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"Motion sickness" is the general term describing a group of common nausea syndromes originally attributed to motion-induced cerebral ischemia, stimulation of abdominal organ afferents, or overstimulation of the vestibular organs of the inner ear. Seasickness, car sickness, and airsickness are commonly experienced examples. However, the identification of other variants such as spectacle sickness and flight simulator sickness in which the physical motion of the head and body is normal or even absent has led to a succession of "sensory conflict" theories that offer a more comprehensive etiologic perspective. Implicit in the conflict theory is the hypothesis that neural and (or) humoral signals originate in regions of the brain subserving spatial orientation, and that these signals somehow traverse to other centers mediating sickness symptoms. Unfortunately, our present understanding of the neurophysiological basis of motion sickness is incomplete. No sensory conflict neuron or process has yet been physiologically identified. This paper reviews the types of stimuli that cause sickness and synthesizes a mathematical statement of the sensory conflict hypothesis based on observer theory from control engineering. A revised mathematical model is presented that describes the dynamic coupling between the putative conflict signals and nausea magnitude estimates. Based on the model, what properties would a conflict neuron be expected to have?
Charles M. Oman (Thu,) studied this question.