Suppression head impulse test paradigm (SHIMP) characteristics in people with Parkinson's disease compared to healthy controls.

The suppression head impulse test paradigm (SHIMP) is a newly described indicator of vestibular function which yields two measures: vestibulo-ocular reflex (VOR) gain and a saccadic response. It is an alternative and complementary test to the head impulse test paradigm (HIMP). Parkinson's disease (PD) has known saccadic and central vestibular pathway dysfunction. This paper is the first description of SHIMP VOR gain and saccade characteristic in this population. This prospective observational study measured the SHIMP VOR gain and saccade characteristics in 39 participants with idiopathic PD and compared this to 40 healthy controls (HC). The effect of group, demographic variables and SHIMP characteristics were evaluated. SHIMP VOR gains were not significantly different between groups (p = 0.10). Compared to HC, the PD group mean SHIMP peak saccade velocity was significantly reduced by an average of 77.07°/sec (p < 0.001), and SHIMP saccade response latency was longer, with an average delay of 23.5 ms (p = 0.003). SHIMP saccade peak velocity was also associated with both head impulse velocity (p = 0.002) and SHIMP VOR gain (p = 0.004) variables, but there was no significant influence of these variables when SHIMP saccade peak velocity was considered as a predictor of PD (p = 0.52-0.91). VOR gains were unaffected by PD. PD-specific saccadic dysfunction, namely reduced peak saccade velocities and prolonged response latencies, were observed in the SHIMP-induced saccade responses. VOR gain using slow phase eye velocity is preferred as the indicator of vestibular function in the SHIMPs paradigm as non-vestibular factors affected saccade peak velocity.

Resolved External Ophthalmoplegia and Hearing Loss in Wernicke's Encephalopathy With Thiamine Replacement.

BACKGROUND: Wernicke encephalopathy (WE) is classically described by a clinical triad consisting of confusion, ataxia, and ophthalmoplegia, but recent reports emphasize a history of malnutrition along with 2 elements of the WE triad (Caine's criteria) to enhance diagnostic sensitivity. The ophthalmoplegia, vestibular, and auditory expeditious improvement with intravenous thiamine usually confirms the diagnosis; serum levels generally provide additional diagnostic certainty. METHODS: Here, we discuss the case of a woman with a distant history of gastric sleeve, poor nutrition and protracted vomiting, who developed acute confusion, imbalance, near-total external ophthalmoplegia (EO), and hearing loss. The baseline thiamine level was 28 πmol/L (Normal: 70-180 πmol/L). We performed serial neurological, vestibular, and audiological examination to document over 5 days, the effect of intravenous (IV) thiamine, and again at 3 months with continued oral supplementation. We provide serial documentation with photographs and video recording of oculomotor abnormalities, audiometric testing, and a video of horizontal head impulse testing, and imaging findings. RESULTS: Over the course of 5 days of IV thiamine supplementation, we demonstrate our patient's resolution of near complete EO. We assessed vestibular paresis with horizontal head impulse testing, after complete resolution of the EO. The initially positive bilateral h-HIT showed decreased gain and overt corrective saccades, it clinically resolved by day 5, but video h-HIT testing demonstrated persistent decreased horizontal vestibulo-ocular reflex (VOR) gain and covert horizontal saccades, which persisted at the 3-month examination. By contrast, the vertical VOR gain was normal without corrective saccades. Bedside audiometry completed during the acute phase demonstrated severely restricted auditory speech comprehension, which normalized 3 months later. Severe truncal ataxia improved as well. CONCLUSIONS: This case is an example of how awareness of the variations in the clinical presentation of WE can be crucial in achieving an early diagnosis and obtaining better outcomes. A history of the poor nutritional status can be an important clue to aid in this early diagnosis.

Vestibular failure managed with osteopathic manipulative treatment: A report of two cases.

