Chen MH, et al. - The aim of this randomized control study was to assess the changes in brain function responsible for the persistent antidepressant effect of a single low-dose ketamine infusion. Researchers reported that the persistent antidepressant effect of a low-dose ketamine infusion was mediated by increased activation in the supplementary motor area (SMA) and dorsal anterior cingulate cortex (dACC). They observed that the higher increase in dACC activation was related to the decline in depressive symptoms after ketamine infusion. They noted that a single optimal low-dose ketamine infusion facilitated the glutamatergic neurotransmission in the SMA and dACC.

Methods

• For this examination, 24 patients with treatment-resistant depression (TRD) were randomized into 3 groups according to the treatment received: 0.5 mg/kg ketamine, 0.2 mg/kg ketamine, and normal saline infusion.
• Standardized uptake values (SUVs) of glucose metabolism measured through ¹⁸F-FDG positron-emission-tomography before infusion and 1 day after a 40-min ketamine or normal saline infusion were utilized for subsequent whole-brain voxel-wise analysis and were associated with depressive symptoms, as defined utilizing the Hamilton Depression Rating Scale-17 (HDRS-17) score.

Results

• The voxel-wise analysis showed that patients with TRD receiving the 0.5 mg/kg ketamine infusion had significantly higher SUVs (corrected for family-wise errors, P = 0.014) in the supplementary motor area (SMA) and dorsal anterior cingulate cortex (dACC) than did those receiving the 0.2 mg/kg ketamine infusion.
• Findings revealed that the increase in the SUV in the dACC was negatively related to depressive symptoms at 1 day after ketamine infusion.