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. According to this theory, when the brain presents the mind with two incongruous states of<unk> ; the result is often nausea and other symptoms of disorientation known as<unk> . 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. According to sensory conflict theory, the cause of terrestrial<unk>  is the opposite of the cause of space<unk> . 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<unk>  relative to its surroundings. The latter can occur when the visual system perceives that one's surroundings are in<unk>  while the vestibular system reports relative bodily immobility (as in zero gravity.) 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<unk> , 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." Defense against poisoning It has also been proposed that<unk>  could function as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling<unk>  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<unk> , but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is 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. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent<unk>  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<unk> . Nystagmus hypothesis Yet another theory, known as the nystagmus hypothesis, 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 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 describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of 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. Thus, 10th nerve stimulation resulting from eye muscle stretch is proposed as the cause of<unk> . The theory explains why labyrinthine-defective individuals are immune to<unk> ; 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<unk>  symptoms. A recent theory argues that the main reason<unk>  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<unk> . For example, there are many sensory conflicts that are associated with<unk>  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).
Motion sickness
Stroke
Sweating sickness
Benign paroxysmal positional vertigo
Ski sickness
Migraine-associated vertigo
Foreign accent syndrome
Morning sickness