INTRODUCTION: Vestibular failure or hypofunction can be generated by pathologies such as vestibular neuritis (VN), causing the onset of rotatory vertigo and the vestibulo-ocular reflex (VOR) hyporeaction. VN is a post-viral inflammation-producing vestibular nerve-axon impairment, which reaches compensation in 70% of cases. Here, we present two cases of vestibular failure that did not respond to pharmacological therapy, but did show modulated vestibular response after an osteopathic manipulative treatment. Dizziness handicap inventory (DHI) was used to assess disability, while VOR was examined by means of video head impulse test (v-HIT). Case 1 showed bilateral VOR areflexia with severe related disability due to chronic vertigo, while case 2 showed sub-acute VN complicated by intense vomiting. After treatment, both cases had a complete remission of symptoms, with a reduction in DHI score of 60 and 70 points respectively, as well as a normalization of the v-HIT exam. CONCLUSION: OMT might work to modulate VOR, through osteopathic manipulation of the fascial-system and interaction with proprioceptive inputs. Further clinical trials should be performed to investigate the OMT clinical efficacy in uncompensated vestibular neuritis.

Electrical Vestibular Stimulation in Humans: A Narrative Review.

BACKGROUND: In patients with bilateral vestibulopathy, the regular treatment options, such as medication, surgery, and/or vestibular rehabilitation, do not always suffice. Therefore, the focus in this field of vestibular research shifted to electrical vestibular stimulation (EVS) and the development of a system capable of artificially restoring the vestibular function. Key Message: Currently, three approaches are being investigated: vestibular co-stimulation with a cochlear implant (CI), EVS with a vestibular implant (VI), and galvanic vestibular stimulation (GVS). All three applications show promising results but due to conceptual differences and the experimental state, a consensus on which application is the most ideal for which type of patient is still missing. SUMMARY: Vestibular co-stimulation with a CI is based on "spread of excitation," which is a phenomenon that occurs when the currents from the CI spread to the surrounding structures and stimulate them. It has been shown that CI activation can indeed result in stimulation of the vestibular structures. Therefore, the question was raised whether vestibular co-stimulation can be functionally used in patients with bilateral vestibulopathy. A more direct vestibular stimulation method can be accomplished by implantation and activation of a VI. The concept of the VI is based on the technology and principles of the CI. Different VI prototypes are currently being evaluated regarding feasibility and functionality. So far, all of them were capable of activating different types of vestibular reflexes. A third stimulation method is GVS, which requires the use of surface electrodes instead of an implanted electrode array. However, as the currents are sent through the skull from one mastoid to the other, GVS is rather unspecific. It should be mentioned though, that the reported spread of excitation in both CI and VI use also seems to induce a more unspecific stimulation. Although all three applications of EVS were shown to be effective, it has yet to be defined which option is more desirable based on applicability and efficiency. It is possible and even likely that there is a place for all three approaches, given the diversity of the patient population who serves to gain from such technologies.

Effect of Intensity Level and Speech Stimulus Type on the Vestibulo-Ocular Reflex.

