomes displaced,deflecting the cupula whichelicits nystagmus <strong>and</strong>vertigo.
Nystagmus Characteristics of h-BPPVThree Subtypes• Bilateral Geotropic Nystagmus (Canalolithiasis)– O<strong>to</strong>conial debris within posterior arm of hSCC• Bilateral Ageotropic Nystagmus– Reverts <strong>to</strong> Geotropic– O<strong>to</strong>conial debris within anterior arm of hSCC• Bilateral Ageotropic Nystagmus (Cupulolithiasis)– Persistent ageotropic nystagmus– O<strong>to</strong>conial debris located on utricular side of hSCC
Geotropic h-BPPV• Geotropic variant: Rotation of the head results inhorizontal nystagmus which beats <strong>to</strong>ward theundermost ear.– With geotropic nystagmus, the location of the debriswithin the canal causes ampullopetal endolymph flowwhich generates excita<strong>to</strong>ry GEOtropic nystagmus (i.e.the affected side generates the MORE intensenystagmus response).
Geotropic-Posterior Arm hSCCHigher SPVLower SPV
Ageotropic h-BPPV• Ageotropic variant: Rotation of the head results inhorizontal nystagmus which beats <strong>to</strong>ward theuppermost ear.• With ageotropic nystagmus, the location of the debriswithin the canal causes ampullofugal endolymph flowwhich generates inhibi<strong>to</strong>ry AGEOtropic nystagmus (i.e.the affected side generates the LESS intensenystagmus response).
Ageotropic-Anterior Arm hSCC(Canal Side)Lower SPVHigher SPV
Ageotropic-Anterior Arm hSCC(Utricular Side)Lower SPVHigher SPV
Flow Chart for the <strong>Treat</strong>ment of hSCC BPPV
Electro-Videonystagmography:Bithermal Caloric TestRemember “COWS”:Cold – OppositeWarm – Same
Bithermal Caloric Norms<strong>and</strong> Terms of Use• Quantification of theVOR:– Slow Phase Velocity(SPV)– Degrees perSecond (deg/sec)• Total Caloric Response– 22% asymmetrysuggest a Unilateralperipheral deficit• DirectionalPreponderance– >28% is abnormal
Rotary Chair• <strong>Assess</strong>es the VOR over a broaderoperational range of frequencies(0.01Hz-0.64Hz).– Calorics assess VOR at~0.003Hz (very low frequencyresponse)• Useful in determining:– Central Compensation ofUnilateral Peripheral Deficits– Degree of Bilateral Peripheral<strong>Vestibular</strong> System Hypofunction– Identification of Central<strong>Vestibular</strong> System Impairments
Rotary ChairPhase: Timing relationship between eye <strong>and</strong> head velocity.Gain: The ratio of peak eye velocity <strong>to</strong> head velocity.Symmetry: The ratio of rightward versus leftward SPV.
Acutely UncompensatedUnilateral Peripheral Deficit
Profound Bilateral Hypofunction
Acoustical Cervical VEMP(cVEMP)P13N23
Acoustically Evoked Sonomo<strong>to</strong>r Response• The cVEMP is a stimulusrelatedattenuation of <strong>to</strong>nicEMG activity.• An acoustically evoked<strong>to</strong>neburst (500Hz) stimulusacts as a hydro-mechanicalforce <strong>to</strong> move theendolymphatic fluid <strong>and</strong>, asa consequence, translateso<strong>to</strong>liths <strong>to</strong> createtransduction.
The Recep<strong>to</strong>r for cVEMP is the Saccule.Halmagyi & Curthoys (1999)• The Saccule is the vestibular endorgan most sensitive <strong>to</strong> sound.• Lies under the stapes footplate.• Neurons from saccular macularespond <strong>to</strong> tilts <strong>and</strong> click stimuli.• Electrical output from the sacculeis routed through the inferiorvestibular nerve.
Central Connections & Efferent Pathway“Vestibulocollic Reflex”(From: Rosengren et al. 2009)• Saccule (a)• Scarpa’s ganglion (a)• Inferior vestibular nerve (a)• <strong>Vestibular</strong> nucleus (a)• Medial vestibulospinal tract(MVST) – (e)• Spinal accessory nucleusof CN XI (e)• CN XI (e)eaeaea = afferent, e = efferent
How do we activate the SCM?Unilateral Activation/Recording<strong>Testing</strong> right<strong>Testing</strong> left
Acoustical Ocular VEMP (oVEMP)(P15)P1N1(N10)
2-Channel oVEMP RecordingVersion 2GroundActive (+)Reference (-)
oVEMP Pathway(after Curthoys et al., 2011 <strong>and</strong> Manzari et al., 2010)• oVEMP Pathway– Utricle– Sup. Vestib. Nerve– Med. Vestib. Nuc.– Medial LongitudinalFasciculus– Mo<strong>to</strong>r Nucleus of ContraCN III– CN III– Contra Inferior Oblique m.UtricleSup. Vestib. N.
