Unilateral Loss Of Vestibular Function Research Articles

Amplification of vibration induced nystagmus in patients with peripheral vestibular loss by head tilt.

In patients with unilateral loss of vestibular function (UVL) vibration of the skull leads to a response of the vestibulo-ocular reflex (VOR) called vibration-induced nystagmus (VIN), with slow phases usually directed toward the paretic ear. This response is thought to result from the difference between the neural discharge in semicircular canal afferents from the healthy and the affected labyrinth. The brain interprets this difference as a sustained imbalance in angular (rotational) vestibular tone, which in natural circumstances would only occur when the head was rotating at a constant acceleration. To study this effect, we used a contemporary model of the neural network that combines sensory information about head rotation, translation, and tilt relative to gravity to estimate head orientation and motion. Based on the model we hypothesize that in patients with UVL, the brain may estimate not only a "virtual" rotation from the induced canal imbalance but also a subsequent "virtual" translation from the incorrect computation of the orientation of the head relative to gravity. If this is the case, the pattern of vibration-induced nystagmus will depend on the orientation of the head relative to gravity during the stimulation. This model predicts that this "virtual" translation will alter the baseline VIN elicited with the head upright; augmenting it when the affected ear is down and diminishing it when the affected ear is up. Confirming this hypothesis, we recorded VIN in 3 patients with UVL (due to vestibular neuritis) in upright, right ear-down, and left ear-down positions and each showed the expected pattern. From a practical, clinical view, our results and modeling suggest that positional VIN might reveal a hidden imbalance in angular vestibular tone in patients with UVL, when patients have equivocal signs of a vestibular imbalance, such as a minute amount of spontaneous or vibration-induced nystagmus with the head upright. This research provides insights into the underlying mechanisms of vestibular processing, the analysis of nystagmus in patients with UVL, and guides the design of a new bedside diagnostic test to assess vestibular function in patients with dizziness and imbalance.

Video Ocular Counter-Roll (vOCR): Otolith-Ocular Function and Compensatory Effect of the Neck Following Vestibular Loss.

Assessment of recovery following vestibular loss has been limited by the lack of bedside measures in clinical settings. Here, we used the video ocular counter-roll (vOCR) test to study otolith-ocular function and compensatory effect of neck proprioception in patients at different stages of vestibular loss. Case-control study. Tertiary care center. Fifty-six subjects were recruited including patients with acute (9 ± 2 days [mean ± standard error of mean]), subacute (61 ± 11 days), and chronic (1009 ± 266 days) unilateral loss of vestibular function, as well as a group of healthy controls. We used a video-oculography method based on tracking the iris for vOCR measurement. To examine the effect of neck inputs, vOCR was recorded during two simple tilt maneuvers in all subjects while seated: 30°head-on-body tilt and 30°head-and-body tilt. The vOCR responses evolved at different stages following vestibular loss with improvement of the gains in the chronic stage. The deficit was more pronounced when the whole body was tilted (acute: 0.08 ± 0.01, subacute: 0.11 ± 0.01, chronic: 0.13 ± 0.02, healthy control: 0.18 ± 0.01), and the gain of vOCR improved when the head was tilted on the body (acute: 0.11 ± 0.01, subacute: 0.14 ± 0.01, chronic: 0.13 ± 0.02, healthy control: 0.17 ± 0.01). The time course of vOCR response was affected as well with reduced amplitude and slower response in the acute stage of vestibular loss. The vOCR test can be valuable as a clinical marker to measure vestibular recovery and compensatory effect of neck proprioception in patients at different stages following loss of vestibular function.

Evaluation of the Video Ocular Counter-Roll (vOCR) as a New Clinical Test of Otolith Function in Peripheral Vestibulopathy

