Abstracts

The purpose of this study was to estimate the relative influence of genetic and environmental factors on the etiology of febrile seizures (FS) overall and of FS partitioned by subtype. Twins with FS were ascertained from the population-based Danish Twin Registry by questionnaire. Twin pairs where both members had FS were considered to be concordant for seizures. Affected pairs were validated and classified according to the ILAE classification of epilepsies/syndromes (1989). Affected pairs with FS were subclassified into the following categories: simple febrile seizures (SFS), complex febrile seizures (CFS) and undetermined febrile seizures (UFS). Pairs where the FS of both twins were of the same type were classified as concordant for FS subtype, while pairs where the FS of pair members were not of the same type were classified as discordant for FS subtype. The similarity of monozygotic (MZ) and dizygotic (DZ) twins was assessed using probandwise concordance rates. It was possible to assign an FS diagnosis for a total of 526 individuals included in 446 complete twin pairs. For FS overall, the probandwise concordance rate for MZ twins was substantially higher than for DZ twins (MZ: 0.43 and DZ: 0.17, p[lt]0.001). For SFS, the probandwise concordance rate was also higher for MZ than for DZ twins (MZ: 0.44 and DZ: 0.13, p[lt]0.001). No significant differences were found in the concordance rates observed for MZ versus DZ pairs for either CFS or UFS (CFS: MZ: 0.06 and DZ:0.02, p=0.30; UFS: MZ: 0.11 and DZ: 0.02, p=0.06). The finding of significantly higher probandwise concordance rates in MZ versus DZ twins with validated FS emphasizes the importance of the role that genetic factors play in the etiology of FS overall. The pattern of concordance rates observed for SFS, CFS and UFS in this sample (significant differences in probandwise concordance rates for SFS in MZ versus DZ twins and no significant differences in the MZ-DZ rates observed for either CFS or UFS) suggests that genetic factors play an important role in determining risk for the occurrence of SFS, but not as important or possibly not as straightforward a role in the etiology of CFS and UFS. (Supported by a grant from NIH NINDS (NS-31564).)