110121 Understanding Vestibular Function Handout

7/27/2019 110121 Understanding Vestibular Function Handout

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VESTIBULARFUNCTION &

DYSFUNCTION:

We would accomplish many more things if we did not think of them as impossible

- Vince Lombardi

Presented by:

Chris ZalewskiNIH, Audiology

[email protected]

American Academy of Audiology

Web Seminar Spring 2011

HOW DO I PUT THE

VESTIBULARPUZZLETOGETHER

We would accomplish many more things if we did not think of them as impossible

- Vince Lombardi

ROM HE ARIOUS IECES

Presented by:


[email protected]



We would accomplish many more things if we did not think of them as impossible- Vince Lombardi

HOW DO I PUT THE

VESTIBULARPUZZLETOGETHER



PIECES ARE MISSING ?Presented by:


[email protected]


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Presentation Objectives

1. Further our comprehensive understanding of vestibular

function (and dysfunction) through a case study approach

2. Review the advantages and limitations of various vestibulartests

1. Computerized dynamic platform posturography

2. Vestibular evoked myogenic potentials

3. Rotational assessment

4. Videonystagmography

3. Example normal, absent and abnormal responses for eachassessment tool

4. Illustrate how the sum of the parts is far better (and oftennecessary) than any individual measure

Understanding Normal Balance Function

a prerequisite

Balance is a Multi-Sensory Interaction

The maintenance of bodyequilibrium and posture ineveryday life is a complex functioninvolving multi-receptor organs

and neural centers.

In particular, the visual,somatosensory, and proprioceptivereflexes must be integrated with thevestibular reflexes in order toensure postural stability.

It is the interaction and intimaterelationship between these systemsthat provide balance and posturalstability.


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Postural Neural Pathways

Lateral SCC

Anterior SCC

Posterior SCC

eftLabyrinth

Eye

MusclesVestibular Ocular Reflex (VOR)

SaccadicSystem Tracking

System

Optokinetic

System NeckReceptors

Other

-Adapted from Canalis & Lambert, 2000

Central Vestibular Nuclei

r c e

Saccule

Lateral SCC

Anterior SCC

Posterior SCC

Utricle

Saccule

RightLabyrinth

L

Adaptation

Skeletal

MusclesVestibular Spinal Reflex (VSR)

Proprioceptive

Visual

Tactile

Other

(cerebellum)

Beyond the Vestibular System

Until recently, clinical vestibular testing was primarily systemoriented.

An isolation of each system the visual, the somatosensory,and the vestibular was controlled to evaluate eachn epen en y w ere y e overa a ance unc on o e

patient was inferred

This approach has significant limitationsbecause the visualsystem (or oculomotor reflexes), the somatosensory system (orvestibulospinal reflexes) AND the vestibular system arecomplex functions that contribute to a coordinated responsewhere one system can have significant impacts on how anothersystem performs.

nevertheless

understanding the primary vestibular

role is imperative

The convergence and interaction of sensoryinformation is primary believed to be coordinated

through the vestibular system specifically thecentra vest u ar system vest u ar nuc e .

The vestibular nuclei can be thought of as thecommon central processorwhich coordinates themassive amounts of sensory input in order toformulate the most appropriate sensory output formaintaining posture and balance.


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therefore

A fundamental understanding of the normal

vestibular system is imperative to the understandingof balance function and postural control

however, keep in mind that a

fundamental understanding of ONLY

the vestibular system leaves balance

assessment extremely limited and

under-investigated

Computerized Dynamic Platform

Posturography (CDPP)

Components of CDPPBalance

using CDPP

Case study:

A new interpretation ofCDPP

Case Study:

A case of uncompensatedvestibular functionor not



CDPP is divided into twoprimary

tests:

The Sensory Organization Test (SOT)

whichmani ulatesthe visual and

proprioceptive inputs while determining

the effects on equilibrium

The Motor Control or Movement

Coordination Test (MCT) which

evaluates the muscle response to various

computer-induced platform perturbations

Other specialty Tests


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Equipment

EquipmentSway referenced surround 4 Ant-Post force pressure gauges

Sway referenced support

1 Shear force pressure gauge

Sensory Organization Test (SOT)

Test paradigm consists of 6subtests which are designed totease out the overallcontributions, as well as thestrengths & weaknesses of the

three sensory components ofequilibrium (visual, vestibular &somatosensory)


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SOT Subtests 1-3:

Fixed Platform

Condition 1

Measures the patients stability while the patient stands on a fixed platform with a fixedvisual surround and with eyes open

All sensory components are active

Condition 2

visual surround and with eyes closed (Romberg Test)

Vestibular and somatosensory systems active, absent visual cues

Should have little effect on balance since the absence of visual cues have been shown tohave minimal effect on equilibrium in the presence of functional vestibular andsomatosensory systems

Condition 3 Measures the patients stability while the patient stands on a fixed platform with eyes open,

however, the visual surround is sway referenced to the A-P sway measured by theplatform

Provides orientational ly inaccurate visual cues does the patient rely too heavily uponvisual cues (visual preference)?

