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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.

Older studies of mammalian otolith physiology have focused mainly on sustained responses to low-frequency (

In superior canal dehiscence (SCD), fluid displacement of the endolymph activates type I vestibular hair cells in the crista of the affected canal and thus irregular superior canal (SC) neurons in Scarpa's ganglion, which provides the neurophysiological basis for the clinical presentation of SCD.Patients with SCD display sound- and vibration-induced vertigo/nystagmus and increased amplitudes of vestibular evoked myogenic potentials.Extracellular recordings from n = 25 primary vestibular neurons of 16 female guinea pigs were analyzed. We recorded from the same vestibular neuron before, during and after creating the dehiscence and after closing the dehiscence. Neurobiotin labeling was employed in n = 11 neurons.After SCD, previously unresponsive irregular SC neurons displayed a stimulus-locked increase in discharge during application of air-conducted sound (ACS) or bone-conducted vibration (BCV) for a broad range of frequencies (ACS: 200-4000 Hz; BCV: 500-1500 Hz). This typical response was only observed for irregular SC neurons (n = 19), but not regular SC neurons, or irregular/regular horizontal canal neurons (n = 2 each), and was abolished after closing the dehiscence. Eleven irregular SC neurons responsive to ACS and/or BCV were traced back to calyx synapses in the central crista of the affected superior canal by neurobiotin labeling.Stimulus-locked activation of irregular SC neurons by ACS and BCV is the neurophysiological basis for sound- and vibration-induced vertigo/nystagmus and increased VEMP amplitudes in SCD. The results of the present study help to improve vestibular diagnostics in patients with suspected SCD.

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.

Hypothesis: Bone-conducted vibration (BCV) at 100 Hz causes endolymph displacement at hair cell stereocilia in semicircular canal (SCC) ducts of the intact bony labyrinth resulting in activation of irregularly discharging afferent neurons. Background: Suprathreshold 100 Hz BCV is employed in the clinic to evoke skull vibration-induced nystagmus, an indicator for peripheral vestibular asymmetry. Recently, this stimulus has also been used in vestibular-evoked myogenic potentials, a selective test for otolithic function. Methods: We performed extracellular recordings from utricular and SCC afferents in guinea pigs during application of suprathreshold BCV stimuli (100-500 Hz) to the animal's skull. Vibration was administered in a way that the animal, the vibrator, and the recording electrode moved as one. Results: In summary, 19 of 43 recorded SCC afferents displayed a stimulus- and phase-locked increase in firing during stimulation at 100 Hz BCV with no perstimulatory adaptation and no poststimulatory silencing. All of the 19 activated SCC afferents had an irregular resting discharge. Neuronal activation of SCC afferents was less pronounced at 200 Hz and largely absent at 500 Hz. On the contrary, a stimulus- and phase-locked increase in firing was observed for irregularly discharging utricular neurons at all frequencies tested. Conclusions: At intensities usually applied in the clinic, 500 Hz BCV is a largely selective otolithic stimulus, while 100 Hz BCV can activate both otolith and SCC afferents. Therefore, while 100 Hz BCV is ideally suited for evoking skull vibration-induced nystagmus in peripheral vestibular asymmetry, it is not recommended for vestibular-evoked myogenic potentials, as it lacks otolithic specificity.

Hypothesis: Build a biologic geometry based computational model to test the hypothesis that, in some circumstances, endolymphatic hydrops can mechanically cause enhanced eye velocity responses during clinical conditions of the head impulse test. Background: Some recent clinical and experimental findings had suggested that enhanced eye velocity responses measured with the video head impulse test could not only be caused by recording artifacts or central disfunction but also could be directly caused by the mechanical effect of endolymphatic hydrops on horizontal semicircular canal receptor. Methods: Data from clinical video head impulse test was computed in three biologic-based geometry models governed by Navier-Stokes equations; six head impulses of incrementally increasing peak head velocity were computed in each one of the three different geometric models, depending on absence, canal or utricular hydrops. Results: For all computed head impulses an increased endolymphatic pressure was measured at the ampullar region of the horizontal semicircular canal on both canal and utricular hydrops models. The mean of aVOR gain was 1.01 ± 0.008 for the no-hydrops model, 1.14 ± 0.010 for the canal hydrops model was, and 1.10 ± 0.007 for the utricular hydrops model. Conclusion: The results of the physical computation models support-the hypothesis that in endolymphatic hydrops conditions, which are affecting horizontal semicircular canal and utricular region on moderate dilatations, the eye velocity responses output-by the aVOR will be enhanced by a 1.14 factor and aVOR gain values will be enhanced by over 1.1 for impulses to the right side.

