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What is Being Tested in DifferentVestibular Function Tests

Kamran Barin, Ph.D.Assistant Professor, Emeritus

Department of OtolaryngologyThe Ohio State University

barin.1@osu.eduDisclosure: Consultant to Otometrics

Marco Jurado, Au.D., CCC-A, FAAAClinical Support Audiologist

Otometrics, Schaumburg, Illinoismjurado@gnotometrics.com

American Academy of AudiologyOrlando, FL, March 26, 2014

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Overview

• Purpose of vestibular function tests– Is there a lesion?– If yes, can the site and side of lesion be localized?

• Traditional vestibular function tests (ENG/VNG, rotation chair, active rotation) fail to provide adequate answer to the above questions in about 60% of the dizzy patients

• Can recent developments in vestibular testing such as video head impulse test (vHIT) or vestibular evoked myogenic potentials (VEMP), provide more accurate information about the site and side of lesion?

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Anatomical Sites Involved in Vestibular Tests

• Vestibular tests evaluate VOR (VNG, rotation tests, vHIT), VSR (posturography), or a combination of both (VEMP)– No direct access to the labyrinth or vestibular nerve– Peripheral → Labyrinthine structures and two branches of vestibular nerve from

the end organ to brainstem → Otologic disease?– Central → All structures beyond the root entry zone of vestibular nerve including

the vestibular nuclei → Neurologic disease?

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Differentiating Peripheral vs Central Lesions

• Exhaustive search for central lesions– Oculomotor tests in ENG/VNG, but currently not able to identify every

possible central lesion

• Subtracting out central pathways through repeated stimulations– Unilateral weakness in the caloric test (subject to caloric test limitations)

• Differentiate based on response characteristics (frequency/velocity/latency)– Oculomotor responses are much slower than vestibular responses

• Hair cell response characteristics in vHIT or BPPV-type eye movements in Dix-Hallpike

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Site of Lesion in VNG/ENG Oculomotor Tests

• Tests of oculomotor function (with fixation)– Saccade (fast eye movements)– Tracking (slow voluntary eye movements)– Optokinetic (reflexive eye movements but the test performed as a part of

ENG/VNG is not a true test of optokinetic pathways)– With very few exceptions (one?), abnormalities in the oculomotor tests

indicate a central finding– Oculomotor tests provide hard and localizing findings but only about 5%

of dizzy patients have abnormal findings in oculomotor tests

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Non-Central Finding in Oculomotor Tests

• Borderline unilateral defective tracking caused by strong spontaneous nystagmus (in the direction of fast phases)– Effect of superimposed nystagmus and not

abnormal tracking

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Site of Lesion in VNG/ENG Gaze Stabilization Tests

• Tests of gaze stabilization with fixation– Gaze test (effect of gaze position on presence/characteristics of nystagmus)– With very few exceptions, abnormalities in the gaze test with fixation

indicate a central finding

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Site of Lesion in VNG/ENG Gaze Stabilization Tests

• Tests of gaze stabilization without fixation– Spontaneous nystagmus test (recording eye movements in the primary gaze

position with and without fixation)– Static position test (effect of head position on presence/characteristics of

nystagmus)– Abnormalities in gaze stabilization tests without fixation are typically non-

localizing but can support localizing findings in other vestibular tests– Gaze stabilization tests with fixation provide hard, localizing findings but without

fixation, the findings are often non-localizing– About 15% of dizzy patients will have abnormal findings in gaze stabilization tests

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Non-Central Findings in Gaze Stabilization Tests

• When unilateral gaze nystagmus is observed with fixation, observe the response without fixation– If intensity increases significantly, it is not gaze-evoked nystagmus! It is spontaneous

nystagmus (usually follows Alexander’s law)

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Site of Lesion in VNG/ENG Caloric Test

• Test of lateral canals and the superior portion of vestibular nerve– Unilateral weakness (canal paresis) indicates a peripheral vestibular lesion

involving the lateral (horizontal) canal or its afferent pathways on the side of the weaker response (the involved pathway extends from the end-organ to the root entry zone of the vestibular nerve in the brain stem)

– Other abnormalities are either non-localizing (directional preponderance/ bilateral weakness) or central (hyperactive/failure of fixation suppression)

– Caloric testing provides often unique hard localizing findings (abnormal in ~20% of dizzy patients)

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Site of Lesion in VNG/ENG Dynamic Position Tests

• Dix-Hallpike or sidelying maneuver– Most common finding is a BPPV-type nystagmus (transient torsional-

vertical nystagmus with delayed-onset) that localizes to the undermost posterior semicircular canal and inferior portion of vestibular nerve

• Roll maneuver– For the diagnosis of lateral canal BPPV

• Dynamic position tests are the definitive diagnostic tests for BPPV (abnormal in ~20% of dizzy patients)

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Non-Peripheral Findings in Dynamic Position Tests

• Some patients exhibit repeated reversal of nystagmus direction during canalith repositioning therapy (Epley’s maneuver), which has been associated with unsuccessful treatment outcomes

