Aerosp Med Hum Perform. 2024 Oct;95(10):733-740. doi: 10.3357/AMHP.6445.2024.
The pathophysiological basis of neurological decompression sickness and the association between cerebral subcortical white matter (WM) change and nonhypoxic hypobaria remain poorly understood. Recent study of altitude decompression sickness risk evaluated acute WM responses to intensive hypobaric exposure using brain magnetic resonance imaging.
Six healthy men (20 to 50 yr) completed 6 h of hyperoxic hypobaria during three same-day altitude chamber decompressions to pressure altitudes ≥ 22,000 ft (6706 m). Research magnetic resonance imaging sequences, conducted on the days preceding and following decompression, evaluated subcortical WM integrity, cerebral blood flow, neuronal integrity (fractional anisotropy), and neurometabolite concentrations.
No subcortical lesions were evident on diffusion weighted imaging and WM fractional anisotropy was unaffected. Mean WM blood flow was upregulated by 20% to over 25 mL · 100 g-1 · min-1. Gray matter flow was unchanged. There were no changes in gray matter or cerebellar neurometabolites. In parietal subcortical WM, levels of γ-aminobutyric acid (GABA) fell from (mean ± SD) 1.68 ± 0.2 to 1.35 ± 0.3 institutional units while glutathione (GSH) fell from 1.71 ± 0.4 to 1.25 ± 0.3 institutional units. Lactate increased postexposure in five subjects.
Postexposure decrements in GABA and GSH imply WM insult with loss of neuroprotection and oxidative stress. An association between decrements in GABA and GSH support a common origin, while GSH decrements also correlate with WM blood flow responses. WM lactate increments are prone to error but suggest dysregulation of subcortical microvascular flow. WM neurometabolite and blood flow indices did not normalize by 24 h postexposure. Connolly D, Davagnanam I, Wylezinska-Arridge M, Mallon D, Wastling S, Lee VM. Brain magnetic resonance imaging responses to nonhypoxic hypobaric decompression. Aerosp Med Hum Perform. 2024; 95(10):733-740.
神经减压病的病理生理基础以及脑皮质下白质（WM）变化与非缺氧性低气压之间的关联仍知之甚少。最近对高原减压病风险的研究评估了使用脑磁共振成像对强化低压暴露下急性 WM 反应。
6 名健康男性（20 至 50 岁）在 3 天内完成了 6 小时的高氧低压暴露，减压至 22000 英尺（6706 米）以上的压力高度。在减压前和减压后的几天进行了研究性磁共振成像序列，评估了皮质下 WM 完整性、脑血流、神经元完整性（各向异性分数）和神经代谢物浓度。
在弥散加权成像上未见皮质下病变，WM 各向异性分数不受影响。WM 平均血流量增加 20%，超过 25 毫升·100 克-1·分钟-1。灰质血流无变化。灰质或小脑神经代谢物无变化。在顶叶皮质下 WM 中，γ-氨基丁酸（GABA）水平从（平均值±标准差）1.68±0.2 降至 1.35±0.3 个机构单位，而谷胱甘肽（GSH）从 1.71±0.4 降至 1.25±0.3 个机构单位。5 名受试者在暴露后出现乳酸增加。
暴露后 GABA 和 GSH 的减少意味着 WM 损伤，导致神经保护和氧化应激丧失。GABA 和 GSH 减少之间的关联支持其共同起源，而 GSH 减少也与 WM 血流反应相关。WM 乳酸的增加容易出错，但表明皮质下微血管血流失调。WM 神经代谢物和血流指数在暴露后 24 小时内未恢复正常。Connolly D、Davagnanam I、Wylezinska-Arridge M、Mallon D、Wastling S、Lee VM。非缺氧性低压减压的脑磁共振成像反应。航空航天医学与人类绩效。2024;95（10）：733-740。
