Skull Vibration-induced Nystagmus Research Articles

Vestibular Assessment with the vHIT and Skull Vibration-Induced Nystagmus Test in Patients with Nonprogressive Vestibular Schwannoma.

Background: Our primary objective was to monitor nonprogressive unilateral vestibular schwannomas (VSs) to assess the efficiency of rapid bedside examinations, such as the video head impulse test (vHIT) and skull vibration-induced nystagmus test (SVINT), in identifying vestibular damage. Methods: An observational study was conducted from March 2021 to March 2022 on all adult patients (>18 years old) with a confirmed nonprogressive VS (no active treatment). The SVINT (using a 100 Hz vibrator with two (SVINT2) or three (SVINT3) stimulation locations) and vHIT (for the six semicircular canals (SCCs)) were performed on all patients. The asymmetry of function between the vestibules was considered significant when the gain asymmetry was greater than 0.1. Rapid and repeatable assessment of VSs using two- and three-stimulation SVINT plus vHIT was performed to quantify intervestibular asymmetry. Results: SVINT3 and SVINT2 triggered VIN in 40% (24/60) and 65% (39/60) of patients, respectively. There was significant asymmetry in the vestibulo-ocular reflex (VOR), as shown by a VS-side gain < healthy-side gain in 58% (35/60) of the patients. Among the patients with significant gain asymmetry between the two vestibules according to the vHIT (VS-side gain < healthy-side gain), the proportion of patients expressing vestibular symptomatology was significantly greater than that of patients without any symptoms [67% (29/43) vs. 35% (6/17), respectively; p = 0.047]. Conclusions: The SVINT2 can be combined with the vHIT to form an interesting screening tool for revealing vestibular asymmetry. This work revealed the superiority of mastoid stimulation over vertex stimulation for SVINT in patients with unilateral vestibular loss.

Skull Vibration-Induced Nystagmus in Superior Semicircular Canal Dehiscence: A New Insight into Vestibular Exploration-A Review.

The third window syndrome, often associated with the Tullio phenomenon, is currently most often observed in patients with a superior semicircular-canal dehiscence (SCD) but is not specific to this pathology. Clinical and vestibular tests suggestive of this pathology are not always concomitantly observed and have been recently complemented by the skull-vibration-induced nystagmus test, which constitutes a bone-conducted Tullio phenomenon (BCTP). The aim of this work was to collect from the literature the insights given by this bedside test performed with bone-conducted stimulations in SCD. The PRISMA guidelines were used, and 10 publications were included and analyzed. Skull vibration-induced nystagmus (SVIN), as observed in 55 to 100% of SCD patients, usually signals SCD with greater sensitivity than the air-conducted Tullio phenomenon (ACTP) or the Hennebert sign. The SVIN direction when the test is performed on the vertex location at 100 Hz is most often ipsilaterally beating in 82% of cases for the horizontal and torsional components and down-beating for the vertical component. Vertex stimulations are more efficient than mastoid stimulations at 100 Hz but are equivalent at higher frequencies. SVIN efficiency may depend on stimulus location, order, and duration. In SCD, SVIN frequency sensitivity is extended toward high frequencies, with around 400 Hz being optimal. SVIN direction may depend in 25% on stimulus frequency and in 50% on stimulus location. Mastoid stimulations show frequently diverging results following the side of stimulation. An after-nystagmus observed in 25% of cases can be interpreted in light of recent physiological data showing two modes of activation: (1) cycle-by-cycle phase-locked activation of action potentials in SCC afferents with irregular resting discharge; (2) cupula deflection by fluid streaming caused by the travelling waves of fluid displacement initiated by sound or vibration at the point of the dehiscence. The SVIN direction and intensity may result from these two mechanisms' competition. This instability explains the SVIN variability following stimulus location and frequency observed in some patients but also discrepancies between investigators. SVIN is a recent useful insight among other bedside examination tests for the diagnosis of SCD in clinical practice.

