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BACKGROUND: Parkinson’s disease (PD) is a common multi-system neurodegenerative disorder with possible vestibular system dysfunction, but prior vestibular function test findings are equivocal. OBJECTIVE: To report and compare vestibulo-ocular reflex (VOR) gain as measured by the video head impulse test (vHIT) in participants with PD, including tremor dominant and postural instability/gait dysfunction phenotypes, with healthy controls (HC). METHODS: Forty participants with PD and 40 age- and gender-matched HC had their vestibular function assessed. Lateral and vertical semicircular canal VOR gains were measured with vHIT. VOR canal gains between PD participants and HC were compared with independent samples t-tests. Two distinct PD phenotypes were compared to HC using Tukey’s ANOVA. The relationship of VOR gain with PD duration, phenotype, severity and age were investigated using logistic regression. RESULTS: There were no significant differences between groups in vHIT VOR gain for lateral or vertical canals. There was no evidence of an effect of PD severity, phenotype or age on VOR gains in the PD group. CONCLUSION: The impulsive angular VOR pathways are not significantly affected by the pathophysiological changes associated with mild to moderate PD.

Introduction: On video head impulse testing (vHIT) of semicircular canal function, some patients reliably show enhanced eye velocity and so VOR gains >1.0. Modeling and imaging indicate this could be due to endolymphatic hydrops. Oral glycerol reduces membranous labyrinth volume and reduces cochlear symptoms of hydrops, so we tested whether oral glycerol reduced the enhanced vHIT eye velocity.Study Design: Prospective clinical study and retrospective analysis of patient data.Methods: Patients with enhanced eye velocity during horizontal vHIT were enrolled (n = 9, 17 ears) and given orally 86% glycerol, 1.5 mL/kg of body weight, dissolved 1:1 in physiological saline. Horizontal vHIT testing was performed before glycerol intake (time 0), then at intervals of 1, 2, and 3 h after the oral glycerol intake. Control patients with enhanced eye velocity (n = 4, 6 ears) received water and were tested at the same intervals. To provide an objective index of enhanced eye velocity we used a measure of VOR gain which captures the enhanced eye velocity which is so clear on inspecting the eye velocity records. We call this measure the initial VOR gain and it is defined as: (the ratio of peak eye velocity to the value of head velocity at the time of peak eye velocity). The responses of other patients who showed enhanced eye velocity during routine clinical testing were analyzed to try to identify how the enhancement occurred.Results: We found that oral glycerol caused, on average, a significant reduction in the enhanced eye velocity response, whereas water caused no systematic change. The enhanced eye velocity during the head impulses is due in some patients to a compensatory saccade-like response during the increasing head velocity.Conclusion: The significant reduction in enhanced eye velocity during head impulse testing following oral glycerol is consistent with the hypothesis that the enhanced eye velocity in vHIT may be caused by endolymphatic hydrops.

In current clinical practice, when in response to vHIT testing the observed slow-phase eye-velocity responses are significantly higher than head velocity, the most probable cause is considered to be an inadequate collection method or a recording artifact. We present two cases with clinical diagnoses of Menière's Disease: for both cases, enhanced eye velocity responses were measured with a rigorous vHIT testing protocol. In the first case we measured these enhanced responses on each test performed during a 5 year time series; in the second case multiple measurements were obtained from a patient after the radiologic diagnosis of vestibulo-cochlear hydrops. The two cases presented and the new evidence reported by other researchers suggest that owing to the low probability of artifact and the high consistency of the vHIT measurements, we should consider the hypothesis of a physio-pathologic cause for the enhanced eye responses to vHIT testing of some patients with vestibular dysfunction.

To measure horizontal semicircular canal function over days, weeks, and months after an acute attack of vestibular neuritis.The video head impulse test (vHIT) was used to measure the eye movement response to small unpredictable passive head turns at intervals after the attack.Two patients diagnosed with acute right unilateral vestibular neuritis.There was full restoration of horizontal canal function in one patient (A) as shown by the return of the slow phase eye velocity response to unpredictable head turns, while in the other patient (B) there was little or no recovery of horizontal canal function. Instead this second patient generated covert saccades during head turns.Despite the objective evidence of their very different recovery patterns, both patients reported, at the final test, being happy and feeling well recovered, even though in one of the patients there was clear absence of horizontal canal function. The results indicate covert saccades seem a successful way of compensating for loss of horizontal canal function after unilateral vestibular neuritis. Factors other than recovery of the slow phase eye velocity are significant for patient recovery.