Video-oculography (VOG) goggles have been integrated into the assessment of semicircular canal function in patients with vestibular disorders. However, a similar bedside VOG method for testing otolith function is lacking. To evaluate the use of VOG-based measurement of ocular counter-roll (vOCR) as a clinical test of otolith function. A case-control study was conducted to compare vOCR measurement among patients at various stages of unilateral loss of vestibular function with healthy controls. The receiver operating characteristic curve method was used to determine the diagnostic accuracy of the vOCR test in detecting loss of otolith function. Participants were recruited at a tertiary center including the Johns Hopkins outpatient clinic and Johns Hopkins Hospital, Baltimore, Maryland. Participants included 56 individuals with acute (≤4 weeks after surgery), subacute (4 weeks-6 months after surgery), and chronic (>6 months after surgery) unilateral vestibular loss as well as healthy controls. A simple bedside maneuver with en bloc, 30° lateral tilt of the head and trunk was used for vOCR measurement. The study was conducted from February 2, 2017, to March 10, 2019. In each participant vOCR was measured during static tilts of the head and trunk en bloc. The vOCR measurements and diagnostic accuracy of vOCR in detecting patients with loss of vestibular function from healthy controls. Of the 56 participants, 28 (50.0%) were men; mean (SD) age was 53.5 (11.4) years. The mean (SD) time of acute unilateral vestibular loss was 9 (7) days (range, 2-17 days) in the acute group, 61 (39) days (range, 28-172 days) in the subacute group, and 985 (1066) days (range 185-4200 days) in the chronic group. The vOCR test showed reduction on the side of vestibular loss, and the deficit was greater in patients with acute and subacute vestibular loss than in patients with chronic loss and healthy controls (acute vs chronic: -1.81°; 95% CI, -3.45° to -0.17°; acute vs control: -3.18°; 95% CI, -4.83° to -1.54°; subacute vs chronic: -0.63°; 95% CI, -2.28° to 1.01°; subacute vs control: -2.01°; 95% CI, -3.65° to -0.36°; acute vs subacute: -1.17°; 95% CI, -2.88° to 0.52°; and chronic vs control: -1.37°; 95% CI, -2.96° to 0.21°). The asymmetry in vOCR between the side of vestibular loss and healthy side was significantly higher in patients with acute vs chronic loss (0.28; 95% CI, 0.06-0.51). Overall, the performance of the vOCR test in discriminating between patients with vestibular loss and healthy controls was 0.83 (area under the receiver operating characteristic curve). The best vOCR threshold to detect vestibular loss at the 30° tilt was 4.5°, with a sensitivity of 80% (95% CI, 0.62%-0.88%) and specificity of 82% (95% CI, 0.57%-1.00%). The findings of this case-control study suggest that the vOCR test can be performed with a simple bedside maneuver and may be used to detect or track loss of otolith function.

High-risk Allele for Herpes Labialis Severity at the IFNL3/4 Locus is Associated With Vestibular Neuritis.

Objective: Vestibular neuritis (VN) is a peripheral vestibular disorder leading to a sudden loss of unilateral vestibular function. Although the underlying etiological mechanisms for disease development are not yet known, there is evidence that a latent infection with herpes simplex virus type 1 (HSV-1) might be involved. The polymorphism rs12979860 has been associated with the severity of recurrent herpes labialis and hepatitis C virus (HCV) clearance and treatment outcome and is located within the first intron of the IFNL4 gene on chromosome 19.q13.2. This case control study was conducted to evaluate the association of rs12979860 with VN occurrence.Methods: DNA was extracted from EDTA blood of 151 VN patients and 1,775 healthy controls. Genotyping of rs12979860 was performed using iPLEX and MassARRAY Matrix Assisted Laser Desorption Ionization—Time of Flight (MALDI-TOF) mass spectrometry. For association analyses, an additive, dominant and recessive logistic regression model was calculated, using age and sex as covariates.Results: A significant association of rs12979860 with VN was obtained for the additive [OR = 1.51 (1.18–1.92); p = 9.23 × 10−4] and dominant models [OR = 2.15 (1.48–3.13); p = 5.86 × 10−5], with the T allele being more frequent in the VN group.Conclusion: By detecting a significant association of the rs12979860-T risk allele for herpes labialis severity with susceptibility to VN, this study gives further indirect evidence for an involvement of HSV-1 in VN pathology, thereby strengthening the virus hypothesis.

