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Reduced eye velocity and overt or covert compensatory saccades during horizontal head impulse testing are the signs of reduced vestibular function. However, here we report the unusual case of a patient who had enhanced eye velocity during horizontal head impulses followed by a corrective saccade. We term this saccade a “backup saccade” because it acts to compensate for the gaze position error caused by the enhanced velocity (and enhanced VOR gain) and acts to return gaze directly to the fixation target as shown by eye position records. We distinguish backup saccades from overt or covert compensatory saccades or the anticompensatory quick eye movement (ACQEM) of Heuberger et al. (1) ACQEMs are anticompensatory in that they are in the same direction as head velocity and so, act to take gaze off the target and thus require later compensatory (overt) saccades to return gaze to the target. Neither of these responses were found in this patient. The patient here was diagnosed with unilateral definite Meniere's disease (MD) on the right and had enhanced VOR (gain of 1.17) for rightward head impulses followed by backup saccades. For leftwards head impulses eye velocity and VOR gain were in the normal range (VOR gain of 0.89). As further confirmation, testing with 1.84 Hz horizontal sinusoidal head movements in the visual-vestibular (VVOR) paradigm also showed these backup saccades for rightwards head turns but normal slow phase eye velocity responses without backup saccades for leftwards had turns. This evidence shows that backup saccades can be observed in some MD patients who show enhanced eye velocity responses during vHIT and that these backup saccades act to correct for gaze position error caused by the enhanced eye velocity during the head impulse and so have a compensatory effect on gaze stabilization.

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.

In current clinical practice, when in response to vHIT testing the observed slow-phase eye-velocity responses are significantly higher than head velocity, the most probable cause is considered to be an inadequate collection method or a recording artifact. We present two cases with clinical diagnoses of Menière's Disease: for both cases, enhanced eye velocity responses were measured with a rigorous vHIT testing protocol. In the first case we measured these enhanced responses on each test performed during a 5 year time series; in the second case multiple measurements were obtained from a patient after the radiologic diagnosis of vestibulo-cochlear hydrops. The two cases presented and the new evidence reported by other researchers suggest that owing to the low probability of artifact and the high consistency of the vHIT measurements, we should consider the hypothesis of a physio-pathologic cause for the enhanced eye responses to vHIT testing of some patients with vestibular dysfunction.

In current clinical practice, when in response to vHIT testing the observed slow-phase eye-velocity responses are significantly higher than head velocity, the most probable cause is considered to be an inadequate collection method or a recording artifact. We present two cases with clinical diagnoses of Menière's Disease: for both cases, enhanced eye velocity responses were measured with a rigorous vHIT testing protocol. In the first case we measured these enhanced responses on each test performed during a 5 year time series; in the second case multiple measurements were obtained from a patient after the radiologic diagnosis of vestibulo-cochlear hydrops. The two cases presented and the new evidence reported by other researchers suggest that owing to the low probability of artifact and the high consistency of the vHIT measurements, we should consider the hypothesis of a physio-pathologic cause for the enhanced eye responses to vHIT testing of some patients with vestibular dysfunction. [ABSTRACT FROM AUTHOR]

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., (Copyright © 2020 Rey-Martinez, Altuna, Cheng, Burgess and Curthoys.)