Early Onset Absence Epilepsy

J Gordon Millichap
2003 Pediatric Neurology Briefs  
autosomal dominant epilepsy with FS plus, generalized epilepsy with FS plus, and with severe myoclonic epilepsy in infancy that often begins with a prolonged FS. Various Na channels and GABAa receptors in the brain are probably involved in the pathogenesis of frequent FS and also, in simple FS. Genetic linkage analyses have mapped FS to four loci, FEB1,2,3 and 4, in chromosomes 8ql3, 19p, 2q23-q24, and 5ql4-ql5, respectively. (Hirose S, Mohney RP, Okada M et al. The genetics of febrile seizures
more » ... and related epilepsy syndromes. Brain Dev August 2003;25:304-312). (Respond: COMMENT. The determination of the molecular genetic mechanism of FS may lead to more specific therapies. FS occur with increased frequency among family members of patients with FS. Tsuboi (1977) reported 17% of parents and 22% of siblings of FS probands affected; 30% of siblings are affected if one parent has a history of FS (Hauser WA. In: Febrile Seizures. Ed by Nelson and Ellenberg, Raven Press, 1981). An analysis of 2,109 patients with FS reported between 1948 and 1963 in 12 different publications showed a mean familial incidence of 17% (range 2 to 58%) (Millichap, 1968).
doi:10.15844/pedneurbriefs-17-7-4 fatcat:3fqmzwl2hve33h5uhi7r47g7eq