Clinical significance of bedside dynamic visual acuity test

Objective: Dynamic visual acuity (DVA) is defined as the visual acuity when there are relative movements between subjects and visual targets. The purpose of this study was to discuss the correlation between bedside DVA test and other examinations of vestibular function, and to assess the value of DVA test for clinical diagnosis. Methods: Retrospective analysis of 323 cases with peripheral vestibular disorder, and analyzing the correlation between bedside DVA results and caloric test were performed. Results: Out of these 323 cases, 113 cases showed positive results of DVA.Among these 113 cases with positive DVA test, 109 cases were bilateral or unilateral vestibular function loss according to the results of caloric test or VEMP. The disease with the highest positive rate of DVA was bilateral vestibulopathy(BVP), followed by vestibular neuritis (VN) and profound sudden sensorineural hearing loss (pSSNHL). Conclusions: Bedside DVA is effective to determine the cases with BVP and severe unilateral vestibular function loss.

An fMRI study of visuo-vestibular interactions following vestibular neuritis.

Vestibular neuritis (VN) is characterised by acute vertigo due to a sudden loss of unilateral vestibular function. A considerable proportion of VN patients proceed to develop chronic symptoms of dizziness, including visually induced dizziness, specifically during head turns. Here we investigated whether the development of such poor clinical outcomes following VN, is associated with abnormal visuo-vestibular cortical processing. Accordingly, we applied functional magnetic resonance imaging to assess brain responses of chronic VN patients and compared these to controls during both congruent (co-directional) and incongruent (opposite directions) visuo-vestibular stimulation (i.e. emulating situations that provoke symptoms in patients). We observed a focal significant difference in BOLD signal in the primary visual cortex V1 between patients and controls in the congruent condition (small volume corrected level of p < .05 FWE). Importantly, this reduced BOLD signal in V1 was negatively correlated with functional status measured with validated clinical questionnaires. Our findings suggest that central compensation and in turn clinical outcomes in VN are partly mediated by adaptive mechanisms associated with the early visual cortex.

Chapter 15 - Acute unilateral loss of vestibular function

Sudden unilateral loss of vestibular function is the most severe condition that can occur in the vestibular system. The clinical syndrome is caused by the physiologic properties of the vestibulo-ocular reflex (VOR) arc. In the normal situation, the two peripheral vestibular end organs are connected to a functional unit in coplanar pairs of semicircular canals working in a push-pull mode. "Push-pull" mode means that, when one side is excited, the other side is inhibited, and vice versa due to two mechanisms. First, first-order vestibular afferents are bipolar cells. They have a tonic firing rate that is modulated up or down depending on the direction of rotation. Second, via inhibitory neural connections of second-order vestibular neurons between the vestibular nuclei (vestibular commissural system), the excited side inhibits further the contralateral side. The neural signals are encoded as the difference of the change in firing rate of the vestibular neurons modulating the tonic firing rate on both sides in opposite directions (one side up, the contralateral side down). When the head is not moving, the two peripheral vestibular end organs generate a resting firing rate, which is exactly equal on both sides. When the head is rotated, for example, to the right, the right-sided first-order vestibular afferents increase their discharge rate and the left-sided ones decrease their firing rate. This leads to increase in firing rate of also the type I second-order vestibular neurons in the vestibular nuclei, which synapse with inhibitory type II neurons on the contralateral side, further decreasing the firing rate in the second-order vestibular neurons in the contralateral vestibular nucleus. When the direction of head rotation is reversed, the behavior of the type I neurons on the two sides of the head is reversed. The same relation exists between the coplanar vertical canal afferents on the two sides of the head. When there is unilateral damage to the end organ or the vestibular nerve, the resting firing frequency is drastically reduced or even silenced on the lesioned side, thereby creating a tonic imbalance between the normal resting firing on the healthy side and the lesioned side. This tonic imbalance mimics a permanent rotation toward the healthy side (the side with the higher firing rate), resulting, via the VOR, in a slow-phase drift of the eyes toward the side of the lesion, interrupted by rapid quick-phase resetting eye movements toward the healthy side. This leads to the typical vestibular spontaneous horizontal-torsional nystagmus together with rotational vertigo and postural imbalance, with the tendency to fall toward the lesioned side. The tonic imbalance with the hallmark of spontaneous nystagmus usually recovers within days to weeks after the lesion due to the central restoration of tonic activity on the lesioned side. The dynamic changes, however, might be long-lasting when the peripheral sensors do not recover their function. This causes asymmetric VOR responses, with weaker responses when the head is rotated rapidly toward the lesioned side, leading to transient oscillopsia.

