Lombroso C T
Department of Neurology, Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Epilepsia. 1997 Jul;38(7):797-812. doi: 10.1111/j.1528-1157.1997.tb01467.x.
To describe the evolution of interictal findings in serial EEGs from patients with primary generalized epilepsy.
A cohort of 89 subjects with various primary generalized epilepsies were reviewed. Thirty-one did not meet a priori criteria. Of the 58 patients analyzed, 12 had only absence seizures, 28 had absence seizures followed by one or more generalized tonic-clonic seizures, 9 had generalized tonic-clonic seizures followed by absence and/or myoclonic seizures. and 9 had juvenile myoclonic epilepsy. Patients were followed for a mean of 16 years. An average of 39 EEGs were obtained on each patient.
Thirty-two patients (56%) had focal features present in up to 65% of the EEGs in each of the patients. Accepted focalities were only those that were consistent in lateralization, location and, often, morphology across the span of the study. Focal findings were most often temporal or frontal.
Patients with typical primary generalized epilepsies show a high incidence of focal EEG features that cannot be explained on the basis of structural lesions, coincidental factors, or to artifacts of the selection criteria. Although the data do not allow a definitive explanation, possible mechanisms include associated focal cortical pathology such as microdysgenesis, and development over time of localized, self-sustaining hyperexcitability in low-threshold cortical structures subjected to repeated generalized spike-wave activity. Either hypothesis implies the participation and interaction of genetic, ontogenic, and environmental factors.
描述原发性全身性癫痫患者系列脑电图发作间期表现的演变。
回顾了89例患有各种原发性全身性癫痫的受试者队列。31例不符合预先设定的标准。在分析的58例患者中,12例仅有失神发作,28例失神发作后伴有一次或多次全身性强直阵挛发作,9例全身性强直阵挛发作后伴有失神和/或肌阵挛发作,9例患有青少年肌阵挛癫痫。患者平均随访16年。每位患者平均进行了39次脑电图检查。
32例患者(56%)在每次患者高达65%的脑电图中存在局灶性特征。公认的局灶性仅指在研究期间在定位、位置以及通常形态上一致的那些。局灶性表现最常见于颞叶或额叶。
典型原发性全身性癫痫患者脑电图局灶性特征的发生率很高,这无法基于结构病变、偶然因素或选择标准的假象来解释。尽管数据无法给出确切解释,但可能的机制包括相关的局灶性皮质病理,如微小发育异常,以及在反复全身性棘波 - 慢波活动作用下低阈值皮质结构中随时间发展的局部性、自我维持的过度兴奋性。任何一种假设都意味着遗传、个体发育和环境因素的参与和相互作用。