What is Being Tested in Different Vestibular Function Tests Kamran Barin, Ph.D. Assistant Professor, Emeritus Department of Otolaryngology The Ohio State University barin.1@osu.edu Disclosure: Consultant to Otometrics Marco Jurado, Au.D., CCC-A, FAAA Clinical Support Audiologist Otometrics, Schaumburg, Illinois mjurado@gnotometrics.com American Academy of Audiology Orlando, FL, March 26, 2014 Anatomical Sites Involved in Vestibular Tests 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? Differentiating Peripheral vs Central Lesions 1 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? 2 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 3 Page 1
Site of Lesion in VNG/ENG Oculomotor Tests Non-Central Finding in 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 Borderline unilateral defective tracking caused by strong spontaneous nystagmus (in the direction of fast phases) Effect of superimposed nystagmus and not abnormal tracking 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 4 5 Site of Lesion in VNG/ENG Gaze Stabilization Tests 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 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 indicate a central finding nystagmus) Abnormalities in gaze stabilization tests without fixation are typically nonlocalizing 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 6 Page 2 7
Non-Central Findings in Gaze Stabilization Tests Site of Lesion in VNG/ENG Caloric Test 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) Site of Lesion in VNG/ENG Dynamic Position Tests 8 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) Non-Peripheral Findings in Dynamic Position Tests 9 Dix-Hallpike or sidelying maneuver Most common finding is a BPPV-type nystagmus (transient torsionalvertical 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) 10 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 11 Page 3
Intractable BPPV Possible Mechanism Head Left Head Right Geotropic Site of Lesion in Rotation Tests Positional Alcohol Nystagmus before 2-6 hours after Ageotropic 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 12-48 hours after Patients with intractable BPPV may have heavy/light cupula/endolymph caused by metabolic changes in the relative density of cupula to endolymph 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 12 13 VEMP cvemp and ovemp Pathways VEMP Definition cvemp and ovemp are NOT the same test! 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 Not possible to differentiate between utricular or saccular responses based on the type of stimulus BUT differentiation 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 15 14 Page 4
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 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) 16 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 = * 100 Amplitude Right + Amplitude Left Amplitude and latency parameters are derived by averaging values from 2 or 3 trials Site of Lesion in VEMP Tests Central Sometimes when P1/N1 is absent, secondary waves are misinterpreted as VEMP response 17 18 19 Page 5
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 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 20 22 Site of Lesion in VEMP Tests Peripheral From Rauch (2006) 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 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 21 23 Page 6
Head Impulse Test Changes in Neural Firing Head Impulse Test Right Vestibular Lesion 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 Head Impulse Test Catch-Up Saccades 24 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) Head Impulse Test Catch-Up Saccades 25 Overt Saccade Overt Saccade Catch-Up Overt Covert Saccade Catch-Up Overt Saccade Covert Saccade 5⁰ 5⁰ Head Position Eye Position Head Position Eye Position 100 msec 100⁰/sec Head Velocity Eye Velocity 100 msec 100⁰/sec Head Velocity Eye Velocity 100 msec 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 100 msec Catch-up saccades that occur during head impulses are called covert saccades Covert saccades are practically impossible to detect without specialized equipment 26 27 Page 7
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 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 Lateral (right HIT) RALP (downward HIT) LARP (upward HIT) cvemp (ipsilateral SCM) ovemp (contralateral eye) 28 29 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 31 Page 8
Identifying Site of Lesion SITE Lateral HIT Vertical HIT (RALP/LARP) cvemp ovemp Healthy Subject Lateral Canal Abnormal for impulses Anterior Canal Abnormal for downward impulses with the head turned Posterior Canal Abnormal for upward impulses with the head turned Utricle from the eye muscle Saccule from the neck muscle Superior Vestibular Nerve Abnormal for impulses Abnormal for downward impulses with the head turned from the eye muscle Inferior Vestibular Nerve Abnormal for upward impulses with the head turned from the neck muscle Total Unilateral Vestibular Loss Abnormal for impulses Abnormal for downward impulses with the head turned from the neck muscle from the eye muscle 30 Page 9
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