Ocular vestibular-evoked myogenic potentials (oVEMPs) in response to bone-conducted vertex vibration

ObjectiveTo investigate low-frequency vertex bone-conducted (BC) vibration for evoking ocular vestibular myogenic potentials (oVEMPs) and its ability to discriminate between lesioned and healthy ears. MethodsoVEMPs were analysed in response to 125-Hz single cycle vertex BC vibration in healthy subjects (n=50) and in patients with severe unilateral vestibular loss (n=10). Both positive and negative initial stimulus motions were used. ResultsIn most healthy subjects, vertex BC vibration oVEMPs was successfully and symmetrically evoked from both ears. The response was dependent on the direction of the stimulus motion. The latency was shorter with negative initial stimulus motion; however, a positive initial stimulus motion generated somewhat larger amplitudes. Furthermore, there was no significant response from lesioned ears, whereas oVEMPs from the patients’ healthy ears were similar to the responses in healthy subjects. ConclusionThe oVEMP low-frequency BC response was dependent on the direction of the initial stimulus motion. Testing oVEMPs in response to low-frequency vertex vibration can discriminate patients with unilateral vestibular function loss from healthy controls. SignificanceLow-frequency vertex BC vibration oVEMPs should be considered a possible clinical screening test to evaluate vestibular function.

Is vestibular neuritis an immune related vestibular neuropathy inducing vertigo?

Objectives. To review the current knowledge of the aetiology of vestibular neuritis including viral infections, vascular occlusion, and immunomediated mechanisms and to discuss the pathogenesis with relevance to pharmacotherapy. Systematic Review Methodology. Relevant publications on the aetiology and treatment of vestibular neuritis from 1909 to 2013 were analysed. Results and Conclusions. Vestibular neuritis is the second most common cause of peripheral vestibular vertigo and is due to a sudden unilateral loss of vestibular function. Vestibular neuronitis is a disorder thought to represent the vestibular-nerve equivalent of sudden sensorineural hearing loss. Histopathological studies of patients who died from unrelated clinical problems have demonstrated degeneration of the superior vestibular nerve. The characteristic signs and symptoms include sudden and prolonged vertigo, the absence of auditory symptoms, and the absence of other neurological symptoms. The aetiology and pathogenesis of the condition remain unknown. Proposed theories of causation include viral infections, vascular occlusion, and immunomediated mechanisms. The management of vestibular neuritis involves symptomatic treatment with antivertiginous drugs, causal treatment with corticosteroids, and physical therapy. Antiviral agents did not improve the outcomes.

Vestibular Neuritis

Vestibular neuritis is the most common cause of acute spontaneous vertigo. Vestibular neuritis is ascribed to acute unilateral loss of vestibular function, probably due to reactivation of herpes simplex virus in the vestibular ganglia. The diagnostic hallmarks of vestibular neuritis are spontaneous horizontal-torsional nystagmus beating away from the lesion side, abnormal head impulse test for the involved semicircular canals, ipsilesional caloric paresis, decreased responses of vestibular-evoked myogenic potentials during stimulation of the affected ear, and unsteadiness with a falling tendency toward the lesion side. Vestibular neuritis preferentially involves the superior vestibular labyrinth and its afferents. Accordingly, the function of the posterior semicircular canal and saccule, which constitute the inferior vestibular labyrinth, is mostly spared in vestibular neuritis. However, because the rare subtype of inferior vestibular neuritis lacks the typical features of vestibular neuritis, it may be misdiagnosed as a central vestibular disorder. Even in the patient with the typical pattern of spontaneous nystagmus observed in vestibular neuritis, brain imaging is indicated when the patient has unprecedented headache, negative head impulse test, severe unsteadiness, or no recovery within 1 to 2 days. Symptomatic medication is indicated only during the acute phase to relieve the vertigo and nausea/vomiting. Vestibular rehabilitation hastens the recovery. The efficacy of topical and systemic steroids requires further validation.

