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.