Effect of Electroconvulsive Therapy on Medial Prefrontal γ-Aminobutyric Acid Among Schizophrenia Patients: A Proton Magnetic Resonance Spectroscopy Study.

Abstract

Electroconvulsive therapy (ECT) has often been applied to augment antipsychotics for schizophrenia patients. However, the underpinning mechanism is still unclear. Previous studies of major depressive disorder reported an increase in γ-aminobutyric acid (GABA) after ECT. The present study investigated the effects of ECT on medial prefrontal GABA in schizophrenia using a proton magnetic resonance spectroscopy. Inpatients fulfilling the diagnostic criteria for schizophrenia (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) were assigned to 2 groups, ECT group (n = 14) receiving ECT plus antipsychotic drugs (APD) and drug group (n = 17) only receiving antipsychotic drugs. Medial prefrontal GABA+/Cr concentrations of all patients were measured with magnetic resonance spectroscopy at baseline and after 4-week treatment. Sex- and age-matched healthy comparisons (n = 19) were scanned at baseline. γ-Aminobutyric acid level did not show a significant difference among 3 groups. However, when 2 patient groups were combined, their GABA level was significantly lower than that in healthy comparisons group. For schizophrenia patients, repeated measures analysis of variance revealed that both the group effect and group × time interaction were insignificant, but the time effect of baseline versus after treatment was significant. Exploratory post hoc paired t test found a significant increase of GABA only in ECT group, but not in drug group. No correlation was found between GABA change and clinical symptom improvement in either group. γ-Aminobutyric acid level in the medial prefrontal lobe was reduced in schizophrenia patients. An increase in GABA concentration in the medial prefrontal cortex is more significantly associated with ECT plus antipsychotics than antipsychotics alone, possibly supporting the hypothesis of ECT augmentation for GABA mediated neural inhibition.