Multifactorial pathogenesis of neonatal seizures--relationships to the benign partial epilepsies

Elevated incidence of neonatal seizures (NS) in children with idiopathic partial epilepsies, as well as reports on the transition of NS into benign partial epilepsy, point to pathogenetic relationships between these conditions. Further insight into the nature of these relationships can be expected only from NS patients with long-term follow-up, which includes the age range of maximum manifestation of subsequent seizures or epilepsies (SSE), and age-dependent genetic EEG traits. A sample of such cases will necessarily be selected and thus prohibit any quantitative inferences regarding the incidence of SSE and special EEG characteristics. Nevertheless, the data provide new aspects with regard to a possibly multifactorial pathogenesis of NS and SSE. Children in the present study were selected applying the following inclusion criteria: cerebral seizures during the first 14 days of life; follow up of more than two years with at least two EEG recordings beyond the age of two. Children with metabolic NS or subsequent West syndrome were not included. Seventy-six cases were confirmed, 42 with SSE, 34 without. The incidence of EEG symptoms of a generalized genetic seizure liability (theta rhythms, generalized spikes and waves, photoparoxysmal response) was significantly elevated, equally in children with and without SSE. Beyond the age of two years, 50% of the probands had focal sharp waves foci characteristic of idiopathic partial epilepsy (e.g. rolandic epilepsy). Among SSE, febrile convulsions and partial epilepsies with benign course dominated. Idiopathic generalized epilepsies were not observed. These findings indicate that in a certain proportion of cases, NS have genetic factors in common with idiopathic partial epilepsies. Quantitative representative data cannot be obtained to determine the incidence of such pathogenetic mechanisms in NS and SSE.