The development of psychosis in epilepsy: a re-examination of the kindling hypothesis.

It is generally acknowledged that psychosis occurs with increased frequency within epileptic populations. There are several possible explanations for this over-representation: (1) psychosis may develop as a result of anti-epileptic drug or surgical treatment, or as a result of the psychosocial effects of living with epilepsy; (2) epilepsy and psychosis may, in some cases, have a common cause: and (3) chronic seizure activity may sometimes cause psychosis. The objective of this review is to evaluate the hypothesis that focal seizure activity may lead to the development of psychosis through a kindling process. There is some evidence to suggest that secondary epileptogenesis may develop following the spread of seizure activity from a primary focus, possible via a kindling mechanism. Although it has been suggested that long-term potentiation (LTP) may result in the development of secondary epileptic foci; LTP is not necessarily implicated. The kindling hypothesis of the development of psychosis in epilepsy must address the neural mechanism by which the spread of seizures might result in psychosis. At present, the neurochemical mechanisms by which psychosis could result from epilepsy are unclear.