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超越迟发性脑血管痉挛:蛛网膜下腔出血患者的梗死模式。

Beyond delayed cerebral vasospasm: infarct patterns in patients with subarachnoid hemorrhage.

机构信息

Institute of Neuroradiology, Goethe University Hospital, Schleusenweg 2-16, 60528, Frankfurt a. M., Germany.

出版信息

Clin Neuroradiol. 2013 Jun;23(2):87-95. doi: 10.1007/s00062-012-0166-x. Epub 2012 Aug 23.

DOI:10.1007/s00062-012-0166-x
PMID:23010691
Abstract

PURPOSE

Angiographic vasospasm (CVS) has been accused to be the main cause of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH). However, treatment success including endovascular treatment remains to be improved. We performed a pattern analysis of ischemic lesions in SAH patients in the absence of angiographic cerebral vasospasm to generate further hypotheses concerning etiology and risk factors of DCI apart from vasospastic narrowing.

METHODS

We retrospectively included 309 patients with cerebral infarcts after SAH. Vasospasm was assessed by means of CT or MR angiography and perfusion measurement or digital subtraction angiography. All clinical and radiological data were used to determine the most probable etiology for new infarcts.

RESULTS

Twenty-seven percent of patients showed infarcts without presence of angiographic vasospasm. Seventy-three percent of these "atypical infarcts" were induced by complications of aneurysm therapy, 7 % by hypoxia, 2 % by ICP-related herniation. In 17 %, the etiology remained unclear; however, disturbances of the microcirculation for different reasons were the most likely cause in these patients.

CONCLUSION

Beyond CVS and treatment complications, a not insignificant number of SAH patients suffered from infarcts of other etiology probably due to disturbance of the microcirculation. Therapeutic approaches for vasodilation of angiographic vasospasm alone should be reconsidered.

摘要

目的

血管造影性血管痉挛(CVS)被指责是蛛网膜下腔出血(SAH)后迟发性脑缺血(DCI)的主要原因。然而,包括血管内治疗在内的治疗成功率仍有待提高。我们对无血管造影性脑血管痉挛的 SAH 患者的缺血性病变进行了模式分析,以生成除血管痉挛性狭窄外关于 DCI 的病因和危险因素的进一步假设。

方法

我们回顾性纳入了 309 例 SAH 后出现脑梗死的患者。通过 CT 或 MR 血管造影和灌注测量或数字减影血管造影评估血管痉挛。所有临床和影像学数据均用于确定新梗死最可能的病因。

结果

27%的患者出现无血管造影性血管痉挛的梗死。这些“非典型梗死”中,73%是由动脉瘤治疗并发症引起的,7%是由缺氧引起的,2%是由 ICP 相关脑疝引起的。在 17%的患者中,病因仍不清楚;然而,这些患者最有可能的原因是微循环紊乱。

结论

除 CVS 和治疗并发症外,相当数量的 SAH 患者可能由于微循环紊乱而发生其他病因的梗死。单独用于血管造影性血管痉挛扩张的治疗方法应重新考虑。

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