USE OF SKULL VIBRATION-INDUCED NYSTAGMUS DURING FOLLOW-UP IN MÉNIÈRE.

Ménière's disease (MD) is an idiopathic disorder that affects patients' hearing and the inner ear balance. Intratympanic gentamicin (ITG) is also considered an effective treatment for uncontrolled MD characterized by persistent vertigo attacks despite therapy. The video head impulse test (vHIT) and the skull vibration-induced nystagmus (SVIN) are both validated test to assess the vestibular function. A progressive linear relationship has also been described between the slow-phase velocity (SPV) of SVIN with a skull vibrator at 100 Hz and the gain difference (healthy ear/affected ear) measured in vHIT. The objective of this study was to determine whether the SPV of the SVIN was correlated with the restoration of vestibular function after ITG and, consequently, whether the SVIN can predict the appearance of new vertigo attacks in patients with MD treated with ITG. A prospective longitudinal case-control study was conducted. We recorded several variables after ITG and during the follow-up and statistical analyses were performed. Two groups were compared, those who presented vertigo attacks 6 months after ITG and those who did not. Our sample included 88 patients with definite MD who were treated with ITG. Among the 18 patients who experienced vertigo attacks again, 15 showed recovery of the gain of the affected ear, while all 18 showed a reduction in the SPV of the SVIN. SPV of SVIN may have more sensitivity than vHIT for detecting recovery of vestibular function after intratympanic gentamicin (ITG) administration. To the best of our knowledge, this is the first study to describe the association between decreased SPV and the probability of vertigo attacks in patients with MD treated with ITG.

A bone-conducted Tullio phenomenon-A bridge to understand skull vibration induced nystagmus in superior canal dehiscence.

Nystagmus produced in response to air-conducted sound (ACS) stimulation-the Tullio phenomenon-is well known in patients with a semicircular canal (SCC) dehiscence (SCD). Here we consider the evidence that bone-conducted vibration (BCV) is also an effective stimulus for generating the Tullio phenomenon. We relate the clinical evidence based on clinical data extracted from literature to the recent evidence about the physical mechanism by which BCV may cause this nystagmus and the neural evidence confirming the likely mechanism. The hypothetical physical mechanism by which BCV activates SCC afferent neurons in SCD patients is that traveling waves are generated in the endolymph, initiated at the site of the dehiscence. We contend that the nystagmus and symptoms observed after cranial BCV in SCD patients is a variant of Skull Vibration Induced Nystagmus (SVIN) used to identify unilateral vestibular loss (uVL) with the major difference being that in uVL the nystagmus beats away from the affected ear whereas in Tullio to BCV the nystagmus beats usually toward the affected ear with the SCD. We suggest that the cause of this difference is a cycle-by-cycle activation of SCC afferents from the remaining ear, which are not canceled centrally by simultaneous afferent input from the opposite ear, because of its reduced or absent function in uVL. In the Tullio phenomenon, this cycle-by-cycle neural activation is complemented by fluid streaming and thus cupula deflection caused by the repeated compression of each cycle of the stimuli. In this way, the Tullio phenomenon to BCV is a version of skull vibration-induced nystagmus.

A Review of Neural Data and Modelling to Explain How a Semicircular Canal Dehiscence (SCD) Causes Enhanced VEMPs, Skull Vibration Induced Nystagmus (SVIN), and the Tullio Phenomenon

Angular acceleration stimulation of a semicircular canal causes an increased firing rate in primary canal afferent neurons that result in nystagmus in healthy adult animals. However, increased firing rate in canal afferent neurons can also be caused by sound or vibration in patients after a semicircular canal dehiscence, and so these unusual stimuli will also cause nystagmus. The recent data and model by Iversen and Rabbitt show that sound or vibration may increase firing rate either by neural activation locked to the individual cycles of the stimulus or by slow changes in firing rate due to fluid pumping (“acoustic streaming”), which causes cupula deflection. Both mechanisms will act to increase the primary afferent firing rate and so trigger nystagmus. The primary afferent data in guinea pigs indicate that in some situations, these two mechanisms may oppose each other. This review has shown how these three clinical phenomena—skull vibration-induced nystagmus, enhanced vestibular evoked myogenic potentials, and the Tullio phenomenon—have a common tie: they are caused by the new response of semicircular canal afferent neurons to sound and vibration after a semicircular canal dehiscence.