While compensatory saccades indicate vestibular loss in the conventional head impulse test paradigm (HIMP), in which the participant fixates an earth-fixed target, we investigated a complementary suppression head impulse paradigm (SHIMP), in which the participant is fixating a head-fixed target to elicit anticompensatory saccades as a sign of vestibular function.HIMP and SHIMP eye movement responses were measured with the horizontal video head impulse test in patients with unilateral vestibular loss, patients with bilateral vestibular loss, and in healthy controls.Vestibulo-ocular reflex gains showed close correlation (R(2) = 0.97) with slightly lower SHIMP than HIMP gains (mean gain difference 0.06 ± 0.05 SD, p0.001). However, the 2 paradigms produced complementary catch-up saccade patterns: HIMP elicited compensatory saccades in patients but rarely in controls, whereas SHIMP elicited large anticompensatory saccades in controls, but smaller or no saccades in bilateral vestibular loss. Unilateral vestibular loss produced covert saccades in HIMP, but later and smaller saccades in SHIMP toward the affected side. Cumulative HIMP and SHIMP saccade amplitude differentiated patients from controls with high sensitivity and specificity.While compensatory saccades indicate vestibular loss in conventional HIMP, anticompensatory saccades in SHIMP using a head-fixed target indicate vestibular function. SHIMP saccades usually appear later than HIMP saccades, therefore being more salient to the naked eye and facilitating vestibulo-ocular reflex gain measurements. The new paradigm is intuitive and easy to explain to patients, and the SHIMP results complement those from the standard video head impulse test.This case-control study provides Class III evidence that SHIMP accurately identifies patients with unilateral or bilateral vestibulopathies.

OBJECTIVE The aim of this study was to investigate the effect of superior semicircular canal dehiscence (SSCD) on the n10 component of the ocular vestibular evoked myogenic potential (oVEMP n10) and the p13-n23 component of the cervical vestibular evoked myogenic potential (cVEMP p13-n23) evoked by 500 Hz bone-conducted vibration (BCV) at the midline forehead at the hairline (Fz) in 26 patients with computed tomography-verified SSCD. Previous evidence has led to the proposal that the oVEMP n10 is of utricular origin whereas the cVEMP p13-n23 is of saccular origin. The question is can the oVEMP n10 to 500 Hz BCV indicate SSCD? DESIGN A hand-held Bruel & Kjaer 4810 Minishaker was used to provide BCV stimulation using surface electromyography electrodes to record oVEMP n10 and cVEMP p13-n23. The stimulus was 7 msec bursts of 500 Hz BCV at either Fz or at the vertex of the skull (Cz). Twenty-seven healthy subjects were tested in the same paradigm. RESULTS In response to 500 Hz Fz BCV in SSCD patients the oVEMP n10 amplitude beneath the contraSSCD eye was substantially and significantly larger than the oVEMP n10 beneath the ipsiSSCD eye, whereas in these same patients the cVEMP p13-n23 amplitude over the ipsiSSCD sternocleidomastoid muscle to Fz BCV was slightly but significantly larger than the cVEMP p13-n23 amplitude over the contraSSCD sternocleidomastoid muscle. In SSCD patients there was a significant relationship between the size of the dehiscence and the amplitude of the contralateral oVEMP n10 potential. The oVEMP n10 to Cz stimulation was still present in SSCD patients, but small or absent in healthy subjects. CONCLUSIONS In response to 500 Hz Fz BCV an asymmetrical oVEMP n10 with a significantly increased amplitude of contralesional oVEMP n10 (compared with population values of healthy subjects) is a simple useful indicator of SSCD, confirmed by the Cz response. oVEMP testing with 500 Hz Fz BCV allows very simple, very fast identification of a probable unilateral SSCD.

