Temporal lobe epilepsy

Abstract

In the last two decades our understanding of MTLE and its pathophysiology has grown remarkably. Perhaps the most important recognition is that it is not a single entity with a uniform pathology. Rather, it is associated with significant variations in pathology that, in turn, are likely associated with different causes, functional anatomies, physiologies, and outcomes to treatment (medi-cal and surgical). There are numerous changes in the expression of channels and receptors that contribute to the development of epilepsy and, perhaps, drug resistance. This progress in our understanding has also been aided immeasurably by the development of animal models with many parallels to the human condition.These models have allowed us to look at changes in anatomy and physiology and to dissect the circuits in ways that have not been possible in humans. The animal models have also allowed us to create hypotheses about the pathophysiology of the disorder that we have started to exam-ine with the new imaging tools. At present, it is best to summarize our understanding of MTLE by saying there are multiple changes in multiple sites that contribute to the development of the chronic condition. For this reason alone, we should consider MTLE to be a systems disorder.