Sensory conflict in motion sickness: An observer theory approach

Abstract

Motion sickness is the general term describing a group of common nausea syndromes originally attributed to motion-induced cerebral ischemia, stimulation of abdominal organ afferent, or overstimulation of the vestibular organs of the inner ear. Sea-, car-, and airsicknesses are the most commonly experienced examples. However, the discovery of other variants such as Cinerama-, flight simulator-, spectacle-, and space sickness in which the physical motion of the head and body is normal or absent has led to a succession of sensory conflict theories which offer a more comprehensive etiologic perspective. Implicit in the conflict theory is the hypothesis that neutral and/or humoral signals originate in regions of the brain subversing spatial orientation, and that these signals somehow traverse to other centers mediating sickness symptoms. Unfortunately, the present understanding of the neurophysiological basis of motion sickness is far from complete. No sensory conflict neuron or process has yet been physiologically identified. To what extent can the existing theory be reconciled with current knowledge of the physiology and pharmacology of nausea and vomiting. The stimuli which causes sickness, synthesizes a contemporary Observer Theory view of the Sensory Conflict hypothesis are reviewed, and a revised model for the dynamic coupling between the putative conflict signals and nausea magnitude estimates is presented. The use of quantitative models for sensory conflict offers a possible new approach to improving the design of visual and motion systems for flight simulators and other virtual environment display systems