BACKGROUND: Accurate vestibulo-ocular reflex (VOR) measurement requires control of extravestibular suppressive factors such as visual fixation. Although visual fixation is the dominant suppressor and has been extensively studied, the mechanisms underlying suppression from nonvisual factors of attention and auditory stimulation are less clear. It has been postulated that the nonvisual suppression of the VOR is the result of one of two mechanisms: (1) activation of auditory reception areas excites efferent pathways to the vestibular nuclei, thus inhibiting the VOR or (2) cortical modulation of the VOR results from directed attention, which implies a nonmodality-specific process. PURPOSE: The purpose of this research was to determine if the VOR is affected by the intensity level and/or type of speech stimulus. RESEARCH DESIGN: A repeated measures design was used. The experiment was single-blinded. STUDY SAMPLE: Participants included 17 adults (14 females, three males) between the ages of 18-34 years who reported normal oculomotor, vestibular, neurological, and musculoskeletal function. DATA COLLECTION AND ANALYSIS: Each participant underwent slow harmonic acceleration testing in a rotational chair. VOR gain was assessed at 0.02, 0.08, and 0.32 Hz in quiet (baseline). VOR gain was also assessed at each frequency while a forward running speech stimulus (attentional) or a backward running speech stimulus (nonattentional) was presented binaurally via insert earphones at 42, 62, and 82 dBA. The order of the conditions was randomized across participants. VOR difference gain was calculated as VOR gain in the auditory condition minus baseline VOR gain. To evaluate auditory efferent function, the medial olivocochlear reflex (MOCR) was assayed using transient-evoked otoacoustic emissions (right ear) measured in the presence and absence of broadband noise (left ear). Contralateral acoustic reflex thresholds were also assessed using a broadband noise elicitor. A three-way repeated measures analysis of variance was conducted to evaluate the effect of frequency, intensity level, and speech type on VOR difference gain. Correlations were conducted to determine if difference gain was related to the strength of the MOCR and/or to the acoustic reflex threshold. RESULTS: The analysis of variance indicated that VOR difference gain was not significantly affected by the intensity level or the type of speech stimulus. Correlations indicated VOR difference gain was not significantly related to the strength of the MOCR or the acoustic reflex threshold. CONCLUSIONS: The results were in contrast to previous research examining the effect of auditory stimulation on VOR gain as auditory stimulation did not produce VOR suppression or enhancement for most of the participants. Methodological differences between the studies may explain the discrepant results. The removal of an acoustic target from space to attend to may have prevented suppression or enhancement of the VOR. Findings support the hypothesis that VOR gain may be affected by cortical modulation through directed attention rather than due to activation of efferent pathways to the vestibular nuclei.

Blast-induced brain injury in rats leads to transient vestibulomotor deficits and persistent orofacial pain.

Blast-induced traumatic brain injury (blast-TBI) is associated with vestibulomotor dysfunction, persistent post-traumatic headaches and post-traumatic stress disorder, requiring extensive treatments and reducing quality-of-life. Treatment and prevention of these devastating outcomes require an understanding of their underlying pathophysiology through studies that take advantage of animal models. Here, we report that cranium-directed blast-TBI in rats results in signs of pain that last at least 8 weeks after injury. These occur without significantly elevated behavioural markers of anxiety-like conditions and are not associated with glial up-regulation in sensory thalamic nuclei. These injuries also produce transient vestibulomotor abnormalities that resolve within 3 weeks of injury. Thus, blast-TBI in rats recapitulates aspects of the human condition.

Pharmacological profile of vestibular inhibitory inputs to superior oblique motoneurons.

Vestibulo-ocular reflexes (VOR) are mediated by three-neuronal brainstem pathways that transform semicircular canal and otolith sensory signals into motor commands for the contraction of spatially specific sets of eye muscles. The vestibular excitation and inhibition of extraocular motoneurons underlying this reflex is reciprocally organized and allows coordinated activation of particular eye muscles and concurrent relaxation of their antagonistic counterparts. Here, we demonstrate in isolated preparations of Xenopus laevis tadpoles that the discharge modulation of superior oblique motoneurons during cyclic head motion derives from an alternating excitation and inhibition. The latter component is mediated exclusively by GABA, at variance with the glycinergic inhibitory component in lateral rectus motoneurons. The different pharmacological profile of the inhibition correlates with rhombomere-specific origins of vestibulo-ocular projection neurons and the complementary segmental abundance of GABAergic and glycinergic vestibular neurons. The evolutionary conserved rhombomeric topography of vestibulo-ocular projections makes it likely that a similar pharmacological organization of inhibitory VOR neurons as reported here for anurans is also implemented in mammalian species including humans.

Right-sided dominance of the bilateral vestibular system in the upper brainstem and thalamus.