Skull Vibration-Induced Nystagmus and High Frequency Ocular Vestibular-Evoked Myogenic Potentials in Superior Canal Dehiscence.

Background: Although diagnostic criteria have been established for superior canal dehiscence syndrome, cases in which the diagnosis is not easy are frequent. On those occasions, some tests such as vibration-induced nystagmus or vestibular-evoked myogenic potentials can offer invaluable help due to their high sensitivity and specificity. Methods: We studied 30 patients showing superior canal dehiscence or “near-dehiscence” in a CT scan. Skull vibration-induced nystagmus and high frequency ocular vestibular-evoked myogenic potentials are performed in each patient. The aim of the study is to determine how useful both tests are for detection of superior canal dehiscence or near-dehiscence. Results: Of the 60 temporal bones studied, no dehiscence was the result in 22, near-dehiscence in 17 and a definite finding in 21. In 10/30 patients, there was no SVIN (Skull vibration induced nystagmus) during otoneurological testing, while in 6/30, induced nystagmus was mainly horizontal, and in 14/30 there was vertical up-beating. All patients had a positive oVEMP (Ocular vestibular evoked myiogenic potentials) at 0.5 kHz in both ears and the HFoVEMP (High frequency ocular vestibular evoked myiogenic potentials) response was positive in 25/60 (41.6%) of the ears studied and in 19/30 of the patients evaluated (in 6 it was positive in both ears). Up-beat SVIN will point to a SCD (Superior Canal Dehiscence) mainly when HFoVEMP are present, and when this is negative there is a high probability that it is not a SCD. Conclusions: When SVIN and HFoVEMP results are added (or combined), they not only improve the possibilities of detecting SCD, but also the affected side.

Is Skull Vibration-Induced Nystagmus Useful in Vestibular Neuritis Follow Up?

The aim of this study was to evaluate the vestibulo-ocular reflex (VOR) gain and the saccade regrouping pattern PR score of the Video Head Impulse Test (vHIT) and its relationship with the slow-phase velocity (SPV) of skull vibration-induced nystagmus (SVIN) in recovery after a unilateral vestibular loss (UVL). A total of 36 patients suffering from vestibular neuritis (VN) were recruited and followed up for twelve months. In every visit, horizontal vHIT and an SVIN were performed, as well as VOR gain; PR score and the SPV of SVIN were measured. We observed a positive association between the VOR gain difference and the SPV of SVIN over time (probability greater than 0.86). Additionally, we obtained a positive association between the SPV of SVIN and the PR score in successive visits (odds ratio (OR) = −0.048; CI [0.898, 1.01]), with a probability of 0.95. Our results confirm that SPV of SVIN; VOR gain difference; and PR score decrease over time after a UVL. Both tests are useful in the follow-up of VN, as they could reflect its clinical compensation or partial recovery.

Fifty Years of Development of the Skull Vibration-Induced Nystagmus Test.

This review enumerates most of the studies on the Skull Vibration-Induced Nystagmus Test (SVINT) in the past 50 years from different research groups around the world. It is an attempt to demonstrate the evolution of this test and its increased interest around the globe. It explores clinical studies and animal studies, both permitting a better understanding of the importance of SVINT and its pathophysiology.

Skull Vibration Induced Nystagmus Test: Correlations with Semicircular Canal and Otolith Asymmetries.

