Schoonman Guus G, Sándor Peter S, Nirkko Arto C, Lange Thomas, Jaermann Thomas, Dydak Ulrike, Kremer Christine, Ferrari Michel D, Boesiger Peter, Baumgartner Ralf W
Department of Neurology, University Medical Center, Leiden, The Netherlands.
J Cereb Blood Flow Metab. 2008 Jan;28(1):198-206. doi: 10.1038/sj.jcbfm.9600513. Epub 2007 May 23.
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 N(2) to obtain arterial O(2) 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, 0.80+/-0.09; 6 h hypoxia, 0.81+/-0.09; P=0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1+/-98.2; 6 h hypoxia, 450.7+/-102.5; 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.
急性高原病在未适应高原环境而登高的人群中很常见；其潜在机制尚不清楚，但可能与脑水肿有关。对9名健康男性学生在等压性低氧暴露6小时前后进行了研究。受试者吸入富含N₂的室内空气，以使动脉血氧饱和度达到75%至80%。用环境症状问卷评估急性高原病，并用3T磁共振成像在脑白质的18个感兴趣区域评估脑水肿。主要观察指标是通过肉眼观察以及对扩散加权成像得出的表观扩散系数和T2加权成像得出的B0信号强度进行定量分析，评估细胞内和细胞外脑白质水肿的发展情况。9名受试者中有7人出现了急性高原病。平均表观扩散系数增加了2.12%（基线值为0.80±0.09；低氧6小时后为0.81±0.09；P = 0.034），平均B0信号强度增加了4.56%（基线值为432.1±98.2；低氧6小时后为450.7±102.5；P < 0.001）。磁共振图像的肉眼观察未发现脑水肿。脑急性高原病评分与表观扩散系数的相对变化呈负相关（r = -0.83，P = 0.006）；与B0信号强度的相对变化无相关性。总之，在大多数受试者中，等压性低氧与轻度细胞外（血管源性）脑水肿有关，无论是否存在急性高原病，而严重急性高原病则伴有额外的轻度细胞内（细胞毒性）脑水肿。
