Does status epilepticus in children cause developmental deterioration and exacerbation of epilepsy?

The aims of this study were to determine predictors of abnormal outcome, ne urodevelopmental deterioration, new-onset epilepsy, refractory epilepsy, an d recurrent status epilepticus in children presenting with status epileptic us. For all children presenting to Royal University Hospital, Saskatoon, Sa skatchewan, Canada, with status epilepticus between January 1987 and Decemb er 1996, demographic data, details of status epilepticus (etiology, duratio n, treatment, and investigations), developmental milestones, seizures prior to and following status epilepticus, recurrent status epilepticus, and neu rologic examination findings at status epilepticus and at follow-up were co llected by chart review, patient interview, and neurologic examination. Neu rodevelopmental outcome was determined for all subjects except those who di ed during the initial hospitalization. Predictors of new-onset epilepsy, re fractory epilepsy, and recurrent status epilepticus were determined for chi ldren followed for 3 months or more after status epilepticus. At follow-up, 79% were abnormal neurologically. Predictors included etiology (nonfebrile or nonidiopathic), perinatal difficulties, preceding developmental delay, abnormal initial neurologic examination; and abnormal neuroimaging. Thirty- four percent showed neurodevelopmental deterioration; predictors included e tiology (nonidiopathic or nonfebrile), young age at status epilepticus (12 months or less), and abnormal neuroimaging. Thirty-six percent with no hist ory of seizures preceding status epilepticus developed epilepsy and 25% dev eloped refractory epilepsy. Fifty percent of children had recurrent status epilepticus. In conclusion, very few children presenting in status epilepti cus were normal at follow-up. Sequelae were seen predominantly in those wit h a nonidiopathic, nonfebrile etiology, whereas those with idiopathic or fe brile status epilepticus did well.