MRI diffusion tensor imaging tractography was performed on the bilateral vestibular brainstem pathways, which run from the vestibular nuclei via the paramedian and posterolateral thalamic subnuclei to the parieto-insular vestibular cortex. Twenty-one right-handed healthy subjects participated. Quantitative analysis revealed a rope-ladder-like system of vestibular pathways in the brainstem with crossings at pontine and mesencephalic levels. Three structural types of right-left fiber distributions could be delineated: (1) evenly distributed pathways at the lower pontine level from the vestibular nuclei to the pontine crossing, (2) a moderate, pontomesencephalic right-sided lateralization between the pontine and mesencephalic crossings, and (3) a further increase of the right-sided lateralization above the mesencephalic crossing leading to the thalamic vestibular subnuclei. The increasing lateralization along the brainstem was the result of an asymmetric number of pontine and mesencephalic crossing fibers which was higher for left-to-right crossings. The dominance of the right vestibular meso-diencephalic circuitry in right-handers corresponds to the right-hemispheric dominance of the vestibular cortical network. The structural asymmetry apparent in the upper brainstem might be interpreted in relation to the different functions of the vestibular system depending on their anatomical level: a symmetrical sensorimotor reflex control of eye, head, and body mediated by the lower brainstem; a lateralized right-sided upper brainstem-thalamic function as part of the dominant right-sided cortical/subcortical vestibular system that enables a global percept of body motion and orientation in space.

Assessment of vestibulo-ocular function without measuring eye movements.

BACKGROUND: The vestibulo-ocular reflex (VOR) maintains stable gaze during head motion. Deficiencies lead to apparent world motion due to incomplete stabilization of eyes in space. VOR measurement requires specialized apparatus, trained operators, and significant setup time. NEW METHOD: We present a system (VON: vestibulo-ocular nulling) for rapid vestibulo-ocular assessment without measuring eye movements per se. VON uses a head-mounted motion sensor, laptop computer with user input control, and laser target whose position is controlled by the computer. As the head moves, the target is made to move in the same manner with a gain set by the subject. When the subject sets the gain so the target appears stationary in space, it is stationary on the retinas. One can determine from this gain the extent to which the eyes move in space when the head moves, which is the amount by which the VOR is deficient. From this the gain of the compensatory eye movements is derived. RESULTS: VON was compared with conventional video-based VOR measures. Both methods track expected changes in gain over 20min of adaptation to minifying spectacles. VON measures are more consistent across subjects, and pre-adaptation values are closer to compensatory. COMPARISON WITH EXISTING METHOD: VON is a rapid means to assess vestibulo-ocular performance. As a functional perceptual measure, it accounts for gaze-stabilizing contributions that are not apparent in the standard VOR, such as pursuit and perceptual tolerance. CONCLUSIONS: VON assesses functional VOR performance. Future implementations will make VOR assessment widely available to investigators and clinicians.

Vertigo with sudden hearing loss: audio-vestibular characteristics.

Acute vertigo with sudden sensorineural hearing loss (SSNHL) is a rare clinical emergency. Here, we report the audio-vestibular test profiles of 27 subjects who presented with these symptoms. The vestibular test battery consisted of a three-dimensional video head impulse test (vHIT) of semicircular canal function and recording ocular and cervical vestibular-evoked myogenic potentials (oVEMP, cVEMP) to test otolith dysfunction. Unlike vestibular neuritis, where the horizontal and anterior canals with utricular function are more frequently impaired, 74 % of subjects with vertigo and SSNHL demonstrated impairment of the posterior canal gain (0.45 ± 0.20). Only 41 % showed impairment of the horizontal canal gains (0.78 ± 0.27) and 30 % of the anterior canal gains (0.79 ± 0.26), while 38 % of oVEMPs [asymmetry ratio (AR) = 41.0 ± 41.3 %] and 33 % of cVEMPs (AR = 47.3 ± 41.2 %) were significantly asymmetrical. Twenty-three subjects were diagnosed with labyrinthitis/labyrinthine infarction in the absence of evidence for an underlying pathology. Four subjects had a definitive diagnosis [Ramsay Hunt Syndrome, vestibular schwannoma, anterior inferior cerebellar artery (AICA) infarction, and traction injury]. Ischemia involving the common-cochlear or vestibulo-cochlear branches of the labyrinthine artery could be the simplest explanation for vertigo with SSNHL. Audio-vestibular tests did not provide easy separation between ischaemic and non-ischaemic causes of vertigo with SSNHL.

