Nonconvulsive Seizures in Subarachnoid Hemorrhage Link Inflammation and Outcome
Nonconvulsive Seizures in Subarachnoid Hemorrhage Link Inflammation and Outcome
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DOI：
10.1002/ana.24166
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发表时间：
2014-05-01
影响因子：
11.2
通讯作者：
Badjatia, Neeraj
中科院分区：
文献类型：
--
作者：
Claassen, Jan;Albers, David;Badjatia, Neeraj
目的：非惊厥性癫痫发作（NCSz）在急性脑损伤后很常见，并且被认为是继发性脑损伤的原因，但引起 NCSz 的机制存在争议。促炎症状态在许多脑损伤后很常见，炎症介导的血脑屏障通透性变化已在实验中与癫痫发作相关。方法：在这项针对动脉瘤性蛛网膜下腔出血 (SAH) 患者的前瞻性观察研究中，我们探讨了 SAH 后的炎症反应与住院 NCSz 研究临床（全身炎症反应综合征）之间的联系。 [SIRS]）和实验室（肿瘤坏死因子受体 1 [TNF-R1]、高敏 C 反应蛋白 [hsCRP]）炎症标志物。采用 Logistic 回归、Cox 比例风险回归和中介分析来调查时间和因果关系。结果：在 479 名 SAH 患者中，53 名 (11%) 患有住院 NCSz。院内 NCSz 患者有更明显的 SIRS 反应（比值比 [OR]=1.9 每点 SIRS 增加，95% 置信区间 [CI]=1.3-2.9），炎症激增更有可能在 NCSz 发病前立即出现，SIRS 对 3 个月功能结果的负面影响部分是通过院内 NCSz 介导的。在具有炎症血清生物标志物的子集中，我们证实了这些发现将较高的血清 TNF-R1 和 hsCRP 与院内 NCSz 联系起来（OR=每 20 点 hsCRP 增加 1.2，95% CI=1.1-1.4；OR=每 100 点 TNF-R1 增加 2.5，95% CI=2.1-2.9）。炎症生物标志物与不良预后的关联部分是通过 NCSz 介导的。解释：院内 NCSz 与 SAH 后的促炎症状态独立相关，这反映在临床症状和炎症的血清生物标志物中。我们的研究结果表明，SAH 后的炎症与不良预后相关，并且这种影响至少部分是通过院内 NCSz 介导的。
Objective: Nonconvulsive seizures (NCSz) are frequent following acute brain injury and have been implicated as a cause of secondary brain injury, but mechanisms that cause NCSz are controversial. Proinflammatory states are common after many brain injuries, and inflammation-mediated changes in blood-brain barrier permeability have been experimentally linked to seizures.Methods: In this prospective observational study of aneurysmal subarachnoid hemorrhage (SAH) patients, we explored the link between the inflammatory response following SAH and in-hospital NCSz studying clinical (systemic inflammatory response syndrome [SIRS]) and laboratory (tumor necrosis factor receptor 1 [TNF-R1], high-sensitivity C-reactive protein [hsCRP]) markers of inflammation. Logistic regression, Cox proportional hazards regression, and mediation analyses were performed to investigate temporal and causal relationships.Results: Among 479 SAH patients, 53 (11%) had in-hospital NCSz. Patients with in-hospital NCSz had a more pronounced SIRS response (odds ratio [OR]=1.9 per point increase in SIRS, 95% confidence interval [CI]=1.3-2.9), inflammatory surges were more likely immediately preceding NCSz onset, and the negative impact of SIRS on functional outcome at 3 months was mediated in part through in-hospital NCSz. In a subset with inflammatory serum biomarkers, we confirmed these findings linking higher serum TNF-R1 and hsCRP to in-hospital NCSz (OR=1.2 per 20-point hsCRP increase, 95% CI=1.1-1.4; OR=2.5 per 100-point TNF-R1 increase, 95% CI=2.1-2.9). The association of inflammatory biomarkers with poor outcome was mediated in part through NCSz.Interpretation: In-hospital NCSz were independently associated with a proinflammatory state following SAH as reflected in clinical symptoms and serum biomarkers of inflammation. Our findings suggest that inflammation following SAH is associated with poor outcome and that this effect is at least in part mediated through in-hospital NCSz.