Acute behavioral symptomatology at disappearance of epileptiform EEG abnormality. Paradoxical or "forced" normalization.

Paradoxical or "forced" normalization of the EEG of patients with epilepsy was first described by Landolt in 1953. It refers to conditions where disappearance of epileptiform discharge from the routine scalp EEG is accompanied by some kind of behavioral disorder. The best known of these is a paranoid psychotic state in clear consciousness, which is also known as "alternative" psychosis. Thus, the issue is related to much older observations which indicated a "biological antagonism" between productive psychotic symptomatology and epileptic seizures, which led to the therapy of psychoses with artificially induced convulsions. Apart from psychotic episodes, the clinical manifestations of PN comprise dysphoric states, hysterical and hypochondriacal syndromes, affective disorders, and miscellanea. PN can be observed in both generalized and localization-related epilepsies as a rare complication. A subset where it is more frequently seen are in adults with persistent absence seizures when the latter become finally controlled by succinimide therapy. These seem to be the drugs with the highest hazard of precipitation of PN, but all other AEDs have also been suspected. Sleep disturbance by succinimide treatment may play a crucial role, but a variety of other factors are also involved, including psychosocial factors. The pathogenesis of this condition has given rise to some debate but remains still unresolved. Eleven of the most important hypotheses have been discussed and seem to converge into a more comprehensive hypothesis which basically assumes that, during PN, the epilepsy is still active subcortically, perhaps with spread of discharge along unusual pathways. This activity is supposed to provide energy and, possibly, some of the symptoms included in the psychotic syndrome. A critical clinical condition results, usually with a dysphoric symptomatology, where a development towards psychosis is impending but still depends on the presence or absence of a variety of risk factors. Along with neurophysiological factors such as powerful inhibition of the spread of epileptic discharge, these may also include biographic factors such as the repeated experience of ictal sudden, unexpected loss of consciousness. Because during PN there presumably is ongoing epileptic activity, the differences with respect to other psychotic conditions in epilepsy are probably subtle rather than fundamental. Thus, it could be that ictal psychosis is characterized by a direct expression of epileptic activity, whereas in postictal psychosis a momentum of exhaustion may be added; moreover, in PN the prevailing pathogenic factor could be an abnormally high level of balance between excitatory and inhibitory processes.