Background: To establish in patients with peripheral vestibular disorders relations between skull vibration-induced nystagmus (SVIN) different components (horizontal, vertical, torsional) and the results of different structurally related vestibular tests. Methods: SVIN test, canal vestibular test (CVT: caloric test + video head impulse test: VHIT), otolithic vestibular test (OVT: ocular vestibular evoked myogenic potential oVEMP + cervical vestibular evoked myogenic potential cVEMP) performed on the same day in 52 patients with peripheral vestibular diseases (age < 65 years), and 11 control patients were analyzed. Mixed effects logistic regression analysis was performed to assert whether the presence of nystagmus in SVIN (3D analysis) have an association with the presence of peripheral vestibular dysfunction measured by vestibular explorations (CVT or OVT). Results: We obtained different groups: Group-Co (control group), Group-VNT (dizzy patients with no vestibular tests alterations), Group-O (OVT alterations only), Group-C (CVT alterations only), Group-M (mixed alterations). SVIN-SPV horizontal component was significantly higher in Group-M than in the other groups (p = 0.005) and correlated with alterations of lateral-VHIT (p < 0.001), caloric test (p = 0.002) and oVEMP (p = 0.006). SVIN-SPV vertical component was correlated with the anterior-VHIT and oVEMP alterations (p = 0.007; p = 0.017, respectively). SVIN-SPV torsional component was correlated with the anterior-VHIT positivity (p = 0.017). SVIN was the only positive test for 10% of patients (83% of Group-VNT). Conclusion: SVIN-SPV analysis in dizzy patients shows significant correlation to both CVT and OVT. SVIN horizontal component is mainly relevant to both vestibular tests exploring lateral canal and utricle responses. SVIN-SPV is significantly higher in patients with combined canal and otolith lesions. In some patients with dizziness, SVIN may be the only positive test.

The Neural Basis of Skull Vibration Induced Nystagmus (SVIN).

I list a summary of the major clinical observations of SVIN in patients with total unilateral vestibular loss (TUVL) and show how basic results from neurophysiology can explain these clinical observations. The account integrates results from single neuron recordings of identified semicircular canal and otolith afferent neurons in guinea pigs in response to low frequency skull vibration with evidence of the eye movement response in cats to selective semicircular canal stimulation (both individual and combined) and a simple model of nystagmus generation to show how these results explain most of the major characteristics of SVIN.

Skull Vibration-Induced Nystagmus Test in a Human Model of Horizontal Canal Plugging.

Background/Aim: the aim of this study was to assess the skull vibration-induced nystagmus test (SVINT) results and vestibular residual function after horizontal semicircular canal (HSCC) plugging. Methods: In this retrospective chart review performed in a tertiary referral center, 11 patients who underwent unilateral horizontal semicircular canal plugging (uHSCCP) for disabling Menière’s disease (MD) were included. The skull vibration-induced nystagmus (SVIN) slow-phase velocity (SPV) was compared with the results of the caloric test (CaT), video head impulse test (VHIT), and cervical vestibular-evoked myogenic potentials (cVEMP) performed on the same day. Results: Overall, 10 patients had a strong SVIN beating toward the intact side (Horizontal SVIN-SPV: 8.8°/s ± 5.6°/s), 10 had a significant or severe ipsilateral CaT hypofunction, 10 had an ipsilateral horizontal VHIT gain impairment, and 3 had altered cVEMP on the operated side. Five had sensorineural hearing worsening. SVIN-positive results were correlated with CaT and horizontal VHIT (HVHIT) results (p < 0.05) but not with cVEMP. SVIN-SPV was correlated with CaT hypofunction in % (p < 0.05). Comparison of pre- and postoperative CaT % hypofunction showed a significant worsening (p = 0.028). Conclusion: SVINT results in a human model of horizontal canal plugging are well correlated with vestibular tests exploring horizontal canal function, but not with cVEMP. SVINT always showed a strong lesional nystagmus beating away from the lesion side. SVIN acts as a good marker of HSCC function. This surgical technique showed invasiveness regarding horizontal canal vestibular function.

Agreement between the Skull Vibration-Induced Nystagmus Test and Semicircular Canal and Otolith Asymmetry.

