Regional differences in the cerebral blood flow velocity response to hypobaric hypoxia at high altitudes.

Symptoms of acute mountain sickness (AMS) may appear above 2,500 m altitude, if the time allowed for acclimatization is insufficient. As the mechanisms underlying brain adaptation to the hypobaric hypoxic environment are not fully understood, a prospective study was performed investigating neurophysiological changes by means of near infrared spectroscopy, electroencephalograpy (EEG), and transcranial doppler sonography at 100, 3,440 and 5,050 m above sea level in the Khumbu Himal, Nepal. Fourteen of the 26 mountaineers reaching 5,050 m altitude developed symptoms of AMS between 3,440 and 5,050 m altitude (Lake-Louise Score ⩾3). Their EEG frontal beta activity and occipital alpha activity increased between 100 and 3,440 m altitude, i.e., before symptoms appeared. Cerebral blood flow velocity (CBFV) in the anterior and middle cerebral arteries (MCAs) increased in all mountaineers between 100 and 3,440 m altitude. During further ascent to 5,050 altitude, mountaineers with AMS developed a further increase in CBFV in the MCA, whereas in all mountaineers CBFV decreased continuously with increasing altitude in the posterior cerebral arteries. These results indicate that hypobaric hypoxia causes different regional changes in CBFV despite similar electrophysiological changes.

Noninvasive assessment of cerebral oxygenation during high altitude trekking in the Nepal Himalayas (2850-5600 m).

Mountain trekking is significantly increasing in popularity. Hypoxia seems to play a key role in the pathogenesis of acute mountain sickness (AMS). The purpose of this study was to investigate regional cerebral (rSO2) and peripheral (SaO2) oxygen saturation for the first time, during 22 days high altitude trekking (measurement points: 3450, 4450, 4750, 5050 and 2850 m) in the Khumbu region of Nepal with near infrared spectroscopy and pulse oximetry. We examined 17 healthy volunteers 19-65 years old (8 female, 9 male; mean age +/- SD, 46.1 +/- 13.1 years). RSO2 and SaO2 were significantly (p < 0.001, ANOVA, Tukey test) decreased at high altitudes (4450, 4750 and 5050 m). The decrease in cerebral oxygen saturation was more pronounced at higher altitudes than in the periphery (rSO2/SaO2 = 0.56 at 5050 m). At higher altitudes (> 4450 m), two subjects showed reversible symptoms of AMS. The present data indicates that acute reduction in rSO2 values might be a primary cause of AMS, however, further studies and analysis are necessary to correlate our findings with cerebral symptom scores.