Many schizophrenia patients experience residual symptoms even after treatment. Electroconvulsive therapy (ECT) is often used in medication-resistant schizophrenia patients when pharmacologic interventions have failed; however, the mechanism of action is unclear. Brain-derived neurotrophic factor (BDNF) levels are reduced in drug-naive, first-episode schizophrenia and are increased by antipsychotic treatment. We tested the hypothesis that ECT increases serum BDNF levels by measuring BDNF concentrations in schizophrenia patients before and after they received ECT.

A total of 160 patients with schizophrenia were examined. The ECT group (n=80) was treated with antipsychotics and ECT (eight to 10 sessions administered every other day). The drug therapy group (n=80) received only antipsychotic treatment. A control group (n=77) was recruited that served as the baseline for comparison.

Baseline serum BDNF level in ECT group was lower than in controls (9.7±2.1 vs. 12.4±3.2ng/ml; P<0.001), but increased after ECT, such that there was no difference between the two groups (11.9±3.3 vs. 12.4±3.2ng/ml; P=0.362). There was no correlation between patients’ Positive and Negative Syndrome Scale (PANSS) score and serum BDNF level before ECT; however, a negative correlation was observed after ECT (total: r=−0.692; P<0.01). From baseline to remission after ECT, serum BDNF level increased (P<0.001) and their PANSS score decreased (P<0.001). Changes in BDNF level (2.21±4.10ng/ml) and PANSS score (28.69±14.96) were positively correlated in the ECT group (r=0.630; P<0.01).

BDNF level was lower in schizophrenia patients relative to healthy controls before ECT and medication. BDNF level increased after ECT and medication, and its longitudinal change was associated with changes in patients’ psychotic symptoms. These results indicate that BDNF mediates the antipsychotic effects of ECT.