Vestibulo-ocular reflex deficits with medial longitudinal fasciculus lesions.

The medial longitudinal fasciculus (MLF) is the final common pathway for all conjugate adducting horizontal eye movements, as well as for the vertical-torsional vestibulo-ocular reflex (VOR). MLF lesion causes adduction paresis of ipsilesional (adducting) eye with dissociated nystagmus of contralesional (abducting) eye-the well-known clinical syndrome of internuclear ophthalmoplegia (INO). We measured the VOR stimulation and also any catch-up saccades, from individual semicircular canal (SCC) evoked by the head impulse test (HIT), using head and binocular 3-dimensional scleral search coils in 27 multiple sclerosis (MS) patients, 8 with unilateral, 19 with bilateral INO. In unilateral INO, VOR gain (normal >0.90) from ipsilesional lateral SCC stimulation was 0.48 for the adducting eye and 0.81 for the abducting eye; 0.61 from contralesional anterior SCC stimulation and only 0.29 from contralesional posterior SCC stimulation. In bilateral INO, there were VOR gain deficits from all six SCCs: lateral SCC gains were asymmetrically reduced to 0.45 in the adducting eye and 0.66 in the abducting eye; anterior SCC gain was 0.48 and posterior SCC gain was only 0.19. Horizontal VOR versional dysconjugacy between adducting and abducting eyes at 0.66 was less severe than horizontal catch-up saccade versional dysconjugacy (0.44); normal >0.80. Unexpected partial preservation of horizontal VOR with greater catch-up saccade impairment from the adducting than abducting eye suggests that the ascending tract of Deiters (ATD), an extra-MLF pathway, also mediates the horizontal VOR, but not adducting horizontal saccades. Vertical VOR deficits will produce vertical oscillopsia with any vertical head movement and measurement of the vertical VOR could help with the diagnosis and quantitative evaluation of MLF lesions in suspected MS. Horizontal VOR deficits and catch-up saccade versional dysconjugacy in INO will cause gaze instability and horizontal oscillopsia during active horizontal head movements.

Axonal conduction in multiple sclerosis: A combined magnetic resonance imaging and electrophysiological study of the medial longitudinal fasciculus.

OBJECTIVE: The objective of this paper is to inform the pathophysiology of medial longitudinal fasciculus (MLF) axonal dysfunction in patients with internuclear ophthalmoplegia (INO) due to multiple sclerosis (MS), and develop a composite structural-functional biomarker of axonal and myelin integrity in this tract. METHODS: Eighteen patients with definite MS and clinically suspected INO underwent electrical vestibular stimulation and search-coil eye movement recording. Components of the electrically evoked vestibulo-ocular reflex (eVOR) were analyzed to probe the latency and fidelity of MLF axonal conduction. The MLF and T2-visible brainstem lesions were defined by high-resolution MRI. White matter integrity was determined by diffusion-weighted imaging metrics. RESULTS: eVOR onset latency was positively correlated with MLF lesion length (left: r = 0.66, p = 0.004; right: r = 0.75, p = 0.001). The mean conduction velocity (±SD) within MLF lesions was estimated at 2.72 (±0.87) m/s. eVOR onset latency correlated with normalized axial diffusivity (r = 0.66, p < 0.001) and fractional anisotropy (r = 0.44, p = 0.02) after exclusion of cases with ipsilateral vestibular root entry zone lesions. CONCLUSIONS: Axonal conduction velocity through lesions involving the MLF was reduced below levels predicted for natively myelinated and remyelinated axons. Composite in vivo biomarkers enable delineation of axonal from myelin processes and may provide a crucial role in assessing efficacy of novel reparative therapies in MS.

Vestibular and Saccadic Abnormalities in Gaucher's Disease.