Dear Sir,It is difficult to obtain objective measures of vestibularfunction from very young children (3- to 7-years-old)because they are unwilling to receive caloric tests whichinduce vertigo, or to undergo bedside examination forspontaneous nystagmus as they must be in darkness forsome minutes [1, 2]. It is also difficult to obtain an accuratemedical history in such young patients in a subacute stage,and in order to understand what really happened, the cli-nician relies on the story told by the parents. These diffi-culties increase when a child comes to a vertigo clinic or anEmergency Department in the acute stage of a vertigoattack complaining that the world is turning around. Underthese circumstances, a clinician can identify the classicalsigns and symptoms which are dependent on the absentfunction of the affected vestibular labyrinth. Such classicalstatic clinical signs are (a) spontaneous nystagmus with thequick phase of the horizontal component directed awayfrom the affected ear, (b) ocular torsion with both eyesrolled away from the affected ear indicating unilaterallyreduced otolithic function of the affected ear, (c) skewdeviation with a vertical misalignment between the twoeyes such that the ipsilesional eye shows a lower positionin the orbit, (d) postural instability with sensations offalling toward the lesioned side, related to reduced functionof the affected ear projecting to ipsilateral vestibulo-spinalresponses. The usual standard tests of dynamic vestibularfunction are (e) the Hallpike–Fitzgerald canal paresismeasure from caloric testing and (f) the clinical sign ofcanal paresis (the head-impulse sign)—during brief, pas-sive, unpredictable, horizontal head turns toward theaffected ear, the patient with reduced unilateral horizontalcanal function fails to maintain fixation on an earth-fixedtarget and so makes corrective (overt) saccades at the endof the head rotation in order to regain fixation [3]. Duringsimilar rotations toward the healthy ear no overt saccadesare evident. The overt saccade is a sign of reduced dynamichorizontal canal function; however, this clinical sign issubjective, in that there is no objective measure of the headvelocity stimulus or the eye velocity response and so noobjective measure of vestibulo-ocular (VOR) gain.Three new objective measures of dynamic vestibularfunction have been reported. These tests are quick, accurateand not demanding for the patients (i.e., they do not inducevertigo), and above all they can be used to obtain objectivemeasures of the dynamic function of all the vestibularreceptors, both semicircular canals and otoliths, even invery young children. Two of the tests use vestibular-evoked myogenic potentials to sound and vibration. Thefirst is the cervical vestibular-evoked myogenic potential(cVEMP) to air-conducted sound (ACS) or bone conductedvibration (BCV) [4, 5]. These stimuli have been shown topreferentially activate otolith irregular afferents from theutricular and saccular macula [5–7]. The cVEMP responseto ACS and BCV indicates dynamic saccular and inferiorvestibular nerve function. In healthy subjects with surfaceelectrodes on the tensed sternocleidomastoid muscles, it isfound that that in response to BCV or intense ACS stim-ulation there is a short-latency positive (inhibitory) poten-tial (p13-n23) at a latency of around 13 ms from stimulusonset, indicating ipsilateral saccular function. The second

OBJECTIVE: To determine whether the first negative component (n10) of the ocular vestibular-evoked myogenic potential (oVEMP) to bone-conducted vibration (BCV) is due primarily to activation of the...

Objective Two indicators of otolithic function were used to measure dynamic otolith function in the same patients both during an acute attack of Meniere’s disease (MD) and in the quiescent period between attacks. Methods The early negative component (n10) of the ocular vestibular-evoked myogenic potential (the oVEMP) to brief 500 Hz bone conducted vibration (BCV) stimulation of the forehead, in the midline at the hairline (Fz) was recorded by surface EMG electrodes just beneath both eyes while the patient looked up. It has been proposed that the n10 component of the oVEMP to 500 Hz Fz BCV indicates utricular function. It has been proposed that the early positive component (p13) of the cervical vestibular-evoked myogenic potential (the cVEMP) recorded by surface electrodes on both tensed SCM neck muscles to 500 Hz Fz BCV indicates saccular function. Results Sixteen healthy control subjects tested on two occasions showed no detectable change in the symmetry of oVEMPs or cVEMPs to 500 Hz Fz BCV. In response to 500 Hz Fz BCV 15 early MD patients tested at both attack and quiescent phases showed a dissociation: there was a significant increase in contralesional of n10 of the oVEMP during the attack compared to quiescence but a significant decrease in the ipsilesional p13 of the cVEMP during the attack compared to quiescence. Conclusions During an MD attack, dynamic utricular function in the affected ear as measured by the n10 of the oVEMP to 500 Hz Fz BCV is enhanced, whereas dynamic saccular function in the affected ear as measured by the p13 of the cVEMP to 500 Hz Fz BCV is not similarly affected. Significance The MD attack appears to affect different otolithic regions differentially.