The brain is asked to ignore the inaccurate visual input and rely on the orientationallyaccurate vestibular and somatosensory (proprioceptive) inputs

PREF

SOT Subtests 4-6:

Moving Platform

Condition 4 Measures the patients stability while the patient stands on an un-fixed platform with a

fixed visual surround and with eyes open

As a result, the proprioceptive input to the brain is inaccurate and balance must bemaintained by the visual and vestibular system

Condition 5 Measures the patients stability while the patient stands on an un-fixed platform with eyes

closed (visual surround is fixed, but with eyes closed this does not matter)

This condition isolates the vestibular system more than any other

Since the visual and proprioceptive systems are compromised, balance and equilibriummust be maintained by the vestibular system alone

Condition 6 Measures the patients stability while the patient stands on an un-fixed platform with eyes

open however, the visual surround is sway referenced to the A-P sway measured by theplatform

This condition also involves the vestibular system but to a lesser degree than condition 5

Both the visual and the proprioceptive systems are compromised, but moreover, the brainmust also ignore the inaccurate visual inputs and rely on the orientationally accuratevestibular system (further evaluates visual preference

PREF

Understanding the SOT

Center of Gravity (COG) In normal subjects standing erect, the

COG is located in the lower abdominal

area and slightly forward of the anklejoints

COG Sway Angle The degree of sway from the vertical

COG using ankle strategy


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Understanding the SOT

Limits of Stability (B)

The maximum A-P or lateral swayangle without losing balance(approx. 12.50 off COG) - when theCOG sway angle exceeds the limitsofstabilit the atientmustste, ,stumble, or grasp to regainequilibrium

The Equilibrium Score (A) Calculated for each condition

Represents the angular differencebetween the patients calculatedmaximum sway angle and the COGtheoretical maximum (12.50)

Result is a percentage with 100%indicating perfect stability

SOT Raw Postural Trace Data

The Composite Equilibrium Score(CES) Calculated percentage score

representing the patient's overallequilibrium ability (compared toage, weight and height-matchednorms)

NORMAL TRACINGS

Examination of the CES provides aglobal determination of normalversus abnormal

SOT DataSensory Analysis Summary

Sensory Analysis When the composite score falls within the abnormal

range, the second interpretation is needed to identify thesensory dysfunction and/or abnormal sensory preferencecontributing to the overall sensory organizationabnormality

When the composite score is significantly below the

most conditions, a specific sensory abnormality orpattern may not be discernible. This patient may have amulti-sensory dysfunction (more to come)

SENSORY ANALYSIS

Rat io Formula Quest ions and Signific ance if ABN ORMAL

SOMQ: Does swayincrease when VIS cues are removed ?

A: Patient makes poor use of SOM references

VISQ: Does swayincrease when SOM cues are inaccurate ?

A: Patient makes poor use of VIS references

VESTQ: Does swayincrease when VIS cues are removed & SOM cues are inaccurate ?

A: Patient makes poor use of VEST references

PREFQ: Do inaccurate VIS cues result in increased swaycompared to no VIS cues ?

A: Patient relies on VIS c ues even when inaccurate

Condition 2Condition 1

Condition 4Condition 1

Condition 5

Condition 1

Condition 3+6Condition 2+5


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Case Stud :

A Different Approach to Interpreting

Dynamic Posturography

History

38 y/o male presents with a previousdiagnosis of USHER Syndrome type I

Diagnosed at 2 years of age was facilitatedby two older siblings with the samediagnosis

Usher Syndrome Types

Type Visual Auditory Vestibular

Onset of RP by ~ 10 Congenital absence ofyears old

function

USH2Onset of RP in late teens-

early 20s

Congenital moderate

to severe SNHLNormal

USH3Onset of RP in late teens-

early 20s

Progressive SNHL,

may be near normal at

birth, deaf when older

Progressive balance

dysfunction


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Hearing History

Believed to be congenitally deaf with most recent audiometric

evaluation in middle school that revealed little if anymeasurable hearing bilaterally

Hearing aid history is significant for use of a body aid duringelementary school and middle school providing little (ifany) success which was limited to sound awareness

Hearing aid use discontinued in high school. After, attendedGallaudet University. ASL user.

Balance History

Self reported balance problems, describing himself asclumsy, uncoordinated and overall not great (oftenwalking like a drunk)

Attempted school sponsored sport activities such as tennis,basketball and baseball with limited proficiency

Unsure of exact age when he started walking, but did reportdelayed ability

Visual History

Retinitis pigmentosa diagnosed at the age of2 years

Visual ability remained fairly good andconsistent through high school

During college, RP reported to beginimpacting visual acuity and peripheralvision

Current visual function:

Right eye totally blinded

Left visual fieldis confined to anapproximate 5-10 degree range that isleft of center field - acuity within FOVis reported to be 20/30

No night vision

X


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Miscellaneous History

Sustained head injury at 6 years of age after running into a tree atnight

Resulted in LOC without skull fracture

Utilizes ASL for communication as well as is fluent in tactile ASL

Audiometric Results

No measurable hearing tospeech or pure tones

bilaterally

orma ympanome rybilaterally

Absent middle ear reflexesbilaterally

Absent DPOAEs

bilaterally

Videonystagmography Results

Oculomotor assessment was WNL - despite the

limited visual field (left eye tested only)

Positional testing was WNL


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Caloric Testing

Caloric testing revealedabsent labyrinthine

reactivity to both cool

an warm a r s mu

Ice water irrigations

further resulted in no

measurable reactivity

bilaterally

Rotational & VEMP Testing

Rotational Vestibular Testing revealed absent VOR gain for the frequency

range of 0.01-0.64 Hz

Absent VEMPs bilaterally

0 ms 0 ms

Conclusions thus far

Profound bilateral SNHL bilaterally

Absence of any peripheral vestibular reactivity evidenced

Absent VOR response by air and ice water caloric irrigations

Absent VOR gain on RVT

Absent saccular activity by VEMP testing

What can functional assessment via dynamic platformposturography reveal ?


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but first,

What is expected on posturography with an

USHER type I patient ?

absence of vestibular function, right?

what to expect

Conditions 5 & 6

on platform SOT

testing isolates

overall

contributions of

the vestibular

system to postural

stability

Typical USHER type I SOT Pattern

Note the absence of vestibular contribution to over postural stability (condition 5/6SOT pattern) concomitant to significantly reduced use of visual input


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Posturography Resultsfor our USHER patient

Computerized Dynamic Platform Posturography Sensory

Organization Test Results (SOT)

What Does SOT Reveal ?

Is there vestibular function ?

Is there any vestibular

contribution when

maintaining posture ?

What can functionally be

said of this patients

performance ?


