Affiliations: [a] Brigham and Women's Hospital, Boston, MA, USA | [b] Massachusetts Institute of Technology, Man Vehicle Laboratory, Cambridge, MA, USA
Correspondence:
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Corresponding author: Scott Sheehan, Department of Radiology, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, USA. Tel.: +1 617 732 5938; E-mail: [email protected]
Abstract: 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.
