ABSTRACT
The central nervous system is exquisitely sensitive to hypoxia, so it is not surprising that impairment of neuropsychological function occurs at high altitude. Brain oxygenation is a function of both the arterial PO2 and cerebral blood flow. The latter is regulated in part by the arterial blood gases. Hypoxemia causes cerebral vasodilatation while a reduced arterial PCO2 results in cerebral vasoconstriction. Therefore, these are conflicting factors at high altitude. Some impairment of neuropsychological function, for example slow learning of complex mental tasks, can be demonstrated at altitudes of less than 2000 m. At higher altitudes many aspects of neuropsychological function have been shown to be impaired including reaction time, hand-eye coordination, and higher functions such as memory and language expression. Several studies have documented residual impairment of neuropsychological function after ascents to very high altitude. An interesting finding is that climbers with a high hypoxic ventilatory response tend to have the most severe residual impairment, possibly because the associated reduced arterial PCO2 causes cerebral vasoconstriction and therefore diminished oxygen delivery, and more severe cere-
improves neuropsychological function at an altitude of 5000 m and therefore improves performance in commuters to mines and telescopes.