VNG, RVT and VEMP testresults support an absence ofvestibular activity in this

patient However, this is a functional

measure

The fundamental question isNOT how much the vestibularsystem is contributing to

postural stability in thispatient, but rather


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How does this patientperform orfunction in an environment that

demands a specific sensory input ?

In other words, how does thispatient function in a vestibular

dependant environment ?

CDPP Case Study

A case of uncompensated

vestibular function

or not?

Case Study 2: History

48 y/o male presents with a previous diagnosis of vonHippel-Lindau (VHL) disease

mutation on 3p25-26 (tumor suppressor gene function)

VHL is characterized by a predisposition to bilateralretinal angiomas, CNS (cerebellar) and spinal cordhemangioblastomas, renal cell carcinomas,

pheochromocytomas, islet cell tumors of the pancreas,endolymphatic sac tumors, and renal / pancreatic &epididymal cysts


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Hearing History

Previously documented bilateral moderate, high frequency,notched sensorineural hearing loss

Persistent com laints of difficult with s eech understandin

- particularly in adverse listening environments

No history of hearing aid use

Hearing history is positive for noise exposure with reported

consistent use of hearing protection devices

Complaints of pruritis for two months

Balance History

Previous vestibular testing in 2000 revealed: Bilateral failure of fixation suppression,

Saccadic tracking during smooth pursuit testing,

Robust caloric response to cold (only) irrigations, and

Rotational vestibular testing (RVT) revealed reduced VOR gain above 0.16Hz with concomitant abnormal phase lead times above this frequency

Patient reports a subjective complaint of continued worseningin balance - particularly when maneuvering over slopes andunstable surfaces.

Has experienced increasing fainting episodes over the lastyear.

Balance History

During routine otoneurologicevaluation, patient was noted to have anabnormal Romberg and tandem walkingtest

Patient noted to have significant posturalstability problems and often utilized hissurroundings for support. Despite this,

patient was noted to lose his stabilityand fall into the exam chair.

Patient regularly used the wall duringambulation


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Miscellaneous History

Multiple VHL related tumors

resection of hemangioblastomas

Patient reports monitoring of cerebellar tumors with noimmediate plans for resection

Audiometric Results

Bilateral mild-to-moderate /moderately severe SNHL(right slightly greater thanleft). Normal speech

.

Normal tympanometrybilaterally

Middle ear reflexes presentcontra-lateral at appropriatesensation levels

DPOAEs not performed

Videonystagmography Results

Previous findings in

2000 revealed:

Bilateral failure of

fixation suppression

Bilateral cog-wheeling

on smooth pursuit


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Caloric Testing Only

Caloric testing revealed (borderline) reduced vestibular response in the right ear (20%) with no

evidence of directional preponderance

No evidence to support failure of fixation suppression (improvement from 2000)

RIGHTLEFT

Conclusions thus far

Mild-to-Moderate / Moderately Severe SNHL bilaterally

Right peripheral vestibular pathology secondary to rightRVR on caloric irrigations

Previous VNG results suggesting a central (cerebellar)pathology contributing to his dizziness

Significant central lesion(s) suspected on otoneurologicbedside evaluation

Posturography Results - SOT

Multi-sensory dysfunction with unique sway patterns


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Posturography Results - MCT

Abnormal MCT postural reflexes with backward translations

with unique sway patterns

A closer look

Postural sway patterns arenot consistent with normal

behavior - even with thoseof atholo ic atients

CDP can be a very reliabletest to differentiate non-organic sway from organicsway

A closer look

7 criteria believed to be

consistent with aphysiologic

response to CDP

1. Substandard performance onSOT 1

2. Lower scores on SOT 1 and 2,

higher scores on SOT 5 & 6

3. Repetitive large-amplitude

anteroposterior sway without

falling

4. Excessive lateral sway without

falling

5. Excessive variability on SOTs 1

& 2Goebel, J. et al. (1996)


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A closer look (cont)

7 criteria believed to be

consistent withaphysiologic response to

CDPMCT Results

1. Exaggerated motor responses

to small platform translations

2. Inconsistent motor responses

to small and large, forward

and backward translations

Normal responseGoebel, J. et al. (1996)

Another objective measure of

aphysiologic sway

9 criteria presented by Mallinson et

al. (2005) believed to be consistent

with aphysiologic response to CDP

1. Better performance of first trial of

SOT1 and 2 (when unaware of

being measured) than on trials 2 & 3

2. Scores on SOT 5 & 6 relatively

better than scores on SOT 1 & 2

3. SOT 1 & 2 scores all below 75

(markedly below normal)

4. High inter-trial variability seen in

scores across all SOT trials

5. Circular sway patterns with falls

6. Repetitive large amplitude

suspicious anteroposterior swaywithout falls

Mallinson (cont)

(Continued)

1. Exaggerated motor responses to

small platform translations

.

small and large, forward and

backward translations. Non

repetitive motor responses to all

translations

3. Clinical judgment (gut feeling)

Normal response


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Score analysis for determination of

patients aphysiologic sway

Mallison & Longridgeaphysiologic Criteriascore 4 of9 score indicatin

DETERMINATION OFAPHYSIOLOGIC PERFORMANCECHARACTERISTICS

MALLINSON CRITERION

Comrehens ive Report Enter Score1 . B et t er P er f or m an c e o n f ir s t tr i al o f S OT 1 & 2 ( wh e n u n aw a re o f be i ng m e as u re d ) th a n o n 0

2 . H ig he r i nt er -t ri al v ar ia bi li ty se en i n s co re s a cr os s a ll S OT t ri al s 0

3. Lower scores on SOT 1 & 2, higher scores in SO 5 & 6 0

4. SOT 1 & 2 scores all below 75 0.5

SOT COGX-Y Plot

5. Circular sway patterns withoutany falls 0.5

Excessive Lateralsway withoutfalls (>2.5 deg)

Sway,Shearand Alignment Data

6 . Re pe t it i ve l a rg e -a m pl i tu d e " s us p ic i ou s " a n te r io r -p o st e ri o r s w ay w i th o ut f a ll s 0 . 5probable aphysiologicperformance

