Brigham and Women's Hospital, Boston, MA, USA.
J Vestib Res. 2011;21(4):209-17. doi: 10.3233/VES-2011-0417.
Motion sickness has been defined as a set of physiological signs and symptoms produced as a result of prolonged sensory conflict in central nervous system vestibular centers. It has long been noted that the particular pattern of motion sickness signs and symptoms does not fit the conventional "fight or flight vs. rest and digest" autonomic synergy. We argue that most of the progression of symptoms is consistent with a new etiologic hypothesis: that an as-yet-unidentified ganglionic cholinomimetic agent is slowly released in proportion to sensory conflict. The agent accumulates systemically and stimulates the peripheral sympathetic and parasympathetic ganglia, the adrenal medulla, and potentiates the response of central cholinergic emetic pathways to the same conflict stimulus. The predominant effects of ganglionic stimulation on each autonomic organ, determined by resting tone, are selectively enhanced or inhibited by adrenal catecholamine release, producing the atypical pattern of autonomic changes seen in motion sickness. The adrenergic response may eventually also counter the central emetic drive. The hypothesis could be experimentally pursued via human and animal experiments employing a nicotinic antagonist that has both central and peripheral ganglionic actions such as mecamylamine.
运动病被定义为由于中枢神经系统前庭中枢的长期感觉冲突而产生的一系列生理体征和症状。长期以来，人们注意到运动病的特定症状模式不符合传统的“战斗或逃跑与休息和消化”自主协同作用。我们认为，大多数症状的进展与一个新的病因假说一致：一种尚未确定的神经节胆碱能激动剂是根据感觉冲突缓慢释放的。该试剂在体内累积并刺激外周交感神经和副交感神经节、肾上腺髓质，并增强中枢胆碱能催吐途径对相同冲突刺激的反应。神经节刺激对每个自主器官的主要影响取决于静息张力，被肾上腺儿茶酚胺释放选择性增强或抑制，产生运动病中所见的自主变化的非典型模式。肾上腺素能反应最终也可能对抗中枢催吐驱动。可以通过用人和动物实验来实验性地研究该假说，实验中可以使用具有中枢和外周神经节作用的烟碱拮抗剂，如美加明。
