Editing Motion sickness (section)

=== 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}}