Test-specific Topological Localization• Caloric Test– Horizontal Semicircular Canal– Ampullary Branch of the Superior<strong>Vestibular</strong> Nerve• oVEMP– Utricle– Utricular Branch of the Superior<strong>Vestibular</strong> Nerve• cVEMP– Saccule– Inferior <strong>Vestibular</strong> NerveImage from Manzari et al., 2010
Possible Patterns of Impairment<strong>and</strong> Their Clinical SignificanceType Caloric cVEMP oVEMP Impairment1 Nl Nl Nl None2 Abn Abn Abn Large end organ, or inf. <strong>and</strong> sup.vestibular nerve3 Nl Abn Nl Saccule or inf. vestibular nerve4 Abn Nl Abn Sup. vestibular n.5 Abn Nl Nl hSCC6 Nl Nl Abn Utricle7 Nl Abn Abn Utricle + saccule or inf. vestibular nerve?8 Abn Abn Nl hSCC + saccule, <strong>and</strong>/or inf. vestibular n.?9 Nl Abn* Abn* SSCD Syndrome* = Abnormally reduced VEMP thresholds
Insensitivity of the Romberg Test of St<strong>and</strong>ing Balance on Firm <strong>and</strong>Compliant Support Surfaces (RTSBFCSS) in Diagnosing<strong>Vestibular</strong> System Disorders(Jacobson et al., 2011)• Using the NHANES subject selection criteriawith the RTSBFCSS offers poor sensitivity(
Excellent Reference Materials
A Case of ConcomitantVestibulopathy <strong>and</strong> BPPVPat Flemming PT DSc GCS
Background.. Case One• Dizziness is one of the most frequent clinical drivers for avisit <strong>to</strong> a physician or other health care provider.• <strong>Treat</strong>ment may be provided by a MD, nurse practitioner& others in a variety of clinical settings (i.e. ER, out-pt.)• Common diagnoses referred <strong>to</strong> PTs specializing investibular rehabilitation therapy (VRT) are BenignParoxysmal Positional Vertigo (BPPV) <strong>and</strong> UnilateralPeripheral Hypofunction.• Many times, however, a definitive diagnosis has notbeen reached; the referring diagnosis is non-specific ormisleading, i.e. Dizziness, Ataxia.
Background.. continued• Sophisticated diagnostic equipment or therapistsspecializing vestibular rehabilitation with may not beavailable in all communities.• BPPV may present alone or in combination with othervestibular dysfunction.• In some cases, a peripheral hypofunction may gountreated since the most provoking <strong>and</strong> urgentsymp<strong>to</strong>ms are related <strong>to</strong> BPPV.• <strong>Vestibular</strong> function testing can assist in identifyingunderlying vestibulopathy which may benefit fromvestibular rehabilitation.
Purpose• The primary purpose of this case is <strong>to</strong> describe apatient presenting with concomitant unilateralperipheral vestibulopathy <strong>and</strong> BPPV.• Secondary purposes include:– Increase therapist awareness of vestibular comorbiditiesin patients they may evaluate <strong>and</strong> treat– Increase therapist awareness of the benefits ofaudiological vestibular function testing in diagnostics– Describe bedside tests that may be utilized bytherapists for screening when vestibular functiontesting is not available in the community
BPPV Etiology <strong>and</strong> Characteristics• Often occurs spontaneously; remission can alsobe spontaneous.• May follow trauma <strong>to</strong> the head, labyrinthitis,<strong>and</strong>/or ischemia.• Symp<strong>to</strong>ms evoked with looking down or up,rolling over in bed, putting head back for anappointment, i.e. dentist.• Vertigo often fleeting, but symp<strong>to</strong>ms ofimbalance, lightheadedness may persist.S. Herdman, <strong>Vestibular</strong> Rehabilitation,Ch.17, 2007.
<strong>Vestibular</strong> Hypofunction: Etiology <strong>and</strong>Characteristics• <strong>Vestibular</strong> neuritis, <strong>and</strong> labyrinthitis arecommon causes.• Symp<strong>to</strong>ms may include vertigo,dysequilibrium, acute nausea/ vomiting,oscillopsia, tinnitus, dizziness, imbalance,blurred vision, falls his<strong>to</strong>ry, fear ofmovement, <strong>and</strong> hearing loss.Herdman, S. <strong>Vestibular</strong> Rehabilitation, Ch.19, 2007.
Diagnostics:<strong>Vestibular</strong> Hypofunction• Bithermal caloric test is considered a significanttest in diagnosis of vestibular dysfunction• A difference of more than 20-23% betweenresponses from the ears is considered clinicallysignificant for a weak vestibular system.• A unilateral weakness implies vestibular disorderon the side of the decreased response; there isasymmetry in the magnitude of informationentering the brainstem, resulting in differentnystagmus characteristics from each ear.Jacobson et al., 1997; Jonkees et al., 1962.
Concomitant Vestibulopathy <strong>and</strong> BPPV• Numerous disorders may cause the presence ofboth disorders.– <strong>Vestibular</strong> neuritis– Labyrinthitis– Meniere’s Disease– Cerebrovascular disease, including CVA, TIA,migraines, basilar artery insufficiency,vertebrobasilar insuffiency– Head TraumaPollack et al., 2002; Hughes&Proc<strong>to</strong>r 1997;Katsakas &Kirkham, 1978; Karlberg et al.,2000.
