Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology
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...
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| Format: | Article |
| Language: | English |
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Springer Berlin Heidelberg
2016
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| Online Access: | http://hdl.handle.net/1721.1/103177 https://orcid.org/0000-0002-5576-3510 |
| _version_ | 1826213223852933120 |
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| author | Oman, Charles M. Cullen, Kathleen E. |
| author2 | Massachusetts Institute of Technology. Department of Aeronautics and Astronautics |
| author_facet | Massachusetts Institute of Technology. Department of Aeronautics and Astronautics Oman, Charles M. Cullen, Kathleen E. |
| author_sort | Oman, Charles M. |
| collection | MIT |
| description | 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 self-generated movement (estimated with an internal model—presumably located in the cerebellum) with the actual sensory feedback. The un-canceled 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 self-generated 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 sickness. |
| first_indexed | 2024-09-23T15:45:24Z |
| format | Article |
| id | mit-1721.1/103177 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T15:45:24Z |
| publishDate | 2016 |
| publisher | Springer Berlin Heidelberg |
| record_format | dspace |
| spelling | mit-1721.1/1031772022-10-02T03:55:01Z Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology Oman, Charles M. Cullen, Kathleen E. Massachusetts Institute of Technology. Department of Aeronautics and Astronautics Oman, Charles M. Cullen, Kathleen E. 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 self-generated movement (estimated with an internal model—presumably located in the cerebellum) with the actual sensory feedback. The un-canceled 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 self-generated 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 sickness. National Space Biomedical Research Institute (NASA NCC 9-58) Canadian Institutes of Health Research National Institutes of Health (U.S.) (DC002390) Fonds québécois de la recherche sur la nature et les technologies (FQNRT) National Institutes of Health (U.S.) (Grant R01 DC2390) 2016-06-21T20:17:55Z 2016-06-21T20:17:55Z 2014-05 2014-01 2016-05-23T12:09:29Z Article http://purl.org/eprint/type/JournalArticle 0014-4819 1432-1106 http://hdl.handle.net/1721.1/103177 Oman, Charles M., and Kathleen E. Cullen. “Brainstem Processing of Vestibular Sensory Exafference: Implications for Motion Sickness Etiology.” Experimental Brain Research 232, no. 8 (May 18, 2014): 2483–2492. https://orcid.org/0000-0002-5576-3510 en http://dx.doi.org/10.1007/s00221-014-3973-2 Experimental Brain Research Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. Springer-Verlag Berlin Heidelberg application/pdf Springer Berlin Heidelberg Springer Berlin Heidelberg |
| spellingShingle | Oman, Charles M. Cullen, Kathleen E. Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology |
| title | Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology |
| title_full | Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology |
| title_fullStr | Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology |
| title_full_unstemmed | Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology |
| title_short | Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology |
| title_sort | brainstem processing of vestibular sensory exafference implications for motion sickness etiology |
| url | http://hdl.handle.net/1721.1/103177 https://orcid.org/0000-0002-5576-3510 |
| work_keys_str_mv | AT omancharlesm brainstemprocessingofvestibularsensoryexafferenceimplicationsformotionsicknessetiology AT cullenkathleene brainstemprocessingofvestibularsensoryexafferenceimplicationsformotionsicknessetiology |