P Sachdev1. 1. Neuropsychiatric Institute, Prince Henry Hospital and School of Psychiatry, University of New South Wales, Sydney, Australia.
Abstract
OBJECTIVE: Current knowledge of the relationship between epilepsy and schizophrenia-like psychosis is examined, and the proposed pathogenetic mechanisms are evaluated. METHOD: The author provides an overview of the published literature on epilepsy and schizophrenia-like psychosis. RESULTS: The schizophrenia-like psychoses of epilepsy are inadequately categorized by the current classifications. Their categorization into ictal, postictal, and interictal psychoses is clinically useful, but it does not imply distinct pathophysiology for each. The recent interest in postictal psychoses has opened an important avenue for research. Brief interictal psychoses, involving alternation between epilepsy and psychosis and accompanied by forced normalization, are uncommon. Many aspects of the relationship with chronic interictal psychosis remain controversial. The majority of investigators support a special but not exclusive relationship with mediobasal temporal lobe epilepsy, and left temporal bias receives only limited support. The chronic psychosis resembles schizophrenia phenomenologically. Some suggested risk factors are severe and intractable epilepsy, epilepsy of early onset, secondary generalization of seizures, certain anticonvulsant drugs, and temporal lobectomy. Different neuropathological studies suggest the presence of cortical dysgenesis or diffuse brain damage. CONCLUSIONS: There are many mechanisms by which epilepsy may be associated with schizophrenia-like psychosis. It is likely that structural brain abnormalities, e.g., cortical dysgenesis or diffuse brain lesions, underlie both epilepsy and psychosis, and that the seizures modify the presentation of the psychosis, and vice versa, thus producing a clinical picture of both an affinity and an antagonism between the two disorders.
OBJECTIVE: Current knowledge of the relationship between epilepsy and schizophrenia-like psychosis is examined, and the proposed pathogenetic mechanisms are evaluated. METHOD: The author provides an overview of the published literature on epilepsy and schizophrenia-like psychosis. RESULTS: The schizophrenia-like psychoses of epilepsy are inadequately categorized by the current classifications. Their categorization into ictal, postictal, and interictal psychoses is clinically useful, but it does not imply distinct pathophysiology for each. The recent interest in postictal psychoses has opened an important avenue for research. Brief interictal psychoses, involving alternation between epilepsy and psychosis and accompanied by forced normalization, are uncommon. Many aspects of the relationship with chronic interictal psychosis remain controversial. The majority of investigators support a special but not exclusive relationship with mediobasal temporal lobe epilepsy, and left temporal bias receives only limited support. The chronic psychosis resembles schizophrenia phenomenologically. Some suggested risk factors are severe and intractable epilepsy, epilepsy of early onset, secondary generalization of seizures, certain anticonvulsant drugs, and temporal lobectomy. Different neuropathological studies suggest the presence of cortical dysgenesis or diffuse brain damage. CONCLUSIONS: There are many mechanisms by which epilepsy may be associated with schizophrenia-like psychosis. It is likely that structural brain abnormalities, e.g., cortical dysgenesis or diffuse brain lesions, underlie both epilepsy and psychosis, and that the seizures modify the presentation of the psychosis, and vice versa, thus producing a clinical picture of both an affinity and an antagonism between the two disorders.