Primary <strong>and</strong> Secondary BPPV• Patients without his<strong>to</strong>ry of o<strong>to</strong>logic pathologyhave been described as presenting with primaryBPPV; with a definite his<strong>to</strong>ry of o<strong>to</strong>logicpathology, secondary BPPV.• Prevalence of vestibulopathy in individuals withBPPV has been reported in range of 13 -50%.Karlberg et al, 2000; Blesing et al, 1986;Hughes &Proc<strong>to</strong>r, 1997; Pollack et al., 2002.
Prevalence of Vestibulopathy in Benign Positional VertigoPatients With <strong>and</strong> Without Prior O<strong>to</strong>logic His<strong>to</strong>ryInt J Aud 2005;44:191-196 Roberts et al.• Purpose: determine prevalence of vestibulopathy intwo groups of participants presenting with posteriorcanal BPPV; retrospective review of 157 charts.• Patients divided in<strong>to</strong> two groups based on o<strong>to</strong>logicalhis<strong>to</strong>ry: 49 patients with positive prior his<strong>to</strong>ry, 108with negative his<strong>to</strong>ry.• Caloric testing performed on all patients as part ofassessment of vertigo.• Findings: Vestibulopathy present in 53.1% of patientswith positive Hx, 30.6% in patients with negative Hx.
Clinical Significance of Concomitant BPPV<strong>and</strong> Vestibulopathy• Patients with BPPV <strong>and</strong> additional vestibulopathymay have a greater incidence of symp<strong>to</strong>ms followingBPPV Rx than those with BPPV alone.• Underlying vestibular disorder may result indysequilibrium, lightheadedness, increase falls risk.• Vestibulopathy may be caused by varied conditions:uncompensated peripheral hypofunction, anunidentified vertical canal, o<strong>to</strong>lith, or centralvestibular dysfunction.Roberts et.al, 2005.
Case Description• 54 y.o. female reported <strong>to</strong> ER in Oc<strong>to</strong>ber via ambulanceafter 1 week of mild dizziness <strong>and</strong> lightheadedness.Chief complaint: Onset of constant dizziness. Severeepisode of nausea, imbalance, unable <strong>to</strong> walk alone,vertigo with certain head movements on day presenting<strong>to</strong> ER. She had vomited x2. Hypertension noted enroute. Initial concern: possible CVA.• MRI at time of ER visit– Negative for acute infarct; Old infarct of left centrumsemivale; MRA of head/ neck negative for stenosis,dissection/ or aneurysm
Patient His<strong>to</strong>ry <strong>and</strong> Hospital Course• Patient his<strong>to</strong>ry included heart murmur, + TB skin test(completed INH 20 years prior), G3G4 (twins),hearing loss in L ear, vertigo, tinnitus x1 day• Employed as RN, married, working one full <strong>and</strong> onepart-time job.• Neurology consult in ER: “ most likely viral acutelabyrinthitis or vestibular neuronitis; onset <strong>to</strong>oabrupt with constant symp<strong>to</strong>ms unlikely <strong>to</strong> be BPPV.<strong>Treat</strong> with steroids, meclizine, fluids, refer <strong>to</strong> ENT”.Patient admitted for overnight observation.
Hospital Course.. Continued• ENT consult during in-patient stay:– Audiogram revealed L sided high-frequency SNHL; patientreported long st<strong>and</strong>ing hearing loss vs. acute loss– Dix Hallpike Test: positive <strong>to</strong> the left– Epley maneuver performed, followed by patient vomiting.After recovery, Dix Hallpike repeated with < vertigo <strong>and</strong>rotary nystagmus. Canal involvement not documented.– Discharge following one overnight; referral for audiologicbalance function testing as out-patient.– ENT resident assessment “ Findings consistent with BPPV”.
<strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong>(28 Days s/p Hospital Discharge)• Impressions:– BPPV affecting the L horizontal semi-circular canal;geotropic nystagmus (treated x1 with Bar-b-q Roll)– Caloric testing : L peripheral vestibular systemdisorder (50% weakness)– Absent cVEMP <strong>and</strong> oVEMP on the left– Rotary Chair Test: Uncompensated weakness.Asymmetries <strong>to</strong> the right consistent with L beatingrecovery nystagmus.– 46/100 Dizziness H<strong>and</strong>icap Inven<strong>to</strong>ry (severeperceived h<strong>and</strong>icap); abnormal anxiety rating (HADS)
Recovery Nystagmus• Fine, left-beatingnystagmus
Roll TestsHead LeftHead RightGeotropic Nystagmus(Greater SPV Head LEFT)
VNG• NORMAL– Ocular motility• ABNORMAL– Fine, left-beatingrecoverynystagmus– Geotropicnystagmus c/wLEFT hSCC BPPV– 50% unilateralweakness in theLEFT ear.
