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Title of Journal: Exp Brain Res

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Abbravation: Experimental Brain Research

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Springer Berlin Heidelberg

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DOI

10.1007/bf00761999

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1432-1106

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Brainstem processing of vestibular sensory exaffer

Authors: Charles M Oman Kathleen E Cullen
Publish Date: 2014/05/18
Volume: 232, Issue: 8, Pages: 2483-2492
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Abstract

The origin of the internal “sensory conflict” stimulus causing motion sickness has been debated for more than four decades Recent studies show a subclass of neurons in the vestibular nuclei and deep cerebellar nuclei that respond preferentially to passive head movements During active movement the semicircular canal and otolith input “reafference” to these neurons are canceled by a mechanism comparing the expected consequences of selfgenerated movement estimated with an internal model—presumably located in the cerebellum with the actual sensory feedback The uncanceled component “exafference” resulting from passive movement normally helps compensate for unexpected postural disturbances Notably the existence of such vestibular “sensory conflict” neurons had been postulated as early as 1982 but their existence and putative role in posture control and motion sickness have been long debated Here we review the development of “sensory conflict” theories in relation to recent evidence for brainstem and cerebellar reafference cancelation and identify some open research questions We propose that conditions producing persistent activity of these neurons or their targets stimulate nearby brainstem emetic centers—via an as yet unidentified mechanism We discuss how such a mechanism is consistent with the notable difference in motion sickness susceptibility of drivers as opposed to passengers human immunity to normal selfgenerated movement and why head restraint or lying horizontal confers relative immunity Finally we propose that fuller characterization of these mechanisms and their potential role in motion sickness could lead to more effective scientifically based prevention and treatment for motion sicknessDr Oman was supported in part by the National Space Biomedical Research Institute through NASA NCC 958 Dr Cullen’s research was supported by the Canadian Institutes of Health Research CIHR the National Institutes of Health DC002390 the Fonds Québécois de la Recherche sur la Nature et les Technologies FQNRT and US National Institute of Health Grant R01 DC2390

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