Gaucher's disease (GD) is a hereditary lysosomal storage disease characterized by abnormal deposition of glucocerebroside due to the enzyme glucocerebrosidase deficiency, resulting in multi-organ pathology. GD type III has a progressive neurological involvement. We studied the vestibular and saccadic abnormalities in GD type III to determine if these parameters may be useful for assessing neurological involvement. We evaluated the vestibular and saccadic responses of two siblings with genetically identified GD type III on enzyme replacement therapy. Vestibular functions were assessed with the head impulse test (HIT), vestibular evoked myogenic potentials (VEMPs), and electrical vestibular stimulation (EVS). Saccadic functions were investigated with volitional horizontal and vertical saccades to ±20°. Three-dimensional head and eye movements were recorded with dual-search coils and VEMP with surface electrodes. HIT showed impaired individual semicircular canal function with halved angular vestibulo-ocular reflex (VOR) gains and absent horizontal refixation saccade. Ocular and cervical VEMPs to air-conducted clicks were absent in the older sibling, and only cervical VEMP was present in the younger sibling indicating otolithic dysfunction. EVS showed prolonged onset latency and attenuated tonic and phasic responses suggesting impaired neural conduction and vestibular function. Horizontal saccadic velocity was miniscule (<30°/s) and multiple back-to-back saccades with saccade-vergence interaction were utilized to minimize eye position error in the older sibling. Vertical saccades were slightly abnormal, but vergence and smooth pursuit were normal in both siblings. Our findings suggest that GD affected the vestibular nuclei in addition to the paramedian pontine reticular formation. These vestibular and saccadic abnormalities may be useful biomarkers to monitor neurological deterioration.

Vestibular schwannoma mimicking horizontal cupulolithiasis.

Positional vertigo and nystagmus can be due to canalithiasis, cupulolithiasis and less commonly, an underlying peripheral or central vestibular disorder. We present a patient with vestibular schwannoma who initially sought treatment for positioning vertigo. Video-oculography on the roll-test revealed direction-changing horizontal apogeotropic nystagmus, consistent with horizontal cupulolithiasis. However, further audio-vestibular investigations and imaging confirmed a right vestibulopathy attributable to a schwannoma of the right vestibular nerve. This case report suggests that vestibular schwannoma should be considered as another potential mimicker of horizontal cupulolithiasis.

Enhanced vestibulo-ocular reflex to electrical vestibular stimulation in Meniere's disease.

Meniere's disease is characterized by sporadic episodes of vertigo, nystagmus, fluctuating sensorineural hearing loss, tinnitus and aural pressure. Since Meniere's disease can affect different regions of the vestibular labyrinth, we investigated if electrical vestibular stimulation (EVS) which excites the entire vestibular labyrinth may be useful to reveal patchy endorgan pathology. We recorded three-dimensional electrically evoked vestibulo-ocular reflex (eVOR) to transient EVS using bilateral, bipolar 100-ms current steps at intensities of 0.9, 2.5, 5.0, 7.5 and 10.0 mA with dual-search coils in 12 unilateral Meniere's patients. Their results were compared to 17 normal subjects. Normal eVOR had tonic and phasic spatiotemporal properties best described by the torsional component, which was four times larger than horizontal and vertical components. At EVS onset and offset of 8.9 ms latency, there were phasic eVOR initiation (M = 1,267 °/s(2)) and cessation (M = -1,675 °/s(2)) acceleration pulses, whereas during the constant portion of the EVS, there was a maintained tonic eVOR (M = 9.1 °/s) at 10 mA. However in Meniere's disease, whilst latency of EVS onset and offset was normal at 9.0 ms, phasic eVOR initiation (M = 1,720 °/s(2)) and cessation (M = -2,523 °/s(2)) were enlarged at 10 mA. The initiation profile was a bimodal response, whilst the cessation profile frequently did not return to baseline. The tonic eVOR (M = 20.5 °/s) exhibited a ramped enhancement of about twice normal at 10 mA. Tonic eVOR enhancement was present for EVS >0.9 mA and disproportionately enhanced the torsional, vertical and horizontal components. These eVOR abnormalities may be a diagnostic indicator of Meniere's disease and may explain the vertigo attacks in the presence of declining mechanically evoked vestibular responses.

