Neurology:SAH 后早期脑损伤与早期播散去极化有关

2019-02-23 杨中华 脑血管病及重症文献导读

动脉瘤破裂后,脑实质损害决定了患者的预后。初期的全面缺血会引起弥漫性全脑水肿(global cerebral edema,GCE)和不良预后。在介入前的 CT 扫描中,脑出血(ICH)周围往往环绕着局灶损害。早期或延迟局灶性损害更常见于被血液填充的脑沟和脑裂周围的皮质。在传统的病理文献中,这些损害被称为『局灶性贫血坏死(“focal anemic necroses)』,在 CT 上表现为明显的低密


动脉瘤破裂后,脑实质损害决定了患者的预后。初期的全面缺血会引起弥漫性全脑水肿(global cerebral edema,GCE)和不良预后。在介入前的 CT 扫描中,脑出血(ICH)周围往往环绕着局灶损害。早期或延迟局灶性损害更常见于被血液填充的脑沟和脑裂周围的皮质。在传统的病理文献中,这些损害被称为『局灶性贫血坏死(“focal anemic necroses)』,在 CT 上表现为明显的低密度,MRI 上表现为细胞毒性水肿。

在不同的灰质结构包括新皮质中,播散去极化(Spreading depolarization,SD)是触发细胞毒性水肿的基本原理。以此类推,SD 也可以发生于动脉瘤蛛网膜下腔出血(aSAH)、创伤性脑损伤(TBI)、自发性ICH、恶性半球卒中和心脏骤停后几分钟内。SD 是否会发展为细胞损伤依赖于局部组织的状态。SD 这个概念一直强调了波形的变化特征,后者是由局部状态决定的。

SD 会特征性引起自发性活性停止(播散抑制)。在代谢紊乱区和其周围,播散抑制持续致使组织无电活动(等电位)。在这些组织中,SD称为等电位 SD,与 TBI 后不良预后有关。同样,延长抑制的 SD 与 aSAH 后更坏的预后有关。2019年1月来自丹麦的Nina Eriksen等在 Neurology 上公布了他们的研究结果,探究 aSAH 后两个不同的时间段内(1-4天河5-8天)的SD 相关变量是否与干预前 CT上早期局灶性脑损伤体积有关。

这个观察性多中心研究共纳入了54例患者,评估了(stereologically estimated)未受累脑组织、脑室、小脑、aSAH、ICH 和局灶脑实质低密度的体积。采用硬膜下电极进行脑电监测(electrocorticographically monitored),在1-4天时间段平均监测81.8h,5-8天时间段平均监测75.9h。按照研究推荐方案记录一个记录天中峰总 SD-诱导抑制持续时间(Peak total SD-induced depression duration,PTDDD)和 SD/等电位 SD/播散抑制的峰数量。

在SAH 1-4天时间段中,SD 患者中89%存在早期局灶性脑损伤,而无 SD 患者中41%存在早期局灶性脑损伤(敏感性:89% [95% CI, 75% - 97%],特异性:59% [CI,33% - 82%],阳性预测值:83% [CI:67% - 97%],阴性预测值:71% [CI,42% - 92%],Fisher exact test,P< 0.001)。在1-4天时间段中,所有4项 SD 相关参数皆与早期局灶脑损伤的体积有关(Spearman rank order correlations)。multiple ordinal回归分析发现 PTDDD 是最重要的预测指标。

最终作者认为SAH 后早期局灶性脑损伤与早期 SD 有关,支持 SD 为局灶性脑损伤的生物学标志物。

原始出处:

RIKSEN, NINA ,et al.Early focal brain injury after subarachnoid hemorrhage correlates with spreading depolarizations.Neurology. 2019 Jan 22;92(4):e326-e341. doi: 10.1212/WNL.0000000000006814. Epub 2018 Dec 28.

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    2019-03-23 yinhl1978
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    2019-02-25 zexyw03
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    2019-02-24 飛歌

    学习了很有用不错

    0

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Neurology:低剂量阿司匹林不增加颅内出血风险,反而降低SAH风险

低剂量阿司匹林广泛应用于缺血性血管事件的二级预防,甚至用于一级预防。随机对照试验或随机对照试验联合队列研究的meta分析把阿司匹林和颅内出血风险增加联系起来,发现二者未达到统计学意义或处于边缘状态。观察性研究的结果更是模棱两可,甚至有研究认为长期服用阿司匹林能够降低蛛网膜出血的风险。

Stroke:蛛网膜下腔出血后骨质疏松症与脑积水的关系

蛛网膜下腔出血(SAH)后蛛网膜颗粒的病理性阻塞可阻碍脑脊液向静脉窦外流并引起脑积水。由于骨骼和蛛网膜颗粒具有相同的胶原类型,研究者评估了SAH后骨密度和分流依赖性脑积水的可能关系。相关研究结果于近期发表在Stroke杂志。

Neurology:同时脑梗死和蛛网膜下腔出血是什么原因?

47岁,男性。既往抽烟和高血压病史。因为突发剧烈头痛就诊。

Stroke:诱导性高血压预防 SAH 后 脑梗死

动脉瘤蛛网膜下腔出血(SAH)的发病率为6-7/10万人-年,占所有卒中的5%。一半的患者年龄低于55岁,不良预后超过50%。24h 内幸存患者不良预后最重要的原因为迟发性脑缺血(DCI),DCI 通常发生在 SAH 后4-10天。截止到目前为止,L-型钙离子拮抗剂尼莫地平是唯一被证明能够预防 SAH 后 DCI 的措施。