Abstracts

Rationale: Temporal lobe epilepsy (TLE) secondary to mesial temporal sclerosis (MTS) is the most frequent cause of focal refractory epilepsy in adults. In addition to severe neurological symptoms, these patients present a high prevalence of psychiatric symptoms. The prevalence of schizophrenia-like psychotic symptoms in patients with MTS ranges from 7% to 11% and are thus higher than the expected 1% in the general population. Given the clinical similarities, it is conceivable that psychosis in epilepsy may share some common pathological substrate with schizophrenia. One consistent biochemical finding in schizophrenia is an increased activity of the enzymes phospholipases A2 (PLA2). This family of enzymes is responsible for the metabolism of membrane phospholipids and it is composed by three main groups: cPLA2, sPLA2 and iPLA2. This pioneer study, evaluated the activity of PLA2 subgroups in the hippocampal tissue of patients with refractory TLE with MTS, aiming to ascertain whether patients with TLE-MTS with psychosis have increased PLA2 activity compared to those patients with TLE-MTS without psychosis. Methods: We determined PLA2 activity by radioenzimatic assays in hippocampal tissue from 7 patients with TLE-MTS and psychosis, as compared to 9 TLE-MTS patients without psychosis. Hippocampal tissue was obtained from subjects who underwent a surgical procedure (anterior temporal lobectomy) indicated due to a therapy-resistant epilepsy. Results: TLE-MTS patients with psychosis showed a significantly higher brain iPLA2 activity as compared to patients without psychosis (p= 0,016). No significant differences were found between both groups regarding sPLA2 and cPLA2 activities (table). The group of patients with psychosis had somewhat higher mean ages and duration of the illness, but these differences were not significant, and the activities of the PLA2 subgroups did not correlate with age, duration of the disease and frequency of epileptic seizures. Conclusions: This is the first study that analyses the activity of PLA2 in patients with TLE and psychosis shading a new light in the complex mechanisms that underlie this association. Our findings reinforce the concept of common etiopathogenic mechanisms for psychiatric disorders in epilepsy. Supported by: FAPESP/ABADHS