Recent advances in vestibular testing now permit functional testing of all peripheral vestibular sense organs (all three semicircular canals, utricle, and saccule). This makes it possible to identify patients with isolated dysfunction of the utricle or saccule, even though parallel pathways for vestibular information are ultimately integrated centrally. Selective, isolated unilateral loss of utricular function as measured by ocular vestibular-evoked myogenic potentials (VEMPs) has been observed in patients with normal semicircular canal function as measured by the video head impulse test of all six semicircular canals, and normal bilateral saccular function as determined by symmetrical cervical VEMPs. How these patients present clinically and how they recover is discussed and contrasted with acute vestibular neuritis. In some patients, the unilateral loss of otolith organ (utricle or saccule) function persists and yet the patient recovers functionally to their usual lifestyle. Until the testing of all peripheral vestibular sense organs is routine, the frequency of isolated loss of otolith function cannot be gauged.

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.

Phase-locking of cochlear neurons to sound has been of great value in understanding cochlear transduction. Phase-locking has also been reported previously in irregular vestibular afferents, but detailed information about it is sparse. We measured the phase-locking of guinea pig irregular otolithic neurons and canal neurons (after a semicircular canal dehiscence allowed them to respond) to both sound and vibration stimuli. Irregular vestibular afferents from both otoliths and canals have a range of preferred phase angles which systematically increase as frequency is increased from 250 Hz to above 1000 Hz. Surprisingly vestibular afferents show more precise phase-locking than comparable auditory afferents as reported by Palmer and Russell (1986), and they do so up to higher frequencies. This high precision implies a very sharp, fast threshold for evoking an action potential with minimal variability, and so has implications for the current controversy about hair-cell-afferent transmission in the vestibular system. Following recent evidence, we suggest that potassium in the unique type I-calyx synapse may be a major factor in generating this very precise phase-locking.

Air-conducted sound and bone-conduced vibration activate otolithic receptors and afferent neurons in both the utricular and saccular maculae, and trigger small electromyographic (EMG) responses [called vestibular-evoked myogenic potentials (VEMPs)] in various muscle groups throughout the body. The use of these VEMPs for clinical assessment of human otolithic function is built on the following logical steps: (1) that high-frequency sound and vibration at clinically effective stimulus levels activate otolithic receptors and afferents, rather than semicircular canal afferents, (2) that there is differential anatomical projection of otolith afferents to eye muscles and neck muscles, and (3) that isolated stimulation of the utricular macula induces short latency responses in eye muscles, and that isolated stimulation of the saccular macula induces short latency responses in neck motoneurons. Evidence supports these logical steps, and so VEMPs are increasingly being used for clinical assessment of otolith function, even differential evaluation of utricular and saccular function. The proposal, originally put forward by Curthoys in 2010, is now accepted: that the ocular vestibular-evoked myogenic potential reflects predominantly contralateral utricular function and the cervical vestibular-evoked myogenic potential reflects predominantly ipsilateral saccular function. So VEMPs can provide differential tests of utricular and saccular function, not because of stimulus selectivity for either of the two maculae, but by measuring responses which are predominantly determined by the differential neural projection of utricular as opposed to saccular neural information to various muscle groups. The major question which this review addresses is how the otolithic sensory system, with such a high density otoconial layer, can be activated by individual cycles of sound and vibration and show such tight locking of the timing of action potentials of single primary otolithic afferents to a particular phase angle of the stimulus cycle even at frequencies far above 1,000 Hz. The new explanation is that it is due to the otoliths acting as seismometers at high frequencies and accelerometers at low frequencies. VEMPs are an otolith-dominated response, but in a particular clinical condition, semicircular canal dehiscence, semicircular canal receptors are also activated by sound and vibration, and act to enhance the otolith-dominated VEMP responses.

