通过脑影像、血管超声、神经电生理、血液指标等临床标记物，探讨癫痫后头痛可能的发病机制。

选择2013年10月至2018年10月于天津市环湖医院癫痫监测诊疗中心的住院患者40例为研究对象，20例癫痫发作后头痛患者为试验组，20例癫痫发作后不伴头痛的患者为对照组，分别测量癫痫发作间期、癫痫发作停止后试验组患者头痛开始5 min内及对照组在癫痫发作停止后5 min内的血清5-羟色胺（5-HT）、一氧化氮（NO）、谷氨酸水平，经颅多普勒（TCD）血流变化，视频脑电图（VEEG），头部磁共振（MRI）。采用t检验比较癫痫发作间期和癫痫发作后5-HT、NO、谷氨酸和大脑前、中、后动脉血流变化的差异，采用χ²检验比较2组脑电异常放电比例和弥散加权成像（DWI）高信号比例的差异。

试验组患者与对照组患者相比，癫痫发作后血清NO含量均升高，2组升高值比较［（46.37±18.17）μmol/L vs （19.83±5.78）μmol/L］，差异具有统计学学意义（t=12.157，P=0.034）。试验组脑电图异常放电部位顶枕部放电比例高于对照组（55.0% vs 25.0%），弥散性放电比例低于对照组（25.0% vs 60.0%），差异均具有统计学意义（χ²=3.750、5.103，P=0.043、0.025）。而2组间血清5-HT含量、谷氨酸含量、大脑前中后动脉血流速度、出现DWI高信号的比例差异均无统计学意义（P均＞0.05）。

神经递质NO的升高、顶枕部放电以及癫痫发作引起的局灶性损伤可能与癫痫发作后头痛有关。

To investigate the possible pathogenesis of post-seizure headache by brain imaging, vascular ultrasound, neuroelectrophysiology, blood indicators and other clinical markers.

Forty inpatients who had been treated at the Epilepsy Monitoring Center of Tianjin Huanhu Hospital were enrolled between October 2013 and October 2018, 20 patients with post-seizure headache as the experimental group, and other 20 patients without post-seizure headache as the control group. The serum 5-hydroxytryptamine (5-HT), nitric oxide (NO), and glutamic acid (Glu), transcranial Doppler (TCD), video electroencephalogram (VEEG) and magnetic resonance imaging (MRI) of each patient were measured before the epileptic seizure in both groups, within 5 minutes of headache after the cease of epileptic seizure in the experimental group, and within 5 minutes after the cease of epileptic seizure in the control group, respectively. The t-test was used to compare the differences of 5-HT, NO, Glu and blood flow changes in the front, middle, and posterior arteries of the brain during and after seizures. The χ² test was used to compare the difference of proportion of abnormal EEG discharges and the high signal ratio in diffusion-weighted imaging (DWI) in the two groups.

Compared with patients without headache after epilepsy, patients with post-seizure headache had significantly higher serum NO levels after seizures [(46.37±18.17) μmol/L vs (19.83±5.78) μmol/L, t=12.157, P=0.034]. The proportion of parietooccipital abnormal discharge was significantly higher than the control group (55.0% vs 25.0%, χ²=3.750, P=0.043). The diffuse discharge ratio was significantly lower than the control group (25.0% vs 60.0%, χ²=5.103, P=0.025). There were no significant differences in 5-HT, Glu, blood flow velocity in anterior cerebral artery, middle cerebral artery, posterior cerebral artery, and the proportion of intensive DWI signals between the two groups (P＞0.05).

The increase in serum NO level, the discharge of the parietooccipital, and the focal damage caused by epileptic seizures may be involved in the mechanism of post-seizure headache.