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The Critical Role of Velocity Storage in Production of Motion Sickness
aDepartment of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA bDepartment of Computer and Information Sciences, Brooklyn College of the City University of New York, Brooklyn, New York 11210, USA
Address for correspondence: Bernard Cohen, Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029. Voice: 212-241-7068; fax: 212-831-1610. bernard.cohen{at}mssm.edu Ann. N.Y. Acad. Sci. 1004: 359-376 (2003).
We 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.
Key Words: head movements • nystagmus • vestibular • vertigo • roll while rotating • nodulus • uvula • vestibulocerebellum This article has been cited by other articles:
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