Cevette et al.aphysiologic criteria

Highest score of 117.9designated to the groupaphysiologic

MotorControl Test

7 . E xa gg er at ed m ot or r e sp on se t o s ma ll f or wa rd & b a ck wa rd p la tf or m t ra ns la ti on s 1

8 . I nc o ns i st e nt , n on - re p et i ti v e mo t or r e sp o ns e t o a l l tr a ns l at i on s a nd b o th a d ap t ai o ns 0 . 5

Clinical Impression

9. Clinical judgement ("gut feeling") 1

TOTALSCORE 4

0 o f 9 No suspi c i on of aphys io l ogi c ("mal i ngeri ng")behavi our

1 of 9

2 of 9

3 o f 9 Possi b l e susp i c ion ra i sed(assessmento fen repea ted)

4 of9 ProbableAphys iologicPer formance("malingering 4 of 9

5/9 to 9/9 Definite Aphysiologic Performance ("malingering")

CEVETTEAPHYSIOLOGIC CRITERION

Average Tri al 1 Trial 2 Trial 3

C1 87.33333333 87 88 87

C2 66.33333333 80 68 51

C4 28 0 55 29

C6 26 0 36 42

A ph ys io lo gi c 1 17 .9 9

Normal 97.89

V es ti bu la r 9 0. 5 23 33 33 3

"The highestoverallvalue designates the groupto which the patient

References: is mostlikely to belong" with 95.5%certainty (Cevette etal 676)

Mallinson Al, Longridge NS;

A NewSetof Criteria for Evaluating Malingering in Work-RelatedVestibular Injury.

OtolNeurotol26:000-000, 2005 (in press)

Ceve tte MJ,Pue tz B ,Ma r ion MS ,We r tz ML ,Muen te r MD Aphysio log i c pe r fo rman ce on dynamic postu rog raphy

OtolaryngolHeadNeck Surg. 112(6):676-88, 1995.

Conclusions ?

An underlying vestibular

pathology with an

overlaying functional

component

Evidence to support

components of a central

and peripheral etiology to

patients pathology

Neurotologic Rotational Testing

Components of RotationalTesting

Normal Vestibulareactv ty

Interpretation ofRotational Testing

Case Study:

Vestibular loss or sensoryintegration dysfunction


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Rotational Vestibular Testing

Test Paradigm

Patients head is tilted 300

forward toplace the H-SCC in the plane ofrotation

Chair is situated in a lightproofenclosure

Standard electrode placement and / orvideo-oculography

Chair is turned by a torque motor forseveral cycles of sinusoidal rotation ateach of seven test frequencies (0.01,0.02, 0.04, 0.08, 0.16, 0.32, & 0.64 Hz)and possibly higher

Patient is kept mentally alert similar tothe caloric & positional subtests of theVNG

Contraindicated medications must alsobe ceased 48 hours prior to the test

Rotational Vestibular Testing

Test Paradigm Head rotation is inferred

from the chair rotation

e pa en s or zon a eyeposition is measured throughvideo-oculography, and anystagmus tracing isgenerated by the computer

program

The clinician can thenexamine the relationship

between the patients headand eye movement

Passive Rotational Vestibular Testing

Two primary stimuli employed during passive rotationaltesting:

1. Velocity Step Testing

.

Other tests employed during passive rotational testing:

1. VOR Suppression

2. Oculomotor Assessment

3. Unilateral Centrifugation

4. Visual-Vestibular Enhancement

5. OVAR


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Velocity Step Testing

Velocity step testing involves a

quick angular acceleration of1000 / second2 lasting for onesecond (to the left)

At the end of the acceleration,the patient is rotating at aconstant velocityof 600, 1000,2400 / second which ismaintained through the entiretrial


In response to this stimulus, aburst of (left-beating) horizontalnystagmus is observed

Wh left beatin ? Excitation of the left h-SCC

causes a rightward slow-phasepull with a leftward fast phasequick saccade to bring the eyesback to primary position (i.e.,repeated left-beatingnystagmus)

The response graduallydissipates (without visual

fixation), and can be followed bya few beats of nystagmus in theopposite direction


After the completion of the test,

the computer eliminates the

quick-phases (fast-phases), and

calculates the velocity (intensity)- -

yielding a plot ofslow-phase eye

velocity

This plot evidences a rapid burst

of SPV, an exponential decline

back to zero, and finally a weak

reversal


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VOR Time Constant

Despite on-going velocity, thecupula of the h-SCC returns to itsresting position at about 6-7seconds.

However, the VOR responsecontinueswell past this time frame

The persistence of VOR is due tovelocity storage

The point at which the VORresponse decays 37% from its peakresponse is known as the timeconstant of the VOR and should begreater than 10 seconds.

Normal Velocity Step Test

Abnormal Velocity Step Test


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Velocity Step Testing Abnormalities

Velocity Step TestingAbnormality Possible Interpretation Rule Out

1. Peripheral UVL if oculomotor testing is normal, likelyInattention;

600 / sec

Low time constant

(0.3; if not, consider migraine

;

too much

blinking; bilat

loss; fixation

If 3 of 4 time

constants are

abnormal

1. Abnormal study; non-localizingInattention;

too much

blinking

2400 / sec

Consider peak

slow phase

velocity; >30%

difference

between CW &

CCW directions?

1. Significant asymmetric results in peak SPV indicate

peripheral UVL and side of lossEye closure

(eyes must be

open when

chair starts &

stops)

Slow Sinusoidal Oscillation Testing

As the chair and patient begin to

rotate, a slow, compensatory eye

movement is observed in the

rec on oppos e e ro a on.

