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Idiopathic Epilepsies with a Complex Mode of Inheritance

In the last decade, major advances have been made in the understanding of the molecular bases of simple mendelian genetic epilepsies (1). However, epilepsies following a simple mendelian pattern of inheritance are rare, and most common human genetic epilepsies (most idiopathic epilepsies) follow a complex mode of inheritance. The idiopathic epilepsies, those for which there is no detectable underlying cause other than a possible hereditary predisposition (2), account for almost 50% of all epilepsies. According to the International League Against Epilepsy (Commission on Classification and Terminology), idiopathic epilepsies are defined by agerelated onset, clinical and electroencephalographic characteristics, and a presumed genetic etiology (2). The presumed genetic etiology of the idiopathic epilepsies may be difficult to prove in many cases, making the effort necessary to map and clone the responsible genes a considerable task. Informative families containing enough affected members to be useful for linkage analysis are not common, and other methods that require a high number (in the hundreds) of affected individuals (such as nonparametric sib-pair analysis) may be necessary to map and clone the responsible genes. The main problems associated with the genetic dissection of complex traits are incomplete penetrance, phenocopies, genetic heterogeneity, bilineality due to high frequency of diseasecausing alleles, and polygenic inheritance (3). Besides the problems inherent in complex traits, genetic analysis of the epilepsies is limited by the difficulties related to the definition of affectedness in a disorder characterized by paroxysmal events. There is now evidence supporting the hypothesis that most idiopathic epilepsies are caused by the interaction of a few gene variants, which by themselves are not sufficient to cause an epilepsy phenotype (1,4). Environmental factors may also have some influence in the epilepsy phenotype. Because of the difficulties in mapping epilepsy genes responsible for common epilepsies, most mapping efforts have been directed to mapping and clon-