Ocular vestibular evoked myogenic potentials: Skull taps can cause a stimulus direction dependent double-peak

Objective To explore the mechanisms for skull tap induced ocular vestibular evoked myogenic potentials (oVEMP). Methods An electro-mechanical “skull tapper” was used to test oVEMP in response to four different stimulus sites (forehead, occiput and above each ear) in healthy subjects ( n = 20) and in patients with unilateral loss of vestibular function ( n = 10). Results In normals, the oVEMP in response to forehead taps and the contra-lateral oVEMP to taps above the ears were similar. These responses had typical oVEMP features, i.e. a short-latency negative peak (n10) followed by a positive peak (p15). In contrast, the ipsi-lateral oVEMP to the laterally directed skull taps, as well as the oVEMP to occiput taps, had an initial double negative peak (n10 + n10b). In patients with unilateral loss of vestibular function, the crossed responses from the functioning labyrinth were very similar to the corresponding oVEMP in normals. Conclusions The present data support a theory that skull tapping may cause both a response that is more stimulus direction dependent and one that is less so. Significance Whereas the stimulus direction dependent occurrence of the negative double-peak might reveal the functional status of one part of the labyrinth, the rather stimulus direction-independent response might reveal the functional status of other parts.

Recovery of Vestibulogastrointestinal Symptoms During Vestibular Compensation After Unilateral Labyrinthectomy in Rats

The loss of unilateral vestibular function causes vestibulogastrointestinal symptoms that include nausea and vomiting. However, the temporal changes occurring on vestibular compensation are unclear. Thus, the temporal changes and the role of the cerebellum in the recovery of vestibulogastrointestinal symptoms after unilateral labyrinthectomy (UL) were investigated in this study. Vestibulogastrointestinal symptoms were evaluated for intestinal transit and geometric center, whereas vestibulo-ocular symptoms were represented by spontaneous nystagmus. Expression of the c-Fos protein was observed in the vestibular nuclei. These were measured at 30 minutes and at 2, 6, and 24 hours after UL in rats. Intestinal transit was 66.3% +/- 7.6% in the control animals but significantly decreased to 40.7% +/- 7.8%, 46.3% +/- 6.3%, and 48.6% +/- 10.8% at 30 minutes (p < 0.01), 2 hours (p < 0.01), and 6 hours (p < 0.05) after UL, respectively. The intestinal transit showed a recovery to control levels 24 hours after UL. The geometric center was 5.6 +/- 0.4 in control animals but significantly decreased to 2.1 +/- 0.4, 2.9 +/- 0.3, and 4.0 +/- 0.3 at 30 minutes, 2 hours, and 6 hours after UL, respectively (p < 0.01). Recovery of the geometric center to control levels, 24 hours after UL, was reported. Uvulonodullectomy significantly decreased the intestinal transit and geometric center for 24 hours after surgery (p < 0.01). Moreover, UL in uvulonodullectomized animals significantly decreased the intestinal transit and geometric center for 24 hours after surgery (p < 0.01). Pretreatment of the UL animals with MK-801 significantly increased the geometric center 30 minutes after surgery (p < 0.01). Unilateral labyrinthectomy produced spontaneous nystagmus, 28.9 +/- 1.5, 23.3 +/- 1.4, 17.5 +/- 1.5, and 9.2 +/- 0.9 beats per 10 seconds at 30 minutes and at 2, 6, and 24 hours after UL, respectively. Expression of the c-Fos protein was significantly increased in the medial vestibular nuclei and inferior vestibular nuclei at 1, 2, and 6 hours after UL, and the expression was significantly decreased in animals that were pretreated with MK-801 (p < 0.01). These results suggest that the recovery of vestibulogastrointestinal symptoms is faster than that of vestibulo-ocular symptoms and that the cerebellum and glutamate have an important role to play in the recovery of symptoms after UL.

Vestibular evoked myogenic potentials in response to lateral skull taps are dependent on two different mechanisms