Objective: Bone-conducted vibration (BCV) in the midline at the hairline (Fz), results in short latency potentials recorded by surface electrodes beneath the eyes - the ocular vestibular-evoked myogenic potential (oVEMP). The early negative component of the oVEMP, n10, is due to vestibular stimulation, however it is similar to the early R1 component of the blink reflex. Here we seek to dissociate n10 from R1. Methods: Surface potentials were recorded from the infraorbital electromyogram of 10 healthy subjects, 6 patients with bilateral vestibular loss, 2 with unilateral vestibular loss, 4 with facial palsy and 3 with facial and vestibular nerve lesions on the same side. BCV was delivered at Fz, the inion, the glabella or the supra-orbital ridge using a tendon hammer or a bone-conduction vibrator. Results: Onset latencies of the n10 evoked by taps at Fz or inion were significantly shorter than the R1 components of blink responses to supraorbital and glabellar stimuli. Upward gaze increased the amplitude of The n10 was absent bilaterally in patients with bilateral vestibular loss and beneath the contralesional eye in patients with unilateral vestibular loss, but in both these groups of patients R1 was preserved. In severe facial palsy the R1 component was absent or delayed and attenuated ipsilesionally, but n10 was preserved bilaterally. In subjects with unilateral facial and vestibular nerve lesions (Herpes Zoster of the facial and vestibulocochlear nerves) the dissociation was complete - the ipsilesional R1 was absent or attenuated whereas the ipsilesional n10 was preserved. Conclusions: n10 is distinguished from R1 by its earlier onset, laterality, modulation by gaze position and dissociation in patient groups. Significance: The n10 component evoked by BCV at Fz is not the R1 component of the blink reflex. (C) 2009 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Background/hypothesis The video Head Impulse Test (vHIT) is now widely used to test the function of each of the six semicircular canals individually by measuring the eye rotation response to an abrupt head rotation in the plane of the canal. The main measure of canal adequacy is the ratio of the eye movement response to the head movement stimulus, i.e., the gain of the vestibulo-ocular reflex (VOR). However, there is a need for normative data about how VOR gain is affected by age and also by head velocity, to allow the response of any particular patient to be compared to the responses of healthy subjects in their age range. In this study, we determined for all six semicircular canals, normative values of VOR gain, for each canal across a range of head velocities, for healthy subjects in each decade of life. Study design The VOR gain was measured for all canals across a range of head velocities for at least 10 healthy subjects in decade age bands: 10–19, 20–29, 30–39, 40–49, 50–59, 60–69, 70–79, 80–89. Methods The compensatory eye movement response to a small, unpredictable, abrupt head rotation (head impulse) was measured by the ICS impulse prototype system. The same operator delivered every impulse to every subject. Results Vestibulo-ocular reflex gain decreased at high head velocities, but was largely unaffected by age into the 80- to 89-year age group. There were some small but systematic differences between the two directions of head rotation, which appear to be largely due to the fact that in this study only the right eye was measured. The results are considered in relation to recent evidence about the effect of age on VOR performance. Conclusion These normative values allow the results of any particular patient to be compared to the values of healthy people in their age range and so allow, for example, detection of whether a patient has a bilateral vestibular loss. VOR gain, as measured directly by the eye movement response to head rotation, seems largely unaffected by aging.

We recently conducted experiments where 24 seated participants were subjected (with eyes closed) to small amplitude, high-jerk impulses of linear acceleration. Responses were distributed as a continuum between two extremes. The "stiff" participants showed little movement of the head relative to the trunk, whereas the "floppy" participants showed a large head rotation in the direction opposite the sled movement. We hypothesized that the stiff behavior resulted from the spontaneous use of an imagined visual frame of reference and undertook this larger-scale study to test that idea. The distribution along the "stiff-floppy" continuum was compared with the scores on psychophysiological tests measuring vividness of imagery, visual field-dependence and motion sickness susceptibility. Multivariate regression analysis revealed that the "stiffness" of individuals was loosely, but significantly related to the vividness of their imagery. However, "stiffness" was not linked to visual field-dependence or motion sickness susceptibility. Even if it explains only 20% of the variance of the data, the increase of "stiffness" with vividness of imagery fits our hypothesis. With eyes closed, stiff people may use imagined external visual cues to stabilize their head and trunk. Floppy people, who are poorer imagers, may rely more on "egocentric", proprioceptive and vestibular inputs.

The aim of this paper was to characterise the conditions under which the quick phase of vestibular nystagmus is generated in response to sinusoidal horizontal angular accelerations in guinea pig and to determine whether the characteristics of the quick phase are altered following unilateral vestibular deafferentation (UVD). In experiment 1, the quick-phase response to 2-Hz sinusoidal stimuli with different peak head velocities was measured before and after UVD. In experiment 2, lower-frequency stimuli with a fixed amplitude (+/-20 degrees ) were used to measure the eye-movement response. In experiment 1, at 2 Hz, the most noticeable difference between UVD animals and normal animals was a reduction in the number of quick phases generated, particularly when rotating towards the lesioned side: the onset of the quick phase was delayed and occurred at a lower value of peak head velocity compared to normals. However, both these measures probably reflect the depressed slow-phase eye-velocity gain rather than a change in the quick-phase mechanism itself, because if a quick phase was generated there was no difference between UVDs and normals on a variety of measures (duration, position, peak eye velocity) for a 2-Hz stimulus. For both UVD and normal animals there did appear to be a position threshold for the onset of a quick-phase eye movement (approximately +/-7.5 degrees ), although it should be noted that the threshold is not an absolute value. In experiment 2, with lower-frequency stimuli, the characteristics of the quick phase itself were altered in UVD animals. At these lower accelerations, although the head velocity and average eye position for the onset of the quick phase did not differ between UVD and normal animals, there were significant differences between UVD and normal animals in the number of quick phases generated (fewer), the duration of the quick phase (longer) and the peak eye velocity of the quick phase (slower). For lower-frequency stimuli there was no evidence of a specific eye-position threshold for the generation of a quick phase, although the position at which a quick phase occurred rarely exceeded the +/-7.5 degrees value obtained in experiment 1. The behavioural data were used to produce a biologically based neural-network simulation of both the slow- and quick-phase components of the vestibulo-ocular reflex, the results of which are presented in a companion paper.

