Transient neurological disorders during a simulated ascent of Mount Everest

Transient neurological disorders are often observed at high altitude but are poorly documented under field conditions. The mechanism usually invoked is a hypocapnic vasoconstriction due to severe hypoxic hyperventilation. During a simulated ascent of Mount Everest in a hypobaric chamber by eight volunteer alpinists (Operation Everest III, Comex '97), three subjects presented neurological symptoms. We report here on the clinical observations and testing to detect mechanisms in addition to hypocapnic vasoconstriction.

The experiment was designed to investigate factors limiting physiological performance at altitude and the pathophysiology of acute mountain sickness. A retrospective analysis was made comparing the three cases of transient neurological disorder at high altitude (TNDHA) with the five subjects who had no neurological symptoms.

Analysis of clinical and blood parameters showed no difference between cases and controls. The cases showed no neurological sequelae following the experiment and were normal on cardiac imaging. However, one case had a history of migraine in his youth, leading us to hypothesize that segmental vasoconstriction was a factor. In another case, gas bubbles were detected in the pulmonary artery by transthoracic echocardiography when he was symptomatic, suggesting that gas emboli may have played a role. All three cases shared a possible triggering factor in that each experienced hyperventilation alternating with straining against a closed glottis shortly before the onset of symptoms.

Mechanisms other than hypocapnic vasoconstriction in hypoxia may be causal factors of TNDHA. The existence of triggering factors and evidence of a possible embolic mechanism should be further explored.