To explore the mechanisms for skull tap induced vestibular evoked myogenic potentials (VEMP). The muscular responses were recorded over both sternocleidomastoid (SCM) muscles using skin electrodes. A skull tapper which provided a constant stimulus intensity was used to test cervical vestibular evoked myogenic potentials (VEMP) in response to lateral skull taps in healthy subjects (n=10) and in patients with severe unilateral loss of vestibular function (n=10). Skull taps applied approximately 2 cm above the outer ear canal caused highly reproducible VEMP. There were differences in VEMP in both normals and patients depending on side of tapping. In normals, there was a positive-negative ("normal") VEMP on the side contra-lateral to the skull tapping, but no significant VEMP ipsi-laterally. In patients, skull taps above the lesioned ear caused a contra-lateral positive-negative VEMP (as it did in the normals), in addition there was an ipsi-lateral negative-positive ("inverted") VEMP. When skull taps were presented above the healthy ear there was only a small contra-lateral positive-negative VEMP but, similar to the normals, no VEMP ipsi-laterally. The present data, in conjunction with earlier findings, support a theory that skull-tap VEMP responses are mediated by two different mechanisms. It is suggested that skull tapping causes both a purely ipsi-lateral stimulus side independent SCM response and a bilateral and of opposite polarity SCM response that is stimulus side dependent. Possibly, the skull tap induced VEMP responses are the sum of a stimulation of two species of vestibular receptors, one excited by vibration (which is rather stimulus site independent) and one excited by translation (which is more stimulus site dependent). Skull-tap VEMP probably have two different mechanisms. Separation of the two components might reveal the status of different labyrinthine functions.

Skull tap induced vestibular evoked myogenic potentials: An ipsilateral vibration response and a bilateral head acceleration response?

Objective To explore the mechanisms for skull tap induced vestibular evoked myogenic potentials (VEMP). Methods An electro-mechanical “skull tapper” (that provided a constant stimulus intensity) was used to test the effects of different midline stimulus sites/directions in healthy subjects ( n = 10) and in patients with severe unilateral loss of vestibular function ( n = 8). Results The standardized midline skull taps caused highly reproducible VEMP. There were highly significant differences in amplitude and latency in both normals and patients depending on site/direction of tapping (suggesting a stimulus direction dependency). Occiput skull taps caused, in comparisons to forehead and vertex taps, larger amplitude VEMP with more pronounced differences between the lesioned and the healthy side in the patients. Conclusions The present data, in conjunction with earlier findings, support a theory that skull tap VEMP are mediated by two different mechanisms. It is suggested that skull tapping causes both skull vibration and head acceleration. Further, the VEMP would be the sum of the direction-independent vibration-induced response (from the sound-sensitive part of the saccule) and the direction-dependent head acceleration response (from other parts of the labyrinth). Significance Skull tap VEMP, as a diagnostic test, is not equivalent to sound-induced VEMP.

Abnormal Eye Movements Associated with Unilateral Loss of Vestibular Function

Acute unilateral loss of peripheral vestibular function causes spontaneous nystagmus. Initially, nystagmus is present during visual fixation.

Response to Galvanic Vestibular Stimulation in Patients with Unilateral Vestibular Loss

This study sought to characterize various responses to galvanic vestibular stimulation (GVS) by comparing GVS-induced eye movements in healthy subjects and patients with vestibular function loss. The study also aimed to estimate the clinical significance of GVS tests. Finally, an effort was made to localize the primary excitation site of stimulation in the vestibular system. Three parameters of response to GVS, spontaneous nystagmus, galvanic stimulating nystagmus (GSN), and postgalvanic stimulating nystagmus (PGSN), were evaluated in 20 normal subjects and 14 patients with complete unilateral vestibular function loss resulting from labyrinthectomy or vestibular neurectomy using a three-dimensional video-electronystagmography technique. In normal subjects, GSN was detected in all subjects and was directed toward the negative electrode. PGSN was also detected but was directed toward the opposite electrode. When the negative electrode was attached to the intact side in unilateral vestibular loss subjects, GSN was always directed toward the negative electrode and PGSN was never observed. When the negative electrode was attached to the lesion side, however, GSN was detected in only one case, and PGSN was observed and directed to the intact side in 13 patients. The response to GVS in vestibular loss patients differed from that in normal subjects, which suggests that GVS could be useful for estimating the extent of vestibular function loss. The fact that the patterns of GVS response differed so significantly suggests that the primary site of excitation is not central but is instead the peripheral vestibular organ.

Episodisch auftretendes Schwindelgef�hl

While an acute loss of unilateral vestibular function (for example in case of neuritis vestibularis or temporal bone fracture) leads to long-term vertigo, this paper deals with the phenomenon of episodic vertigo (duration: seconds up to hours).Both peripheral-vestibular and central disturbances can be responsible for this symptom. The aim of this paper is to present otological and neurological diseases which can lead to episodic attacks of vertigo.