An indirect measure of

vestibular sensitivity to

rotational stimuli

Assesses the h-SCC, central

systems and the vestibular

nuclei

Head Movement

Calorics

Normal Head

Max VOR

Operational. otary a r0.01 Hz -2.0 Hz

Motion0.5 Hz 5 Hz

VOR linear range 0.1 Hz 10 Hz

Range 26 Hz


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Maximum Velocities During typical

Daily Life Tasks

Walking Horizontal 36 deg/sec

Vertical 32 deg/sec

Running

Horizontal 62 deg/sec

Vertical 87 deg/sec

Driving at 30 mph

84 deg/sec

Competitive sports and high performance

120 deg/sec

Grossman G, Leigh R, et al. (1988, 1990)

Sinusoidal Oscillation Testing

The most widely used rotational test isthe slow-harmonic acceleration test

Patient undergoes sinusoidaloscillations about a vertical axis atseveral different frequencies (0.01,

(0.16 Hz)

. , . , . , . , . .

Constant-changing accelerations (+/-)achieving a peak 600/sec head velocity

The saccadic (fast) eye movementreturns the eye to its primary centralposition and is noted to be in the samedirection as the rotation Right-Beating on rightward rotation Left-Beating on leftward rotation

However, the slow phase is what ismeasured / calculated (fast-phases areremoved by the analysis)

Parameters of Sinusoidal Oscillation Testing

The relationship between slow-phase eye velocity and head velocity isdescribed by three parameters:1. Spectral Purity: A measure of the quality of the data collected

2. Gain: the ratio of peak eye velocity to head velocity

3. Phase Angle: The reaction time of eye movement in response to head

movement4. Symmetry: The ratio of rightward and leftward slow-phase eye velocities

NORMAL PATTERN


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Again, if the VOR function is to

produce equal and opposite eyemovements to that of headmovement than the SPEV plot ind would have been the exact

(0.16 Hz)

mirror image of head velocity b

However, it was not. The gainwas only 0.66 (0.4 / 0.6)

That is, the eyes did not movequite quick enough during thenystagmus slow-phase tocompensate for, or entirelymatch head/chair movement

d

b


A note on VOR Gain

Shown here is an

absence ofVOR ain

Phase and Symmetry are

calculated from Gain

Phase and Symmetry

should be analyzed /

interpreted with caution

when VOR gain is 10-

15%


There are two things that are critical to RVT, which, if you donot control for, you may as well not test your patient

Head restraint

Tasking


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There are two things that are critical to RVT, which, if you donot control for, you may as well not test your patient

Head restraint

Tasking


The relationship between slow-

phase eye velocity and head

velocity is described by three

arameters:

(0.16 Hz)

Gain: the ratio of peak eye

velocity to head velocity

Phase Angle: The reaction

time of eye movement in

response to head movement

Symmetry: The ratio of

rightward and leftward slow-

phase eye velocities

VOR Phase The temporal relationship between the velocity of the head (chair) and that of

the slow-phase component of the rotational-induced nystagmus.

Again, as the chair and patient begin to rotate, the slow, compensatorynystagmus is observed to move in the opposite direction of the chair (head)

. ,moves at exactly the same time and pace as the chair only in the oppositedirection.

BUT THIS DOES NOT HAPPEN in

fact, eye movement tends to be ahead of

(or lead) chair movement the slower the

chair/head rotation


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0.01 Hz Average SPV 0.16 Hz Average SPV

Phase Lead by Frequency - Normal

0.02 Hz Average SPV

0.04 Hz Average SPV

0.08 Hz Average SPV

0.32 Hz Average SPV

0.64 Hz Average SPV


VOR phase approaches zero (exactly 1800 out of phase) around 0.08 or 0.16 Hz

NORMAL PATTERN

Sinusoidal Oscillation Abnormalities

Sinusoidal Harmonic Acceleration TestingParameter Abnormal Result Possible Interpretation Rule Out

Low VOR gain for

low Hzs (


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RVT Case Study

Vestibular Loss or Sensory-Integration

Dysfunction ?

56 y/o male disabled geologist

Occasional non-localizing tinnitus since Aug 2008

Occupational noise history of 10+ years from machinery for specimens as a geologist

Repeated sensations of dysequilibrium which he characterizes as occurring once per weekwith each episodes duration being several minutes each time

CaseStudyHistory:

Reports vague sensations during ambulation and has a very difficult time recoveringfrom unexpected disturbances in his environment

He further reports a definitive unsteadiness particularly while maintaining a crouchingposition

Reports hyperacusis to sounds such as pots and pans and coffee scooping

1998 Bells Palsy

1999 ri ght pinna edema

Aug 2008 single episode of true vertigo with movement x 1day

MRI of brain in June 2008 was WNL CN exam II-VII, IX-XII grossly intact

Audiometry

Normal tympanometry with the exception of hyper-mobility in the left ear

Present acoustic stapedial reflexes bilaterally


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Videonystagmography (VNG)

Cool Left Cool Ri ht

Nooculomotorabnormalities Noevidence ofanypositionalorspontaneousnystagmus Calorictestingrevealedrobustlabyrinthine reactivity tostandardaircaloricstimuli. Noevidence ofanyfailureoffixationsuppression

290 RB 220 LB

260 LB 240 RB

Warm Left Warm Right

Incidence of ENG Abnormalities

2584 ENG results reviewed from a variety of

settings - private otolaryngology, neurology, and

audiology and neurology departments.