Recent studies have shown that responses to surface galvanic vestibular stimulation (GVS) show substantial interindividual variation. Between-subject variability may be due to individual differences between subjects, or to the poor reliability of the test, or to differences in test details, or to host factors. The aim of the present study was to compare variability between and within subjects in binocular 3-D eye-movement responses to long-duration, maintained, large-amplitude, bilateral, bipolar, surface GVS. Subjects were seated and restrained, and in one condition fixated a small, centrally located visual target; in the other condition, testing was carried out in complete darkness. Surface GVS of 5 mA, with a rectangular waveform was delivered bilaterally for 5 min while eye movements were measured using computerised video-oculography (VTM). In the first experiment, ten subjects participated in both conditions in one session, and in the second experiment, two subjects participated in both conditions for a total of five repeated sessions. The stimulation was well tolerated by all subjects and produced a change in torsional position with the upper pole of both eyes rolling towards the anode and away from the cathode in all subjects in both conditions. Although little vertical nystagmus was evident in either condition, most subjects showed relatively strong horizontal nystagmus (slow phases towards the anode) in darkness. This study confirms previous observations that the torsional response to GVS is highly variable between subjects, whilst also showing for the first time that eye-movement responses to GVS show good within-subject repeatability. This study also demonstrates considerable between-subject variability in the relative ratios of response components (torsional and horizontal nystagmus, torsional position), whereas the relatively small within-subject variability can be characterised more by changes in the overall amplitude of the eye-movement response. Subjects show idiosyncratic oculomotor response patterns to GVS, varying slightly in absolute magnitude between sessions. Thus, GVS may be a more reliable stimulus than may have been anticipated from the literature.

The aim of this study was to determine how context and on-line sensory information are combined to control posture in seated subjects submitted to high-jerk, passive linear accelerations. Subjects were seated with eyes closed on a servo-controlled linear sled. They were asked to relax and received brief accelerations either sideways or in the fore-aft direction. The stimuli had an abrupt onset, comparable to the jerk experienced during a minor car collision. Rotation and translation of the head and body were measured using an Optotrak system. In some of the subjects, surface electromyographic (EMG) responses of selected neck and/or back muscles were recorded simultaneously. For each subject, responses were highly stereotyped from the first trial, and showed little sign of habituation or sensitisation. Comparable results were obtained with sideways and fore-aft accelerations. During each impulse, the head lagged behind the trunk for several tens of milliseconds. The subjects' head movement responses were distributed as a continuum in between two extreme categories. The 'stiff' subjects showed little rotation or translation of the head relative to the trunk for the whole duration of the impulse. In contrast, the 'floppy' subjects showed a large roll or pitch of the head relative to the trunk in the direction opposite to the sled movement. This response appeared as an exaggerated 'inertial' response to the impulse. Surface EMG recordings showed that most of the stiff subjects were not contracting their superficial neck or back muscles. We think they relied on bilateral contractions of their deep, axial musculature to keep the head-neck ensemble in line with the trunk during the movement. About half of the floppy subjects displayed reflex activation of the neck muscles on the side opposite to the direction of acceleration, which occurred before or during the head movement and tended to exaggerate it. The other floppy subjects seemed to rely on only the passive biomechanical properties of their head-neck ensemble to compensate for the perturbation. In our study, proprioception was the sole source of sensory information as long as the head did not move. We therefore presume that the EMG responses and head movements we observed were mainly triggered by the activation of stretch receptors in the hips, trunk and/or neck. The visualisation of an imaginary reference in space during sideways impulses significantly reduced the head roll exhibited by floppy subjects. This suggests that the adoption by the central nervous system of an extrinsic, 'allocentric' frame of reference instead of an intrinsic, 'egocentric' one may be instrumental for the selection of the stiff strategy. The response of floppy subjects appeared to be maladaptive and likely to increase the risk of whiplash injury during motor vehicle accidents. Evolution of postural control may not have taken into account the implications of passive, high-acceleration perturbations affecting seated subjects.

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.

