Abstract
It is now generally accepted that acute mountain sickness (AMS) is caused by a mild form of high-altitude cerebral edema (HACE). In susceptible individuals AMS may progress to a lethal form of HACE and/or high-altitude pulmonary edema (3). Two hypotheses have been promulgated to account for HACE: the vasogenic edema hypothesis and the cytotoxic edema hypothesis (3,4). Since cerebral energetics are unchanged during AMS-HACE in an experimental sheep model (7), evidence favors the view that HACE is vasogenic in nature, although cytotoxic edema has not been ruled out specifically.
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Krasney, J.A. (1999). Frontiers in Neuroscience. In: Roach, R.C., Wagner, P.D., Hackett, P.H. (eds) Hypoxia. Advances in Experimental Medicine and Biology, vol 474. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4711-2_9
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DOI: https://doi.org/10.1007/978-1-4615-4711-2_9
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