Piccinelli Paolo, Borgatti Renato, Nicoli Francesca, Calcagno Patrizia, Bassi Maria Teresa, Quadrelli Marta, Rossi Giorgio, Lanzi Giovanni, Balottin Umberto
Child Neuropsychiatry Unit, University of Insubria, Macchi Foundation Hospital, Varese, Italy.
Headache. 2006 Mar;46(3):413-21. doi: 10.1111/j.1526-4610.2006.00373.x.
Many studies have supported the hypothesis of alteration of cortical hyperexcitability as a possible pathological mechanism underlying the onset of migraine and epileptic attacks. Different biochemical pathways involving cellular structures may increase or decrease the excitability of neuronal membranes. The aim of this study was to identify a possible link between migraine and epilepsy from a clinical and neurophysiologic point of view.
One-hundred thirty-seven children and adolescents consecutively diagnosed for tension-type headache and idiopathic migraine with and without aura were studied. Anamnestic, clinical, and instrumental data were collected by a neurological examination, a specific questionnaire, and awake electroencephalogram (EEG) registrations. EEG features of nonheadache and nonseizures control group were compared.
Fourteen cases (10.2%) had a positive history for seizures with fever, isolated seizures, or epilepsy. Distribution differed according to headache diagnosis; migraine with aura (MWA) was largely prevalent. Specific electroencephalographic abnormalities were present in 11.7% of the sample, with a significant different distribution across the groups of children with headache and the control group: specific interictal abnormalities were found in 10 of 23 (43.5%) children with MWA. Two factors, seizures and specific interictal electroencephalographic abnormalities, showed a different distribution in patients with MWA compared to other classes of headache and control group (P < or = .01).
The present study supports the hypothesis of a possible clinical continuum between some types of MWA and epileptic syndromes as entities due to altered neuronal excitability with similar genetic substrates.
许多研究支持皮质兴奋性改变这一假说，认为其可能是偏头痛和癫痫发作起始的病理机制。涉及细胞结构的不同生化途径可能会增加或降低神经元膜的兴奋性。本研究旨在从临床和神经生理学角度确定偏头痛与癫痫之间可能存在的联系。
对137名连续诊断为紧张型头痛以及伴或不伴先兆的特发性偏头痛的儿童和青少年进行研究。通过神经学检查、特定问卷和清醒脑电图（EEG）记录收集既往史、临床和仪器检查数据。比较非头痛和非癫痫发作对照组的脑电图特征。
14例（10.2%）有发热性惊厥、孤立性惊厥或癫痫的阳性病史。其分布因头痛诊断而异；伴先兆偏头痛（MWA）最为普遍。11.7%的样本存在特定的脑电图异常，在头痛儿童组和对照组之间分布有显著差异：23例MWA儿童中有10例（43.5%）发现有特定的发作间期异常。癫痫发作和特定的发作间期脑电图异常这两个因素在MWA患者中的分布与其他类型头痛患者及对照组不同（P≤0.01）。
本研究支持这样一种假说，即某些类型的MWA和癫痫综合征之间可能存在临床连续性，它们是由于具有相似遗传底物的神经元兴奋性改变而形成的实体。
