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Updated: Dec 30, 2025

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Transient Cerebral Ischemia at High Altitude and Hyper-Responsiveness to Hypoxia
Jean-Paul Richalet1,2,3, Philippe Larmignat2, Patricia Poignard4
1INSERM U1272 Hypoxie et Poumon, Université Paris 13, Bobigny, France.
Abstract:
A 36-year-old woman with no medical history participated in a trekking in Ladakh up to 5300 m of altitude. She was well acclimatized and presented no previous sign of acute mountain sickness, high altitude pulmonary edema or high altitude cerebral edema. After an intense effort to catch up with her group, she became breathless and complained of visual disturbances, fatigue, dizziness, and confusion. During her descent to a lower altitude (4800 m), with the help of companions, she lost consciousness several times. After a 14-hour sleep, she recovered and all symptoms disappeared so that she was able to walk along with the group for 20 km. On returning home, she went through a battery of examinations that were all normal: cerebral magnetic resonance imaging, Doppler of supra-aortic arteries, 24 hours Holter, and cardiac transthoracic and transesophageal echography. A hypoxia exercise test revealed a hyper-response to hypoxia with severe hypocapnia. The etiology of this neurological episode is discussed (transient embolic ischemic attack, migraine, cerebral edema, and global amnesia). The patchy distribution of neurological symptoms is not in favor of a thrombotic event. The most probable diagnosis proposed is a transient cerebral ischemia due to local cerebral vasoconstriction related to hyperventilation-induced hypocapnia in a context of acute severe exercise. Special attention should be given to subjects who show a hyper-responsiveness to hypoxia before a sojourn at high altitude: they should avoid unnecessary hyperventilation due to any kind of stress, emotion, or exhaustive exercise.
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