Editing Motion sickness (section)

==Pathophysiology==
There are various hypotheses that attempt to explain the cause of the condition.

=== Sensory conflict theory ===
Contemporary sensory conflict theory, referring to "a discontinuity between either visual, proprioceptive, and somatosensory input, or semicircular canal and otolith input", is probably the most thoroughly studied.<ref>{{Cite journal |pmid = 6870740|year = 1983|last1 = Kohl|first1 = R. L.|title = Sensory conflict theory of space motion sickness: An anatomical location for the neuroconflict|journal = Aviation, Space, and Environmental Medicine|volume = 54|issue = 5|pages = 464–5}}</ref> According to this theory, when the brain presents the mind with two incongruous states of motion, the result is often nausea and other symptoms of disorientation known as motion sickness.{{why|reason=This restates the causes section without explaining why the body responds in this way.|date=April 2024}} Such conditions happen when the [[vestibular system]] and the [[visual system]] do not present a synchronized and unified representation of one's body and surroundings.<ref>{{Cite web |title=How To Cure Motion Sickness Permanently |url=https://curemotionsickness.com/ |access-date=2022-11-16 |website=Captain Arthur's |language=en-US}}</ref>

According to sensory conflict theory, the cause of terrestrial motion sickness is the opposite of the cause of space motion sickness. The former occurs when one perceives visually that one's surroundings are relatively immobile while the [[vestibular system]] reports that one's body is in motion relative to its surroundings.<ref name="Benson 2002" /> The latter can occur when the visual system perceives that one's surroundings are in motion while the vestibular system reports relative bodily immobility (as in zero gravity.){{citation needed|date=July 2021}}

=== Neural mismatch ===
A variation of the sensory conflict theory is known as neural mismatch, implying a mismatch occurring between ongoing sensory experience and long-term memory rather than between components of the vestibular and visual systems. This theory emphasizes "the limbic system in the integration of sensory information and long-term memory, in the expression of the symptoms of motion sickness, and the impact of anti-motion-sickness drugs and stress hormones on limbic system function. The limbic system may be the neural mismatch center of the brain."<ref>{{Cite journal |pmc = 4112051|year = 2014|last1 = Lackner|first1 = J. R.|title = Motion sickness: More than nausea and vomiting|journal = Experimental Brain Research|volume = 232|issue = 8|pages = 2493–2510|pmid = 24961738|doi = 10.1007/s00221-014-4008-8}}</ref>

=== Defense against poisoning ===
It has also been proposed that motion sickness could function as a defense mechanism against [[neurotoxin]]s.<ref name="Treisman1977" /> The [[area postrema]] in the [[human brain|brain]] is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in the cabin of a ship with no portholes), the [[inner ear]] transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is [[hallucination|hallucinating]] and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis.<ref name="Lawson 20142"/> The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.{{citation needed|date=July 2021}}

=== Nystagmus hypothesis ===
Yet another theory, known as the nystagmus hypothesis,<ref name="Ebenholtz et al 1994" /> has been proposed based on stimulation of the [[vagus nerve]] resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., [[semicircular canals]] and [[Otolith|otolith organs]], and a change in tonus among various of each eye's six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of [[Sherrington's law of reciprocal innervation|Sherrington's Law]]<ref name="Sherrington1893" /> describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of [[Extraocular muscles|extraocular muscle]] that must occur whenever Sherrington's Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction.<ref name="pmid6671149" /> Thus, tenth nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness;<ref name="Kennedy et al 1968" /><ref name="pmid1859339" /> why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.<ref name="Ebenholtz 2005" />

A recent theory <ref name="Previc 2018" /> argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals ([[nauseogenic]]) vs. [[otolith]] organs (anti-nauseogenic). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., in [[free fall]]) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic).{{citation needed|date=July 2021}}