Altered neural activity in the reward-related circuit and executive control network associated with amelioration of anhedonia in major depressive disorder by electroconvulsive therapy.

Anhedonia is a core characteristic of depression, the amelioration of which accounts for depressive symptom improvement. Electroconvulsive therapy (ECT) has been shown remarkable antidepressive effect, however, less is known about the effect of ECT on anhedonia and its underlying neural mechanism. Herein, we investigated local and global intrinsic brain functional alterations during the resting state in 46 patients with pre- and post-ECT major depressive disorder using the amplitude of low-frequency fluctuations (ALFF) and degree centrality (DC) approach. Functional connectivity (FC) was also calculated between nodes with significant local and global intrinsic brain functional alterations. The severity of anhedonia and depression was assessed with the Temporal Experience of Pleasure Scale and Hamilton Depression Rating Scale, respectively. The relationship between the change in anhedonia and depressive symptoms and brain functional alterations was determined. Increased ALFF and DC were observed in the bilateral dorsal medial prefrontal cortex (dmPFC), right dorsal lateral prefrontal cortex (dlPFC), left orbitofrontal cortex, and right orbitofrontal cortex (ROFC) after ECT. Correlational analysis between the change in anhedonia and ALFF had positive results in the dmPFC. Similarly, there was a positive correlation between the change in anhedonia and change in DC in the dmPFC, right dlPFC, ROFC, and middle frontal gyrus. Furthermore, there was a significant relationship between the change in anhedonia and altered dmPFC-dlPFC FC. These results revealed that amelioration of anhedonia may be associated with intrinsic neural activity alteration in the reward-related circuit and executive control network following ECT.