A mathematical model of human semicircular canal geometry: a new basis for interpreting vestibular physiology.

We report a precise, simple, and accessible method of mathematically measuring and modeling the three-dimensional (3D) geometry of semicircular canals (SCCs) in living humans. Knowledge of this geometry helps understand the development and physiology of SCC stimulation. We developed a framework of robust techniques that automatically and accurately reconstruct SCC geometry from computed tomography (CT) images and are directly validated using micro-CT as ground truth. This framework measures the 3D centroid paths of the bony SCCs allowing direct comparison and analysis between ears within and between subjects. An average set of SCC morphology is calculated from 34 human ears, within which other geometrical attributes such as nonplanarity, radius of curvature, and inter-SCC angle are examined, with a focus on physiological implications. These measurements have also been used to critically evaluate plane fitting techniques that reconcile many of the discrepancies in current SCC plane studies. Finally, we mathematically model SCC geometry using Fourier series equations. This work has the potential to reinterpret physiology and pathophysiology in terms of real individual 3D morphology.

Impulsive testing of semicircular canal function.

After acute vestibular loss in humans or animals, eye-movement responses to rapid horizontal ipsilesional head rotations ("head impulses") show that there is severe, permanent impairment of the angular vestibulo-ocular reflex. The basis for this appears to be an inhibitory saturation of ipsilesional vestibular nerve, and perhaps vestibular nucleus afferents, in response to high-acceleration, off-direction stimulation of the sole functioning member of any pair of semicircular canals. For the clinician, impulsive testing is an easy and reliable way to identify severe unilateral as well as bilateral impairment of semicircular canal function.

Inter-ocular differences of the horizontal vestibulo-ocular reflex during impulsive testing.

Impulsive testing, which accurately measures the gain of the vestibulo-ocular reflex (VOR) is mostly recorded from only one eye. We measured the horizontal VOR of both eyes in response to graded velocity head impulses in 14 normal subjects. VOR acceleration gains were similar for each eye in both directions at low accelerations, but as head acceleration increased, gains of the adducting eye exceeded gains of the abducting eye. These inter-ocular VOR gain differences were due to longer latencies but higher accelerations of the adducting eye compared to the abducting eye. Consequently, directional VOR gain asymmetry occurred at high accelerations if the same eye was always analysed--with an average inter-ocular difference of 15.3%. If only the abducting eye was analysed, VOR gains were symmetrical in both directions. For accurate measurements of the VOR at high accelerations, the inter-ocular VOR gain differences require binocular recording.

Vestibular, saccadic and fixation abnormalities in genetically confirmed Friedreich ataxia.

Friedreich ataxia (FRDA), the commonest of the inherited ataxias, is a multisystem neurodegenerative condition that affects ocular motor function. We assessed eye movement abnormalities in 20 individuals with genetically confirmed FRDA and compared these results to clinical measures. All subjects were assessed with infrared oculography. Fifteen individuals underwent a full protocol of eye movement recordings. Ten subjects were analysed using two-dimensional scleral coil equipment and five using three-dimensional scleral coil recording equipment. We also recorded visual quality of life, Sloan low contrast letter acuity and Friedreich Ataxia Rating Scale scores to compare to the visual measures. Whilst saccadic velocity was essentially normal, saccadic latency was prolonged. The latency correlated with clinical measures of disease severity, including the scores for the Friedreich Ataxia Rating Scale and the Sloan low contrast letter acuity tests. Fixation abnormalities consisting of square wave jerks and ocular flutter were common, and included rare examples of vertical square wave jerks. Vestibular abnormalities were also evident in the group, with markedly reduced vestibulo-ocular reflex gain and prolonged latency. The range of eye movement abnormalities suggest that neurological dysfunction in FRDA includes brainstem, cortical and vestibular pathways. Severe vestibulopathy with essentially normal saccadic velocity are hallmarks of FRDA and differentiate it from a number of the dominant spinocerebellar ataxias. The correlation of saccadic latency with FARS score raises the possibility of its use as a biomarker for FRDA clinical trials.

