Introduction

The epilepsies represent a heterogeneous group of disorders with diverse etiologies, electrographical and behavioral seizure patterns, and pharmacological sensitivities. The subtype termed complex partial epilepsy (Commission on Classification and Terminology of the ILAE, 1981) is one of the most devastating forms of human epilepsy. Complex partial seizures (CPSs) constitute the single most common seizure type, accounting for approximately 40% of all cases in adults (Hauser & Kurland, 1975). CPSs are often quite resistant to available anticonvulsant drugs; only 25% of adults with CPS experience complete seizure control despite optimal contemporaneous treatment (Mattson et al., 1985). CPSs induce impairment of consciousness, thereby limiting performance of many tasks, such as driving a motor vehicle; as a result, finding and maintaining employment is difficult for sufferers. Complex partial epilepsy is a major public health problem affecting at least 800 000 people in the United States alone.

Insight into the mechanisms underlying this disorder is limited. Three main questions arise, (a) What is(are) the mechanism(s) underlying the expression of the hyperexcitability? (b) How does hyperexcitability develop? (c) Why does hyperexcitability persist? Developing answers to these questions in cellular and molecular terms may lead to more effective therapy, prevention, or even cure of this disorder.