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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.

As previously reported, a single test measuring oVEMP n10 to 4000 Hz stimuli (bone-conducted vibration (BCV) or air-conducted sound (ACS)) provides a definitive diagnosis of semicircular canal dehiscence (SCD) in 22 CT-verified patients, with a sensitivity of 1.0 and specificity of 1.0. This single short screening test has great advantages of speed, minimizing testing time, and the exposure of patients to stimulation. However, a few studies of the 4000 Hz test for SCD have reported sensitivity and specificity values which are slightly less than reported previously. We hypothesized that the rise time of the stimulus is important for detecting the oVEMP n10 to 4000 Hz, similarly to what we had shown for 500 and 750 Hz BCV. We measured oVEMP n10 in 15 patients with CT-verified SCD in response to 4000 Hz ACS or BCV stimuli with rise times of 0, 1, and 2 ms. As a result, increasing the rise time of the stimulus reduced the oVEMP n10 amplitude. This outcome is expected from the physiological evidence of guinea pig primary vestibular afferents, which are activated by sound or vibration. Therefore, for clinical VEMP testing, short rise times are optimal (preferably 0 ms).

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.

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.

INTRODUCTION: We have previously shown that bone-conducted vibration to each mastoid in humans results in small stimulus-locked horizontal and vertical eye movements suggesting that the ipsilateral superior oblique and the contralateral inferior rectus are activated. However, as torsional responses were not measured we have repeated the study by measuring torsional as well as horizontal and vertical responses in seven adult subjects during different directions of gaze. METHODS:Wemeasured stimulus-locked horizontal (H), vertical (V) and torsional (T) eye movements during brief stimulation to the mastoid unilaterally and bilaterally using a high-speed, high-resolution video technique. Bone-conducted vibrations were delivered to each mastoid separately as well as bilaterally using a Radioear B71 bone oscillator while the subjects viewed targets 2 metres away situated straight ahead and 10 ◦ to the right and left. RESULTS: For unilateral stimulation the eyes moved downwards when directed away from the stimulated mastoid, along with bilateral counter-rolling away from the side of stimulation. Horizontal movements were small, with little effect of gaze position. Bilateral stimulation enhanced the downward responses. CONCLUSIONS: Bone conducted vibration to the mastoid in humans produces vertical and torsional eye movements consistent with activation of the ipsilateral superior oblique muscle, and the contralateral inferior oblique muscle to produce counter rolling of the eyes away from the stimulated mastoid.

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.

This study sought to characterize the response of mammalian primary otolithic neurons to sound and vibration by measuring the resting discharge rates, thresholds for increases in firing rate and supra-threshold sensitivity functions of guinea pig single primary utricular and saccular afferents. Neurons with irregular resting discharge were activated in response to bone conducted vibration (BCV) and air conducted sound (ACS) for frequencies between 100 Hz and 3000 Hz. The location of neurons was verified by labelling with neurobiotin. Many afferents from both maculae have very low or zero resting discharge, with saccular afferents having on average, higher resting rates than utricular afferents. Most irregular utricular and saccular afferents can be evoked by both BCV and ACS. For BCV stimulation: utricular and saccular neurons show similar low thresholds for increased firing rate (around 0.02 g on average) for frequencies from 100 Hz to 750 Hz. There is a steep increase in rate change threshold for BCV frequencies above 750 Hz. The suprathreshold sensitivity functions for BCV were similar for both utricular and saccular neurons, with, at low frequencies, very steep increases in firing rate as intensity increased. For ACS stimulation: utricular and saccular neurons can be activated by high intensity stimuli for frequencies from 250 Hz to 3000 Hz with similar flattened U-shaped tuning curves with lowest thresholds for frequencies around 1000–2000 Hz. The average ACS thresholds for saccular afferents across these frequencies is about 15–20 dB lower than for utricular neurons. The suprathreshold sensitivity functions for ACS were similar for both utricular and saccular neurons. Both utricular and saccular afferents showed phase-locking to BCV and ACS, extending up to frequencies of at least around 1500 Hz for BCV and 3000 Hz for ACS. Phase-locking at low frequencies (e.g. 100 Hz) imposes a limit on the neural firing rate evoked by the stimulus since the neurons usually fire one spike per cycle of the stimulus. Conclusion These results are in accord with the hypothesis put forward by Young et al. (1977) that each individual cycle of the waveform, either BCV or ACS, is the effective stimulus to the receptor hair cells on either macula. We suggest that each cycle of the BCV or ACS stimulus causes fluid displacement which deflects the short, stiff, hair bundles of type I receptors at the striola and so triggers the phase-locked neural response of primary otolithic afferents.