The response of guinea pig primary utricular and saccular irregular neurons to bone-conducted vibration (BCV) and air-conducted sound (ACS).

UNLABELLED: 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.

How imagery changes self-motion perception.

Imagery and perception are thought to be tightly linked, however, little is known about the interaction between imagery and the vestibular sense, in particular, self-motion perception. In this study, the observers were seated in the dark on a motorized chair that could rotate either to the right or to the left. Prior to the physical rotation, observers were asked to imagine themselves rotating leftward or rightward. We found that if the direction of imagined rotation was different to the physical rotation of the chair (incongruent trials), the velocity of the chair needed to be higher for observers to experience themselves rotating relative to when the imagined and the physical rotation matched (on congruent trials). Accordingly, the vividness of imagined rotations was reduced on incongruent relative to congruent trials. Notably, we found that similar effects of imagery were found at the earliest stages of vestibular processing, namely, the onset of the vestibular-ocular reflex was modulated by the congruency between physical and imagined rotations. Together, the results demonstrate that mental imagery influences self-motion perception by exerting top-down influences over the earliest vestibular response and subsequent perceptual decision-making.

The role of cervical and ocular vestibular evoked myogenic potentials in the assessment of patients with vestibular schwannomas.

OBJECTIVES: To investigate the clinical utility of VEMPs in patients suffering from unilateral vestibular schwannoma (VS) and to determine the optimal stimulation parameter (air conducted sound, bone conducted vibration) for evaluating the function of the vestibular nerve. METHODS: Data were obtained in 63 patients with non-operated VS, and 20 patients operated on VS. Vestibular function was assessed by caloric, cervical and ocular VEMP testing. 37/63 patients with conclusive ACS ocular VEMPs responses were studied separately. RESULTS: In the 63 non-operated VS patients, cVEMPs were abnormal in 65.1% of patients in response to AC STB and in 49.2% of patients to AC clicks. In the 37/63 patients with positive responses from the unaffected side, oVEMPs were abnormal in 75.7% of patients with ACS, in 67.6% with AFz and in 56.8% with mastoid BCV stimulation. In 16% of the patients, VEMPs were the only abnormal test (normal caloric and normal hearing). Among the 26 patients who did not show oVEMP responses on either side with ACS, oVEMPs responses could be obtained with AFz (50%) and with mastoid stimulation (89%). CONCLUSIONS: The VEMP test demonstrated significant clinical value as it yielded the only abnormal test results in some patients suffering from a unilateral vestibular schwannoma. For oVEMPs, we suggest that ACS stimulation should be the initial test. In patients who responded to ACS and who had normal responses, BCV was not required. In patients with abnormal responses on the affected side using ACS, BCV at AFz should be used to confirm abnormal function of the superior vestibular nerve. In patients who exhibited no responses on either side to ACS, BCV was the only approach allowing assessment of the function of the superior vestibular nerve. We favor using AFz stimulation first because it is easier to perform in clinical practice than mastoid stimulation.

Loss of α-calcitonin gene-related peptide (αCGRP) reduces the efficacy of the Vestibulo-ocular Reflex (VOR).