While there is agreement that unilateral vestibular deafferentation (UVD) invariably produces an immediate severe horizontal vestibulo-ocular reflex (HVOR) deficit, there is disagreement about whether or not this deficit recovers and, if so, whether it recovers fully or only partly. We suspected that this disagreement might mainly be due to experimental factors, such as the species studied, the means chosen to carry out the UVD, or the nature of the test stimulus used. Our aim was to sort out some of these factors. To do this, we studied the HVOR of alert guinea pigs in response to low and high acceleration sinusoidal and high acceleration impulses after UVD by either labyrinthectomy or by vestibular neurectomy. The HVOR in response to high acceleration impulsive yaw rotations was measured before, and at various times after, either unilateral labyrinthectomy or superior vestibular neurectomy. Following UVD, there was a severe impairment of the HVOR for ipsilesional rotations and a slight impairment for contralesional rotations, after either operation. This asymmetrical HVOR deficit in the guinea pig parallels the deficit observed in humans. Between the first measurement, which was made 1 week after UVD, and the last, which was made 3 months after UVD, there was no change in the HVOR. This lack of recovery was the same after labyrinthectomy as after vestibular neurectomy. The HVOR to low and high acceleration sinusoidal yaw rotations were measured after UVD, and the results were compared with those in response to impulsive rotations. For low acceleration sinusoidal rotations (250 degrees/s2), the gain was symmetrical, although reduced bilaterally. As the peak head acceleration increased, the HVOR became increasingly asymmetric. The HVOR asymmetry for sinusoidal rotations was significantly less than for impulsive rotations that had the same high peak head acceleration (2500 degrees/s2). Our results show that the HVOR deficit after UVD is the same in guinea pigs as in humans; that it is the same after vestibular neurectomy as after labyrinthectomy; that it is lasting and severe in response to high acceleration rotations; and, that it is more obvious in response to impulses than to sinusoids.

Objectives The negative potential at 10 msec (called n10) of the ocular vestibular-evoked myogenic potential (oVEMP) recorded beneath the eyes in response to bone-conducted vibration (BCV) delivered to the skull at the midline in the hairline (Fz) is a new indicator of otolithic, and in particular utricular, function. Our aim is to find the optimum combination of frequency and rise-time for BCV stimulation, to improve the sensitivity of oVEMP testing in the clinic. Design We tested 10 healthy subjects with 6 msec tone bursts of BCV at three stimulus frequencies, 250, 500, and 750 Hz, at rise-times ranging between 0 and 2 msec. The BCV was delivered at Fz. Results The n10 response was significantly larger at the shorter rise-times, being largest at zero rise-time. In addition, we examined the effect of stimulus frequency in these same subjects by delivering 6 msec tone bursts at zero rise-time at a range of frequencies from 50 to 1200 Hz. The main effect of rise-time was significant with shorter rise-times leading to larger n10 responses and the Rise-Time × Frequency interaction was significant so that at low frequencies (100 Hz) shorter rise-times had a modest effect on n10 whereas at high frequencies (750 Hz) shorter rise-times increased n10 amplitude substantially. The main effect of frequency was also significant: The n10 response tended to be larger at lower frequency, being largest between 250 and 500 Hz. Conclusions In summary, in this sample of healthy subjects, the most effective stimulus for eliciting oVEMP n10 to BCV at Fz was found to be a tone burst with a rise-time of 0 msec at low stimulus frequency (250 or 500 Hz).

The n10 component of the ocular vestibular evoked myogenic potential (oVEMP) to sound and vibration stimuli is a crossed response that has enhanced amplitude and decreased threshold in patients with CT-verified superior semicircular canal dehiscence (SSCD). However, demonstrating enhanced VEMP amplitude and reduced VEMP thresholds requires multiple trials and can be very time consuming and tiring for patients, so a specific indicator of probable SCD that is fast and not tiring would be preferred. Here we report a 1-trial indicator: that the oVEMP n10 in response to a very high frequency stimulus (4000 Hz), either air-conducted sound (ACS) or bone conducted vibration (BCV), is such a fast indicator of probable SCD. In 22 healthy subjects, oVEMP n10 at 4000 Hz was not detectable; however, in all 22 CT-verified SSCD patients tested, oVEMP n10 responses were clearly present to 4000 Hz to either ACS or BCV stimuli.

Objective: In 26 patients with CT-verified SSCD, to investigate the effect of frequency on the n10 component of the ocular vestibular-evoked myogenic potential (oVEMP n10) evoked by air conducted sound (ACS) and bone conducted vibration (BCV) at the midline forehead at the hairline (Fz).Methods: A handheld Bruel and Kjaer 4810 minishaker provided BCV stimulation was used, using surface EMG electrodes beneath both eyes to record oVEMP n10. The stimulus ACS and BCV at either Fz or at the vertex of the skull (Cz) were tone bursts ranging from 125 Hz to 8000 Hz. Twenty-seven healthy subjects were tested in the same paradigm.Results: In response to ACS and Fz BCV from 125 Hz until 8000 Hz in SSCD patients the oVEMP n10 amplitude beneath the contraSSCD eye was substantially and significantly larger than the oVEMP n10 beneath the ipsiSSCD eye. In normal patients, ACS oVEMPs n10 is present and reproducible until 1000 Hz, while in SSCD ACS oVEMPs n10 is present up to far higher frequencies (8000 Hz). To Fz BCV oVE...