61% (1571 tests) showed no abnormalities

- Stockwell, 2000




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Dynamic Posturography

SOT

Across the Board Pattern

Rule out:

Anxiety,

Non-Organic, &

Multi-Sensory

SOT Raw Sway Data

Center of Gravity Raw DataRaw Sway Data

Non-Organicity DeterminationDETERMINATION OFAPHYSIOLOGIC PERFORMANCECHARACTERISTICS

MALLINSON CRITERION

Comrehensive Report Enter Score

1 . Bet ter Per forman ce on f i rst t r ia lof SO T 1 & 2 ( wh en u naware of be ing measu red ) t h an on 0

2. Higher inter-trial variability seen in scores across all SOT tri al s 0

3. Lower scores on SOT 1 & 2, higher scores in SO 5 & 6 0

4. SOT 1 & 2 scores all below 75 0

SOT COGX-Y Plot

5. Circular sway patterns withoutany falls 0

Excessive Lateralsway withoutfalls (>2.5 deg)

Sway,ShearandAlignment Data

6 . R ep et it iv e l ar ge -a mp li tu de " su sp ic io us " a nt er io r- po st er io r s wa y w it ho ut f a ll s 0

MotorControl Testo o r o n r o es

7 . E xa gg er at ed m ot or re sp on se to sm al l f or wa rd & ba ck wa rd p la tf or m t ra ns la ti on s 0 .5

8 . I nc on si st en t, n o n- re pe ti ti ve m ot or r e sp on se t o a ll t r an sl at io ns a nd b ot h ad ap ta io ns 0

Clinical Impression

9. Clinical judgement ("gut feeling") 0

TOTALSCORE 0.5

0 of 9 No suspicion of aphysiologic ("malingering")behaviour

1 of 9

2 of 9

3 of 9 Possible suspicion raised(assessmentofen repeated)

4 of9 ProbableAphysiologicPerformance("malingering")

5/9 to 9/9 Definite Aphysiologic Performance ("malingering")

CEVETTEAPHYSIOLOGIC CRITERION

Average Trial 1 Trial 2 Trial 3

C1 92.33333333 94 94 89

C2 84.33333333 88 81 84

C4 51 73 80 0

C6 49.33333333 52 55 41

A ph ys io lo gi c 1 75 .3 2

N or ma l 171 .256 666 7

Vestibular 159.73

"The highestoverallvalue designates the groupto which the patient

is mostlikely to belong" with 95.5%certainty (Cevette etal 676)

POSITIVE for Cevette (et al) ???Black etal,(1999) & Longridge &Mallinson,( 2005)


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Dynamic Posturography - MCT

Prolonged postural motor reflexlatencies to backward translations

Essentially normal amplitude scaling

Rotational Vestibular Testing (RVT)

Slow HarmonicAcceleration (0.01-0.64Hz)

600 Trapezoidal StepTesting

VOR Suppression testing(0.16 Hz & 064 Hz)

RVT Slow Harmonic Acceleration

Summary

Increased VOR phase lead

Normal VOR gain


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RVT - 600 Step Testing

RVT - 600 Step Testing

T =1

(2f)tan

T = 1 / (20.01)tan580

T = 1 / (0.0628)1.6

Phase & Time-Constant:

An Inverse Relationship

T = 1 / 0.10048

T = 9.95 sec

If no step testing was conducted, a time constant c an be calculated from the phase value of

your random sinusoidal oscillation testin g at 0.01Hz (generally restricted to 0.0 4 Hz and

below)

An inverse relationship exists: as phase angle increases, time constant decreases

Increased abnormal phase leads, related to a decrease in time constant, suggests a pathology

of the peripheral system

however, damage to the central vestibular nuclei within the brainstem may also result

in abnormally low time constants


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VOR Fixation Suppression 0.16 Hz

Average Cycle

VOR Fixation Suppression 0.64 Hz

Average Cycle 0.4 gain

Clinical Summary

Asymmetrical, high frequency SNHL (L>R)

Normal middle ear function bilaterally

Normal VNG

Abnormal Dynamic Posturography Across the Board SOT pattern

Prolonged backward MCT latencies

Abnormal RVT Abnormal phase lead across the entire frequency

range in the presence of normal VOR gain

Abnormal Time Constants

Failure of fixation suppression

Normal Visual-Vestibular Enhancement


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Patient diagnosed with a positive Lyme titer

Sensory integration dysfunction likely involving central vestibularnuclei and motor sensory input (long loop motor pathways)evidenced on CDP

Conclusions

Central vestibular pattern on RVT suggesting central vestibularvelocity storage integration dysfunction

Vestibular compensation outlook is questionable given cerebellardysfunction in regulating vestibular input/output

Sensory integration trainingsuggested to reorganize / retrainsensory management

Vestibular Evoked Myogenic Potentials

(VEMP)

Components of VEMPTesting

Normal VEMP Responses

Case Study:

Answering a question ofIAC compromise,

or

Here comes VEMP

to save the day

Vestibular Evoked Myogenic Potentials

Short latency myogenic

response to loud clicks

recorded on the ipsilateral

sternocleidomastoid muscle

Contraction of the SCM is

held at a relatively constant

throughout the recording

VEMP is an inhibitory

response of the SCM


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Vestibular Evoked Myogenic Response Testing

(VEMP)

Since 1916 (Tullio), it has been known thatthe vestibular system (of pigeons) wassensitive to sound.

It has been also suggested that the VEMPresponse may be a consequence of the

proximity of the saccule to the stapesfootplate and eddy currents set up in theendolymph by sudden movement of thestapes.

The VEMP is abolished by selectivevestibular neurectomy, but may be presentdespite profound deafness, as long as there isnot significant conductive component

present to attenuate the stimulus


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VEMP Waveform

The P1-N1 response, whilestill an evoked potential, isgenerated by synchronouschanges in motor unit

potential

An additional consequenceof the myogenic nature ofthis response is that theseevoked potentials are ofrelatively large sizecompared with mostneurogenic evoked

potentials.

VEMP Norms

Normative Parameters of the waveform are identified(Ochi, Ohashi & Nishino, 2001)

Absolute latencies of P1 (11.30 ms

1.50)

so u e a enc es o .

ms 2.81)

Inter-aural amplitude differences for

P1 (0.86 ms 0.61)

Inter-aural amplitude differences for

N1 (1.68 ms 1.31)

P1-N1 ratio (%) (13.6 12.1)

VEMP threshold (87.78 dB nHL 4.54)

Inter-aural threshold difference (1.67 dBnHL 2.43)

EMG Monitoring Techniques Intelligent Hearing Systems

(IHS)

Target EMG activity range

EP sweeps are rejected if EMG

activity is outside target range

Target Level EMG Monitoring

Bio-feedback of SCM muscle

activation


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VEMP Case Study

Answering a Question of IAC

Compromise ?