The neuroactive peptide calcitonin-gene related peptide (CGRP) is known to act at efferent synapses and their targets in hair cell organs, including the cochlea and lateral line. CGRP is also expressed in vestibular efferent neurons as well as a number of central vestibular neurons. Although CGRP-null (-/-) mice demonstrate a significant reduction in cochlear nerve sound-evoked activity compared with wild-type mice, it is unknown whether and how the loss of CGRP influence vestibular system function. Vestibular function was assessed by quantifying the vestibulo-ocular reflex (VOR) in alert mice. The loss of CGRP in (-/-) mice was associated with a reduction of the VOR gain of ≈50% without a concomitant change in phase. Using immunohistochemistry, we confirmed that, although CGRP staining was absent in the vestibular end-organs of null (-/-) mice, cholinergic staining appeared normal, suggesting that the overall gross development of vestibular efferent innervation was unaltered. We further confirmed that the observed deficit in vestibular function of null (-/-) mice was not the result of nontargeted effects at the level of the extraocular motor neurons and/or their innervation of extraocular muscles. Analysis of the relationship between vestibular quick phase amplitude and peak velocity revealed that extraocular motor function was unchanged, and immunohistochemistry revealed no abnormalities in motor endplates. Together, our findings show that the neurotransmitter CGRP plays a key role in ensuring VOR efficacy.

Neural basis of new clinical vestibular tests: otolithic neural responses to sound and vibration.

Extracellular single neuron recording and labelling studies of primary vestibular afferents in Scarpa's ganglion have shown that guinea-pig otolithic afferents with irregular resting discharge are preferentially activated by 500 Hz bone-conducted vibration (BCV) and many also by 500 Hz air-conducted sound (ACS) at low threshold and high sensitivity. Very few afferent neurons from any semicircular canal are activated by these stimuli and then only at high intensity. Tracing the origin of the activated neurons shows that these sensitive otolithic afferents originate mainly from a specialized region, the striola, of both the utricular and saccular maculae. This same 500 Hz BCV elicits vestibular-dependent eye movements in alert guinea-pigs and in healthy humans. These stimuli evoke myogenic potentials, vestibular-evoked myogenic potentials (VEMPs), which are used to test the function of the utricular and saccular maculae in human patients. Although utricular and saccular afferents can both be activated by BCV and ACS, the differential projection of utricular and saccular afferents to different muscle groups allows for differentiation of the function of these two sensory regions. The basic neural data support the conclusion that in human patients in response to brief 500 Hz BCV delivered to Fz (the midline of the forehead at the hairline), the cervical VEMP indicates predominantly saccular function and the ocular VEMP indicates predominantly utricular function. The neural, anatomical and behavioural evidence underpins clinical tests of otolith function in humans using sound and vibration.

Ocular vestibular evoked myogenic potentials: the effect of head and body tilt in the roll plane.

OBJECTIVE: To explore effects of whole-head/body tilt in the roll plane on ocular-vestibular evoked myogenic potentials (oVEMP). METHODS: Twenty healthy subjects were randomly tilted in an Eply Omniax rotator across a series of eight angles from 0° to 360° (at 45° separations) in the roll plane. At each position, oVEMPs to air-conducted (AC) and bone-conducted (BC) stimulation were recorded from unrectified infra-orbital surface electromyography during upward gaze. oVEMP amplitudes, latencies and amplitude asymmetry were compared across each angle of orientation. RESULTS: Head orientation had a significant effect on oVEMP reflex amplitudes for both AC and BC stimulation (p<0.001). For both stimuli there was a trend for lower amplitudes with increasing angular departure from the upright position. Mean amplitudes decreased by 42.6-56.8% (AC) and 23.2-25.5% (BC) when tilted 180°. Roll-plane tilt had a significant effect on amplitude asymmetry ratios recorded in response to AC stimuli (p<0.001), indicating a trend for lower amplitudes from the dependent (down) ear. Amplitude asymmetry ratios for BC stimuli were unaffected by head and body orientation. CONCLUSIONS: The results confirm an effect of head and body orientation on oVEMP reflexes recorded in response to air- and bone-conducted stimuli. SIGNIFICANCE: The upright position yields an optimal oVEMP response.

