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Background: The head impulse test (HIT) is a useful bedside test to identify peripheral vestibular deficits. However, such a deficit of the vestibulo-ocular reflex (VOR) may not be diagnosed because corrective saccades cannot always be detected by simple observation. The scleral search coil technique is the gold standard for HIT measurements, but it is not practical for routine testing or for acute patients, because they are required to wear an uncomfortable contact lens., Objective: To develop an easy-to-use video HIT system (vHIT) as a clinical tool for identifying peripheral vestibular deficits. To validate the diagnostic accuracy of vHIT by simultaneous measures with video and search coil recordings across healthy subjects and patients with a wide range of previously identified peripheral vestibular deficits., Methods: Horizontal HIT was recorded simultaneously with vHIT (250 Hz) and search coils (1,000 Hz) in 8 normal subjects, 6 patients with vestibular neuritis, 1 patient after unilateral intratympanic gentamicin, and 1 patient with bilateral gentamicin vestibulotoxicity., Results: Simultaneous video and search coil recordings of eye movements were closely comparable (average concordance correlation coefficient r(c) = 0.930). Mean VOR gains measured with search coils and video were not significantly different in normal (p = 0.107) and patients (p = 0.073). With these groups, the sensitivity and specificity of both the reference and index test were 1.0 (95% confidence interval 0.69-1.0). vHIT measures detected both overt and covert saccades as accurately as coils., Conclusions: The video head impulse test is equivalent to search coils in identifying peripheral vestibular deficits but easier to use in clinics, even in patients with acute vestibular neuritis.

Background: Parenteral antibiotic therapy with gentamicin, even in accepted therapeutic doses, can occasionally cause bilateral vestibular loss (BVL) due to hair cell toxicity., Objective: To quantify in patients with gentamicin vestibulotoxicity (GVT) the extent of acceleration gain deficit of the horizontal vestibulo-ocular reflex at different accelerations with a graded head impulse test (HIT) in comparison with standard caloric and rotational testing. To characterize the corresponding HIT catch-up saccade pattern to provide the basis for its salience to clinicians., Methods: Horizontal HIT of graded acceleration (750 degrees-6,000 degrees/sec2) was measured with binocular dual search coils in 14 patients with GVT and compared with 14 normal subjects and a control subject with total surgical BVL., Results: Patients showed mostly symmetric HIT gain deficits with a continuous spectrum from almost normal to complete BVL. Gain deficits were present even at the lowest head accelerations. HIT gain correlated better with caloric (Spearman rho = 0.85, p = 0.0001) than rotational testing (rho = 0.55, p = 0.046). Cumulative amplitude of overt saccades after head impulses was 5.6 times larger in patients than in normal subjects. Compared with previously published patients after unilateral vestibular deafferentation, GVT patients with BVL generated only approximately half the percentage of covert saccades during head rotation (23% at 750 degrees/sec2 to 46% at 6,000 degrees/sec2)., Conclusions: Head impulse testing is useful for early bedside detection of gentamicin vestibulotoxicity because most patients, even those with partial bilateral vestibular loss (BVL), have large overt saccades. Covert saccades, which can conceal the extent of BVL, are only approximately half as frequent as in unilateral patients, but may be present even in total BVL.

Objective: Patients with superior canal dehiscence (SCD) have large sound-evoked vestibular reflexes with pathologically low threshold. We wished to determine whether a recently discovered measure of the vestibulo-ocular reflex-the ocular vestibular evoked myogenic potential (OVEMP)-produced similar high-amplitude, low-threshold responses in SCD, and could differentiate patients with SCD from normal control patients., Methods: Nine patients with CT-confirmed SCD and 10 normal controls were stimulated with 500 Hz, 2 ms tone bursts and 0.1 ms clicks at intensities up to 142 dB peak SPL. Conventional VEMPs were recorded from the ipsilateral sternocleidomastoid muscle to determine threshold, and OVEMPs were recorded from electrode pairs placed superior and inferior to the eyes. Three-dimensional eye movements were measured with scleral dual-search coils., Results: In patients with SCD, OVEMP amplitudes were significantly larger than normal (p<0.001) and thresholds were pathologically low. The n10 OVEMP in the contralateral inferior electrode became particularly large with increasing stimulus intensity (up to 25 microV) and with up-gaze (up to 40 microV). Sound-evoked (slow-phase) eye movements were present in all patients with SCD (vertical: upward; torsional: upper pole away from the affected side; and horizontal: towards or away from the affected side), but began only as the OVEMP response became maximal, which is consistent with the surface potentials being produced by activation of the extraocular muscles that generated the eye movements., Conclusions: OVEMP amplitude and threshold (particularly the contralateral inferior n10 response) differentiated patients with SCD from normal controls. Our findings suggest that both the OVEMPs and induced eye movements in SCD are a result of intense saccular activation in addition to superior canal stimulation.

