Brain structural changes underlying clinical symptom improvement following fast-acting treatments in treatment resistant depression.

Electroconvulsive therapy, ketamine infusion, and total sleep deprivation all reduced depressive symptoms in 127 patients with treatment-resistant depression, but they affected other clinical measurements and brain structures differently. All three treatments increased gray matter volume in the left caudate. Only electroconvulsive therapy increased gray matter volume in the hippocampus, parahippocampus, amygdala, insula, fusiform gyrus, and several occipital and temporal areas. Neither baseline gray matter volume nor its change correlated with depressive symptom improvement for any treatment. The findings suggest that different rapid interventions for treatment-resistant depression have distinct effects on brain structure, which may help personalize treatment.

Study at a glance

Abstract

Electroconvulsive therapy (ECT), ketamine infusion (KI), and total sleep deprivation (TSD) are effective and fast in treating patients with treatment-resistant depression (TRD). However, it remains unclear whether the three treatments have the same effect on clinical symptom improvement and have common brain structural mechanisms. The current study included 127 TRD patients and 37 healthy controls, which were obtained from the Perturbation of the Treatment Resistant Depression Connectome Project. We aimed to investigate the shared and distinct brain structural changes underlying clinical symptom improvement among ECT, KI, and TSD treatments. All of the three treatments significantly reduced the depressive symptoms in TRD patients, but they differently affected other clinical measurements. Neuroimaging results also revealed that all of ECT, KI, and TSD treatments significantly increased gray matter volume of left caudate after treatment in TRD patients. However, the gray matter volume of other brain regions including hippocampus, parahippocampus, amygdala, insula, fusiform gyrus, several occipital and temporal areas was increased only after ECT treatment. Still, the baseline or the change of gray matter volume did not correlate with the depressive symptom improvement for all of the three treatments. A higher sample size would be required to further validate our findings. The results observed in the current study suggested that the ECT, KI, and TSD treatments differently affected clinical measurements and brain structures in TRD patients, though all of them were effective in depressive symptom improvement, which might facilitate the development of personalized treatment protocol for this disease.