Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-6219
Schoonman, G G; Sàndor, P S; Nirkko, A C; Lange, T; Jaermann, T; Dydak, U; Kremer, C; Ferrari, M D; Boesiger, P; Baumgartner, R (2008). Hypoxia-induced acute mountain sickness is associated with intracellular cerebral edema: a 3 T magnetic resonance imaging study. Journal of Cerebral Blood Flow and Metabolism, 28(1):198-206.
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Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N2 to obtain arterial O2 saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80plusminus0.09; 6 h hypoxia, 0.81plusminus0.09; P=0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1plusminus98.2; 6 h hypoxia, 450.7plusminus102.5; P<0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients (r=-0.83, P=0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Institute of Biomedical Engineering|
04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurology
610 Medicine & health
|Deposited On:||10 Dec 2008 14:38|
|Last Modified:||27 Nov 2013 22:10|
|Publisher:||Nature Publishing Group|
|Citations:||Web of Science®. Times cited: 24|
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