Left EarcVEMPRight Ear• Abnormal cVEMPexamination– Absent LEFT cVEMP• Amplitude AsymmetryRatio:– 100% <strong>to</strong> the LEFT– >47% is Abnormal• Impaired Saccule <strong>and</strong>/orInferior <strong>Vestibular</strong> Nerve
Left EaroVEMPRight Ear• Abnormal oVEMPexamination– Absent LEFT oVEMP• Amplitude AsymmetryRatio:– 100% <strong>to</strong> the LEFT– >33% is Abnormal• Impairment affecting atleast the Superior<strong>Vestibular</strong> Nerve
Rotary ChairMulti-frequency Asymmetries (0.01Hz-0.04Hz)Presence of Multi-frequency asymmetriesIndicates INCOMPLETE Compensation
Physical Therapy Initial Evaluation• Subjective: inability <strong>to</strong> work currently as RN.• PT Eval: 4 days post vestibular function testing.• InVision <strong>Testing</strong> initiated, but discontinued duringGaze Stabilization Test. Static <strong>and</strong> dynamic visualacuity then assessed with Snellen chart seated from10’. 20/16 static visual acuity; 20/50 (5 Line Dropwith imposed horizontal head movements.)• Video goggles utilized <strong>to</strong> perform Dix Hallpike <strong>and</strong>Roll Tests: Left beating horizontal nystagmus > 1 min.duration noted with Roll Test bilaterally, indicating Lhorizontal canal cupuloliathiasis.
Physical Therapy Initial Intervention• Quick bar-b-q Roll initiated from the left, followed byCasani (modified Semont maneuver.)• Patient instruction : prolonged positioning at night,lying initially on the left, then rolling <strong>to</strong> the right.Patient instructed <strong>to</strong> repeat process if out of bedduring night or aware she had changed position.• Patient instruction : Casani maneuver for followthrough daily at home.• VOR 1 viewing <strong>and</strong> two target eye/ head substitutionexercises.
Second PT Visit• Subjective report: still dizzy, no true vertigo,performing prolonged positioning & Casani• Negative for BPPV using video goggles• No subjective report of vertigo• Left beating nystagmus of lesser degree.• Progression <strong>to</strong> VOR 1 view full field stimulus.• Self canalith repositioning maneuverdiscontinued due <strong>to</strong> resolution of BPPV.
Third PT Visit• Progression <strong>to</strong> VOR 2 viewing ex. , negative DixHallpike/ Roll Tests.• Completion of InVision <strong>Testing</strong>.– Perception Time: 30 msec.– Gaze Stabilization : 83 degrees/ second left; 90degrees second/ right– Dynamic Visual Acuity: .12 Logmar loss <strong>to</strong> L, .32Logmar loss <strong>to</strong> R with horizontal headmovements; WNL with vertical head movements
Fourth PT (VRT) Visit• Subjective report: feeling better, off FMLA, able<strong>to</strong> return <strong>to</strong> work part-time. Continuing with gazestabilization / VOR program. Still reportingdizziness with quick head movements.• Gaze Stabilization Test: 87 degrees/ second <strong>to</strong>the left; 127 degrees/ second <strong>to</strong> right (19%asymmetry).• Progressed <strong>to</strong> Week 5/6 of the gaze stabilizationprogram (VOR1 <strong>and</strong> 2, two target eye/ head).
Discharge Visit (#5): Patient Outcomes• 5 PT visits over 10 weeks (December <strong>to</strong> February)• 30/30 on the <strong>Function</strong>al Gait <strong>Assess</strong>ment• 12/100 Dizziness H<strong>and</strong>icap Inven<strong>to</strong>ry (absentperceived h<strong>and</strong>icap vs. 46/100 initially)• Snellen Chart: accurate at 2 line drop with imposedhorizontal head movements at 2 Hz.• Subjective report of return <strong>to</strong> work at 36 hr/ week asRN, looking for supplemental prn work as well• Instruction in continuing gaze stabilization programover next several months.
Use of <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong> Results:Patient with BPPV <strong>and</strong> Hypofunction• > collaboration between healthcare providers• <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong> alerted therapist <strong>to</strong> multipleareas of vestibulopathy which could affect patient’sfunctional status:– Absent VEMPs on the left– L peripheral system disorder (50% weakness)– Left beating recovery nystagmus– Identification of canal affected 4 days prior <strong>to</strong> PTevaluation; Left horizontal SCC BPPV canaliathiasis– High perceived dizziness h<strong>and</strong>icap; high anxiety
Benefit of Collaborative <strong>Testing</strong>• Without benefit of vestibular function testing,increased possibility of “ tunnel vision” bytherapist <strong>and</strong>/or patient, focusing solely on theBPPV.• Audiologists skilled in performing VEMPs, ENG/VNG, Rotary Chair, etc.• PTs skilled in assessing postural control, gait,functional balance.• The patient “wins” with comprehensiveassessment/ Rx from the vestibular rehab team.
Take Home Message: Case One• Consider underlying vestibulopathy when a referralfor BPPV is received or when you identify a patientwith BPPV; consider referral for vestibular functiontesting.• Perform “ bedside tests” if vestibular function testingis not available in your community: Head ImpulseTest, screening with Snellen chart.• Don’t assume that if the BPPV is resolved, thepatient’s functional deficits are resolved.• Create a vestibular rehabilitation network withinyour region <strong>to</strong> provide optimal care for patients.
