Physiological basis and pharmacology of motion sickness: An update

Motion sickness can occur when sensory inputs regarding body position in sp ace are contradictory or are different from those predicted from experience , Signals from the vestibular system are essential for triggering motion si ckness. The evolutionary significance of this malady is unclear, although i t may simply represent the aberrant activation of vestibuloautonomic pathwa ys that typically subserve homeostasis. The neural pathways that produce na usea and vomiting during motion sickness are presumed to be similar to thos e that generate illness after ingestion of toxins. The neural substrate of nausea is unknown but may include neurons in the hypothalamus and inferior frontal gyrus of the cerebral cortex, The principal motor act of vomiting i s accomplished through the simultaneous contractions of inspiratory and exp iratory respiratory muscles and is mediated by neurons in the lateral medul lary reticular formation and perhaps by cells near the medullary midline, C ocontraction of the diaphragm and abdominal muscles increases pressure on t he stomach, which causes gastric contents to be ejected through the mouth. Effective drugs for combating motion sickness include antihistamines, antim uscarinics, 5-HT1A (serotonergic) receptor agonists and neurokinin type 1 r eceptor antagonists. However, considerable information concerning the physi ological basis and pharmacology of motion sickness is unknown; future resea rch using animal models will be required to understand this condition. (C) 1999 Elsevier Science Inc.