Ocular vestibular evoked myogenic potentials (OVEMPs) produced by air- and bone-conducted sound.

OBJECTIVE: To determine the origin and properties of short latency extraocular potentials produced by activation of the vestibular apparatus using two modes of acoustic stimulation. METHODS: Extraocular potentials were measured in 10 normal subjects using a bipolar montage to increase selectivity. Three dimensional eye movements were also recorded in five subjects. The subjects were stimulated with both air-conducted (AC) and bone-conducted (BC) sound using a single cycle of a 500Hz sine wave. RESULTS: Short latency positive and negative potentials that peaked at 8.1-12.7ms for AC and 7.5-13.9ms for BC stimulation were recorded, which were distinct for the two eyes and for the two modes of stimulation. The extraocular potentials began prior to the onset of eye movements, which peaked at 16.5-20.1ms for AC, 17.8-25.0ms for BC stimulation. CONCLUSIONS: The pattern of short latency eye movements and extraocular potentials induced by AC and BC vestibular stimulation are distinct. As the potentials preceded the eye movements and were not correlated morphologically with them, the source of the observed potentials is not an eye movement and thus we refer to them as ocular vestibular evoked myogenic potentials (OVEMPs). SIGNIFICANCE: The potentials had properties consistent with modulation of the electromyogenic activity of the extraocular muscles and if interpreted as originating from displacement of the eye will give misleading results. AC and BC acoustic stimulation are likely to activate differing profiles of vestibular end organs.

MRI of the vestibular nerve after selective vestibular neurectomy.

CONCLUSION: In patients with Ménière's disease and persisting vertigo attacks after vestibular neurectomy (VNx) MRI of the vestibulocochlear nerve can identify residual vestibular nerve fibres that could be responsible for the vertigo attacks. OBJECTIVE: To test if MRI of the vestibulocochlear nerve can corroborate the presence of residual vestibular nerve fibres in patients with persisting vertigo attacks and residual vestibular function after VNx. MATERIALS AND METHODS: Vestibulocochlear nerve bundles of seven post-VNx unilateral Ménière's patients were imaged using 1.5 Tesla MRI with steady state free precession (SSFP) sequences. Reformatted MR images orthogonal to the vestibulocochlear nerve axis in internal auditory canal were compared on the VNx and intact sides. Vestibular function was assessed with caloric tests, three-dimensional head impulse tests and vestibular evoked myogenic potentials. Of the seven patients only one was asymptomatic (totally free of vertigo); six had continued to experience vertigo attacks, albeit not as long or as severe as before VNx. RESULTS: On the VNx side, MRI showed intact facial and cochlear nerves in all seven patients. In the six symptomatic patients, although superior and inferior vestibular nerve bulk and signal were reduced, residual bulk suggestive of inferior vestibular nerve was evident, correlating with evidence of residual posterior canal function on impulsive testing in all six symptomatic patients. In the asymptomatic patient, superior and inferior vestibular nerves were absent on MRI and impulsive testing revealed no residual posterior canal function.

Latency and initiation of the human vestibuloocular reflex to pulsed galvanic stimulation.