A Case of Bilateral <strong>Vestibular</strong> HypofunctionCathey Nor<strong>to</strong>n, PT
Background• Bilateral <strong>Vestibular</strong> Hypofunction (BVH) is less commonthan unilateral hypofunction <strong>and</strong> less often diagnosed asa cause of dizziness.• Imbalance, lightheadedness <strong>and</strong> oscillopsia are commoncomplaints.• BVH leads <strong>to</strong> increased risk for falls, decreasedvocational ability, participation in leisure activities, driving<strong>and</strong> social isolation.• Since symp<strong>to</strong>ms mimic many nonvestibular causes ofdizziness, <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong> is beneficial indetermining proper treatment <strong>and</strong> functional outcomesfor patients with bilateral vestibular hypofunction.Schubert, 2004; Brown et al, 2001
Purpose• Describe common presenting symp<strong>to</strong>ms <strong>and</strong>causes of bilateral vestibular hypofunction(BVH)• Discuss benefits of <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong>results in planning appropriate treatment• Present appropriate clinical tests <strong>and</strong> measures• Describe rationale for treatment of BVH• Discuss expected outcomes for patients withBVH
Common Causes of BVH• O<strong>to</strong><strong>to</strong>xicity• Meningitis• Labyrinthine infection /bilateral neuritis• O<strong>to</strong>sclerosis• Paget’s disease• Bilateral tumors• Endolymphatic Hydrops• Polyneuropathy• Au<strong>to</strong>immune Disease• Congenital• O<strong>to</strong><strong>to</strong>xic medications (e.g.,aminoglycosides, cisplatin)• Idiopathic vestibular loss• Bilateral Meniere’s disease• Cerebellar ataxia withneuropathy <strong>and</strong> bilateralvestibular areflexiasyndrome (CANVAS)• Trauma• Au<strong>to</strong>immune disease• Genetic disease• Meningitis• Neurofibroma<strong>to</strong>sis type 288Herdman 2007; McCall, et al 2009
Causes of BVH• The cause of BV remains unclear in about half ofall patients.• A large subgroup of these patients haveassociated cerebellar dysfunction <strong>and</strong> peripheralpolyneuropathy.• This suggests a new syndrome that may becaused by neurodegenerative or au<strong>to</strong>immuneprocesses.McCall et al, 2009
Case Description• Referral from O<strong>to</strong>laryngology Nurse Practitioner.• Referring Diagnosis - Vertigo, peripheral- 386.10• Initial evaluation 9/3/09• 30 year old female• Onset: 2-3 years ago• Chief complaints – Patient reports 2-3 years of feelingwobbly in her head with multiple brief episodes of vertigowhich only last minutes <strong>and</strong> does not return for weeks.• Described as an episode of her eyes shifting "likesomeone hit me in the head" <strong>and</strong> feeling off balance inthe dark.
Patient His<strong>to</strong>ry• Subjective : "I feel off balance <strong>and</strong> like my eyes will not staystill at times“• Patient Goals : “I want <strong>to</strong> have better balance <strong>and</strong> get back <strong>to</strong>normal. I need <strong>to</strong> be able <strong>to</strong> drive with my kids in the car.”• Neurology consult: 4/28/09 - Impression: “Recurrent dizzinessof uncertain cause. I do not think that she has a vestibularmigraine. I do not have a clear explanation for her recentepisodes of transient/fleeting visual shift. The comprehensiveexamination shows no evidence for cerebellar syndrome orbenign positional vertigo.”• Diagnostic testing: MRI 5/7/09 – normal• Referred <strong>to</strong> O<strong>to</strong>laryngology• <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong>: 6/2/09
Medical His<strong>to</strong>ry• DM - TYPE I since age 3 (has insulin pump)• Normal pregnancy 2002/2003, second pregnancy 2006-07, EDC5/31/07. Scheduled C-section 2003 & 5/17/07.• UTI 3/04-Cipro• PYELONEPHRITIS - April 2001• NPDR OU (non proliferative diabetic retinopathy)• Graves Disease 2005, I-131 treatment (radioiodine treatment)• Hypothyroidism after ablation• Dysuria 4/04• URI 2/09• Elevated blood pressure 04-09• Four wisdom teeth removed• Renal cyst left drained '99.
VFT Results• VNG (ABNORMAL)– Fine spontaneous versuscentral positional nystagmus– Abnormally Reduced TotalCaloric Response• 9 deg/sec – 2009• 11 deg/sec – 2010•
Rotary ChairMulti-frequency VOR gain reductionswith asymmetries <strong>and</strong> phase leads(Note preserved high frequency function)
Impression• Bilateral <strong>Vestibular</strong> hypofunction based on:– Visual disturbances (oscillopsia)– Imbalance – especially in the dark– <strong>Vestibular</strong> function testing– Normal MRI
Examination• ROM, Strength, coordination, muscle <strong>to</strong>ne, bedmobility, transfers <strong>and</strong> ambulation normal• Sensation testing performed in Diabetic Clinic <strong>and</strong>reported as normal.• Oculomo<strong>to</strong>r exam normal• Head Impulse test: abnormal bilaterally• Dynamic Gait Index: 22/24
DGI Videos
Intervention• Patient elected <strong>to</strong> attend therapy at a facilitycloser <strong>to</strong> her home as she is not comfortabledriving <strong>and</strong> lives 25 miles from the clinic.• She was referred <strong>to</strong> a facility with a PT who hasexperience in <strong>Vestibular</strong> Rehabilitation. Theclinic is 5 miles from her home <strong>and</strong> she feels shewill be able <strong>to</strong> attend therapy there.