• When repositioning maneuvers are unsuccessful (Intractable BPPV), non-peripheral causes should be ruled out– Intracranial, vascular, metabolic abnormalities can mimic BPPV

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Intractable BPPV – Possible Mechanism

2-6 hours after

12-48 hours after

before

Geotropic

Ageotropic

Head Left

Head Right

• Patients with intractable BPPV may have heavy/light cupula/endolymphcaused by metabolic changes in the relative density of cupula to endolymph

Positional Alcohol Nystagmus

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Site of Lesion in Rotation Tests

• Rotation about vertical axis that passes through center of the head– Most common stimulus is sinusoidal at frequencies of 0.01-0.64 Hz– Tests both lateral SCCs and their central pathways– Usually does not provide localizing findings (for unilateral lesions, tests the

effect of loss on the velocity storage mechanism)– Is a useful test for bilateral vestibular loss but only ~3-5% of dizzy patients

will have abnormal findings not detected in VNG/ENG

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VEMP – Definition

• Short-latency electromyographic (EMG) potentials evoked in response to high-level acoustic stimuli

• Most common recording sites:– Neck/sternocleidomastoid (SCM) muscle – Cervical VEMP or cVEMP– Extraocular/inferior oblique muscle – Ocular VEMP or oVEMP

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VEMP – cVEMP and oVEMP Pathways

• cVEMP and oVEMP are NOT the same test!– Not possible to

differentiate between utricular or saccularresponses based on the type of stimulus BUTdifferentiation based on motor projections is possible

– Saccular neurons have a strong projection to neck muscles but weak projection to eye muscles

– Utricular neurons have a strong projection to eye muscles but weak projection to neck muscle

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VEMP – Optimal Clinical Protocol

• Use 500 Hz tone burst stimulus for both cVEMP and oVEMP– If no response in older patients, consider 750 Hz or 1000 Hz stimulus (Piker

et al, 2013)– Test in other frequencies may be helpful in patients with suspected superior

canal dehiscence (SCD) and in patients with suspected Meniere’s disease

• Perform air-conducted cVEMPs unless the patient has conductive hearing loss and bone-conducted oVEMPs except for suspected SCD patients

• Standardize muscle contraction levels (monitoring/normalization) for cVEMPs and set the gaze direction at 30⁰ upward for oVEMPs

• Use more conservative criteria (presence or absence/high asymmetry ratio) for interpretation of VEMPs– Consider the patient’s age

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VEMP – Response Parameters

• Presence – Ability to produce an identifiable response at any stimulus type and level

• Latency – Time of positive and negative peaks measured from the onset of stimulus (p1 and n1 in milliseconds)

• Amplitude – Difference between positive and negative averaged EMG levels (p1-n1 in microvolt)– Absolute amplitudes of p1 and n1 measured from 0 baseline can also be useful

• Threshold – Minimum sound intensity level to produce an identifiable VEMP response (usually in dB nHL, dB SPL, or dB FL )

• Asymmetry ratio – Normalized difference between right and left amplitudes (in percent) Amplitude Right – Amplitude Left

Asymmetry Ratio = * 100Amplitude Right + Amplitude Left

Amplitude and latency parameters are derived by averaging values from 2 or 3 trials

 

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Site of Lesion in VEMP Tests – Central

• Prolonged latencies usually indicate a central lesion– cVEMP latencies are affected by the distance of the electrode from the motor

point of the muscle (motor point is usually around the upper 1/3 of the muscle at length about 4” below the mastoid)

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Site of Lesion in VEMP Tests – Central

– Sometimes when P1/N1 is absent, secondary waves are misinterpreted as VEMP response

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Site of Lesion in VEMP Tests – Peripheral

• Low thresholds, elevated amplitudes, or elevated asymmetries usually indicate a peripheral lesion

• In vestibular neuritis, can determine involvement of different vestibular nerve branches– Superior branch – Abnormal oVEMP– Inferior branch – Abnormal cVEMP

• In SCD, can determine the side– Low threshold in air-conducted cVEMP– Elevated n1-p1 or n1 amplitude in air-conducted oVEMP (Zuniga et al., 2013)– Presence of response at high-frequency (4k) air-conducted oVEMP (Manzari

et al., 2013)

• In Meniere’s disease, can determine frequency-tuning abnormalities

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Site of Lesion in VEMP Tests – Peripheral

• In Meniere’s disease, can determine frequency-tuning abnormalities– Findings are similar in cVEMP and oVEMP– Due to the difficulty of obtaining thresholds, some have used the amplitude ratio of

500 versus 1k tone bursts– Using amplitude ratio can help differentiate between Meniere's disease and migraine

associated vertigo (Taylor et al, 2012) – Addition of caloric results improve sensitivity

From Rauch (2006)

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Head Impulse Test (HIT) – Overview

• A quick test of vestibular function that consists of monitoring eye movements as the patient fixates on a stationary target while the head is rotated right or left unexpectedly using small-amplitude high-velocity high-acceleration movements