Background: Quantitative head impulse test (HIT) measures the gain of the angular vestibulo-ocular reflex (VOR) during head rotation as the ratio of eye to head acceleration. Bedside HIT identifies subsequent catch-up saccades after the head rotation as indirect signs of VOR deficit., Objective: To determine the VOR deficit and catch-up saccade characteristics in unilateral vestibular disease in response to HIT of varying accelerations., Methods: Eye and head rotations were measured with search coils during manually applied horizontal HITs of varying accelerations in patients after vestibular neuritis (VN, n = 13) and unilateral vestibular deafferentation (UVD, n = 15) compared to normal subjects (n = 12)., Results: Normal VOR gain was close to unity and symmetric over the entire head-acceleration range. Patients with VN and UVD showed VOR gain asymmetry, with larger ipsilesional than contralesional deficits. As accelerations increased from 750 to 6,000 degrees /sec(2), ipsilesional gains decreased from 0.59 to 0.29 in VN and from 0.47 to 0.13 in UVD producing increasing asymmetry. Initial catch-up saccades can occur during or after head rotation. Covert saccades during head rotation are most likely imperceptible, while overt saccades after head rotation are detectable by clinicians. With increasing acceleration, the amplitude of overt saccades in patients became larger; however, initial covert saccades also became increasingly common, occurring in up to about 70% of trials., Conclusions: Head impulse test (HIT) with high acceleration reveals vestibulo-ocular reflex deficits better and elicits larger overt catch-up saccades in unilateral vestibular patients. Covert saccades during head rotation, however, occur more frequently with higher acceleration and may be missed by clinicians. To avoid false-negative results, bedside HIT should be repeated to improve chances of detection.

Taps to the forehead on the midline, at the hairline (Fz), with a reflex hammer or powerful bone conduction vibrator caused short-latency surface potentials from beneath both eyes in all healthy subjects. The earliest negative responses were invariably absent from the eye contralateral to the side of a previous vestibular nerve section but were preserved despite sensorineural hearing loss. These responses probably reflect vestibular function via crossed otolith-ocular pathways.

Using an acute scleral search coil technique for measuring eye position in alert animals we have shown that after UVD the yaw VOR in the guinea pig shows a permanent gain asymmetry. There is a reduced gain during the first 100 ms of brief, high acceleration horizontal head rotations ("yaw head impulses") towards the operated side, but only a small loss in gain for similar rotations towards the intact side. This result confirms that the horizontal E response during the first 100 ms of an abrupt high acceleration head rotation is a clear indicator of the function of the horizontal canal. These results are similar to those in human patients after unilateral acoustic neuroma operations. The asymmetry in response is large shortly after UVD and decreases over time but is permanent.

Using dual torsion scleral search coils we have recorded 3-dimensional eye position during yaw angular accelerations of 20 degrees/s2 about an earth vertical axis in healthy subjects and in patients with unilateral vestibular deafferentation (UVD). These experiments produced two interesting results: i) even in healthy subjects, the axis of eye velocity did not coincide with the (earth vertical) stimulus axis during centred rotation; ii) Patients with UVD had torsional eye velocity components that were systematically different from those in normal subjects. While in normals the direction of the torsional component of the eye velocity depended on the direction of rotation and was on average approximately symmetric for CW and CCW yaw rotation, there was a clear asymmetry in patients, which was distinctly different for left and right UVD.

Three new, simple, clinically applicable tests of vestibular function are described. The first is a test of the response of the lateral semicircular canals to high accelerations. The test can even be done at the bedside where it can reveal severe unilateral or bilateral loss of lateral canal function. The test can also be recorded in a laboratory where it might show a less severe deficit of lateral canal function. The second is a simple, laboratory test of utricular function which depends on a subject's ability to align a bar with the subjective visual vertical. Patients with acute unilateral peripheral vestibular lesions invariably set the bar toward the side of the lesion. The third is a laboratory test of saccular function relying on a click-evoked inhibitory vestibulo-collic reflex recorded in the ipsilateral sternomastoid muscle. It can be done with equipment used for auditory evoked potentials.