Here comes VEMP to save the day...

Case History 12 year old female with Fanconi Anemia

Fanconi Anemia is a type of Inherited Bone Marrow Failure Syndrome

Most people with Fanconi's anemia have these types of symptoms Skin pigment change (darkened areas of the skin, cafe-au-lait spots, vitiligo)

Short height

Upper limb problems (missing, extra or misshapen thumbs; small or missing radius bone in;the forearm; problems of the hands and the forearm bone in the lower arm)

Small testicles, genital changes

Abnormal bones (abnormalities of the hip, spine or rib; curved spine (scoliosis); small head)

Abnormal eye/eyelid

Malformed kidney

Abnormal ears/deafness

Abnormal hip, leg, and toe

Abnormal digestive tract/heart and lungs

Hearing loss

Other possible symptoms Mental retardation

Learning disability Low birth weight

Failure to thrive

Patient History

Presents with otitis media in the rightear and a recent CT scan that identifieda narrowing of the left IAC.

Histor of rofound nomeasurablehearing in the left ear with normalhearing in the right ear.

Nuerotologic concern regardingconstriction of neural tracts (Facial,Auditory & Vestibular) through left IAC

No balance / dizziness complaintsreported from patient or her parents

Picture is NOT case study presentation

but is Fanconi Anemia (www.google/images.com)


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Audiogram History

Initial audiometric evaluation at the NIH (3/28/2006)

SRT RE: 20 dB HL; SAT LE: 94 dB HL

Normal tympanometry LE; Flat tympanogram RE (normal volume)

Follow-up Audiometric Evaluation(5/3/2007)

Profound SNHL previously documented in the left ear (2006)

OME diagnosed in the right ear on this evaluation

No response LE

RE

CT Axial Imaging

Right IACLeft IAC

Normal widthSignificant

narrow width


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Auditory Brainstem Response

Left Ear Right Ear

No response LE

Summed response Summed response

Cochlear Microphonic

Left Ear Right Ear

No response LE

VEMP RecordingsCHL

No response LE


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Summary

LEFT

EAR

VEMP Cochlear Microphonic

ABR

NoresponseLE

RIGHTEAR

CHL effect

VEMPCochlear Microphonic

ABR

No response LE

Conclusions

Although no left-sided facial nerve effects wereobserved, VEMP was instrumental in providingthe only objective / measurable evidence that IACstenosis was not im actin vestibular inte rit

Although the ABR and CM was most likelyabsent secondary to the degree of peripheralhearing loss, VEMP was possible in spite of thishearing loss

Caloric irrigations were not possible with this

patient secondary to tolerance problems

Videonystagmography (VNG)

A comprehensivelook at VNG?

A ComprehensiveCase Study

An Unfortunate

Vestibular Demise


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a look at VNG testing

Normal results are easy (64%?)

o are no response pa en s or estraightforward unilateral weakness patients)

Its everything else in between that causes theproblemsand no two are (ever or seldom)alike

VNG Testing;The Didactic Approach - Teaching the Puzzle

Oculomotor Assessment

Positional Assessment

Caloric Assessment

Providing all the VNG puzzle pieces during didactic presentations likethis is difficult as you hope you can provide all the critical pieces (rulesand guidelines) so one can still interpret the entire picture independentof the puzzle (patient). This is difficult as no two patients are alike andcan often lead to a dangerous path of misinterpretation

Pitfalls and Errors

Rules and Guidelines for Interpretation

Anatomy and Physiology

Often your best tool of interpretation

PATIENCE, PRACTICE AND PRUDENCE

Comprehensive

Case Study

An unfortunate vestibular demise


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History

27 year old male presents to the NIH with an unknown

diagnosis First symptoms of visual blurriness in October of 2000

First began noticing balance difficulties following a brain

biopsy in May of 2006

Onset of bilateral tinnitus approximately 2 years ago

History significant for two distinct episodes of vertigo

Each persisted for 1-2 days

First in July / August of 2010

Second episode October / November of 2010

Second episode was noted to be in the vertical plane (backwards)

Medical history Admitting Sxs: Recurrent encephalopathy, headache, and gastrointenstinal

disorder

Onset of Sxs of severe headache at age 6-7 complicated by recurrent sinusitis

Migraine with visual scintillations (2-3/month) in teens

De ression

Recurrent kidney stones

Encepaholopathy (age 13) - experienced first episode of transient dysarthria and left upperextremity weakness; CT at this time was unrevealing

Second episode of focal neurological dysfunction three years later (age 16); CT consistent withabnormality in left basal ganglia

Between 2000-2004 imaging (19 cranial MRIs) showed waxing and waning signal changes witha working diagnosis of an indeterminate forebrain inflammatory process

Age 22 (2006) extensively evaluated at Mayo Clinic with non-specific myelin damage andinflammatory cell infiltrate; again given Dx of indeterminate inflammatory process

April-July of 2010 self-described his condition as much worse with fatigue, headache, severevertigo ,blurred vision, oscillopsia, and significant ataxia

Medication history

Prednisone (antiinflammatory)

Neurontin (control seizures / neuralgia pain relief)

Diazepam (anti-anxiety)

Xanax (anti-anxiety) Zoloft (depression)

Baclofen (spasticity)

Colazal (ulcerative colitis)

Fosamax (osteoporosis)

Immunosupressive therapy

Note: when possible, meds were

suspended for vestibular testing


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Vestibular Assessment

VNG

Positionals Caloric Irrigations

Rotational Oculomotor

SHA

600 & 2400 Step Testing

VOR Suppression

VEMP

Deferred CDPP secondaryto significant ataxia

SpontaneousVision denied - gaze right

30

Left-Beating

Vision denied - gaze left

Supine Head LEFT

Positional Testing - SupineSupine Head RIGHT

6-70 left-beating

50

left-beating

Horizontal / vision denied Horizontal / vision denied

Vertical / vision denied Vertical / vision denied

Horizontal / fixationHorizontal / fixation

40 down-beating


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Lateral LEFT Lateral RIGHT

Positional Testing - Laterals

Horizontal / vision denied Horizontal / vision denied

40 left-beating 70 left-beating

Vertical / vision denied Vertical / vision denied

30 down-beating

Horizontal / fixationHorizontal / fixation

Caloric Position (Positional)

40 Left-Beating

Summary thus far.