How significant asymmetries in otolith organ function in the presence of symmetrical and asymmetrical semicircular canal function influence skull vibration-induced nystagmus testing (SVINT) has not been well described. The aim of the study is to examine the agreement between SVINT and caloric testing, ocular vestibular-evoked myogenic potentials (oVEMP), and cervical vestibular-evoked myogenic potentials (cVEMP) for detecting asymmetric vestibular function. This is a retrospective study of patients presenting with the chief complaint of vertigo, dizziness, or imbalance. A total of 812 patients were studied with a median age at testing of 59 years (interquartile range 46-70; range 18-93) and included 475 (59%) women. Either the monothermal warm caloric test or alternate binaural bithermal caloric test, oVEMP, and cVEMP tests were administered to all patients. All patients underwent the SVINT prior to vestibular laboratory testing. Agreement between tests categorized as normal versus abnormal was summarized using percent concordance (PC). Sensitivity and specificity values were calculated for SVINT compared with other tests of vestibular function. There was higher agreement between ipsilateral and contralateral SVINT with the caloric test (PC = 80% and 81%, respectively) compared with oVEMP (PC = 63% and 64%, respectively) and cVEMP (PC = 76% and 78%, respectively). Ipsilateral and contralateral SVINT showed higher sensitivity for the caloric test (sensitivity = 47% and 36%, respectively) compared with oVEMP (sensitivity = 26% and 21%, respectively), or cVEMP (sensitivity = 33% vs. 27%, respectively). Specificity of SVINT was high (>80%) for all assessments of vestibular function. The presence of SVIN is a useful indicator of the asymmetry of vestibular function between the two ears when making judgments about semicircular canal asymmetry but is less sensitive to asymmetries in otolith organ function.

The Skull Vibration-induced Nystagmus Test (SVINT) for Vestibular Disorders: A Systematic Review.

To determine the specificity and sensitivity of the skull vibration-induced nystagmus test (SVINT) for detecting vestibular hypofunction. The Cochrane Library, MEDLINE, PubMed, EMBASE, and SciELO. A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Databases were searched using a comprehensive search strategy including the terms "Vibration-induced nystagmus" or "SVINT" or "skull vibration-induced nystagmus test" or "skull vibration-induced nystagmus" from inception to May 2020. A total of 79 articles were identified, and 16 studies met the inclusion criteria. The methodology for performing the SVINT and determining positivity is varied. Most authors refer to reproducibility, sustained response, ending with withdrawal of stimulus, nondirection changing, and response in more than one point of stimulation, as necessary for a positive test. Only seven studies included a slow phase velocity of 2 degrees/s or 2.5 degrees/s as a criterion. Most studies employed 100 Hz stimulus for 10 seconds, while longer duration is suggested for pediatric patients. For partial and total unilateral vestibular loss, positivity varied from 58 to 60%, and 93 to 100%, respectively. Sensitivity ranged from 50 to 100%, and specificity from 62 to 100%. Importantly, the SVINT may decrease with time but does not usually disappear, hence, can provide information of past/compensated vestibular events. The SVINT can be used in pediatric and adult patients. It provides information regarding unilateral vestibular loss, acute, or compensated. It is a quick, safe, and noninvasive test, and is complementary to the dynamic vestibular and positional tests.

How to do and why perform the skull vibration-induced nystagmus test

The skull vibration-induced nystagmus test (SVINT) is a global vestibular test stimulating otoliths and semicircular canals at a frequency of 100Hz, not modified by vestibular compensation, which may reveal vibration-induced nystagmus (VIN). Bone-conducted vibration applied to the mastoid processes and the vertex instantaneously induces predominantly low-velocity (∼10°/s) horizontal nystagmus, with rapid phases beating away from the affected side in patients with unilateral vestibular loss (UVL). VIN starts and stops immediately with stimulation, is continuous, reproducible, beats in the same direction irrespective of which mastoid process is stimulated, with no or little habituation. The SVINT acts like a vestibular Weber test. In peripheral UVL, the SVINT is a good marker of vestibular asymmetry and demonstrates pathological nystagmus beating towards the healthy side in 90% of cases of vestibular neuritis, 71% of cases of Menière's diseases and 44 to 78% of vestibular schwannomas. In superior semicircular canal dehiscence, VIN usually beats towards the affected side due to facilitation of bone conduction related to the presence of a third window. Stimulation of the vertex is more effective than in UVL patients, with sensitivity extending to higher frequencies, up to 700Hz. Observation of vibration-induced nystagmus then reveals equally represented vertical, torsional, and horizontal components beating towards the affected ear, suggesting dominant, but not exclusive, stimulation of the dehiscent superior semicircular canal.

