ABSTRACT
Idiopathic epilepsies account for a substantial proportion of all epilepsies and are considered to be largely genetically determined (Steinlein 2008). e inheritance of these epilepsies may be Mendelian, whereby a single identied mutation results in epilepsy and/or febrile seizures. However, there is oen interfamilial and intrafamilial variability in the clinical phenotype, suggesting an eect of other genetic variants. e inheritance is more oen non-Mendelian or complex, whereby the phenotype is thought to be determined by several more minor genetic defects as well as environmental eects. Epilepsies inherited in a complex or multifactorial manner will arise when a chance combination of certain susceptibility alleles come together with sucient eect in the individual to push neuronal hyperexcitability over the seizure threshold (Mulley et al. 2005), but where each susceptibility allele alone is insucient to cause seizures. Susceptibility genes with minor eect have hitherto been much harder to identify, and most genes conrmed to be implicated in idiopathic epilepsy have thus far been Mendelian.