• Normal individuals can maintain a steady gaze but patients with deficient VOR cannot keep up with high-velocity head turns and generate “catch-up” or refixation saccades after head impulses toward the damaged side

• Can be performed in the planes of lateral, right anterior/left posterior (RALP), right posterior/left anterior (LARP) canal pairs to provide independent assessment of all 6 semicircular canals

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Head Impulse Test – Mechanism

• There is an asymmetry between excitatory and inhibitory neural responses of each semicircular canal (greater dynamic range for excitation)– Excitation from tonic level of ~100 up to a maximum of ~400 spikes/sec– Inhibition from tonic level of ~100 down to a minimum of 0 spikes/sec

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Head Impulse Test – Changes in Neural Firing

• Head impulses toward the canal cause excitation from that canal– Change in the neural firing is proportional to the head velocity

• Head impulses away from the canal cause inhibition from that canal– Neural firing is clipped (saturates) at 0 spikes/sec and the canal does not

provide an accurate measure of head velocity

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Head Impulse Test – Right Vestibular Lesion

• For head impulses toward the side of lesion, the neural input to the oculomotor system is no longer proportional to head velocity– The resulting eye velocity does not match head velocity and the eyes fall

short of target– VOR Gain = Eye Move./Head Move. << 1 (decreases rapidly with increasing

head velocity)

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Head Impulse Test – Catch-Up Saccades

• Catch-up saccades reposition the eyes on the target• Catch-up saccades that occur after head impulses are called overt saccades• Overt saccades are visible and can be detected by an experienced examiner during

the bedside test without any additional equipment

100⁰/sec

100 msec

Head VelocityEye Velocity

5⁰

100 msec

Head Position

Eye Position

5⁰

100 msec

Head Position

Eye Position

100⁰/sec

100 msec

Head VelocityEye Velocity

Overt Saccade Overt Saccade

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Head Impulse Test – Catch-Up Saccades

• Catch-up saccades that occur during head impulses are called covert saccades• Covert saccades are practically impossible to detect without specialized equipment

100⁰/sec

100 msec

Head VelocityEye Velocity

5⁰

100 msec

Head PositionEye Position

5⁰

100 msec

Head PositionEye Position

Catch-Up Saccade

100⁰/sec

100 msec

Head VelocityEye Velocity

Catch-Up SaccadeOvert Saccade Overt Saccade

5⁰

100 msec

Head PositionEye Position

100⁰/sec

100 msec

Head VelocityEye Velocity

Covert Saccade Covert Saccade

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Site of Lesion in Video Head Impulse Test

• Presence of abnormal catch-up saccades (overt or covert) denotes a peripheral vestibular lesion involving the semicircular canal or its afferent neural pathway on the side of head impulse– Normal individuals may have catch-up saccades but abnormal catch-up

saccades can be identified based on their direction, timing, velocity, and consistency

– VOR gain (slow eye movement / head movement) can be used to support abnormal HIT results

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Site of Lesion in New Vestibular Tests• Combination of vHIT, cVEMP, and oVEMP results provides a

complete evaluation of the labyrinth and both branches of vestibular nerve– Caloric testing adds low-frequency evaluation of lateral canals and their

afferent neural pathways

Right Labyrinth RALP (downward HIT)

Lateral (right HIT)

LARP (upward HIT)

oVEMP (contralateral eye)cVEMP (ipsilateral SCM)

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Summary

• New vestibular tests have the potential to provide more specific information about different structures within the vestibular system

• More widespread clinical studies are needed to verify and validate the new methods

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Identifying Site of LesionSITE Lateral HIT Vertical HIT (RALP/LARP) cVEMP oVEMP

Healthy Subject Within normallimits

Within normallimits

Within normallimits

Within normallimits

Lateral Canal Abnormal for impulses toward side of lesion

Within normallimits

Within normallimits

Within normallimits

Anterior Canal Within normallimits

Abnormal for downward impulses with the head turned

away from side of lesion

Within normallimits

Within normallimits

Posterior Canal Within normallimits

Abnormal for upward impulses with the head turned

toward side of lesion

Within normallimits

Within normallimits

Utricle Within normallimits

Within normallimits

Within normallimits

Abnormal recordings from the eye muscle

away from side of lesion

Saccule Within normallimits

Within normallimits

Abnormal recordings from the neck muscle toward side of lesion

Within normallimits

Superior Vestibular Nerve

Abnormal for impulses toward side of lesion

Abnormal for downward impulses with the head turned

away from side of lesion

Within normallimits

Abnormal recordings from the eye muscle

away from side of lesion

Inferior Vestibular Nerve

Within normallimits

Abnormal for upward impulses with the head turned

toward side of lesion

Abnormal recordings from the neck muscle toward side of lesion

Within normallimits

Total Unilateral Vestibular Loss

Abnormal for impulses toward side of lesion

Abnormal for downward impulses with the head turned

away from side of lesion

Abnormal recordings from the neck muscle toward side of lesion

Abnormal recordings from the eye muscle

away from side of lesion

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