Second Evaluation• 6/29/10 (9 months following initial evaluation)• Patient did not attend therapy at the local facility• Chief complaints - She has been unable <strong>to</strong> drivefor the past month due <strong>to</strong> increase in symp<strong>to</strong>msof dizziness when driving. She feels dizzy whenshopping in the grocery s<strong>to</strong>re, at church <strong>and</strong> inrestaurants. She reports nausea when she getsdizzy.• Physical exam unchanged• DGI 22/24 remains unchanged
<strong>Treat</strong>ment• Adaptation exercises <strong>to</strong> improve use of remainingvestibular function• Substitution exercises <strong>to</strong> improve use of alternatesensory systems for improving visual stability <strong>and</strong>balance.• Safety <strong>and</strong> falls prevention education
<strong>Treat</strong>ment• Adaptation refers <strong>to</strong> the potential for theremaining vestibular system <strong>to</strong> adjust its outputaccording <strong>to</strong> the dem<strong>and</strong>s placed on it.• Achieve long-term change in the neuronalresponse <strong>to</strong> reduce symp<strong>to</strong>ms <strong>and</strong> normalizinggaze <strong>and</strong> postural stability.• A critical signal <strong>to</strong> induce adaptation is retinalslip during head movements.• VORx1 ,VOR x2 (use if some functions remains)Cox & Hall, 2009
<strong>Treat</strong>ment• Substitution – use of alternative strategies formissing vestibular function.• Substitution for the VOR includes the cervicalocular reflex, use of smooth pursuit eyemovements, <strong>and</strong> central preprogramming of eyemovements.• Substitution includes the use of visual cues,soma<strong>to</strong>sensory cues, or both <strong>to</strong> maintainstability.Cox & Hall, 2009
<strong>Treat</strong>ment• Substitution exercises– Saccades – two targets central preprograming– Imaginary targets – COR– Visual substitution exercises – walk <strong>to</strong> a target– Soma<strong>to</strong>sensory inputs- firm surface, proprioceptivetraining at ankles• Precautions– Light in home –carry a flashlight– Watch uneven terrain– Use of assistive device if necessary
Outcomes• Patient received 9 visits over 2 months (6-29 <strong>to</strong> 9-2-10).• SOT composite score declined from 47 <strong>to</strong> 39.• DVA unchanged from 0.19 left 0.26 right <strong>to</strong> 0.11logMar left, 0.26 logMar right.• <strong>Function</strong>al: patient reports decreased symp<strong>to</strong>ms ofoscillopsia, when shopping or at church she can usevisual fixation <strong>to</strong> feel less “dizzy”, limited driving, ingood weather, close <strong>to</strong> home <strong>and</strong> during daylighthours. Does not drive when she is “having a badday”.
Conclusion• Patients with bilateral vestibular loss improve in theirperception of dizziness <strong>and</strong> imbalance.• 33% <strong>to</strong> 55% improved with individualized vestibularphysical therapy program.• Most patients with BVH continue <strong>to</strong> be at risk forfalls.• Recovery is longer than UVH – up <strong>to</strong> 2 years.• Patients should be referred <strong>to</strong> physical therapist withtraining in vestibular rehabilitation.• Some may be able <strong>to</strong> return <strong>to</strong> driving• Refer for VFT <strong>to</strong> determine BVL.Brown, et al 2001; MacDougall, et al 2009
A Case of Dizziness With ConcomitantCentral <strong>and</strong> Peripheral DysfunctionAmy Pause, PT, DPT
Background• Patient’s presenting with vertigo:– 75% Peripheral vestibular disorders– 25% Central origin• Most Common Causes of Vertigo:– BPPV– <strong>Vestibular</strong> neuritis– Meniere’s syndrome– Vascular disordersKaratas M, 2011
Background• Vertigo of vascular origin is usually limited <strong>to</strong>:– Migraine• Migraine affects as many as 15-20% of the generalpopulation.• A quarter of patients with migraine experiencespontaneous attacks of vertigo.Karatas M, 2011
Background– Transient ischemic attacks– Ischemic or hemorrhagic stroke• 6 - 7% Cerebrovascular disease• 1.5 - 3.6% Cardio-circula<strong>to</strong>ry disease• Cerebrovascular <strong>and</strong> cardio-circula<strong>to</strong>ry causes are:– Relatively uncommon– More serious causes of vertigo– Lead <strong>to</strong> various central or peripheral vestibularsyndromes with vertigoKaratas M, 2011
Purpose• Present a patient with symp<strong>to</strong>ms of dizziness ofvascular origin.• Discuss benefits of <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong><strong>to</strong> guide clinical tests <strong>and</strong> measures.• Describe use of tests <strong>and</strong> measures <strong>to</strong> formulatecus<strong>to</strong>mized treatment interventions <strong>to</strong> maximizeoutcomes.
