脑卒中后颅内压升高:机制和后果

R. Hood, Daniel J. Beard, D. McLeod, L. Murtha, N. Spratt
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引用次数: 1

摘要

脑卒中后颅内压(ICP)升高一直被认为是大面积恶性梗死后继发性恶化的原因,而显著的颅内压升高通常是终末期事件。然而,越来越多的证据表明,小卒中后,通常在梗死后24小时内,ICP也会升高。这种上升的时间提示它可能在早期梗死扩张相关的侧支衰竭中起重要作用。尽管人们越来越认识到颅内压升高对患者预后的重要性,但目前对脑卒中后颅内压升高的潜在机制知之甚少。传统的理解认为颅内压升高仅仅是由于脑水肿引起的,然而,这似乎并不适用于轻中度梗死。相反,最近的研究表明脑脊液(CSF)容量的变化起作用。在这篇文章中,我们将讨论最近的机制观察,以及卒中后颅内压升高的后果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Intracranial pressure elevation post-stroke: Mechanisms and consequences
Intracranial pressure (ICP) elevation post-stroke has long been thought of as a cause of secondary deterioration after large, malignant infarction, and dramatic ICP elevation is frequently a pre-terminal event. However, there is an increasing body of evidence to suggest that ICP also rises after small stroke, typically within 24 h of the infarct. The timing of this rise suggests that it may play an important role in the collateral failure associated with early infarct expansion. Despite its increasingly recognized importance to patient outcome, very little is currently known about the underlying mechanisms of ICP elevation post-stroke. The traditional understanding suggests ICP elevation occurs solely due to cerebral edema, however this does not seem to be the case in mild-moderate infarction. Instead, recent studies suggest a role for changes in cerebrospinal fluid (CSF) volume. In this article, we will discuss recent mechanistic observations, as well as the consequences of ICP elevation post-stroke.
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