110121 understanding vestibular function handout
TRANSCRIPT
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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
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:
Chris ZalewskiNIH, Audiology
American Academy of Audiology
Web Seminar Spring 2011
We would accomplish many more things if we did not think of them as impossible- Vince Lombardi
HOW DO I PUT THE
VESTIBULARPUZZLETOGETHER
American Academy of Audiology
Web Seminar Spring 2011
PIECES ARE MISSING ?Presented by:
Chris ZalewskiNIH, Audiology
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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
Computerized Dynamic Platform
Posturography (CDPP)
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 ?
What Does SOT Reveal ?
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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What Does SOT Reveal ?
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
Velocity Step Testing
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
Velocity Step Testing
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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Sinusoidal Oscillation Testing
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
Sinusoidal Oscillation Testing
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%
Sinusoidal Oscillation Testing
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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Sinusoidal Oscillation Testing
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
Parameters of Sinusoidal Oscillation Testing
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
Parameters of Sinusoidal Oscillation Testing
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
Computerized Dynamic Platform
Posturography (CDPP)
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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