Patients were tested 1 day before and 1 week after therapeutic unilateral vestibular neurectomy (UVN) on vestibular tests which are likely determined primarily by otolithic function. UVN causes a maintained ocular torsion: fundus photographs showed that both eyes of every patients were rolled such that the upper pole of both eyes was tonically deviated towards the operated side, and there is a corresponding change in the perceived gravitational horizontal: patients set a small bar of LEDs bar down on the same side as their operation. One week after UVN, patients showed an asymmetrical sensitivity to linear acceleration vectors directed along their interaural axis in comparison to their preoperative settings for the same stimuli.

Asymmetric vestibular function is the basis of vertigo. Whereas caloric tests can identify unilateral peripheral loss or impairment of horizontal semicircular canal function reasonably accurately, there is as yet no single accepted test of unilateral otolith hypofunction. In some advanced vestibular laboratories around the world, new and perhaps diagnostically useful tests of otolith function are being devised. The physiologic basis and the present clinical applications of these tests are reviewed.

Visual suppression of vestibulo-ocular reflexes (induced vestibular nystagmus) differs between normal subjects and patients with various neurological disorders. Abnormalities of VOR suppression were associated consistently with abnormalities of the visual and/or vesitibular oculomotor reflexes and in particular with abnormal smooth pursuit eye movements in the direction of abnormal suppression. Absent VOR suppression in a gaze position of, and in the same direction as, a spontaneous nystagmus was found exclusively in patients with spontaneous nystagmus of central nervous system origin. Conversely, ability to suppress in these circumstances was found only in patients with spontaneous nystagmus of peripheral labyrinthine origin. Suppression of VOR was abnormal ipsilaterally in patients with unilateral cerebral hemisphere lesions and abnormal in both the horizontal and vertical planes in patients with basal ganglia lesions. Failure of VOR suppression in the absence of spontaneous nystagmus indicates a supratentorial lesion.

Objective:To report the outcome of posterior semicircular canal occlusion surgery for intractable benign positional vertigo, regarding vertigo cure rate and hearing and balance outcomes.Methods:Retrospective review of 53 patients presenting with benign positional vertigo, unresponsive to repositioning manoeuvres, who eventually underwent posterior canal occlusion, over a 20 year period.Results:From 1991 to 2011, 5364 benign positional vertigo patients were treated in our balance disorders clinic; 53 of those who failed to respond to repositioning underwent posterior canal occlusion. All 53 were cured of their benign positional vertigo. Nine suffered some symptomatic permanent hearing loss (>20 dB at low and >25 dB at high frequencies). Ten patients suffered caloric vestibular function deterioration, with mild but permanent subjective imbalance in five; a further 10 patients with no post-operative caloric test changes also had some permanent imbalance. Benign positional vertigo later developed in the operated ear lateral canal in two patients and in the opposite ear posterior canal in eight patients. Two patients needed bilateral sequential posterior canal occlusion.Conclusion:Posterior canal occlusion is a highly effective treatment for intractable benign positional vertigo, with what is probably an acceptable risk to hearing and balance: five of six patients will have no hearing problem and nine of 10 no balance problem after surgery. [ABSTRACT FROM PUBLISHER]

If a patient, who is lying supine and looking upward, is given bone-conducted vibration (BCV) of the forehead at the hairline in the midline (Fz) with a clinical reflex hammer or a powerful bone conduction vibrator, short-latency surface potentials called ocular vestibular evoked myogenic potentials (oVEMP) can be recorded from just beneath the eyes. The early negative (excitatory) component (n10) is approximately equal in amplitude for both eyes in healthy subjects, but in patients with unilateral vestibular loss, the n10 component is significantly asymmetrical under the 2 eyes – the n10 component is small or absent under the eye on the side contralateral to the prior unilateral vestibular nerve removal, but of normal amplitude under the eye on the side contralateral to the healthy ear. The n10 component of the oVEMP response to BCV at Fz stimuli reflects vestibular and probably mainly otolithic function via crossed otolithic-ocular pathways, and so n10 asymmetry is a new way of identifying the affected side in patients with unilateral otolithic loss. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]