The presence of spontaneous nystagmus in darkness with a strong horizontal component has been taken to indicate that there is asymmetrical function of the horizontal semicircular canals. If this horizontal spontaneous nystagmus can be suppressed by vision, then it is regarded as due to peripheral horizontal canal dysfunction. However, we report evidence from one patient (61-year-old male), who visited the MSA ENT Clinic, Cassino (FR) Italy, reporting acute, severe vertigo, postural unsteadiness, nausea and vomiting associated with right sudden hearing loss. The patient received instrumental audiovestibular testing to obtain objective measurements of his inner-ear receptors. At the time of the attack, the patient showed spontaneous nystagmus, mainly with horizontal and vertical components (3D infrared video-oculography). Video head-impulse tests of dynamic horizontal canal function showed that the functional status of both horizontal canals was within the normal range. Cervical VEMPs to 500 Hz bone-conducted vibration at Fz showed normal results; ocular VEMPs to the same stimulus showed a reduced n10 amplitude beneath the left eye, corresponding to the right ear. For this reason, the patient was diagnosed as having right unilateral selective utricular macula lesion due to labyrinthitis. There is considerable evidence of convergence of neural input from the otoliths onto horizontal canal neurons in the vestibular nuclei. The firing of such neurons could reflect either asymmetrical horizontal canal function or asymmetrical utricular function. The problem with this patient was not due to asymmetrical horizontal canal function, but only to asymmetrical utricular function, demonstrated by the results of the oVEMP test.

Objective Intense air-conducted sound (ACS) elicits an ocular vestibular-evoked myogenic potential (oVEMP), and it has been suggested that it does so by stimulating saccular receptors and afferents in the inferior vestibular nerve and so activating a crossed sacculo-ocular pathway. Bone conducted vibration (BCV) also elicits an oVEMP probably by activating utricular receptors and a crossed utriculo-ocular pathway. Are there two separate pathways mediating oVEMPs for ACS and BCV? If saccular receptors and afferents are primarily responsible for the oVEMP to ACS, then the oVEMP to ACS should be normal in patients with reduced or absent utricular function – unilateral superior vestibular neuritis (SVN). If utricular receptors and afferents are primarily responsible for oVEMP n10, then oVEMP to ACS should be reduced or absent in SVN patients, and in these patients there should be a close relationship between the size of the oVEMP n10 to BCV and to ACS. Methods The n10 component of the oVEMP to 500 Hz BCV and to 500 Hz ACS was recorded in 10 patients with unilateral SVN but who had saccular and inferior vestibular nerve function preserved, as shown by their normal cVEMP responses to ACS. Results In SVN patients with normal saccular and inferior vestibular nerve function, the oVEMP n10 in response to ACS was reduced or absent. Across SVN patients there was a very close correspondence between the size of oVEMP n10 for ACS and for BCV. Conclusions The n10 component of the oVEMP to ACS is probably mediated predominantly by the superior vestibular nerve and so most likely by utricular receptors and afferents. Significance The n10 component of the oVEMP to either ACS or BCV probably indicates mainly superior vestibular nerve function.

Bone-conducted vibration (BCV) delivered to the skull causes linear acceleration of the mastoids and results in small potentials (oVEMPs) from the extraocular muscles in humans. Very small eye movements to both air- and bone-conducted sound with latencies of around 9 ms and amplitudes up to 16.5 mdeg have also been reported (where mdeg = millidegrees =0.001 degree). To clarify the otolith-ocular responses we investigated the effect of unilateral and bilateral BCV (500 Hz of the mastoid) on eye movements in human subjects, and the effect of gaze position on these movements using a video-based eye-movement recording system. We found very small, short-latency eye-movement responses similar to those previously reported, but these were followed by larger (up to 0.57°) prolonged responses peaking at around 120 ms post-stimulus. For unilateral stimulation the eyes moved downwards when directed away from the stimulated mastoid and upwards when directed towards stimulation. Horizontal movements were towards the stimulated mastoid with little effect of gaze position. Bilateral stimulation enhanced the downward responses, suggesting that the depressor muscles are preferentially activated by BCV. Bilateral stimulation either eliminated the horizontal response or produced convergence of the eyes: the convergence suggests that the eye-movement response is probably primarily driven by the contralateral mastoid.

