Abstract

Febrile seizures (FS) occur in infancy or childhood and are associated with fever without evidence of intracranial infection or prior afebrile seizure. FS are the most common seizure disorder in children,1 affecting 2 to 5% of children by age 6 in the United States, and as many as 8.3% in Japan. After a first FS, children have a 25% to 40% recurrence risk. Genes clearly contribute to the risk of FS. FS are more common in relatives of individuals with a history of FS,2 and risks are consistently higher in monozygotic than dizygotic twins. A positive family history of FS is also a strong risk factor for FS recurrence.3 These data suggest that the predisposition to single FS and recurrence of FS are partially under genetic control. Risk for epilepsy is also increased after a first FS.4 Genetic heterogeneity is evident; recent genetic linkage studies in large pedigrees and nuclear families with FS have pointed to five chromosomal regions likely to harbor FS susceptibility genes (FEB1–FEB5; table 1).5–10⇓⇓⇓⇓⇓ Identification of the responsible genes in these regions is lacking, but has been …

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