Adolescent seizures and epilepsy syndromes

Abstract

Specific epilepsy syndromes begin during adolescence and create a significant neurologic burden. Knowledge of these syndromes has important treatment and prognostic implications, which usually extend into adulthood. Little is known about the effect of menarche on seizures, even though a relationship of seizures to the menstrual cycle has been observed for many years. In general, puberty is not thought to influence seizure frequency. However, estrogen is thought to activate epileptiform activity; testosterone may decrease seizure activity; and progesterone decreases epileptiform discharges. These effects are mediated by effecting gammaaminobutyric acid (GABA) transmission. Idiopathic generalized epilepsies are the most frequent group with adolescent onset. These are probably polygenic in origin and represent a biologic continuum. Juvenile myoclonic epilepsy (JME) is the most common form. This contrasts with a variety of progressive myoclonic epilepsies that also are first seen in adolescence and have a genetic origin and specific treatments. Finally, although temporal lobe epilepsy associated with hippocampal sclerosis may have its origin in childhood, often the child does not come to surgical evaluation until adolescence or young adulthood. The characteristic clinical history, seizure semiology, and magnetic resonance imaging findings have allowed a discrete epilepsy syndrome to be established. Applying these same criteria to children and adolescents reveals that hippocampal sclerosis is the most common lesion responsible for their intractable temporal lobe epilepsy. Hippocampal sclerosis is probably underdiagnosed in children. The safety and efficacy of epilepsy surgery in the age group is excellent. Knowledge of the epilepsy syndromes that remit before adolescence, may persist into adolescence, or begin in adolescence is central to the treatment of this age group.