全身性强直阵挛性癫痫发作(GTCS)与皮肤电活动(EDA)升高和全身脑电图抑制(PGES)有关,可能表明癫痫突然意外死亡(SUDEP)风险的标记。这项研究调查了GTCS符号学的关联,EDA,癫痫儿童的PGES。
波士顿儿童医院长期视频脑电图监测单元收治的患者佩戴了记录EDA的传感器。我们选择了至少有一个GTCS的患者,并回顾了视频EEG的符号学,强直和阵挛性阶段持续时间,总临床癫痫发作持续时间,电图开始,偏移,和PGES。我们将患者分为三个符号学类别:GTCS1:双侧对称强直性手臂伸展,GTCS2:没有特定的强直手臂伸展或弯曲,GTCS3:单侧或不对称手臂伸展,不适合GTCS1或2的强直臂屈曲或姿势。我们分析了符号学之间的相关性,EDA,和PGES,并测量发作EDA(癫痫发作至一小时后)的曲线下面积(AUC),减去基线EDA(癫痫发作前1小时无癫痫发作)。利用广义估计方程(GEE)和线性回归,我们分析了每位患者的所有癫痫发作和单次发作.
我们纳入了30名患者(中位年龄13.8±3.6岁,46.7%女性)和53次癫痫发作。有了GEE,与GTCS2相比,GTCS1与更长的PGES持续时间相关(估计值(β)=-26.32s,95%置信区间(CI):-36.46至-16.18,p<0.001),PGES的存在与更大的EDA变化相关(β=429604μS,95%CI:3550.96至855657.04,p=0.048)。通过单集分析,GTCS1的EDA变化大于GTCS2((β=-601339μS,95%CI:-1167016.56至-35661.44,p=0.047)。EDA随PGES的存在而增加(β=637500μS,95%CI:183571.84至1091428.16,p=0.01)和持续时间(β=16794μS,95%CI:5729.8至27858.2,p=0.006)。与GTCS2相比,GTCS1患者的PGES持续时间更长(β=-30.53s,95%CI:-44.6至-16.46,p<0.001)和GTCS3(β=-22.07s,95%CI:-38.95至-5.19,p=0.016)。
在患有癫痫的儿童中,PGES与较大的发作性EDA相关。GTCS1与更长的PGES持续时间相关,并可能与更大的发作EDA间接相关。我们的研究表明,在这些患者中监测和预防SUDEP的潜在应用。
Generalized tonic-clonic seizures (GTCS) are associated with elevated electrodermal activity (EDA) and postictal generalized electroencephalographic suppression (
PGES), markers that may indicate sudden unexpected death in epilepsy (SUDEP) risk. This study investigated the association of GTCS semiology, EDA, and
PGES in children with epilepsy.
Patients admitted to the Boston Children\'s Hospital long-term video-EEG monitoring unit wore a sensor that records EDA. We selected patients with at least one GTCS and reviewed video-EEGs for semiology, tonic and clonic phase duration, total clinical seizure duration, electrographic onset, offset, and PGES. We grouped patients into three semiology classes: GTCS 1: bilateral symmetric tonic arm extension, GTCS 2: no specific tonic arm extension or flexion, GTCS 3: unilateral or asymmetrical arm extension, tonic arm flexion or posturing that does not fit into GTCS 1 or 2. We analyzed the correlation between semiology, EDA, and
PGES, and measured the area under the curve (AUC) of the ictal EDA (seizure onset to one hour after), subtracting baseline EDA (one-hour seizure-free before seizure onset). Using generalized estimating equation (GEE) and linear regression, we analyzed all seizures and single episodes per patient.
We included 30 patients (median age 13.8 ± 3.6 years, 46.7% females) and 53 seizures. With GEE, GTCS 1 was associated with longer PGES duration compared to GTCS 2 (Estimate (β) = -26.32 s, 95% Confidence Interval (CI): -36.46 to -16.18, p < 0.001), and the presence of PGES was associated with greater EDA change (β = 429604 μS, 95% CI: 3550.96 to 855657.04, p = 0.048). With single-episode analysis, GTCS 1 had greater EDA change than GTCS 2 ((β = -601339 μS, 95% CI: -1167016.56 to -35661.44, p = 0.047). EDA increased with PGES presence (β = 637500 μS, 95% CI: 183571.84 to 1091428.16, p = 0.01) and duration (β = 16794 μS, 95% CI: 5729.8 to 27858.2, p = 0.006). Patients with GTCS 1 had longer PGES duration compared to GTCS 2 (β = -30.53 s, 95% CI: -44.6 to -16.46, p < 0.001) and GTCS 3 (β = -22.07 s, 95% CI: -38.95 to -5.19, p = 0.016).
In children with epilepsy,
PGES correlates with greater ictal EDA. GTCS 1 correlated with longer
PGES duration and may indirectly correlate with greater ictal EDA. Our study suggests potential applications in monitoring and preventing SUDEP in these patients.