Ritsner M S
Genetika. 1985 Jun;21(6):1047-55.
Estimation of genetic and environmental components of phenotypical dispersion of paroxysmal and nonparoxysmal EEG abnormalities in epilepsy (118 probands and 179 relatives) in two phenotypical model frames has been obtained. The alternative phenotypical model was shown to be more adequate than quasicontinual for EEG abnormalities, and the part of additive genetic component (GA) comprises 15.7% for paroxysmal abnormalities and 49.4% for nonparoxysmal type. In the component type "belonging to one generation" joint influence of genetic and environmental factors on the process of forming EEG abnormalities in ontogeny was observed. The GA value for "epilepsy manifestation" symptom equal to 72.9% in general selection of probands increases to 97.4% in the subgroup of patients with nonparoxysmal abnormalities and 67.4% in the subgroup of patients with paroxysmal EEG abnormalities. It has been suggested that paroxysmal EEG abnormalities reflect their own epileptic process, and as far as nonparoxysmal abnormalities are concerned, they present phenotypical manifestation of the genetic system of predisposition to epilepsy.
在两种表型模型框架下，对癫痫患者（118名先证者和179名亲属）阵发性和非阵发性脑电图异常表型离散的遗传和环境成分进行了估计。结果表明，对于脑电图异常，替代表型模型比准连续模型更合适，加性遗传成分（GA）在阵发性异常中占15.7%，在非阵发性异常中占49.4%。在“属于同一代”的成分类型中，观察到遗传和环境因素对个体发育中脑电图异常形成过程的联合影响。在先证者的总体选择中，“癫痫表现”症状的GA值为72.9%，在非阵发性异常患者亚组中增至97.4%，在阵发性脑电图异常患者亚组中为67.4%。有人提出，阵发性脑电图异常反映了其自身的癫痫过程，而就非阵发性异常而言，它们是癫痫易感性遗传系统的表型表现。