Selective effects of head posture on ocular vestibular-evoked myogenic potential (oVEMP) by bone-conducted vibration.

OBJECTIVE: By altering head postures from sitting, supine to head hanging, this study investigated the effects of gravitational force on ocular vestibular-evoked myogenic potential (oVEMP) via either air-conducted sound (ACS) or bone-conducted vibration (BCV) stimuli. METHODS: Twenty healthy volunteers underwent the oVEMP test via ACS or BCV stimuli with the sitting, supine, and head hanging positions on the same day in a randomized order. RESULTS: All subjects had clear BCV oVEMPs in the three head postures. No significant differences existed in terms of mean nI and pI latencies, the nI-pI interval, and asymmetry ratio regardless of various positions. However, the mean nI-pI amplitude with the head hanging position (15.9 ± 6.4 µV) was significantly larger than that with the sitting position (13.8 ± 6.0 µV), but not significantly larger than that with the supine position (14.7 ± 6.1 µV). Nevertheless, such a difference in reflex amplitude does not exist in oVEMPs elicited by ACS stimuli. With the sitting position, mean linear acceleration at the mastoids in response to BCV stimuli was -0.06 ± 0.02, 0.20 ± 0.04 and -0.04 ± 0.02 g along the x-, y-, and z-axis, respectively, which did not differ significantly from those with the head hanging position. CONCLUSION: By altering head postures from sitting to head hanging, gravitational force can exert a selective effect on the reflex amplitude of oVEMPs elicited by BCV stimuli, but not by ACS stimuli. SIGNIFICANCE: Compared to ACS mode, BCV mode can provoke higher response rate, generate earlier and larger waveforms, and be influenced by both dynamic shearing force and static gravitational force to enlarge the reflex amplitude of oVEMPs.

Electrical vestibular stimulation after vestibular deafferentation and in vestibular schwannoma.

BACKGROUND: Vestibular reflexes, evoked by human electrical (galvanic) vestibular stimulation (EVS), are utilized to assess vestibular function and investigate its pathways. Our study aimed to investigate the electrically-evoked vestibulo-ocular reflex (eVOR) output after bilateral and unilateral vestibular deafferentations to determine the characteristics for interpreting unilateral lesions such as vestibular schwannomas. METHODS: EVOR was recorded with dual-search coils as binocular three-dimensional eye movements evoked by bipolar 100 ms-step at EVS intensities of [0.9, 2.5, 5.0, 7.5, 10.0] mA and unipolar 100 ms-step at 5 mA EVS intensity. Five bilateral vestibular deafferented (BVD), 12 unilateral vestibular deafferented (UVD), four unilateral vestibular schwannoma (UVS) patients and 17 healthy subjects were tested with bipolar EVS, and five UVDs with unipolar EVS. RESULTS: After BVD, bipolar EVS elicited no eVOR. After UVD, bipolar EVS of one functioning ear elicited bidirectional, excitatory eVOR to cathodal EVS with 9 ms latency and inhibitory eVOR to anodal EVS, opposite in direction, at half the amplitude with 12 ms latency, exhibiting an excitatory-inhibitory asymmetry. The eVOR patterns from UVS were consistent with responses from UVD confirming the vestibular loss on the lesion side. Unexpectedly, unipolar EVS of the UVD ear, instead of absent response, evoked one-third the bipolar eVOR while unipolar EVS of the functioning ear evoked half the bipolar response. CONCLUSIONS: The bidirectional eVOR evoked by bipolar EVS from UVD with an excitatory-inhibitory asymmetry and the 3 ms latency difference between normal and lesion side may be useful for detecting vestibular lesions such as UVS. We suggest that current spread could account for the small eVOR to 5 mA unipolar EVS of the UVD ear.