Cathodal galvanic currents activate primary vestibular afferents, whereas anodal currents inhibit them. Pulsed galvanic vestibular stimulation (GVS) was used to determine the latency and initiation of the human vestibuloocular reflex. Three-dimensional galvanic vestibuloocular reflex (g-VOR) was recorded with binocular dual-search coils in response to a bilateral bipolar 100-ms rectangular pulse of current at 0.9 (near-threshold), 2.5, 5.0, 7.5, and 10.0 mA in 11 normal subjects. The g-VOR consisted of three components: conjugate torsional eye rotation away from cathode toward anode; vertical divergence (skew deviation) with hypertropia of the eye on the cathodal and hypotropia of the eye on the anodal sides; and conjugate horizontal eye rotation away from cathode toward anode. The g-VOR was repeatable across all subjects, its magnitude a linear function of the current intensity, its latency about 9.0 ms with GVS of >or=2.5 mA, and was not suppressed by visual fixation. At 10-mA stimulation, the g-VOR [x, y, z] on the cathodal side was [0.77 +/- 0.10, -0.05 +/- 0.05, -0.18 +/- 0.06 degrees ] (mean +/- 95% confidence intervals) and on the anodal side was [0.79 +/- 0.10, 0.16 +/- 0.05, -0.19 +/- 0.06 degrees ], with a vertical divergence of 0.20 degrees . Although the horizontal g-VOR could have arisen from activation of the horizontal semicircular canal afferents, the vertical-torsional g-VOR resembled the vestibuloocular reflex in response to roll-plane head rotation about an Earth-horizontal axis and might be a result of both vertical semicircular canal and otolith afferent activations. Pulsed GVS is a promising technique to investigate latency and initiation of the human vestibuloocular reflex because it does not require a large mechanical apparatus nor does it pose problems of head inertia or slippage.

Benign paroxysmal positional vertigo can interfere with the cardiac response to head-down tilt.

OBJECTIVE: To assess the pulse rate and the respiratory rate responses to head-down tilt of the whole body in the plane of the posterior canals in healthy subjects and in patients with benign paroxysmal positional vertigo (BPPV). BACKGROUND: Although BPPV attacks are usually accompanied by autonomic symptoms, there are no studies assessing autonomic responses during triggering maneuvers for BPPV, neither in healthy subjects nor in patients. METHODS: We evaluated nine healthy subjects and four BPPV patients (3 unilateral and 1 bilateral). Using a two-axis rotator, from an upright position they were rotated 135 degrees backwards to head-down tilt, either in the plane of the right or the left posterior canal. RESULTS: In healthy subjects, head-down tilt always induced a significant decrease of the pulse rate, which was similar after rotation to the right and to the left posterior canals. This response was observed in patients with unilateral BPPV only when they were rotated toward the nonaffected side, and it was not evident when they were rotated toward the affected side (p < 0.025). In the patient with bilateral BPPV, no change of the pulse rate was observed after rotation toward the right or to the left posterior canal. Although, in all the patients, the respiratory rate increased during the tilt, a similar increase was observed in two healthy subjects. CONCLUSION: After rotation in the plane of the affected semicircular canal, BPPV can interfere with the cardiac response to head-down tilt of the whole body.

Vergence-mediated changes in Listing's plane do not occur in an eye with superior oblique palsy.

PURPOSE: As a normal subject looks from far to near, Listing's plane rotates temporally in each eye. Since Listing's plane relates to the control of torsional eye position, mostly by the oblique eye muscles, the current study was conducted to test the hypothesis that a patient with isolated superior oblique palsy would have a problem controlling Listing's plane. METHOD: Using the three-dimensional scleral search coil technique, binocular Listing's plane was measured in four patients with congenital and in four patients with acquired unilateral superior oblique palsy during far- (94 cm) and near- (15 cm) viewing. The results were compared to previously published Listing's plane data collected under exactly the same conditions from 10 normal subjects. RESULTS: In patients with unilateral superior oblique palsy, either congenital or acquired, Listing's plane in the normal eye rotated temporally on near-viewing, as in normal subjects, while in the paretic eye it failed to do so. In patients with acquired superior oblique palsy, Listing's plane was already rotated temporally during far-viewing and failed to rotate any farther on near-viewing, whereas in patients with congenital superior oblique palsy Listing's plane in the paretic eye was oriented normally during far-viewing and failed to rotate any farther on near-viewing. CONCLUSIONS: These results suggest that the superior oblique muscle, at least in part, is responsible for the temporal rotation of Listing's plane that occurs in normal subjects on convergence.