We report enhanced symmetrical cervical vestibular evoked myogenic potential (cVEMP) but asymmetrical ocular VEMP (oVEMP) responses in a patient with CT-verified bilateral superior semicircular canal dehiscence (SCD) but with acute vestibular syndrome. This implies that absence of unilateral utricular macula function alone is sufficient to cause symptoms of acute vertigo. Acute vertigo should not automatically be presumed to originate from semicircular canal dysfunction.To identify the cause of an acute vertigo attack in a patient with bilateral SCD.The functional state of all peripheral vestibular sense organs was tested using the video head impulse test (vHIT) for all semicircular canals and VEMPs to air-conducted sound (ACS) or bone-conducted vibration (BCV) to test all otolith organs. The cVEMP tested mainly saccular function and the oVEMP mainly utricular function.All semicircular canals showed normal function. The cVEMPs showed enhanced, but symmetrical saccular function. In contrast, oVEMPs showed an enhanced but asymmetric n10 component - it was greatly reduced beneath the left eye, implying decreased function in the right utricular macula. That result was confirmed using very high frequency stimuli which are effective in SCD: 4000 Hz BCV stimuli showed that oVEMP n10 was present beneath the right eye but absent beneath the left eye.

Summary 1. Extracellular single neuron recording and labelling studies of primary v estibular afferents in Scarpa’ s ganglion have shown that guinea pig otolithic afferents with irregular resting discharge are preferentially acti vated by 500Hz bone-conducted vibration (BCV) and man ya lso by 500Hz air-conducted sound (ACS) at lo wt hreshold and high sensitivity .V ery fe wa fferent neurons from any semicircular canal are activated by these stimuli and then only at high intensity. 2. Tracing the origin of the acti vated neurons shows that these sensitive otolithic afferents originate mainly from as pecialized region ‐ the striola ‐ of both the utricular and saccular maculae. 3. This same 500Hz BCV elicits vestibulardependent eye mo vements in alert guinea pigs and also in health yh umans. These stimuli evoke myogenic potentials (VEMPs) which are used to test the function of the utricular and saccular maculae in human patients. 4. Although utricular and saccular afferents can both be activated by BCV and ACS, the differential projection of utricular and saccular afferents to dif ferent muscle groups allows for differentiation of the function of these tw o sensory regions. The basic neural data support the conclusion that in human patients in response to brief 500Hz BCV delivered to Fz (the midline of the forehead at the hairline) the cervical VEMP (cVEMP) indicates predominantly saccular function and the ocular VEMP (oVEMP) indicates predominantly utricular function. 5. The neural, anatomical and behavioural evidence underpins clinical tests of otolith function in humans using sound and vibration.

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.

Background and aims:Previous evidence shows that the n10 component of the ocular vestibular evoked myogenic potential indicates utricular function, while the p13 component of the cervical vestibular evoked myogenic potential indicates saccular function. This study aimed to assess the possibility of differential utricular and saccular function testing in the clinic, and whether loss of saccular function affects utricular response.Methods:Following vibration conduction from the mid-forehead at the hairline, the ocular n10 component was recorded by surface electromyograph electrodes beneath both eyes, while the cervical p13–n23 component was recorded by surface electrodes over the tensed sternocleidomastoid muscles.Results:Fifty-nine patients were diagnosed with probable inferior vestibular neuritis, as their cervical p13–n23 component was asymmetrical (i.e. reduced or absent on the ipsilesional side), while their ocular n10 component was symmetrical (i.e. normal beneath the contralesional eye).Conclusion:The sense organ responsible for the cervical and the ocular vestibular evoked myogenic potentials cannot be the same, as one response was normal while the other was not. Reduced or absent saccular function has no detectable effect on the ocular n10 component. On vibration stimulation, the ocular n10 component indicates utricular function and the cervical p13–n23 component indicates saccular function.

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

Extracellular single neuron recordings of primary vestibular neurons in Scarpa's ganglion in guinea pigs show that low-intensity 500 Hz bone-conducted vibration (BCV) or 500 Hz air-conducted sound (ACS) activate a high proportion of otolith irregular neurons from the utricular and saccular maculae but few semicircular canal neurons. In alert guinea pigs, and humans, 500 Hz BCV elicits otolith-evoked eye movements. In humans, it also elicits a myogenic potential on tensed sternocleidomastoid muscles. Although BCV and ACS activate both utricular and saccular maculae, it is possible to probe the functional status of these two sense organs separately because of their differential neural projections. Saccular neurons have a strong projection to neck muscles and a weak projection to the oculomotor system. Utricular afferents have a strong projection to eye muscles. So measuring oculomotor responses to ACS and BCV predominantly probes utricular function, while measuring neck muscle responses to these stimuli predominantly probes saccular function.