First degree spontaneous

nystagmus

Direction-fixed, obliquepositional nystagmus (left-

beating ; up beating) that fails to

abate with visual fixation

Left-beating nystagmus in the

caloric position

40 Left-Beating


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Caloric Testing

LEFT Cool

90 right-beating

LEFT Warm

120 left-beating

Caloric Testing

RIGHT Cool

40 Left-Beatin

40 Left-Beating

RIGHT Warm

40 Left-Beating

Caloric Summary

LEFT CoolRIGHT Cool

40 Left-Beating 80 Right-Beating

LEFT WarmRIGHT Warm

40 Left-Beating

Absent RIGHT ear labyrinthine reactivity, present left ear response

11.50Left-Beating


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Oculomotor Testing - Saccades

Normal Saccades

Oculomotor Testing Smooth Pursuit

Oculomotor Testing - Optokinetic

200 OKN Stimulus 400 OKN Stimulus

600 OKN Stimulus

Asymmetry with

increasing stimulus300/sec (50%)

400/sec (67%)

~17%


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SHA Testing 0.01 Hz

SHA Testing 0.04 Hz

SHA Testing 0.16 Hz


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SHA Testing Summary Data

Velocity Step Testing - 600

37% VOR decay

time constant

Velocity Step Testing - 2400


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Velocity Step Testing 2400

Per LEFT Per RIGHT

379.03 LEFT

203.06 RIGHT

Post RIGHT Post LEFT

Stronger Left

VOR response

(Right DP)

VOR Suppression Testing

0.08 Hz 0.32 Hz

0.16 Hz 0.64 Hz

Failure of VOR

fixation suppression

VEMP Testing

108.03 V 96.70 V

NORMAL VEMP Bilaterally


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MRI Scan Mild-to-moderate volume loss

Extensive leukomalacia involving the periventricular

white matter and some subcortical white matter(right>left)

Probable lacunar infarct involving the tail of the leftputamen as well as a possible cyst in theperiventricular white matter of the right parietal lobe

xglobus pallidus bilaterally as well as the dentatenuclei

Petechial deposition of iron (or other metal) atmultiple locations within the brain parenchyma andalong the right central sulcus

Creatine in the parietal gray matter is mildly elevated

Deficit of NAA in the superior cerebellar vermis andthe left thalmus

Cysts or adhesions within the trigones of the lateralventricles (right > left)

Several inspissated mucus retension cysts in themaxillary sinuses

Thornwaldt cyst in the nasopharynx

SUMMARY - VERY ABNORMAL BRAIN MRI

Conclusions

CentralIndicators Saccadic tracking

on smooth pursuit

Non-LocalizingIndicators Right-VOR

asymmetry on SHA

PeripheralIndicators Absence of

labyrinthine

a ure ofixationsuppression

OKN asymmetry(secondary to SNor cerebellardysfunction?)

Positionalnystagmus withfixation

gn can yshortened time-constants

Grossly abnormalVOR phase leadacross entire Hzrange

Direction-fixed,oblique positionalnystagmus

caloric stimulus

Asymmetriclabyrinthinereactivity onhigh-velocity steptesting

Conclusions

Collectively, these results identify both central and peripheral sites of lesions

Evidence supports a cerebellar SOL with a right ear peripheral SOL

Results provide further evidence to support partial compensation for theeri heralinsult normalVOR ain owever his rocess ma be

incomplete (persistent VOR asymmetry)

Central compensation is primarily modulated through the cerebellum wherethere is evidence of a concomitant lesion

In light of this evidence, prognosis for full central compensation for theperipheral vestibulopathy is questionable and may be expected to besignificantly altered or delayed

This may help to explain patients continued (uncompensated) vestibularsymptoms


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Wrap up.

Vestibular Assessment if

a dynamic process ofdiscovery

pieces which is difficultwhen every patient is adifferent puzzle

In balance function assessment it should be the clinician's end goal to be one-step

ahead during the assessment.the hypothesis generating process should continue as

each bit of new information is acquired through [qualitative and/or] quantitative

testing

- Jacobson, et al. (2008)

Wrap up.

The truth of the matter is.thatsometimes the pieces fit together nicely,

but many times they do not

or worse, they seem to fit together butsome pieces are red herrings that leadyou to the wrong interpretation

The information may be correct, but ourinterpretation, experience, knowledge, orcomprehensiveness of testing limitsour understanding of how the pieces fit

together

Final thoughts.

Ill leave you with this


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My vestibular testing tenets(for whatever theyre worth)

If no two vestibular puzzles / results are the same, then it only

stands to reason that1. vestibular assessment and interpretation is just as dynamic andnonconforming (and sometimes downright confusing)

2. experience in vestibular interpretation is the sum of ones mistakes (and

3. if you never have ALL the pieces, youll only see a portion of the finalpicture

4. despite countless hours of didactic teaching and tutorials on the pitfalls and(correct) procedures of vestibular assessment, interpretation largely hingesupon fundamentals in anatomy and physiology.

5. if one piece of the puzzle changes (or is placed incorrectly), all the otherpieces are just as likely to change which could shift your entire interpretation

6. while good vestibular testing comes from patience, practice, and prudence;great vestibular interpretation comes from better vestibular testing (yepits acircular thought but one that thankfully builds upon itself)

Thanks

There is no such thing as failure. There are only results. - Anthony Robbins

Documents

110121 Understanding Vestibular Function Handout