Case Description• The patient is a 28 year old male who works in audioengineering at a local hotel resort.• Past medical his<strong>to</strong>ry includes:• Congenital heart disease - double outlet right ventricle• Pulmonary valve replacement• 1st <strong>and</strong> 2nd degree AV block with pacemakerplacement• Atrial tachycardia with ablation procedure• Cardioembolic stroke/TIA x 5• Psychogenic non-epileptic seizures• Suspected migraines
His<strong>to</strong>ry• Complex congenital heart disease resulted in multiplesurgeries <strong>and</strong> pacemaker placement.– Age 19, experienced a brainstem stroke resulting in:• Left-sided facial weakenss, extremity weakness,significant dysarthria, difficulty managing hisairway, diplopia.– Recovered well <strong>and</strong> discharged• Had remaining supranuclear paralysis of left eyewith convergence <strong>and</strong> retraction nystagmus– Inpatient rehab for 6 days– Outpatient rehab 2x/week
His<strong>to</strong>ry– Between ages 20 <strong>and</strong> 22 years - emergencydepartment for headaches, dizziness, <strong>and</strong> seizures.– Age 25, he had a TIA event <strong>and</strong> prescribedCoumadin.– Five months later he presented <strong>to</strong> ED with:• left eyelid droop• right arm weakness• Surgery <strong>to</strong> remove a 13 cm plastic fragment fromhis left atrium. This was thought <strong>to</strong> be the cause ofclot formation, <strong>and</strong> thus his strokes, <strong>and</strong> eventuallyhe was taken off Coumadin.
His<strong>to</strong>ry– Age 26, brief TIA with:• Diplopia & Left sided weakness– Age 27, sudden onset of:• Headache, double vision, dizziness, heaviness inleft arm• Evaluated in the ED– CTA of the head <strong>and</strong> neck was normal <strong>and</strong> hewas discharged.– Neurology consult with stroke specialist. Started onCoumadin with no further episodes; although,dizziness persisted.
O<strong>to</strong>laryngology Consult• O<strong>to</strong>laryngology referral, three months later, for persistentdizziness.– Describes dizziness as a sensation of acutedisequilibrium.• Episodes of dizziness occur in frequency of a ~ 10times each day• Usually last for 5-10 seconds.• Dizziness is not related <strong>to</strong> changes of headposition.
O<strong>to</strong>laryngology Consult– Falling <strong>to</strong>wards the left direction.– His<strong>to</strong>ry of headaches that are sometimesassociated with the dizziness.– Problems with double vision secondary <strong>to</strong> hisCVAs.– Has been prescribed Antivert in the past withoutimprovement of symp<strong>to</strong>ms.– Referred for CT scan <strong>and</strong> <strong>Vestibular</strong> <strong>Function</strong><strong>Testing</strong>.
VNG• NORMAL– Ocular motility– Positional <strong>and</strong>positional testing• ABNORMAL– Fine, left-beatingspontaneousnystagmus– 30% unilateralweakness in theRIGHT ear– >22% is Abnormal
Rotary ChairVOR Phase, Gain & Symmetry (0.08Hz-0.32) WNL(Isolated asymmetry at 0.01Hz is in keeping with the presenceof spontaneous nystagmus)
Left EarcVEMPRight Ear• Bilaterally normalcVEMP examination• AmplitudeAsymmetry Ratio:– 36% <strong>to</strong> the LEFT– > 47% is Abnormal• Intact Saccule <strong>and</strong>Inferior <strong>Vestibular</strong>Nerve
Left EaroVEMPRight Ear• Bilaterally normaloVEMP examination• AmplitudeAsymmetry Ratio:– 8% <strong>to</strong> the RIGHT– > 33% is abnormal• Intact Utricle <strong>and</strong>Superior <strong>Vestibular</strong>Nerve
<strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong>Overall Impression• Abnormal VNG examination– Bithermal caloric testing yielded a significant(30%) weakness on the right side.– Overall results suggest the presence of aperipheral vestibular system disorder affectingthe right side.
Neurology Consult• Referred <strong>to</strong> neurology for assessment ofmigraines <strong>and</strong> central etiology.– Started on Gabapentin/Neurontin <strong>to</strong> helpreduce episodes of dizziness <strong>and</strong> headache.– Reports significantly reduced frequency of hisepisodes over the next few months.
