The developmental/congenital disorders are a gray area between core idiopathic and core acquired epilepsies, and their inclusion under the term symptomatic epilepsy reflects the inevitably artificial nature of all classification schemes. This chapter talks about epilepsy syndromes, temporal characteristics of acquired epilepsy, and provoked epilepsies. The term 'acquired' is used to refer to symptomatic epilepsies excluding the predominately genetic or developmental causes. The main reason for considering epilepsy a symptom is that there are so many different causes, and it is therefore perhaps ironical to note that the current classifications of epilepsy pay no heed to etiology at all, focused as they are on clinical and electrographic semiology. It is clear that the distinctive natures of the underlying pathological and physiological processes underlying symptomatic epilepsy after acute brain insults are very different from those underlying idiopathic epilepsy, and so are the clinical, therapeutic, and prognostic features.

In this introductory chapter, a classification of the etiology of epilepsy is proposed, and this forms the basis of the sectional divisions in the rest of the book. In constructing such a classification, it is necessary to take cognisance of five particular points: Definitions, Multifactorial cause of epilepsy, Cause versus mechanism, Focal versus generalized epilepsy and Flexibility. The chapter presents the definitions of the epilepsies which are divided into four main categories: Idiopathic epilepsy, Symptomatic epilepsy, Provoked epilepsy and Cryptogenic epilepsy. The ILAE Commission recommended that a classification should be a database forming the basis of a diagnostic manual; the etological schema in this chapter should be viewed as such for instance in relation to the benign focal epilepsies or even the idiopathic generalized epilepsies. It is clear that in the future, as further knowledge accrues, some of these epilepsies may be reclassified and revised.

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.