Electroencephalography, Hospital Complications, and Longitudinal Outcomes After Subarachnoid Hemorrhage.

Electroencephalography, Hospital Complications, and Longitudinal Outcomes After Subarachnoid Hemorrhage.
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DOI:
10.1007/s12028-020-01177-x
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发表时间:
2021-10
期刊:
影响因子:
3.5
通讯作者:
Rosenthal ES
Rosenthal ES
中科院分区:
医学3区
文献类型:
--
作者:
Lissak IA;Locascio JJ;Zafar SF;Schleicher RL;Patel AB;Leslie-Mazwi T;Stapleton CJ;Koch MJ;Kim JA;Anderson K;Rosand J;Westover MB;Kimberly WT;Rosenthal ES

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在非创伤性蛛网膜下腔出血(SAH)后,院内迟发性脑缺血可通过连续EEG(cEEG)上的两个主要事件预测:新发或恶化的癫痫样异常(EAs)和cEEG背景频率恶化。我们评估了纵向结果与这些cEEG生物标志物之间的关联。我们还评估了纵向结果与其他住院并发症之间的关系。接受cEEG监测≥ 3天的非创伤性SAH患者入组了一项前瞻性研究,评价纵向结局。在出院时以及3个月和6个月随访时间点评估改良兰金量表(mRS)。在累积比例优势模型中调整基线严重程度,我们对mRS进行了顺序建模,并测量了mRS与两种形式的院内cEEG恶化之间的相关性:(1)新发或恶化的癫痫样异常的cEEG证据和(2)新发背景恶化的cEEG证据。我们比较了每个时间点这些关联的程度与mRS和其他院内并发症之间的关联:(1)迟发性脑缺血(DCI),(2)医院获得性感染(HAI)和(3)脑积水。在二次分析中,我们采用线性混合效应模型来检查随时间推移的mRS(二分为0-3 vs. 4-6)与cEEG恶化的生物标志物和其他院内并发症的相关性。总共对59例患者进行了175次mRS评估。23例(39%)患者发生新发或恶化的EA,24例(41%)发生新发背景恶化。在cEEG生物标志物中,新发或恶化的EA分别与出院、3个月和6个月时的mRS独立相关(校正的累积比例比值为4.99,95% CI 1.60-15.6; 3.28,95% CI 1.14-9.5;和2.71,95% CI 0.95-7.76),但cEEG背景恶化缺乏相关性。在住院并发症中,DCI与出院、3个月和6个月结局相关(调整后的累积比例优势4.75,95% CI 1.64-13.8; 3.4; 95% CI 1.24-9.01;和2.45,95% CI 0.94-6.6),但HAI和脑积水缺乏相关性。混合效应模型表明,这些协会持续纵向评估没有与时间的相互作用。尽管新发或恶化的EA和cEEG背景恶化均被证明可预测DCI,但只有新发或恶化的EA与功能结局的持续损害相关。这一新的发现提高了确定可能影响结果的治疗靶点的可能性。本文的在线版本(10.1007/s12028-020-01177-x)包含补充材料,可供授权用户使用。
Following non-traumatic subarachnoid hemorrhage (SAH), in-hospital delayed cerebral ischemia is predicted by two chief events on continuous EEG (cEEG): new or worsening epileptiform abnormalities (EAs) and deterioration of cEEG background frequencies. We evaluated the association between longitudinal outcomes and these cEEG biomarkers. We additionally evaluated the association between longitudinal outcomes and other in-hospital complications. Patients with nontraumatic SAH undergoing ≥ 3 days of cEEG monitoring were enrolled in a prospective study evaluating longitudinal outcomes. Modified Rankin Scale (mRS) was assessed at discharge, and at 3- and 6-month follow-up time points. Adjusting for baseline severity in a cumulative proportional odds model, we modeled the mRS ordinally and measured the association between mRS and two forms of in-hospital cEEG deterioration: (1) cEEG evidence of new or worsening epileptiform abnormalities and (2) cEEG evidence of new background deterioration. We compared the magnitude of these associations at each time point with the association between mRS and other in-hospital complications: (1) delayed cerebral ischemia (DCI), (2) hospital-acquired infections (HAI), and (3) hydrocephalus. In a secondary analysis, we employed a linear mixed effects model to examine the association of mRS over time (dichotomized as 0–3 vs. 4–6) with both biomarkers of cEEG deterioration and with other in-hospital complications. In total, 175 mRS assessments were performed in 59 patients. New or worsening EAs developed in 23 (39%) patients, and new background deterioration developed in 24 (41%). Among cEEG biomarkers, new or worsening EAs were independently associated with mRS at discharge, 3, and 6 months, respectively (adjusted cumulative proportional odds 4.99, 95% CI 1.60–15.6; 3.28, 95% CI 1.14–9.5; and 2.71, 95% CI 0.95–7.76), but cEEG background deterioration lacked an association. Among hospital complications, DCI was associated with discharge, 3-, and 6-month outcomes (adjusted cumulative proportional odds 4.75, 95% CI 1.64–13.8; 3.4; 95% CI 1.24–9.01; and 2.45, 95% CI 0.94–6.6), but HAI and hydrocephalus lacked an association. The mixed effects model demonstrated that these associations were sustained over longitudinal assessments without an interaction with time. Although new or worsening EAs and cEEG background deterioration have both been shown to predict DCI, only new or worsening EAs are associated with a sustained impairment in functional outcome. This novel finding raises the potential for identifying therapeutic targets that may also influence outcomes. The online version of this article (10.1007/s12028-020-01177-x) contains supplementary material, which is available to authorized users.
DOI: 10.1002/ana.25232
发表时间: 2018-05
影响因子: 11.2
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Rosenthal ES;Biswal S;Zafar SF;O'Connor KL;Bechek S;Shenoy AV;Boyle EJ;Shafi MM;Gilmore EJ;Foreman BP;Gaspard N;Leslie-Mazwi TM;Rosand J;Hoch DB;Ayata C;Cash SS;Cole AJ;Patel AB;Westover MB
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DOI: 10.1093/brain/awl297
发表时间: 2006-12-01
期刊: BRAIN
影响因子: 14.5
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Dreier, Jens P.;Woitzik, Johannes;Strong, Anthony J.
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DOI: 10.1212/wnl.0000000000006903
发表时间: 2019-02-12
期刊: NEUROLOGY
影响因子: 9.9
作者:
Subramaniam, Thanujaa;Jain, Aditya;Struck, Aaron F.
通讯作者: Struck, Aaron F.
DOI: 10.1016/j.clinph.2004.06.017
发表时间: 2004-12-01
影响因子: 4.7
作者:
Claassen, J;Hirsch, LJ;Mayer, SA
通讯作者: Mayer, SA
DOI: 10.1097/wnp.0000000000000281
发表时间: 2016-06
期刊: Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society
影响因子: --
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Muniz CF;Shenoy AV;OʼConnor KL;Bechek SC;Boyle EJ;Guanci MM;Tehan TM;Zafar SF;Cole AJ;Patel AB;Westover MB;Rosenthal ES
通讯作者: Rosenthal ES