背景:癫痫性脑病(EE-SWAS)是一种儿童综合征,特征为非快速眼动睡眠期间脑电图中的弥漫性或广泛性尖峰波活动。在一些研究中已经证明神经肽在睡眠-觉醒周期中起作用并且显示惊厥和抗惊厥特征。在这项研究中,我们的目的是调查EE-SWAS和神经肽如强啡肽,甘丙肽,ghrelin,瘦素,褪黑激素,和Orexin.
方法:这项多中心研究于2019年7月至2021年1月进行。分为三组:第1组包含EE-SWAS患者。第2组包括儿童自限性局灶性癫痫(SeLFE)患者,第3组为对照组。比较这三组血清中神经肽的水平。
结果:有59名年龄在4至15岁之间的儿童。第一组有14名儿童,第二组有24个孩子,第3组有21名儿童。与第3组相比,第1组的瘦素水平较高,褪黑素水平较低(分别为P=0.01和P=0.005)。在第3组中,食欲素水平低于第2组和第3组(P=0.01和P=0.01)。
结论:这些数据表明,与对照组相比,EE-SWAS患者的瘦素水平较高,褪黑素水平较低。此外,EE-SWAS患者的食欲素水平低于对照组和SeLFE患者.需要进一步的研究来了解这些神经肽在EE-SWAS病理生理学中的潜在作用。
Epileptic encephalopathy with spike-and-wave activation in sleep (EE-SWAS) is a syndrome of childhood, characterized by diffuse or generalized spike-wave activity in electroencephalography during non-rapid eye movement sleep. Neuropeptides have been demonstrated in several studies to function in the sleep-wake cycle and display convulsant and anticonvulsant features. In this study, we aimed to investigate the relationship between EE-SWAS and neuropeptides such as dynorphin, galanin, ghrelin, leptin, melatonin, and orexin.
This multicenter study was conducted from July 2019 to January 2021. There were three groups: Group 1 contained patients with EE-SWAS. Group 2 consisted of patients with self-limited focal epilepsy of childhood (SeLFE), and group 3 was the control group. Levels of neuropeptides were compared in the sera of these three groups.
There were 59 children aged between four and 15 years. Group 1 contained 14 children, group 2 contained 24 children, and group 3 contained 21 children. The level of leptin is higher and the level of melatonin is lower in group 1 than in group 3 (P = 0.01 and P = 0.005, respectively). In group 3, the level of orexin was lower than in both groups 2 and 3 (P = 0.01 and P = 0.01).
These data show that the level of leptin was higher and the level of melatonin was lower in patients with EE-SWAS than in the control group. Furthermore, patients with EE-SWAS had lower orexin levels than both the control group and patients with SeLFE. Further research is required to understand the potential role of these neuropeptides in the pathophysiology of EE-SWAS.