Objective: To provide the empirical basis for using ocular vestibular evoked myogenic potentials (oVEMPS) in response to Fz bone conducted vibration (BCV) stimulation to indicate vestibular function in human subjects. To show the generality of the response by testing a large number of unselected healthy subjects across a wide age range and the repeatability of the response within subjects. To provide evidence that the response depends on otolithic function. Methods: The early negative component (n10) of the oVEMP to brief BCV of the forehead, in the midline at the hairline (Fz) is recorded by surface EMG electrodes just beneath the eyes. We used a Bruel and Kjaer 4810 Mini-Shaker or a light tap with a tendon hammer to provide adequate BCV stimuli to test a large number (67) of unselected healthy people to quantify the individual differences in n10 magnitude, latency and symmetry to Fz BCV. A Radioear B-71 bone oscillator at Fz is not adequate to elicit a reliable n10 response. Results: The n10 oVEMP response showed substantial differences in amplitude between subjects, but is repeatable within subjects. n10 is of equal magnitude in both eyes with an average asymmetry around 11%. The average n10 amplitude for Mini Tone Burst BCV is 8.47 lV ± 4.02 (sd), the average latency is 10.35 ms ± 0.63 (sd). The amplitude of n10 decreases and its latency increases with age. Conclusions: oVEMPs are a new reliable, repeatable test to indicate vestibular and probably otolithic function. Significance: This study shows the optimum conditions for recording oVEMPs and provides baseline values for individual differences and asymmetry. oVEMPs can be measured in senior subjects without difficulty. 2008 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

A recent study by Poljac et al. [Poljac, E., Lankheet, M. J. M., & van den Berg, A. (2005). Perceptual compensation for eye torsion. Vision Research, 45(4), 485–496] concluded that there was complete perceptual compensation for ocular torsion, although they did not directly measure ocular torsion. Using a similar eccentric-gaze paradigm to induce changes in torsion, which were directly measured, we found inconsistent torsional eye movements at eccentric fixation, and also failed to detect a significant relationship between ocular torsion and the perception of line orientation. We then used a stimulus known to induce large changes in ocular torsion: on-centre yaw rotation. This stimulus induced a consistent change in the torsional position of the eye which positively correlated to subjects’ visual perception of horizontal.

HYPOTHESIS That disease or dysfunction of vestibular end organs in human patients will reduce or eliminate the contribution of the affected end organs to the total eye-movement response to DC surface galvanic vestibular stimulation (GVS). BACKGROUND It was assumed that DC GVS (at current of 5 mA) stimulates all vestibular end organs, an assumption that is strongly supported by physiological evidence, including the activation of primary vestibular afferent neurons by galvanic stimulation. Previous studies also have described the oculomotor responses to vestibular activation. Stimulation of individual semicircular canals results in eye movements parallel to the plane of the stimulated canal, and stimulation of the utricular macula produces changes in ocular torsional position. It was also assumed that the total three-dimensional eye-movement response to GVS is the sum of the contributions of the oculomotor drive of all the vestibular end organs. If a particular vestibular end organ were to be diseased or dysfunctional, it was reasoned that its contribution to the GVS-induced oculomotor response would be reduced or absent and that patients thus affected would have a systematic difference in their GVS-induced oculomotor response compared with the response of normal healthy individuals. METHODS Three-dimensional video eye-movement recording was carried out in complete darkness on normal healthy subjects and patients with various types of vestibular dysfunction, as diagnosed by independent vestibular clinical tests. The eye-movement response to long-duration bilateral and unilateral surface GVS was measured. RESULTS The pattern of horizontal, vertical, and torsional eye velocity and eye position during GVS of patients independently diagnosed with bilateral vestibular dysfunction, unilateral vestibular dysfunction, CHARGE syndrome (semicircular canal hypoplasia), semicircular canal occlusion, or inferior vestibular neuritis differed systematically from the responses of normal healthy subjects in ways that corresponded to the expectations from the conceptual approach of the study. CONCLUSION The study reports the first data on the differences between the normal response to GVS and those of patients with a number of clinical vestibular conditions including unilateral vestibular loss, canal block, and vestibular neuritis. The GVS-induced eye-movement patterns of patients with vestibular dysfunction are consistent with the reduction or absence of oculomotor contribution from the end organs implicated in their particular disease condition.

Cognitive tasks such as mental arithmetic and fixation of imagined targets are known to affect vestibular nystagmus. Here we show that another cognitive task—subject’s active control of the rotation of a single moving visual line in an otherwise darkened room—influences the gain of the torsional optokinetic response to that single moving visual line.

‘‘For both BCV and ACS, the p13-n23 components of the cVEMPs recorded from the left SCM were greatly reduced or absent, but the p13-n23 recorded from the right SCM was present (Figs. 1, 2). For this reason, and given the other normal vestibular and audiological test results, the patient was diagnosed as having left inferior vestibular neuritis [5–7]. For both BCV and ACS, the oVEMP n10 recorded beneath both eyes is clearly present and approximately symmetrical (i.e. normal).’’