Rapid ascent to high altitude commonly results in acute mountain sickness, and on occasion potentially fatal high-altitude
cerebral edema. The exact pathophysiological mechanisms behind these syndromes remain to be determined. We report a
study in which 12 subjects were exposed to a FiO2¼ 0.12 for 22 h and underwent serial magnetic resonance imaging sequences
to enable measurement of middle cerebral artery velocity, flow and diameter, and brain parenchymal, cerebrospinal fluid and
cerebral venous volumes. Ten subjects completed 22 h and most developed symptoms of acute mountain sickness (mean Lake
Louise Score 5.4; p< 0.001 vs. baseline). Cerebral oxygen delivery was maintained by an increase in middle cerebral artery
velocity and diameter (first 6 h). There appeared to be venocompression at the level of the small, deep cerebral veins (116 cm3
at 2 h to 97 cm3 at 22 h; p< 0.05). Brain white matter volume increased over the 22-h period (574 ml to 587 ml; p < 0.001) and
correlated with cumulative Lake Louise scores at 22 h (p< 0.05).We conclude that cerebral oxygen delivery was maintained by
increased arterial inflow and this preceded the development of cerebral edema. Venous outflow restriction appeared to play a
contributory role in the formation of cerebral edema, a novel feature that has not been observed previously