Dataset Information

Computing Endolymph Hydrodynamics During Head Impulse Test on Normal and Hydropic Vestibular Labyrinth Models.

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

SUBMITTER: Rey-Martinez J

PROVIDER: S-EPMC7193182 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Computing Endolymph Hydrodynamics During Head Impulse Test on Normal and Hydropic Vestibular Labyrinth Models.

Rey-Martinez Jorge J Altuna Xabier X Cheng Kai K Burgess Ann M AM Curthoys Ian S IS

Frontiers in neurology 20200421

<b>Hypothesis:</b> Build a biologic geometry based computational model to test the hypothesis that, in some circumstances, endolymphatic hydrops can mechanically cause enhanced eye velocity responses during clinical conditions of the head impulse test. <b>Background:</b> Some recent clinical and experimental findings had suggested that enhanced eye velocity responses measured with the video head impulse test could not only be caused by recording artifacts or central disfunction but also could be ...[more]

PMID: 32390929

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Project description:ObjectivesVirtual reality (VR) offers an ecological setting and the possibility of altered visual feedback during head movements useful for vestibular research and treatment of vestibular disorders. There is however no data quantifying vestibulo-ocular reflex (VOR) during head impulse test (HIT) in VR. The main objective of this study is to assess the feasibility and performance of eye and head movement measurements of healthy subjects in a VR environment during high velocity horizontal head rotation (VR-HIT) under a normal visual feedback condition. The secondary objective is to establish the feasibility of VR-HIT recordings in the same group of normal subjects but under altered visual feedback conditions.DesignTwelve healthy subjects underwent video HIT using both a standard setup (vHIT) and VR-HIT. In VR, eye and head positions were recorded by using, respectively, an imbedded eye tracker and an infrared motion tracker. Subjects were tested under four conditions, one reproducing normal visual feedback and three simulating an altered gain or direction of visual feedback. During these three altered conditions the movement of the visual scene relative to the head movement was decreased in amplitude by 50% (half), was nullified (freeze) or was inverted in direction (inverse).ResultsEye and head motion recording during normal visual feedback as well as during all 3 altered conditions was successful. There was no significant difference in VOR gain in VR-HIT between normal, half, freeze and inverse conditions. In the normal condition, VOR gain was significantly but slightly (by 3%) different for VR-HIT and vHIT. Duration and amplitude of head impulses were significantly greater in VR-HIT than in vHIT. In all three altered VR-HIT conditions, covert saccades were present in approximatively one out of four trials.ConclusionOur VR setup allowed high quality recording of eye and head data during head impulse test under normal and altered visual feedback conditions. This setup could be used to investigate compensation mechanisms in vestibular hypofunction, to elicit adaptation of VOR in ecological settings or to allow objective evaluation of VR-based vestibular rehabilitation.

Project description:ObjectiveTo determine whether saccadic velocity in the suppression head impulse paradigm (SHIMP) test is a reliable indicator of vestibular loss at the acute and at the chronic stage in patients suffering from different vestibular pathologies.MethodsThirty-five normal subjects and 57 patients suffering from different vestibular pathologies associated with unilateral vestibular loss (UVL) or bilateral vestibular loss (BVL) were tested in the SHIMPs paradigm. SHIMPs were performed by turning the head 10 times at high velocities to the left or right side, respectively. The patients were instructed to fixate on a red spot generated by a head-fixed laser projected on the wall. In this SHIMPs paradigm, healthy subjects made a large anti-compensatory saccade at the end of the head turn (a SHIMP saccade). The peak saccadic velocity, the percentage of the trials completed with saccades in 10 trials, and the latency of the saccades were quantified in each group. A video-head impulse test (v-HIT) was systematically performed in all of our subjects as well as a caloric test. The dizziness handicap inventory questionnaire was also given to chronic UVL and BVL patients.ResultsAt the acute stage after a complete UVL, patients had zero or a few anti-compensatory saccades for low velocity head turns toward the lesioned side. These saccades had lower velocity than the anti-compensatory saccades recorded during head rotation toward the intact side and/or compared with the saccades measured in control subjects. At the chronic stage, some of the patients recovered the ability to perform SHIMP saccades at each head turn toward the lesioned side, but very often these saccades were of significantly lower velocity. In BVL patients, no anti-compensatory saccades, or only significantly smaller ones, could be detected for head turns to both sides.ConclusionSHIMP is a specific and sensitive test to detect a complete horizontal canal loss at the acute stage. In addition, it reflects the ability of patients with moderate horizontal vestibulo-ocular reflex gain decrease to generate anti-compensatory saccades in the chronic stage. In association with v-HIT, it allows determination of the residual vestibular function and to detect anti-compensatory saccades.

Project description:The normal vestibulo-ocular reflex (VOR) generates almost perfectly compensatory smooth eye movements during a 'head-impulse' rotation. An imperfect VOR gain provokes additional compensatory saccades to re-acquire an earth-fixed target. In the present study, we investigated vestibular and visual contributions on saccade production. Eye position and velocity during horizontal and vertical canal-plane head-impulses were recorded in the light and dark from 16 controls, 22 subjects after complete surgical unilateral vestibular deafferentation (UVD), eight subjects with idiopathic bilateral vestibular loss (BVL), and one subject after complete bilateral vestibular deafferentation (BVD). When impulses were delivered in the horizontal-canal plane, in complete darkness compared with light, first saccade frequency mean(SEM) reduced from 96.6(1.3)-62.3(8.9) % in BVL but only 98.3(0.6)-92.0(2.3) % in UVD; saccade amplitudes reduced from 7.0(0.5)-3.6(0.4) ° in BVL but were unchanged 6.2(0.3)-5.5(0.6) ° in UVD. In the dark, saccade latencies were prolonged in lesioned ears, from 168(8.4)-240(24.5) ms in BVL and 177(5.2)-196(5.7) ms in UVD; saccades became less clustered. In BVD, saccades were not completely abolished in the dark, but their amplitudes decreased from 7.3-3.0 ° and latencies became more variable. For unlesioned ears (controls and unlesioned ears of UVD), saccade frequency also reduced in the dark, but their small amplitudes slightly increased, while latency and clustering remained unchanged. First and second saccade frequencies were 75.3(4.5) % and 20.3(4.1) %; without visual fixation they dropped to 32.2(5.0) % and 3.8(1.2) %. The VOR gain was affected by vision only in unlesioned ears of UVD; gains for the horizontal-plane rose slightly, and the vertical-planes reduced slightly. All head-impulse compensatory saccades have a visual contribution, the magnitude of which depends on the symmetry of vestibular-function and saccade latency: BVL is more profoundly affected by vision than UVD, and second saccades more than first saccades. Saccades after UVD are probably triggered by contralateral vestibular function.

Dataset Information

Computing Endolymph Hydrodynamics During Head Impulse Test on Normal and Hydropic Vestibular Labyrinth Models.

Publications

Computing Endolymph Hydrodynamics During Head Impulse Test on Normal and Hydropic Vestibular Labyrinth Models.

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