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脑出血后脑损伤机制

Mechanisms of brain injury after intracerebral haemorrhage.

作者信息

Xi Guohua, Keep Richard F, Hoff Julian T

机构信息

Department of Neurosurgery, University of Michigan, E Medical Centre Drive, Ann Arbor, MI 48109-0338, USA.

出版信息

Lancet Neurol. 2006 Jan;5(1):53-63. doi: 10.1016/S1474-4422(05)70283-0.

Abstract

The past decade has resulted in a rapid increase in knowledge of mechanisms underlying brain injury induced by intracerebral haemorrhage (ICH). Animal studies have suggested roles for clot-derived factors and the initial physical trauma and mass effect as a result of haemorrhage. The coagulation cascade (especially thrombin), haemoglobin breakdown products, and inflammation all play a part in ICH-induced injury and could provide new therapeutic targets. Human imaging has shown that many ICH continue to expand after the initial ictus. Rebleeding soon after the initial haemorrhage is common and forms the basis of a current clinical trial using factor VIIa to prevent rebleeding. However, questions about mechanisms of injuries remain. There are conflicting data on the role of ischaemia in ICH and there is uncertainty over the role of clot removal in ICH therapy. The next decade should bring further information about the underlying mechanisms of ICH-induced brain injury and new therapeutic interventions for this severe form of stroke. This review addresses our current understanding of the mechanisms underlying ICH-induced brain injury.

摘要

在过去十年中,人们对脑出血(ICH)所致脑损伤的潜在机制的认识迅速增加。动物研究表明,血凝块衍生因子以及出血所致的初始物理创伤和占位效应都发挥了作用。凝血级联反应(尤其是凝血酶)、血红蛋白分解产物和炎症在脑出血诱导的损伤中均起作用,并可能提供新的治疗靶点。人体成像显示,许多脑出血在初次发作后仍会继续扩大。初次出血后不久再出血很常见,这也是目前一项使用凝血因子VIIa预防再出血的临床试验的基础。然而,关于损伤机制的问题依然存在。关于缺血在脑出血中的作用存在相互矛盾的数据,并且脑出血治疗中血凝块清除的作用尚不确定。未来十年应该会带来更多关于脑出血诱导脑损伤潜在机制的信息以及针对这种严重中风形式的新治疗干预措施。本综述阐述了我们目前对脑出血诱导脑损伤潜在机制的理解。

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