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Emerging concepts in acute mountain sickness and high-altitude cerebral edema: from the molecular to the morphological

机译:急性高山病和高海拔脑水肿的新兴概念:从分子到形态

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摘要

Acute mountain sickness (AMS) is a neurological disorder that typically affects mountaineers who ascend to high altitude. The symptoms have traditionally been ascribed to intracranial hypertension caused by extracellular vasogenic edematous brain swelling subsequent to mechanical disruption of the blood–brain barrier in hypoxia. However, recent diffusion-weighted magnetic resonance imaging studies have identified mild astrocytic swelling caused by a net redistribution of fluid from the “hypoxia-primed” extracellular space to the intracellular space without any evidence for further barrier disruption or additional increment in brain edema, swelling or pressure. These findings and the observation of minor vasogenic edema present in individuals with and without AMS suggest that the symptoms are not explained by cerebral edema. This has led to a re-evaluation of the relevant pathogenic events with a specific focus on free radicals and their interaction with the trigeminovascular system. (Part of a multi-author review.)
机译:急性高山病(AMS)是一种神经系统疾病,通常会影响到高海拔地区的登山者。传统上,这些症状归因于缺氧时血脑屏障的机械性破坏引起的细胞外血管源性水肿性脑肿胀引起的颅内高压。但是,最近的弥散加权磁共振成像研究已经发现轻度的星形胶质细胞肿胀是由流体从“低氧引发的”细胞外空间向细胞内空间的净再分配所引起的,而没有任何证据表明屏障进一步破坏或脑水肿进一步增加,肿胀或压力。这些发现以及对患有和不患有AMS的个体中存在的轻微血管性水肿的观察表明,脑水肿不能解释症状。这导致对相关致病事件的重新评估,尤其是自由基及其与三叉神经血管系统的相互作用。 (多作者审阅的一部分。)

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