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Are evolutionary hypotheses for motion sickness "just-so" stories?
1Department of Aeronautics and Astronautics, Massachusetts Institute of Technology, Man Vehicle Lab, Cambridge, MA 02139, USA. coman@mit.edu
Journal of Vestibular Research : Equilibrium & Orientation
|September 25, 2012
Summary
Motion sickness may not be an adaptation but a byproduct of the brain
Area of Science:
- Neuroscience
- Evolutionary Biology
- Physiology
Background:
- Vertebrates possess nausea and vomiting reflexes for defense against neurotoxins.
- Treisman's 1977 "poison" theory posits motion sickness is an accidental byproduct of these defense mechanisms.
- This adaptationist explanation is widely cited but faces alternative hypotheses.
Purpose of the Study:
- To review evidence for the "poison" theory and other adaptationist explanations for motion sickness.
- To explore alternative, pluralistic hypotheses for the evolution of motion sickness.
- To examine the neurobiological underpinnings of motion sickness.
Main Methods:
- Review of existing scientific literature and evidence.
- Analysis of adaptationist and pluralistic theories of motion sickness.
- Examination of neuroarchitectural elements and functional interactions within the vertebrate brainstem.
Main Results:
- Evidence supporting adaptationist theories for motion sickness is equivocal and contradictory.
- A pluralistic view suggests the vertebrate reticular formation has multiple functions: maintaining brain oxygenation, processing sensory stimuli, and expelling neurotoxins.
- Sensory conflict signals, particularly during prolonged passive transport, can abnormally activate the neurotoxin expulsion system, leading to motion sickness.
Conclusions:
- Motion sickness may be a maladaptive phenotype resulting from the cross-coupling of independent brain systems.
- The "poison" theory, while plausible, may not fully explain the phenomenon of motion sickness.
- A pluralistic model offers a more parsimonious explanation for the complex etiology of motion sickness.
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