The study was undertaken to determine whether normobaric hypoxia causes elevated brain volume and intracranial pressure in individuals with symptoms consistent with acute mountain sickness (AMS).
Thirteen males age = (26 (sd 6)) years were exposed to normobaric hypoxia (12% O2) and normoxia (21% O2). After 2 and 10 hours, AMS symptoms were assessed alongside ventricular and venous vessel volumes, cerebral blood flow, regional brain volumes, and intracranial pressure, using high-resolution magnetic resonance imaging.
In normoxia, neither lateral ventricular volume (R2 = 0.07, p = 0.40) nor predominance of unilateral transverse venous sinus drainage (R2 = 0.07, p = 0.45) was related to AMS symptoms. Furthermore, despite an increase in cerebral blood flow after 2 hours of hypoxia (hypoxia vs normoxia: Δ148ml/min−1, 95% confidence interval [CI] = 58 to 238), by 10 hours, when AMS symptoms had developed, cerebral blood flow was normal (Δ−51ml/min−1, 95% CI = −141 to 39). Conversely, at 10 hours brain volume was increased (Δ59ml, 95% CI = 8 to 110), predominantly due to an increase in gray matter volume (Δ73ml, 95% CI = 25 to 120). Therefore, cerebral spinal fluid volume was decreased (Δ−40ml, 95% CI = −67 to −14). The intracranial pressure response to hypoxia varied between individuals, and as hypothesized, the most AMS-symptomatic participants had the largest increases in intracranial pressure (AMS present, Δ7mmHg, 95% CI = −2.5 to 17.3; AMS not present, Δ−1mmHg, 95% CI = −3.3 to 0.5). Consequently, there was a significant relationship between the change in intracranial pressure and AMS symptom severity (R2 = 0.71, p = 0.002).
The data provide the strongest evidence to date to support the hypothesis that the “random” nature of AMS symptomology is explained by a variable intracranial pressure response to hypoxia. ANN NEUROL 2014