Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations
Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations
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DOI：
10.1093/brain/awl297
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发表时间：
2006-12-01
期刊：
影响因子：
14.5
通讯作者：
Strong, Anthony J.
中科院分区：
文献类型：
--
作者：
Dreier, Jens P.;Woitzik, Johannes;Strong, Anthony J.
动物中的进行性缺血性损伤与神经元和星形胶质细胞的扩散性质量去极化相关，检测为扩散性负慢电压变化。在过去的60年里，关于人类缺血性卒中是否会发生扩散性去极化的猜测一直在继续。因此，我们进行了一项前瞻性多中心研究，评估了需要动脉瘤手术的严重蛛网膜下腔出血（SAH）患者中扩散性去极化和迟发性缺血性神经功能缺损（DIND）的发生率和时间。将硬膜下电极条放置在大脑皮层上，通过皮层电描记术记录扩展去极化，持续10天。共分析了2110 h的记录时间。每6 h监测一次临床状态。SAH后迟发性梗死通过连续CT扫描和/或MRI证实。皮质电图显示13/18例患者（72%）出现298次扩散性去极化。7例患者在SAH后7.8天（7.3，8.2）观察到临床DIND。在每一个病例中，DIND被时间锁定为一系列复发性扩散去极化（阳性和阴性预测值分别为86%和100%）。在4例患者中，记录区出现迟发性梗死。与动物的缺血半暗带一样，在每种情况下，迟发性梗死之前都会出现与广泛去极化相关的皮质电图抑制期进行性延长至> 60分钟。本研究表明，弥漫性去极化在严重SAH和缺血性卒中中发生率较高。重复的扩散性去极化和延长的抑郁期是SAH后迟发性缺血性脑损伤的早期指标。鉴于实验证据和目前的临床结果，我们认为，扩展性去极化与长期抑郁症是一个很有前途的目标，在SAH和缺血性中风的治疗发展。
Progressive ischaemic damage in animals is associated with spreading mass depolarizations of neurons and astrocytes, detected as spreading negative slow voltage variations. Speculation on whether spreading depolarizations occur in human ischaemic stroke has continued for the past 60 years. Therefore, we performed a prospective multicentre study assessing incidence and timing of spreading depolarizations and delayed ischaemic neurological deficit (DIND) in patients with major subarachnoid haemorrhage (SAH) requiring aneurysm surgery. Spreading depolarizations were recorded by electrocorticography with a subdural electrode strip placed on cerebral cortex for up to 10 days. A total of 2110 h recording time was analysed. The clinical state was monitored every 6 h. Delayed infarcts after SAH were verified by serial CT scans and/or MRI. Electrocorticography revealed 298 spreading depolarizations in 13 of the 18 patients (72%). A clinical DIND was observed in seven patients 7.8 days (7.3, 8.2) after SAH. DIND was time-locked to a sequence of recurrent spreading depolarizations in every single case (positive and negative predictive values: 86 and 100%, respectively). In four patients delayed infarcts developed in the recording area. As in the ischaemic penumbra of animals, delayed infarction was preceded by progressive prolongation of the electrocorticographic depression periods associated with spreading depolarizations to > 60 min in each case. This study demonstrates that spreading depolarizations have a high incidence in major SAH and occur in ischaemic stroke. Repeated spreading depolarizations with prolonged depression periods are an early indicator of delayed ischaemic brain damage after SAH. In view of experimental evidence and the present clinical results, we suggest that spreading depolarizations with prolonged depressions are a promising target for treatment development in SAH and ischaemic stroke.