Les psychoses post-ictales correspondent à l’apparition soudaine d’un état délirant aigu de durée brève après une salve de crises épileptiques. L’existence d’un intervalle libre de pleine lucidité après la crise élimine une confusion postcritique délirante. Le syndrome psychotique est de sémiologie protéiforme, associant en proportions variables des symptômes thymiques, des hallucinations et des idées délirantes avec une conscience globalement préservée. Le risque de comportements dangereux auto- ou hétéro-agressifs est élevé. L’évolution se fait vers la régression spontanée des symptômes en une semaine en moyenne, avec ou sans traitement. Le syndrome psychotique complique une épilepsie focale réfractaire évoluant depuis plus de 10ans. L’EEG est utile au diagnostic différentiel : enregistré lors de l’épisode psychotique, il n’est pas différent de l’EEG prépsychotique. Les travaux neurobiologiques montrent que la survenue du trouble dépend d’une vulnérabilité individuelle et s’accompagne d’anomalies structurelles sur l’imagerie morphologique de l’encéphale. La dynamique du trouble a été évaluée par les enregistrements par électrodes profondes et par l’imagerie fonctionnelle.

Psychosis in epilepsy can be categorized in relation to seizures in two main categories: interictal psychosis and postictal psychosis. Postictal psychosis (PIP) is a specific syndrome in relation to seizure activity: a clear temporal relation exists between the psychotic state of sudden onset and a precipitating bout of complex partial or generalized seizures. However, this very specific syndrome is not included as such within the DSM-5, and PIP belongs to the category “Psychotic disorder due to another medical condition”. Diagnostic criteria are: (1) episode of psychosis within 1 week after a seizure(s); (2) psychosis lasts more than 15hours and less than 2 months; (3) delusions, hallucinations in clear consciousness, bizarre, or disorganized behavior, formal thought disorder, or affective changes; and (4) no evidence AED toxicity, non-convulsive status epilepticus, recent head trauma, alcohol, or drug intoxication or withdrawal, prior chronic psychotic disorder. The presence of a lucid interval between the last seizure and start of changes rules out a simple postictal delirium. The outcome is characterized by a remission of the psychotic symptoms over several days (mean: 1 week), with or without any treatment. Prepsychotic EEG abnormalities persist during the psychosis. Risk factors for PIP include: long standing localization-related epilepsy, extratemporal onset, bilateral epileptiform activity, secondary generalization, slowing of the EEG background activity and personal or family history of psychiatric disorders. Brain MRI frequently shows structural abnormalities. Several functional neuroimaging studies have shown hyperperfusion in various cerebral regions during PIP, suggesting an excessive activation of particular structures of the brain rather than a postictal depression of cerebral activity. Implanted electrode studies have shown that the EEG correlate of psychotic symptoms differs from the ictal EEG correlate of epileptic seizures. The value of antipsychotic treatment in PIP requires further studies. Despite their role in symptomatic relief, there is no clear effect of neuroleptics on duration or prognosis of PIP. Different combinations of pharmaceutical interventions can be tried on a case by case basis: (1) oral administration of benzodiazepine; (2) combined oral administration of benzodiazepine and atypical neuroleptics; (3) intramuscular administration of dopamine-blockers for rapid tranquilization of violent or agitated patients. The notion that neuroleptic drugs lower the seizure threshold has no clinical significance: there is no evidence that antipsychotic drugs increase seizure frequency in epileptic patients treated with antiepileptic drugs.