
pmid: 14662476
AbstractWe propose that motion sickness is mediated through the orientation properties of velocity storage in the vestibular system that tend to align eye velocity produced by the angular vestibulo‐ocular reflex (aVOR) with gravito‐inertial acceleration (GIA). (GIA is the sum of the linear accelerations acting on the head. In the absence of translational accelerations, gravity is the GIA.) We further postulate that motion sickness produced by cross‐coupled vestibular stimulation can be characterized by a metric composed of the disparity between the axis of eye rotation and the GIA, the strength of the response to angular motion, and the response duration, as determined by the central vestibular time constant, that is, by the time constant of velocity storage. The nodulus and uvula of the vestibulocerebellum are likely to be the central sites where the disparity is sensed, where the vestibular time constants are habituated, and where links are made to the autonomic system to produce the symptoms and signs.
Adult, Male, Cross-Over Studies, Eye Movements, Rotation, Motion Sickness, Motion Perception, Nausea, Reflex, Vestibulo-Ocular, Dizziness, Promethazine, Double-Blind Method, Nystagmus, Physiologic, Head Movements, Histamine H1 Antagonists, Humans, Female
Adult, Male, Cross-Over Studies, Eye Movements, Rotation, Motion Sickness, Motion Perception, Nausea, Reflex, Vestibulo-Ocular, Dizziness, Promethazine, Double-Blind Method, Nystagmus, Physiologic, Head Movements, Histamine H1 Antagonists, Humans, Female
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