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Into Thin Air: Mountain Climbing Kills Brain Cells

The neural cost of high-altitude mountaineering

Three attributes of a good mountaineer are high pain threshold, bad memory, and ... I forget the third.                                                                                                                              —Joke in a mountaineering Internet chat room

IN THE LATE 1890s in a laboratory atop a 4,554-meter peak in the Monta Rosa range in the Italian Alps, physiologist Angelo Mosso made the first direct observations of the effects of high altitude on the human brain: by eye and with an apparatus he designed, Mosso peeked into the skull of a man whose brain had been partly exposed in an accident, observing changes in swelling and pulsation.

Now a similar experiment has been done with noninvasive brain imaging, and for those of us who love to climb the results are not elevating. Neurologist Nicolás Fayed and his colleagues in Zaragoza, Spain, performed MRI brain scans on 35 climbers (12 professionals and 23 amateurs) who had returned from high-altitude expeditions, including 13 who had attempted Everest. They found brain damage in virtually every Everest climber but also in many climbers of lesser peaks who returned unaware that they had injured their brain. It seems that climbers of high mountains, whether weekend warrior or seasoned professional, face returning from the high peaks with a brain that is not in the same condition it was in beforehand.

What Gives in a Climber’s Brain?
Although a person’s tolerance to hypoxia (lack of oxygen) varies according to differences in innate physiology and physical conditioning, no one is immune. Those effects can be acute, affecting you only while you are at altitude, or—as the Fayed study found—they can be longer-lasting.

The first acute stage is called, naturally enough, acute mountain sickness. It can cause headache, insomnia, dizziness, fatigue, nausea and vomiting. The next, more serious stage is high-­altitude cerebral edema, also known as HACE, brain swelling that is potentially fatal.

Lack of oxygen can directly damage brain cells. In addition, the walls of blood capillaries begin to leak at high altitudes, and the leaked fluid can cause dangerous swelling, pressing the brain outward against the rigid skull. Sometimes the optic nerves swell so badly they bulge into the back of the eye, degrading vision and causing retinal hemorrhages. Meanwhile blood, concentrated from dehydration and thickened by increased numbers of red blood cells, clots more easily. This clotting, along with the hemorrhage from the thinned capillaries, can cause a stroke. A climber with HACE may experience amnesia, confusion, ­delusions, emotional disturbance, personality changes and loss of consciousness.

Severe cases of acute high-altitude disease have long been known to cause brain damage. But one of the sobering things about the Fayed study is that even when climbers showed no signs of acute sickness, the scans still found brain damage.

The results in the Everest climbers were the starkest. Of the 13 climbers, three had made the 8,848-meter summit, three had reached 8,100 meters, and seven had topped out between 6,500 and 7,500 meters. The expedition had no major mishaps, and none of the 12 professional climbers evinced any obvious signs of high-altitude illness; the only acute case of mountain sickness was a mild one in the expedition’s amateur climber. Yet only one of the 13 climbers (a professional) returned with a normal brain scan. All the scans of the other 12 showed cortical atrophy or enlargement of the Virchow-Robin (VR) spaces. These  spaces surround the blood vessels that drain brain fluid and communicate with the lymph system; widening of these VR spaces is seen in the elderly but rarely in the young. The amateur climber’s brain had also suffered subcortical lesions in the frontal lobes.

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