Evaluation of a large cohort of adult patients with Ménière's disease: bedside and clinical history.

SUMMARYObjectiveThe purpose of this study was to assess vestibular findings and clinical history in a large cohort of patients affected by Ménière’s disease.MethodsWe retrospectively analysed 511 adult patients fulfilling criteria for definite unilateral Ménière’s disease according to Barany Society. Thorough clinical history, audiometric exam, central nervous system MRI, quantification of serum autoantibodies and complete vestibular function test were performed.ResultsMean age at clinical record was 55.4 years, while age at onset of the first vertigo attack was 47.4 ± 14.3 years. Ménière’s disease overlapped with migraine in 43.4% of patients. In 31.7% of cases, positivity was found for at least one autoantibody. Forty-nine patients (9.6%) had family history for Ménière’s disease. Bedside examination resulted in 14.7% positivity for video head impulse test, 58.9% for skull vibration-induced nystagmus, 38.7% for the positional test and 23.1% for the post head shaking test. Complete negative examination was reported in 115 cases.ConclusionsMénière’s disease was seen to present a characteristic phenotypic pattern in our cohort, confirming the crucial role of thorough anamnesis and bedside examination in diagnosis.

Skull vibration-induced nystagmus in vestibular neuritis

Background As described by Dumas, an 80–100 Hz vibration applied to the mastoid produces a horizontal nystagmus, with quick phases beating away from the affected side in patients with unilateral vestibular loss (UVL). Aim/objectives To elucidate the characteristics of skull vibration-induced nystagmus (SVIN) in patients suffering from vestibular neuritis and how these characteristics are related to information provided by the video head impulse test (vHIT). Material and methods Sixty-three patients were enrolled to perform a vHIT to measure the gain in both ears. SVIN was induced with stimulation at 30 Hz, 60 Hz, and 100 Hz. The slow phase velocity (SPV) of the SVIN was measured. Results The SVIN test was positive in 25/63 patients at 30 Hz, 36/63 at 60 Hz and 46/63 at 100 Hz. Mean gain difference between both ears to obtain a positive SVIN at 30 Hz was observed to be 0.38 ± 0.25, decreasing to 0.35 ± 0.23 at 60 Hz, and 0.31 ± 0.24 at 100 Hz (p = .025). We found a significant positive linear correlation between the gain asymmetry measured using horizontal vHIT and SPV in SVIN at 100 Hz. Conclusions and significance There is a close relationship between the difference in the gains of both ears as measured using VHIT and the SPV of the nystagmus induced by SVIN at 100 Hz.

Activation of Guinea Pig Irregular Semicircular Canal Afferents by 100 Hz Vibration: Clinical Implications for Vibration-induced Nystagmus and Vestibular-evoked Myogenic Potentials.

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. 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. 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. 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. 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.

