Boly Melanie, Jones Benjamin, Findlay Graham, Plumley Erin, Mensen Armand, Hermann Bruce, Tononi Guilio, Maganti Rama
Department of Neurology, University of Wisconsin, Madison, USA.
Department of Psychiatry, University of Wisconsin, Madison, USA.
Brain. 2017 Apr 1;140(4):1026-1040. doi: 10.1093/brain/awx017.
In animal studies, both seizures and interictal spikes induce synaptic potentiation. Recent evidence suggests that electroencephalogram slow wave activity during sleep reflects synaptic potentiation during wake, and that its homeostatic decrease during the night is associated with synaptic renormalization and its beneficial effects. Here we asked whether epileptic activity induces plastic changes that can be revealed by high-density electroencephalography recordings during sleep in 15 patients with focal epilepsy and 15 control subjects. Compared to controls, patients with epilepsy displayed increased slow wave activity power during non-rapid eye movement sleep over widespread, bilateral scalp regions. This global increase in slow wave activity power was positively correlated with the frequency of secondarily generalized seizures in the 3-5 days preceding the recordings. Individual patients also showed local increases in sleep slow wave activity power at scalp locations matching their seizure focus. This local increase in slow wave activity power was positively correlated with the frequency of interictal spikes during the last hour of wakefulness preceding sleep. By contrast, frequent interictal spikes during non-rapid eye movement sleep predicted a reduced homeostatic decrease in the slope of sleep slow waves during the night, which in turn predicted reduced daytime learning. Patients also showed an increase in sleep spindle power, which was negatively correlated with intelligence quotient. Altogether, these findings suggest that both seizures and interictal spikes may induce long-lasting changes in the human brain that can be sensitively detected by electroencephalographic markers of sleep homeostasis. Furthermore, abnormalities in sleep markers are correlated with cognitive impairment, suggesting that not only seizures, but also interictal spikes can have negative consequences.
在动物研究中，癫痫发作和发作间期棘波均可诱导突触增强。最近的证据表明，睡眠期间的脑电图慢波活动反映了清醒时的突触增强，而其在夜间的稳态下降与突触重新规范化及其有益作用相关。在此，我们研究了癫痫活动是否会诱导可塑性变化，这种变化能否通过15例局灶性癫痫患者和15名对照受试者睡眠期间的高密度脑电图记录揭示出来。与对照组相比，癫痫患者在非快速眼动睡眠期间双侧广泛头皮区域的慢波活动功率增加。慢波活动功率的这种整体增加与记录前3 - 5天继发性全面性癫痫发作的频率呈正相关。个体患者在与癫痫发作灶对应的头皮位置也显示出睡眠慢波活动功率的局部增加。慢波活动功率的这种局部增加与睡眠前清醒最后一小时内发作间期棘波的频率呈正相关。相比之下，非快速眼动睡眠期间频繁的发作间期棘波预示着夜间睡眠慢波斜率的稳态下降减少，这反过来又预示着白天学习能力下降。患者还表现出睡眠纺锤波功率增加，这与智商呈负相关。总之，这些发现表明，癫痫发作和发作间期棘波均可在人脑中诱导持久变化，这些变化可通过睡眠稳态的脑电图标记物灵敏地检测到。此外，睡眠标记物异常与认知障碍相关，这表明不仅癫痫发作，发作间期棘波也可能产生负面后果。
