There is often disagreement about what constitutes "epileptogenesis" and what is meant by "symptomatic epilepsy". In considering various mechanistic hypotheses, investigators have often divided potential participants in epileptogenesis into two categories: changes that are a direct result of the insult and serve to initiate the epileptogenic process, and processes that give rise to an altered brain condition that is capable of generating/supporting aberrant (hyperexcitable, hypersynchronous) neuronal discharge. These two sets of mechanisms may overlap (or turn out to be functionally inseparable). However, given the assumed temporal distinction (immediate vs. delayed) between these two categories of processes, it makes some sense to discuss them separately. The need to identify mechanisms of epileptogenesis in symptomatic epilepsies arises from a conviction that a better understanding of these processes will lead to effective antiepileptogenic therapies.

Epilepsy is a disease of the brain characterized by recurring unprovoked epileptic seizures, caused by a transient abnormality of neuronal activity which results in synchronized electrical discharges of neurons within the central nervous system (CNS). This chapter focuses on the most important characteristics of voltage- and ligand-gated ion channels, their role in determining neuronal excitability, and the impact of some reported mutations on epileptogenesis in idiopathic epilepsies. It describes the importance of the thalamocortical loop and thalamic ion channels for the generation of generalized seizures. The binding of transmitters and the coupling to channel opening are complex processes which can consequently be influenced by amino acid changes in many different regions of these channels. Most anticonvulsant drugs that are in clinical use today act by modulating the function of ion channels and the chapter describes how ion channel function can be altered by genetic defects associated with idiopathic epilepsies.