Experimental objective To provide a safe, simple, relatively inexpensive, fast, accurate way of quantifying balance performance either in isolation, or in the face of challenges provided by 3D high definition moving visual stimuli as well as by the proprioceptive challenge from standing on a foam pad. This method uses the new technology of the Wii balance board to measure postural stability during powerful, realistic visual challenges from immersive virtual reality. Limitations of current techniques Present computerized methods for measuring postural stability are large, complex, slow, and expensive, and do not allow for testing the response to realistic visual challenges. Protocol Subjects stand on a 6 cm thick, firm, foam pad on a Wii balance board. They wear a fast, high resolution, low persistence, virtual reality head set (Oculus Rift DK2). This allows displays of varying speed, direction, depth, and complexity to be delivered. The subject experiences a visual illusion of real objects fixed relative to the world, and any of these displays can be perturbed in an unpredictable fashion. A special app (BalanceRite) used the same procedures for analyzing postural analysis as used by the Equitest. Power of the technique Four simple “proof of concept” experiments demonstrate that this technique matches the gold standard Equitest in terms of the measurement of postural stability but goes beyond the Equitest by measuring stability in the face of visual challenges, which are so powerful that even healthy subjects fall. The response to these challenges presents an opportunity for predicting falls and for rehabilitation of seniors and patients with poor postural stability. Significance for the field This new method provides a simpler, quicker, cheaper method of measurement than the Equitest. It may provide a new mode of training to prevent falls, by maintaining postural stability in the face of visual and proprioceptive challenges similar to those encountered in life.

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.

We have defined a complete sample of 228 southern radio sources at 408 MHz with integrated flux densities S_408 > 4.0 Jy, Galactic latitude |b| > 10 deg and declination -85 deg < delta < -30 deg. The main finding survey used was the Molonglo Reference Catalogue. We describe in detail how the Molonglo Southern 4 Jy sample (MS4) was assembled and its completeness assessed. Sources in the sample were imaged at 843 MHz with the Molonglo Observatory Synthesis Telescope to obtain positions accurate to about 1 arcsec, as well as flux densities and angular sizes; follow-up radio and optical observations are presented in Paper II. Radio spectra for the MS4 have been compiled from the literature and used to estimate flux densities at 178 MHz. The strong-source subset of MS4, with S_178 > 10.9 Jy (SMS4), provides a southern sample closely equivalent to the well-studied northern 3CRR sample. Comparison of SMS4 with 3CRR shows a reassuring similarity in source density and median flux density between the two samples., 59 pages, 5 Postscript figures. To appear in Astronomical Journal. For a higher-resolution version of Figure 2, see http://www.physics.usyd.edu.au/astrop/rwh/ms4/

When humans are roll-tilted around the naso-occipital axis, both eyes roll or tort in the opposite direction to roll-tilt, a phenomenon known as ocular counterroll (OCR). While the magnitude of OCR is primarily determined by vestibular, somatosensory, and proprioceptive input, direction of gaze also plays a major role. The aim of this study was to measure the interaction between some of these factors in the control of OCR. Videooculography was used to measure 3D eye position during maintained whole body (en bloc) static roll-tilt in darkness, while subjects fixated first on a distant (at 130 cm) and then a near (at 30 cm) head-fixed target aligned with the subject’s midline. We found that while converging on the near target, human subjects displayed a significant reduction in OCR for both directions of roll-tilt––i.e. the interaction between OCR and vergence was not simple addition or subtraction of torsion induced by vergence with torsion induced by roll-tilt. To remove the possibility that the OCR reduction may be associated with the changed horizontal position of the eye in the orbit during symmetric convergence, we ran an experiment using asymmetric convergence in which the distant and near targets were aligned directly in front of one eye. We found the magnitude of OCR in this asymmetric convergence case was also reduced for near viewing by about the same amount as in the symmetric vergence condition, confirming that the convergence command rather than horizontal position of the eye underlies the OCR reduction, since there was no horizontal movement of the aligned eye in the orbit between fixation on the distant and near targets. Increasing vergence from 130 to 30 cm reduced OCR gain by around 35% on average. That reduction was equal in both eyes and occurred in both the symmetric and asymmetric convergence conditions. These results demonstrate the important role vergence plays in determining ocular counterroll during roll-tilt and may support the contention that vergence acts to reduce the conflict facing a stereopsis-generating mechanism.

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.