The role of vertical semicircular canal function in the vertical component of skull vibration-induced nystagmus

Background: Generally, vertical component of the skull vibratory nystagmus (VCN) is ignored in the clinical practise. Thus, the relative contribution of the vestibular organs in the presence of VCN remains unknown.Objectives: To determine the association between vertical semicircular canal (vSCC) function and the presence of VCN.Material and methods: Comparisons were made between Video Head Impulse Test and SVINT (100 Hz) results at the time of the acute peripheral vestibular lesion (PVL) and at the post-acute phase in patients diagnosed PVL. Later on, a paired analysis was performed restricting the assessments to patients with vestibular explorations in both the acute and post-acute phases.Results: In an univariable analysis, larger mean total gain differences (TGD) between vSCC VOR gains, significantly related with the appearance of VCN in nystagmography in the acute phase (p = .001), unlike the post-acute phase (p = .46). After a multivariate analysis, mean TGD was the only predictive factor of the VCN (p = .013). In the paired analysis, we found an increase in the post-acute phase mean TGD, approaching zero value.Conclusions and significance: Global relation between all vertical canals has at least a contributory role in the presence of the vertical component of nystagmus in SVINT.

The skull vibration-induced nystagmus test: A useful vestibular screening test in children with hearing loss

IntroductionSkull-Vibration-Induced-Nystagmus Test (SVINT), a non-invasive first line examination test, stimulates both otolith and canal structures and shows instantaneously a vestibular asymmetry. This study aimed to analyze the SVINT results observed in children with hearing loss (HL) amplified with hearing aids (HA) or unilateral cochlear implant (uCI) and healthy children. Material and methodsThis case-control study compared the results of SVINT, caloric test (CaT) and video head-impulse-test (VHIT) in 120 controls to 30 children with HA and 30 with uCI, aged 5-18 years old. SVINT was recorded with videonystagmography after very high frequency (VHF) stimulation of mastoids and vertex. ResultsSVINT results were non-pathological in 98% of the control group but modified in the HL group (P-value=0.04). In uCI participants, 13.3% had a bilateral weakness (BW) and 16.7% had a unilateral weakness (UW). In the HA group, 26.7% had BW, 10% had UW. SVINT was efficient to show a UW (6 out of 7 confirmed cases) but not efficient to show BW (1/12 confirmed cases). ConclusionSVINT can detect unilateral vestibular deficit in the VHF with a sensitivity of 86% and specificity of 96%. The positive predictive value is 75% and negative predictive value is 98%. In the case of bilateral deficit, the SVINT is inoperant. In amplified participants, a UW was equally detected whether using SVINT, CaT or VHIT. SVINT is a well-tolerated and useful test to screen vestibular asymmetry in children with HL when combined with other vestibular tests and shows its complementary at very high frequencies.

Skull vibration induced nystagmus in patients with superior semicircular canal dehiscence

ObjectiveTo establish optimum stimulus frequency and location of bone conducted vibration provoking a skull vibration induced nystagmus (SVIN) in superior semi-circular canal dehiscences. MethodsSVIN 3D components in 40 patients with semi-circular canal dehiscence (27 unilateral and 13 bilateral) were compared with a group of 18 patients with severe unilateral vestibular loss and a control group of 11 volunteers. ResultsIn unilateral semi-circular canal dehiscences, SVIN torsional and horizontal components observed on vertex location in 88% beat toward the lesion side in 95%, and can be obtained up to 800Hz (around 500Hz being optimal). SVIN slow-phase-velocity was significantly higher on vertex stimulation at 100 and 300Hz (P=0.04) than on mastoids. SVIN vertical component is more often upbeating than downbeating. A SVIN was significantly more often observed in unilateral than bilateral semi-circular-canal dehiscences (P=0.009) and with a higher slow phase velocity (P=0.008). In severe unilateral vestibular lesions the optimal frequency was 100Hz and SVIN beat toward the intact side. The mastoid stimulation was significantly more efficient than vertex stimulation at 60 and 100Hz (P<0.01). ConclusionSVIN reveals instantaneously in unilateral semi-circular canal dehiscences a characteristic nystagmus beating, for the torsional and horizontal components, toward the lesion side and with a greater sensitivity toward high frequencies on vertex stimulation. SVIN three components analysis suggests a stimulation of both superior semi-circular canal and utricle. SVIN acts as a vestibular Weber test, assessing a vestibular asymmetrical function and is a useful indicator for unilateral semi-circular canal dehiscence.