We tested the hypothesis that motion sickness is produced by an integration of the disparity between eye velocity and the yaw-axis orientation vector of velocity storage. Disparity was defined as the magnitude of the cross product between these two vectors. OVAR, which is known to produce motion sickness, generates horizontal eye velocity with a bias level related to velocity storage, as well as cyclic modulations due to re-orientation of the head re gravity. On average, the orientation vector is close to the spatial vertical. Thus, disparity can be related to the bias and tilt angle. Motion sickness sensitivity was defined as a ratio of maximum motion sickness score to the number of revolutions, allowing disparity and motion sickness sensitivity to be correlated. Nine subjects were rotated around axes tilted 10°–30° from the spatial vertical at 30°/s–120°/s. Motion sickness sensitivity increased monotonically with increases in the disparity due to changes in rotational velocity and tilt angle. Maximal motion sickness sensitivity and bias (6.8°/s) occurred when rotating at 60°/s about an axis tilted 30° Modulations in eye velocity during OVAR were unrelated to motion sickness sensitivity. The data were predicted by a model incorporating an estimate of head velocity from otolith activation, which activated velocity storage, followed by an orientation disparity comparator that activated a motion sickness integrator. These results suggest that the sensory-motor conflict that produces motion sickness involves coding of the spatial vertical by the otolith organs and body tilt receptors and processing of eye velocity through velocity storage.
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