Head impulse test reveals residual semicircular canal function after vestibular neurectomy.

Meniere disease patients sometimes report vertiginous Meniere attacks after vestibular neurectomy that spares hearing. To determine why, the authors compared postsurgical semicircular canal function in nine patients with preserved hearing with that of a control group with no preservation of hearing. The three-dimensional head impulse test revealed residual posterior canal function in all patients with vertigo attacks (eight). The control patients had no residual canal function. Thus, residual vestibular function on the ipsilesional side may cause vertiginous Meniere attacks.

Superior semicircular canal dehiscence simulating otosclerosis.

This is a report of a patient with an air-bone gap, thought 10 years ago to be a conductive hearing loss due to otosclerosis and treated with a stapedectomy. It now transpires that the patient actually had a conductive hearing gain due to superior semicircular canal dehiscence. In retrospect for as long as he could remember the patient had experienced cochlear hypersensitivity to bone-conducted sounds so that he could hear his own heart beat and joints move, as well as a tuning fork placed at his ankle. He also had vestibular hypersensitivity to air-conducted sounds with sound-induced eye movements (Tullio phenomenon), pressure-induced nystagmus and low-threshold, high-amplitude vestibular-evoked myogenic potentials. Furthermore some of his acoustic reflexes were preserved even after stapedectomy and two revisions. This case shows that if acoustic reflexes are preserved in a patient with an air-bone gap then the patient needs to be checked for sound- and pressure-induced nystagmus and needs to have vestibular-evoked myogenic potential testing. If there is sound- or pressure-induced nystagmus and if the vestibular-evoked myogenic potentials are also preserved, the problem is most likely in the floor of the middle fossa and not in the middle ear, and the patient needs a high-resolution spiral computed tomography (CT) of the temporal bones to show this.

Vergence-mediated changes in the axis of eye rotation during the human vestibulo-ocular reflex can occur independent of eye position.

The aim of this study was to determine whether vergence-mediated changes in the axis of eye rotation in the human vestibulo-ocular reflex (VOR) would obey Listing's Law (normally associated with saccadic eye movements) independent of the initial eye position. We devised a paradigm for disassociating the saccadic velocity axis from eye position by presenting near and far targets that were centered with respect to one eye. We measured binocular 3-dimensional eye movements using search coils in ten normal subjects and 3-dimensional linear head acceleration using Optotrak in seven normal subjects. The stimuli consisted of passive, unpredictable, pitch head rotations with peak acceleration of approximately 2000 degrees /s(2 )and amplitude of approximately 20 degrees. During the pitch head rotation, each subject fixated straight ahead with one eye, whereas the other eye was adducted 4 degrees during far viewing (94 cm) and 25 degrees during near viewing (15 cm). Our data showed expected compensatory pitch rotations in both eyes, and a vergence-mediated horizontal rotation only in the adducting eye. In addition, during near viewing we observed torsional eye rotations not only in the adducting eye but also in the eye looking straight ahead. In the straight-ahead eye, the change in torsional eye velocity between near and far viewing, which began approximately 40 ms after the start of head rotation, was 10+/-6 degrees /s (mean +/- SD). This change in torsional eye velocity resulted in a 2.4+/-1.5 degrees axis tilt toward Listing's plane in that eye. In the adducting eye, the change in torsional eye velocity between near and far viewing was 16+/-6 degrees /s (mean +/- SD) and resulted in a 4.1+/-1.4 degrees axis tilt. The torsional eye velocities were conjugate and both eyes partially obeyed Listing's Law. The axis of eye rotation tilted in the direction of the line of sight by approximately one-third of the angle between the line of sight and a line orthogonal to Listing's plane. This tilt was higher than predicted by the one-quarter rule. The translational acceleration component of the pitch head rotation measured 0.5 g and may have contributed to the increased torsional component observed during near viewing. Our data show that vergence-mediated eye movements obey a VOR/Listing's Law compromise strategy independent of the initial eye position.

