Functional Dysconnectivity of Frontal Cortex to Striatum Predicts Ketamine Infusion Response in Treatment-Resistant Depression.
Mu-Hong Chen, Wan-Chen Chang, Wei-Chen Lin, Pei-Chi Tu, Cheng-Ta Li, Ya-Mei Bai, Shih-Jen Tsai, Wen-Sheng Huang, Tung-Ping Su
The international journal of neuropsychopharmacology December 29, 2020 DOI: 10.1093/ijnp/pyaa056 via PubMed
Summary
AI-generated from the abstractDepression involves disrupted communication between the frontal cortex and striatum. In 48 patients with treatment-resistant depression, those with lower baseline connectivity in these circuits showed greater symptom improvement after a single low-dose (0.2 mg/kg) ketamine infusion, but not after a higher dose (0.5 mg/kg) or placebo. Reduced connectivity between the superior frontal cortex and striatum predicted treatment response. Patients had weaker frontostriatal connections than healthy controls.
Study at a glance
| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 48 |
| Population | Patients with treatment-resistant depression |
| Interventions | Ketamine Saline placebo |
| Dose | 0.5 mg/kg, 0.2 mg/kg |
| Duration | Single 40-minute infusion, 2-week follow-up |
| Topics | Depression |
| Keywords | Frontostriatal network Low-dose ketamine infusion Treatment response |
| Citations | 28 |
| Key finding | Baseline hypoconnectivity of the bilateral superior frontal cortex to the executive region of the striatum predicted greater reduction of depression symptoms after a single 0.2-mg/kg ketamine infusion. |
Abstract
Frontostriatal disconnectivity plays a crucial role in the pathophysiology of major depressive disorder. However, whether the baseline functional connectivity of the frontostriatal network could predict the treatment outcome of low-dose ketamine infusion remains unknown. In total, 48 patients with treatment-resistant depression were randomly divided into 3 treatment groups (a single-dose 40-minute i.v. infusion) as follows: 0.5 mg/kg ketamine, 0.2 mg/kg ketamine, and saline placebo infusion. Patients were subsequently followed-up for 2 weeks. Resting-state functional magnetic resonance imaging was performed for each patient before infusion administration. In addition, the baseline frontostriatal functional connectivity of patients with treatment-resistant depression was also compared with that of healthy controls. Compared with the healthy controls, patients with treatment-resistant depression had a decreased functional connectivity in the frontostriatal circuits, especially between the right superior frontal cortex and executive region of the striatum and between the right paracingulate cortex and rostral-motor region of the striatum. The baseline hypoconnectivity of the bilateral superior frontal cortex to the executive region of the striatum was associated with a greater reduction of depression symptoms after a single 0.2-mg/kg ketamine infusion. Reduced connectivity of the superior frontal cortex to the striatum predicted the response to ketamine infusion among patients with treatment-resistant depression.