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Molecular Pathogenesis of Cerebral Aneurysms: Current Concepts and Future Directions

机译:脑动脉瘤的分子发病机制:当前的概念和未来方向

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Cerebral aneurysms (CAs) are pathological dilations of cerebral arteries, most commonly seen at points of bifurcation in the major arteries forming the circle of Willis at the base of the brain. CAs are relatively common with a prevalence estimated to be as high as 6% in autopsy specimens [1,2]. Each year in the U.S., more than 30,000 people experience a subarachnoid hemorrhage (SAH) from the rupture of such an aneurysm. Unfortunately, 50% of these patients will die either at the moment of rupture or shortly thereafter. Another 25% will suffer devastating neurological complications resulting in loss of motor or cognitive function with consequent institutionalization and with enormous costs to the individual as well as to the system that has to care for a chronic patient. Finally, even the remaining 25% will experience protracted hospitalization and some degree of cognitive or neurological impairment. In contrast, operative repair of an unruptured CA has a mortality of less than 2.5% and morbidity of less then 6% [3].
机译:脑动脉瘤(CA)是脑动脉,在主要动脉形成威利斯在大脑底部的圆分叉点的最常见的病理性扩张术。 CA是比较常见的与患病率估计为高达在尸检标本[1,2] 6%。每年在美国,有超过30000人体验到这种动脉瘤破裂蛛网膜下腔出血(SAH)。不幸的是,这些患者中的50%将在此刻之后不久破裂或死亡要么。另外25%将遭受毁灭性导致电机或认知功能与随之而来的制度化的损失,并具有巨大的成本对个人以及为有照顾长期病患者的神经系统并发症。最后,即使剩下的25%将经历长期的住院和某种程度的认知或神经损伤。与此相反,未破裂CA的手术修复具有小于2.5%的死亡率和发病率小于6%[3]。

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