The body detects motion through 3 sources: vestibular, visual, and proprioceptive input to the CNS.1-3 Motion sickness can occur when there is conflicting or inconsistent input (vestibular, visual, or proprioceptive) processed within a multimodal sensory system whose function is to ascertain a patient's motion in relation to environment.1,3
The nausea and vomiting associated with motion sickness is a result of overstimulation of the labyrinth (ie, inner ear) apparatus. The labyrinth has 3 semicircular canals, responsible for maintaining equilibrium.1,3 Postural adjustments are made when the brain receives nerve impulses initiated by the fluid in canals.1,3 Motion sickness occurs with acceleration in a direction perpendicular to the longitudinal axis of the body, which explains why head movements in the opposite direction of the body's movement are so stimulating. This type of motion is common when riding in the car, on a boat, or in an airplane. During motion sickness, impulses from the vestibular center in the labyrinth of the inner ear are thought to travel through the chemoreceptor trigger zone (CRTZ) to the vomiting center in the medulla oblongata.1,2 A number of medications have been successfully used to prevent or minimize motion sickness by interrupting signaling pathways between the vestibular apparatus and the vomiting center.