Motion sickness, which is defined as nausea, vomiting, disorientation and related symptoms in association with movement of the subject or the visual surround, can be elicited by rotating subjects about an axis, tilted relative to the gravitational vertical (Off-Vertical Axis Rotation, OVAR) or by having subjects roll their heads while rotating around a vertical axis at a high velocity (RWR). During both stimuli, motion sickness builds until it reaches a level of intolerable nausea, which can culminate in vomiting. The number of rotations subjects make during OVAR or the number of head movements during RWR before reaching intolerable nausea is the measure of motion sickness susceptibility. A model is proposed in which the development of motion sickness is mediated through the orientation and temporal properties of a process in the central vestibular system known as velocity storage. In this model, motion sickness is activated by a difference between the direction of eye movements generated through velocity storage in response to rotation and the orientation vector associated with velocity storage. This orientation vector lies close to the gravitational vertical. We propose that it is the prolonged difference between the velocity storage vector and the orientation vector (gravitational upright) produced by rotation about a tilted axis during OVAR or by head movement during RWR that causes the development of motion sickness. In the proposed study we will characterize the spatial and temporal evolution of motion sickness using OVAR and RWR to test the model in normal subjects and determine whether the administration of baclofen, a drug that reduces the duration of the velocity storage response, also reduces motion sickness susceptibility. Using OVAR and RWR, we will also test the motion sickness susceptibility of cerebellar patients with degeneration of the nodulus and uvula who can no longer orient their eye velocity to the gravitational vertical during rotation. Finally, we will develop therapeutic interventions that will reduce the duration of the vestibular response. We propose that this will also cause a decrease in motion sickness susceptibility by non-pharmacological means. This research, which should lead to a better understanding of the mechanisms that cause motion sickness and provide new therapeutic measures to reduce motion sickness susceptibility, can potentially lead to relief for a wide range of subjects that suffer from motion sickness.
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