Repetitive Transcranial Magnetic Stimulation Improves Amygdale Functional Connectivity in Major Depressive Disorder.

Emotional abnormality in major depressive disorder (MDD) is generally regarded to be associated with functional dysregulation in the affective network (AN). The present study examined the changes in characteristics of AN connectivity of MDD patients before and after repetitive transcranial magnetic stimulation (rTMS) treatment over the left dorsolateral prefrontal cortex, and to further assess how these connectivity changes are linked to clinical characteristics of patients. Functional connectivity (FC) in the AN defined by placing seeds in the bilateral amygdale was calculated in 20 patients with MDD before and after rTMS, and in 20 healthy controls (CN). Furthermore, a linear regression model was used to obtain correlations between FC changes and Hamilton depression scale (HAMD) changes in MDD before and after rTMS. Before rTMS, compared with CN, MDD exhibited significantly lower FC between left insula (INS.L), right superior and inferior frontal gyrus (SFG.R and IFG.R), right inferior parietal lobule (IPL.R), and amygdala, and showed an increment of FC between the bilateral precuneus and amygdala in AN. After rTMS, MDD exhibited a significant increase in FC in the INS.L, IFG.R, SFG.R, IPL.R, and a significant reduction in FC in the precuneus. Interestingly, change in FC between INS.L and left amygdala was positively correlated with change in HAMD scores before and after rTMS treatment. rTMS can enhance affective network connectivity in MDD patients, which is linked to emotional improvement. This study further suggests that the insula may be a potential target region of clinical efficacy for MDD to design rationale strategies for therapeutic trials.

Effect of Cognitive Behavioral Therapy on Improving the Cognitive Function in Major and Minor Depression.

The aim of this study was to investigate the effectiveness of cognitive behavioral therapy (CBT) on improving the cognitive function in minor depression (MiD) and major depression (MaD). The study will constitute a placebo-controlled single-blind parallel-group randomized controlled trial. The selected participants will be randomly allocated into one of two parallel groups with a 1:1 ratio: the CBT-based group and the general health education group. CBT significantly alleviated depressive symptoms of MiD and MaD at 12 weeks (p < 0.001), and the treatment effect was maintained for at least 12 months (p < 0.001). Interestingly, CBT significantly promotes more cognitive function of MiD and partial cognitive function of MaD at 12 weeks in the intervention group than in the control group (p < 0.01). CBT can alleviate depressive symptoms of both minor and MaDs. The effectiveness of CBT is different on improving the cognitive function in MiD and MaD.

Predictors of neurocognitive impairment at 2years after a first-episode major depressive disorder.

BACKGROUND: Neurocognitive impairment is a contributor to major depressive disorder (MDD). However, MDD patients show great variability in the level and course of deficits. The present longitudinal study was to identify predictors of neurocognitive impairment in first-episode MDD patients. METHODS: Neurocognitive performance was analyzed in a cohort of 100 patients at 2years after a first-episode MDD. Subgroups, deficit type vs. non-deficit type, were compared on baseline clinical, neuropsychological, premorbid and sociodemographic characteristics. The analysis was performed using the multivariate logistic regression to obtain a model for neurocognitive impairment determination. The predicted probabilities of multivariate logistic regression were analyzed using receiver operating characteristic (ROC) curve. RESULTS: Fifty-two percent of MDD participants presented general neurocognitive impairment. The regression analyses demonstrated that clinical and sociodemographic characteristics were not predictive variables. A model composed of processing speed, executive function, and attention, dexterity correctly classified 85.8% of the MDD patients with deficit type. ROC curve indicated that the changes of these three cognitions could identify MDD with deficit type from MDD with non-deficit type. In addition, ROC curve also indicated that processing speed and executive function could identify MDD from CN subjects. Finally, processing speed performance was negatively correlated with Hamilton Depression Scale scores in both MDD with deficit and non-deficit type. CONCLUSION: The present study provides novel insights on frequency and neurocognitive profile of subtypes of patients showing impairment. Our results suggest that processing speed impairment is a trait dimension of the disorder related to specific cognitive dysfunctions and the severity of depression.