The enhanced sound- and vibration-induced vestibular evoked myogenic potentials (VEMPs) and their lower threshold in patients with a thinning of the bony wall of the superior semicircular canal (superior canal dehiscence, SCD) have been interpreted as being due to the dehiscence allowing sound and vibration to activate, unusually, the receptors of the dehiscent semicircular canal. We report a patient with bilateral SCD, as verified by high resolution CT scans, who had bilaterally decreased superior semicircular canal function, as shown by rotational tests of canal function. This patient also showed enhanced VEMPs and reduced thresholds. We conclude that in this patient the enhanced VEMP responses are thus probably due to enhanced otolithic stimulation by sound and vibration after dehiscence.

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.

Objective: The n10 component (n10) of the ocular vestibular evoked myogenic potential (oVEMP) to brief bone conducted vibration (BCV) of the forehead at Fz is probably caused by the vibration selectively activating vestibular otolithic receptors. If the n10 is due primarily to utricular activation then diseases which affect only the superior division of the vestibular nerve (SVN) should reduce or eliminate n10. Methods: The n10 component of the oVEMP was measured in 13 patients with unilateral SVN but with inferior vestibular nerve function preserved. Results: We compared the n10 to BCV of these 13 SVN patients to previously published data for healthy subjects and patients after complete unilateral vestibular loss. We found that in 12 out of the 13 patients with SVN, n10 was markedly reduced or absent under the contralesional eye. Conclusion: Since all utricular afferents course in the superior vestibular nerve and in 12/13 of these patients the n10 was reduced we conclude that the n10 component of the oVEMP to BCV is probably mediated by the superior vestibular nerve and probably due to activation of mainly utricular receptors. Significance: The n10 appears to be a simple new test of superior vestibular nerve and probably mainly utricular function.

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.

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.

Background/Hypothesis. With the video Head Impulse Test (vHIT), the vertical VOR gain is defined as (vertical eye velocity/vertical head velocity), but compensatory eye movements to vertical canal stimulation usually have a torsional component. To minimize the contribution of torsion to the eye movement measurement, the horizontal gaze direction should be directed 40º from straight ahead so it is in the plane of the stimulated canal plane pair. Hypothesis: as gaze is systematically moved horizontally away from canal plane alignment, the measured vertical VOR gain should decrease.Study Design. 10 healthy subjects, with vHIT measuring vertical eye movement to head impulses in the plane of the left anterior-right posterior (LARP) canal plane, with gaze at one of 5 horizontal gaze positions (40º (aligned with the LARP plane), 20º, 0º, -20º, -40º).Methods. Every head impulse was in the LARP plane. The compensatory eye movement was measured by the vHIT prototype system. The one operator delivered every impulse. Results. The canal stimulus remained identical across trials, but the measured vertical VOR gain decreased as horizontal gaze angle was shifted away from alignment with the LARP canal plane.Conclusion. In measuring vertical VOR gain with vHIT the horizontal gaze angle should be aligned with the canal plane under test.

Vertigo and vigorous horizontal spontaneous nystagmus in a presenting patient is usually taken to indicate unilaterally reduced horizontal canal function. However here we report results which question that presumption. In three such patients with an acute vestibular syndrome, complete testing of all peripheral vestibular sense organs using new tests of canal and otolith function (vHIT and VEMPs) showed that semicircular canal function was normal, but that there were unilateral otolithic deficits which probably caused their acute syndrome.

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.

A realistic neural-network model was constructed to simulate production of both the slow-phase and quick-phase components of vestibular nystagmus by incorporating a quick-phase pathway into a previous model of the slow phase. The neurons in the network were modelled by multicompartmental Hodgkin-Huxley-style spiking neurons based on known responses and projections of physiologically identified vestibular neurons. The modelling used the GENESIS software package. The slow-phase network consisted of ganglion and medial vestibular nucleus (MVN) neurons; the latter were constructed using biophysical models of MVN type A and B neurons. The quick-phase network contained several types of bursting cells which have been shown to have major roles in the generation of the quick phase: burster-driver neurons, long-lead burst neurons, pause neurons, excitatory burst neurons and inhibitory burst neurons. Comparison of the output neural responses from the model with guinea pig behavioural responses from the companion paper showed consistency between model and animal data for neuron firing patterns, maximal firing rates, and timing, duration and number of quick phases. Comparisons were made for stable head input and for sinusoidal angular stimuli at a range of frequencies from 0.1 to 2 Hz. Except for data at 0.1 Hz, where the simulation produced one more quick phase per half cycle than the animal data, the number of quick phases was consistent between the model and the animal data. The model was also used to simulate the effects both of unilateral vestibular deafferentation (UVD) and of vestibular compensation after UVD, and the responses in the modelled MVN neurons were affected in a way similar to those measured in guinea pig MVN neurons: the number of quick phases and their timing changed in a similar fashion to that observed in behavioural data.

