Abstract
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.
Highlights
IntroductionAcademic Editors: Georges Dumas, Sébastien Schmerber and Philippe P
In with a semicircular canalcanal dehiscence (SCD),(SCD), mastoidmastoid vibrationvibration can induce a reverse with Skull Vibration InducedNystagmus (SVIN): quick phases phases directed toward the ear with the directed toward the ear with the SCD [7,8]
What is still unclear is the exact mechanism at the level of the receptor hair cell by which low frequency vibration deflects the stereocilia of the canal receptors sufficiently to activate them [26]
Summary
Academic Editors: Georges Dumas, Sébastien Schmerber and Philippe P. The third question is to explain the exact direction of the slow phase eye velocity component of the nystagmus and to do this I refer to the results of selective stimulation of nerves from single canals (or combination of canal nerves [5]). These data are used to explain the results from 3-D eye movement measurement of SVIN in different categories of human testing. The records show the horizontal, vertical and torsional eye movement recordings (Synapsys) of a patient with a total left‐sided vestibular loss in response to stimulation of the right mastoid (RM). (TUVL) summarized from summarized from [1] and related papers by papers the Dumas group
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