August 12 Highlights

Murofushi et al. studied the site of lesions in “vestibular neuritis” using galvanic vestibular evoked myogenic potentials. Among the 11 patients diagnosed with vestibular neuritis, eight showed a neuritis pattern whereas three showed a labyrinthitis pattern. see page 417 Commentary by Michael Halmagyi and James Colebatch It is over a decade since Neurology published the first report of a short latency vestibulo-collic reflex we called the vestibular evoked myogenic potential (VEMP), recordable from anterior neck muscles, specifically the sternomastoid, in response to loud clicks.1 Since then, the VEMP has been studied in vestibular laboratories worldwide and has been shown to have application in the assessment of a range of vestibular disorders, including superior semicircular canal dehiscence, Meniere disease, multiple sclerosis, brainstem infarction, vestibular neuritis, and vestibular schwannomas.2 The definition of this vestibulo-collic reflex pathway has allowed the development of other novel methods of vestibular activation such as head tapping, mastoid bone vibration, and the technique used in this article, short duration galvanic (DC) currents. A galvanic current applied to the mastoid directly activates vestibular nerve endings. Murofushi and coworkers have produced much of the new clinical work in the last 5 years on VEMP. They previously reported that galvanic VEMP can separate vestibular nerve (retro- labyrinthine) lesions from vestibular end-organ (labyrinthine) lesions. They now turn their attention to defining the level of the pathology in vestibular neuritis. Sudden, isolated, total or subtotal, unilateral loss of vestibular function can occur during viral infections such as mumps and herpes zoster and perhaps herpes simplex. As a result, this form of unilateral loss of vestibular function has, like sudden unilateral loss of facial nerve function, …

Vestibular evoked myogenic potentials in response to laterally directed skull taps

In recent years it has been demonstrated that loud clicks generate short latency vestibular evoked myogenic potentials (VEMP). It has also been demonstrated that midline forehead skull tap stimulation evokes similar VEMP. In the present study, the influence of skull tap direction on VEMP was studied in 13 normal subjects and in five patients with unilateral vestibular loss. Gentle skull taps were delivered manually above each ear on the side of the skull. The muscular responses were recorded over both sternocleidomastoid muscles using skin electrodes. Among the normals, laterally directed skull taps evoked "coordinated contraction-relaxation responses", i.e. skull taps on one side evoked a negative-positive "inverted" VEMP on that side and a positive-negative "normal" VEMP on the other side. Among patients with unilateral vestibular function loss, skull taps above the lesioned ear evoked similar coordinated contraction-relaxation responses. However, skull taps above the healthy ear did not evoke that type of response. These findings suggest that laterally directed skull taps activate mainly the contralateral labyrinth.

Head-shaking Nystagmus (HSN): the Theoretical Explanation and the Experimental Proof

Head-shaking nystagmus (HSN) is induced by oscillating the head at high frequency in the horizontal plane. This test is used in the clinic to detect the presence of a unilateral loss of vestibular function. HSN has been described as monophasic with fast-phase direction towards either side, or biphasic with the direction of fast phases reversing after a few seconds. Loss of vestibular function amplifies existing non-linearities in the vestibular system, so that imposed sinusoids can induce biases which are the source of HSN. Fifty-one patients suffering from loss of peripheral vestibular function (43 partial, 11 total unilateral tests) were exposed to whole-body sinusoidal stimulation, with increasing head velocities (90-220°/s) at 1/6Hz, to explore the consistency of per-rotatory induced biases. A bias was induced in all cases, but it wandered on either side, healthy or pathologic, unless test head velocities were larger than ~180°/s. Given this condition, the slow-phase bias was located towards the pathologic side for all patients with significant bias (>5°/s). These observations demonstrate that the sign and amplitude of the bias is variable and is not correlated with the lesioned side, unless high head velocities are imposed. This explains why the direction of the initial phase of HSN in the clinic seems so labile. Subsequent monophasic or biphasic characteristics of HSN are simply the reflection of interactions between two main time constants associated with ?velocity storage? and ?gaze holding? in the vestibular central processes.