Vibration-induced ocular torsion and nystagmus after unilateral vestibular deafferentation.

Vibration is an excitatory stimulus for both vestibular and proprioceptive afferents. Vibration applied either to the skull or to the neck muscles of subjects after unilateral vestibular deafferentation induces nystagmus and a shift of the subjective visual horizontal. Previous studies have ascribed these effects to vibratory stimulation of neck muscle proprioceptors. Using scleral search coils, we recorded three-dimensional eye movements during unilateral 92 Hz vibration of the mastoid bone or of the sternocleidomastoid (SCM) muscle in 18 subjects with chronic unilateral vestibular deficits after vestibular neurectomy or neuro-labyrinthitis. Nine subjects had lost function of all three semicircular canals (SSCs) on one side, and the other nine had lost function of only the anterior and lateral SSCs. Vibration of the mastoid bone or of the SCM muscle on either side induced an ipsilesional tonic shift of torsional eye position of up to 6.5 degrees during visual fixation, as well as a nystagmus with horizontal, vertical and torsional components in darkness. Subjects who had lost function of all three SSCs on one side showed a larger shift in ocular torsion in response to SCM vibration than did subjects who had lost function of only two SSCs. The difference between ocular torsion produced by ipsilesional muscle or bone vibration was not significantly different from that produced by contralesional bone or muscle vibration. The vibration-induced nystagmus rotation axis tended to align with the pitch (y) axis of the head in subjects who had lost only anterior and lateral SSC function, and with the roll (x) axis of the head in subjects who had lost function of all three SSCs. We propose that the previously described vibration-induced shift of the subjective visual horizontal can be explained by the vibration-induced ocular torsion, and that the magnitude of ocular torsion is related to the extent of the unilateral vestibular deficit. While altered proprioceptive inputs from neck muscles might be important in the mechanism of vibration-induced ocular torsion and nystagmus after unilateral vestibular deafferentation, vibratory stimulation of vestibular receptors in the intact labyrinth also appears to have an important role.

Vibration-induced shift of the subjective visual horizontal: a sign of unilateral vestibular deficit.

BACKGROUND: Vibration to the head or neck excites vestibular and neck muscle spindle afferents. Can such vibrations improve the sensitivity of the subjective visual horizontal (SVH) test to chronic unilateral deficit of the vestibular system? DESIGN: Controlled experimental study. SETTING: Tertiary referral center. PATIENTS AND CONTROLS: Thirteen healthy subjects and 23 patients with chronic unilateral vestibular deficits after vestibular neurectomy or neurolabyrinthitis. Results of head-impulse test showed unilateral loss of function of all 3 semicircular canals in 14 patients and loss of anterior and lateral semicircular canals in 9 patients. INTERVENTION: Unilateral vibration (92 Hz; 0.6-mm amplitude) applied to sternocleidomastoid muscle (SCM) or mastoid bone. MAIN OUTCOME MEASURE: Results of SVH test (in degrees). RESULTS: Without vibration, 13 of 23 patients and all healthy subjects had SVH of less than 3 degrees (sensitivity, 43%; specificity, 100%). During vibration to the ipsilesional SCM, SVH increased to greater than 3 degrees in 21 of 23 patients but in only 1 of 13 healthy subjects (sensitivity, 91%; specificity, 92%). The patient group had significantly greater SVH shifts to the ipsilesional side than did healthy subjects in response to SCM and mastoid bone vibration on either side. The SVH shift during vibration to the ipsilesional SCM was significantly greater than that during vibration to the contralesional muscle (P<.001) or to the mastoid bone on either side (P<.05). The vibration-induced SVH shift was significantly greater in those patients with loss of 3 semicircular canals than in those with loss of 2 (P<.01). CONCLUSIONS: The sensitivity of the SVH test to chronic unilateral vestibular deficits can be improved by applying vibration to the SCM. The magnitude of vibratory SVH shift is related to the extent of unilateral deficit of the otolithic organs, vertical canals, or both.