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Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis.
Med Hypotheses. 2005; 64(6):1177-81.MH

Abstract

Motion sickness is a common and distressing but poorly understood syndrome associated with nausea/vomiting and autonomic nervous system accompaniments that develops in the air or space as well as on sea or land. A bidirectional aetiologic link prevails between migraine and motion-sickness. Motion sickness provokes jerk nystagmus induced by both optokinetic and vestibular stimulation. Fixation of gaze or closure of eyes generally prevents motion sickness while vestibular otolithic function is eliminated in microgravity of space, indicating a predominant pathogenetic role for visuo-sensory input. Scopolamine, dimenhydrinate, and promethazine reduce motion-related nystagmus. Contraction of extraocular muscles generates proprioceptive neural traffic and can provoke an ocular hypertensive response. It is proposed that repetitive contractions of the extraocular muscles during motion-related jerk nystagmus rapidly augment brain stem afferent input by increasing proprioceptive neural traffic through connections of the oculomotor nerves with the ophthalmic nerve in the lateral wall of the cavernous sinus as well as by raising the intraocular pressure thereby stimulating anterior segment ocular trigeminal nerve fibers. This verifiable hypothesis defines the pathophysiological basis of individual susceptibility to motion sickness, elucidates the preventive mechanism of gaze fixation or ocular closure, advances the aetiologic link between MS and migraine, rationalizes the mechanism of known preventive drugs, and explores new therapeutic possibilities.

Authors+Show Affiliations

Dubai Police Medical Services, P.O. Box 12005, Dubai, United Arab Emirates. docgupta@emirates.net.ae

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15823712

Citation

Gupta, Vinod Kumar. "Motion Sickness Is Linked to Nystagmus-related Trigeminal Brain Stem Input: a New Hypothesis." Medical Hypotheses, vol. 64, no. 6, 2005, pp. 1177-81.
Gupta VK. Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis. Med Hypotheses. 2005;64(6):1177-81.
Gupta, V. K. (2005). Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis. Medical Hypotheses, 64(6), 1177-81.
Gupta VK. Motion Sickness Is Linked to Nystagmus-related Trigeminal Brain Stem Input: a New Hypothesis. Med Hypotheses. 2005;64(6):1177-81. PubMed PMID: 15823712.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis. A1 - Gupta,Vinod Kumar, PY - 2004/11/11/received PY - 2004/11/13/accepted PY - 2005/4/13/pubmed PY - 2005/10/1/medline PY - 2005/4/13/entrez SP - 1177 EP - 81 JF - Medical hypotheses JO - Med Hypotheses VL - 64 IS - 6 N2 - Motion sickness is a common and distressing but poorly understood syndrome associated with nausea/vomiting and autonomic nervous system accompaniments that develops in the air or space as well as on sea or land. A bidirectional aetiologic link prevails between migraine and motion-sickness. Motion sickness provokes jerk nystagmus induced by both optokinetic and vestibular stimulation. Fixation of gaze or closure of eyes generally prevents motion sickness while vestibular otolithic function is eliminated in microgravity of space, indicating a predominant pathogenetic role for visuo-sensory input. Scopolamine, dimenhydrinate, and promethazine reduce motion-related nystagmus. Contraction of extraocular muscles generates proprioceptive neural traffic and can provoke an ocular hypertensive response. It is proposed that repetitive contractions of the extraocular muscles during motion-related jerk nystagmus rapidly augment brain stem afferent input by increasing proprioceptive neural traffic through connections of the oculomotor nerves with the ophthalmic nerve in the lateral wall of the cavernous sinus as well as by raising the intraocular pressure thereby stimulating anterior segment ocular trigeminal nerve fibers. This verifiable hypothesis defines the pathophysiological basis of individual susceptibility to motion sickness, elucidates the preventive mechanism of gaze fixation or ocular closure, advances the aetiologic link between MS and migraine, rationalizes the mechanism of known preventive drugs, and explores new therapeutic possibilities. SN - 0306-9877 UR - https://www.unboundmedicine.com/medline/citation/15823712/Motion_sickness_is_linked_to_nystagmus_related_trigeminal_brain_stem_input:_a_new_hypothesis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-9877(04)00638-3 DB - PRIME DP - Unbound Medicine ER -