O<strong>to</strong>laryngology Follow-up• O<strong>to</strong>laryngology follow-up one year later due <strong>to</strong>reduced effectiveness of Gabapentin /Neurontin.– Increase of dizziness <strong>and</strong> imbalance– Experienced a fall at work due <strong>to</strong> suddenonset of dizziness– Currently on leave from work– Referred for vestibular rehabilitation therapy
Subjective <strong>Assess</strong>ment• Dizziness described as disequilibrium• Dizziness while riding in a car– Magnified with head turns <strong>to</strong> look out window• Dizziness in s<strong>to</strong>res• Dizziness with prolonged walking• Falls regularly– Sudden <strong>and</strong> without provocation• On medical leave due <strong>to</strong> current symp<strong>to</strong>ms
Objective <strong>Assess</strong>ment:• Gait:– No assistive device– Holds on<strong>to</strong> fiancés arm <strong>and</strong> finger <strong>to</strong>uch <strong>to</strong> wall– Minimized head movements– Path deviation <strong>to</strong>wards the left• MMT: Normal• ROM: Normal• Sensation: Intact
Objective <strong>Assess</strong>ment• Oculomo<strong>to</strong>r Exam: normal• VOR cancellation: intact• Head impulse testing (Weber KP, 2008) : negative• BPPV assessment:– Dix-Hallpike testing: negative– Roll testing: negative
Neurocom SMART EquiTest & In-VisionSystem
Sensory Organization <strong>Testing</strong> (SOT)• Composite score of 80• No deficit in the use ofvestibular, visual, orsoma<strong>to</strong>sensory cuesfor balance.Mishra A, 2009
Head Shake SOT• Head Shake SOT(Horizontal)– Equilibrium ScoreRatio:• Fixed Surface .98• SwayRef Surface .90Mishra A, 2009Clinical Integration Seminar. 2005, Neurocom International, Clackamas,OR.
Neurocom In-Vision• Gaze Stabilization Test:– Maintain visual acuityat velocities up <strong>to</strong>:• 156 deg/sec inleftward• 66 deg/sec inrightward
Neurocom In-Vision• Dynamic Visual Acuity:– 0.01 LogMar loss ofvisual acuity withleftward headmovements.– 0.27 LogMar loss ofvisual acuity withrightward headmovements.
Objective Measure• <strong>Function</strong>al gait assessment: 20/30• Slower gait speeds with path deviation, pivot turns,gait with narrow BOS, gait with eyes closed.• Six-minute walk test:– 1600 feet with dizziness <strong>and</strong> imbalance during turns.• Single limb stance: (Bohannon, 2006)– Left LE - 13.06 seconds– Right LE - 1.93 seconds• Motion Sensitivity Quotient:–
Impression• Unilateral <strong>Vestibular</strong> Hypofunction based on thefollowing findings:– Impaired right gaze stability– Impaired right dynamic visual acuity (Herdman, et al, 1998)– Increased dizziness with head turns– Path deviation with head turns during gait– <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong>
<strong>Treat</strong>ment Interventions• Patient seen for 6 visits over an 8 week period.– Gaze Stabilization Adaptation Exercises (Herdman, 2007)• VOR X1 & VOR X2 viewing• Various balance strategies• Incorporated in<strong>to</strong> gait with forwards <strong>and</strong> backwardswalking• Various visual stimulating backgrounds– Op<strong>to</strong>kinetic Stimulation (Pavlou M, 2011)– Visual stimulating videos– Passenger in a car– Walking in s<strong>to</strong>res <strong>and</strong> mall
<strong>Treat</strong>ment Interventions• Balance training on compliant surfaces– Foam st<strong>and</strong>ing, various stance positions,incorporation of head turns, eyes open <strong>and</strong> closed– Turning 180 & 360 degrees• Neurocom Cus<strong>to</strong>m Training– Support <strong>and</strong> surround movement <strong>to</strong> facilitate variousbalance strategies• Single limb stance– Stepping over objects, negotiating stairs at slowspeed– Increasing single limb stance times with homeprogramGiray M, et al., 2009
<strong>Treat</strong>ment Interventions• Gait training on various surface types– Progressive walking program for up <strong>to</strong> 30 minutesdaily– Incorporation of head turns– T<strong>and</strong>em gait activities– Dual task:• Carrying objects of various sizes <strong>and</strong> weight <strong>to</strong>simulate work duties• Gait on various surfaces with reading & cognitiveskills• Treadmill training– Head turns & speed changesGiray M, et al., 2009
Outcomes• Intermittent dizziness• Occasions of sudden imbalance lasting 10 -15 sec ~4per wk• Independent ambulation without UE support on varioussurfaces.– Able <strong>to</strong> incorporate functional head turns with nosignificant veering• Return <strong>to</strong> work with no visual stimulating dizziness whilein the work environment• Improvement in <strong>Function</strong>al Gait <strong>Assess</strong>ment score 30/30• Single limb stance times improved <strong>to</strong> 30 seconds
In-Vision Results:• Improvement in gazestabilization at velocitiesup <strong>to</strong>:– 186 deg/sec inleftward movementdirections– 154 deg/sec inrightward movementdirections
In-vision Results• Improved Dynamic Vision– 0.18 LogMar loss ofvisual acuity withleftward headmovements.– 0.02 LogMar loss ofvisual acuity withrightward headmovements.Clinical Integration Seminar. 2005, Neurocom International, Clackamas, OR.
Outcome• Returned <strong>to</strong> work full time• Independence with a home exercise program <strong>to</strong>help maintain functional gains (Byung In Han, 2011)• Discharged from therapy.
Discussion• <strong>Vestibular</strong> <strong>Function</strong> <strong>Testing</strong> is important in differentialdiagnosis of peripheral versus central vestibularinvolvement.• Cus<strong>to</strong>mized vestibular rehabilitation programs can beprovided based on diagnosis, presentation, <strong>and</strong>symp<strong>to</strong>ms.• When available, develop a working relationship withaudiologists in your area <strong>to</strong> optimize patient care.
Questions
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