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.

We measured the guinea pig horizontal vestibulo-ocular reflex (hVOR) to high acceleration impulsive head rotations following a unilateral lateral semicircular canal (LSCC) occlusion. We found a significant hVOR deficit for rotations toward the side of the occluded LSCC and this deficit did not show systematic changes over 3 months. We considered the LSCC nerve was still functional as shown by the normal appearance of the crista of the LSCC ampulla and also electrical stimulation of the LSCC. We conclude that the VOR during angular acceleration in response to high acceleration shows no adaptive plasticity following a unilateral LSCC occlusion.

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.

Dual search coils were used to record horizontal, vertical and torsional eye movement components of one eye during nystagmus caused by off-center yaw rotation (yaw centrifugation). Both normal healthy human subjects (n=7) and patients with only one functioning labyrinth (n=12) were studied in order to clarify how the concomitant linear acceleration affected the nystagmus response. Each subject was seated with head erect on the arm of a fixed-chair human centrifuge, 1 m away from the center of the rotation, and positioned to be facing along a radius; either towards (facing-in) or away from (facing-out) the center of rotation. Both yaw right and yaw left angular accelerations of 10 degrees s(-2) from 0 to 200 degrees/s were studied. During rotation a centripetal linear acceleration (increasing from 0 to 1.24xg units) was directed along the subject's naso-occipital axis resulting in a shift of the resultant angle of the gravitoinertial acceleration (GIA) of 51 degrees in the subject's pitch plane and an increase in the total GIA magnitude from 1.0 to 1.59xg. In normal subjects during the angular acceleration off-center there were, in addition to the horizontal eye velocity components, torsional and vertical eye velocities present. The magnitude of these additional components, although small, was larger than observed during similar experiments with on-center angular acceleration (Haslwanter et al. 1996), and the change in these components is attributed to the additional effect of the linear acceleration stimulation. In the pitch plane the average size of the shift of the axis of eye velocity (AEV) during the acceleration was about 8 degrees for a 51 degrees shift of the GIA (around 16% of the GIA shift) so that the AEV-GIA alignment was inadequate. There was a very marked difference in the size of the AEV shift depending on whether the person was facing-in [AEV shift forward (i.e. non-compensatory) of about 4 degrees] or facing-out [AEV shift forward (i.e. compensatory) of around 12 degrees]. The linear acceleration decreased the time constant of decay of the horizontal component of the post-rotatory nystagmus: from an average of 24.8 degrees/s facing-in to an average of 11.3 degrees/s facing-out. The linear acceleration dumps torsional eye velocity in an manner analogous to, but independent of, the dumping of horizontal eye velocity. Patients with UVD had dramatically reduced torsional eye velocities for both facing-in and facing-out headings, and there was little if any shift of the AEV in UVD patients. The relatively small effects of linear acceleration on human canal-induced nystagmus found here confirms other recent studies in humans (Fetter et al. 1996) in contrast to evidence from monkeys and emphasizes the large and important differences between humans and monkeys in otolith-canal interaction. Our results confirm the vestibular control of the axis of eye velocity of humans is essentially head-referenced whereas in monkeys that control is essentially space-referenced.

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...

This study sought to identify in guinea pig the peripheral sense organ of origin of otolith irregular primary vestibular afferent neurons having a very sensitive response to both air-conducted sound (ACS) and bone-conducted vibration (BCV). Neurons responding to both types of stimuli were labelled by juxtacellular labelling by neurobiotin. Whole mounts of the maculae showed that some vestibular afferents activated by both ACS and BCV originate from the utricular macula and some from the saccular macula - there is no "afferent specificity" by one sense organ for ACS and the other for BCV - instead some afferents from both sense organs have sensitive responses to both stimuli. The clinical implication of this result is that differential evaluation of the functional status of the utricular and saccular maculae cannot rely on stimulus type (ACS vs BCV), however the differential motor projections of the utricular and saccular maculae allow for differential evaluation of each sense organ.

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.