The pathology of epilepsy is a complex and evolving field, reflecting both rapid developments in diagnostic and therapeutic techniques, and the continued difficulties in translating electrical and functional phenomena into traditional categories of morphological disease. A seizure is an acute neurological event due to sudden excessive disorderly discharge of neurons.1 Lesions that are presumed to cause seizures can be either structural, definable by morphological techniques such as radiology and anatomic pathology, or functional, definable by clinical localization, electrophysiology, and, in some cases, functional imaging defining a focus. Causality is inferred by correlation of morphological findings and location with clinical and electrophysiological data and, in some cases, by the cessation of subsequent seizures after removal of the lesion or focus. Epilepsy is intermittent recurrence of seizures. The finding of structural lesions in some forms of epilepsy suggests and supports causality, but our understanding of the chain between the definable structural lesion and the recurrence of seizures is often less clear.2 Causality may be particularly difficult to determine in conditions producing multiple structural lesions such as tuberous sclerosis, where one lesion is epileptogenic and other similar lesions are not. Even determining how a particular electrically active focus propagates to evolve into a particular seizure or series of intractable seizures is also incompletely understood. To add to the difficulty, seizures or epilepsy itself can be causal, resulting in progressive brain damage and self-perpetuating seizures, particularly in some forms of temporal lobe epilepsy. Moreover, some treatments for epilepsy themselves have been associated with some forms of brain damage.