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Published on: December 14, 2014
The neural basis of motion sickness
Bernard Cohen1,2, Mingjia Dai1,2, Sergei B Yakushin1,2
1Department of Neurology, Icahn School of Medicine at Mount Sinai , New York, New York.
Sensory conflict from motion triggers motion sickness via vestibular pathways. Understanding these neural signals and inhibitory mechanisms, like GABAB receptors, offers new ways to control and treat motion sickness.
Area of Science:
- Neuroscience
- Vestibular System Physiology
- Autonomic Nervous System Function
Background:
- Motion sickness has been linked to body motion for centuries.
- Recent advances have identified the neural basis and signal sources of motion sickness.
- Understanding the sensory conflict is key to managing its symptoms.
Purpose of the Study:
- To review the origins of sensory conflicts causing motion sickness.
- To summarize experimental data on motion sickness generation and control.
- To explore the neural pathways and molecular mechanisms involved.
Main Methods:
- Review of existing experimental data on motion sickness.
- Analysis of vestibular input pathways (semicircular canals, otolith organs).
- Examination of neural control mechanisms in the vestibulo-cerebellum and vestibular nuclei.
Main Results:
- Motion sickness originates from vestibular input processed by the velocity storage integrator.
- The vestibulo-cerebellum, specifically the nodulus, exerts inhibitory control over vestibular nuclei.
- GABAB receptors play a major inhibitory role, and agonists like baclofen can suppress motion sickness.
Conclusions:
- Understanding the neural basis of sensory conflict provides insights into motion sickness.
- Targeting vestibular pathways and inhibitory mechanisms offers potential therapeutic strategies.
- Further research may lead to improved treatments for motion sickness symptoms.
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