Factors associated with relapse and recurrence of major depressive disorder in patients starting mindfulness-based cognitive therapy

Background Mindfulness-based cognitive therapy (MBCT) is effective for relapse prevention in major depressive disorder (MDD). It reduces cognitive reactivity (CR) and rumination, and enhances self-compassion and mindfulness. Although rumination and mindfulness after MBCT are associated with relapse, the association of CR, rumination, self-compassion, and mindfulness with relapse before initiation of MBCT has never been investigated. Methods Data were drawn from two randomized controlled trials, including a total of 282 remitted MDD participants (>= 3 depressive episodes) who had been using maintenance antidepressant medication (mADM) for at least 6 months before baseline. All participants were offered MBCT while either their mADM was maintained or discontinued after MBCT. CR, rumination, self-compassion, and mindfulness were assessed at baseline by self-rated questionnaires and were used in Cox proportional hazards regression models to investigate their association with relapse. Results CR and mindfulness were associated with relapse, independent of residual symptoms, previous depressive episodes, and mADM-use. Higher CR and lower mindfulness increased the risk of relapse. Self-compassion was not associated with relapse. For rumination, a significant interaction with mADM-use was found. Rumination was associated with relapse in patients who discontinued their mADM, while this effect was absent if patients continued mADM. Conclusions These results show that CR, rumination, and mindfulness are associated with relapse in remitted MDD-patients before initiation of MBCT, independent of residual symptoms and previous depressive episodes. This information could improve decisions in treatment planning in remitted individuals with a history of depression.Stress-related psychiatric disorders across the life spa

Decreased reward circuit connectivity during reward anticipation in major depression

An important symptom of major depressive disorder (MDD) is the inability to experience pleasure, possibly due to a dysfunction of the reward system. Despite promising insights regarding impaired reward-related processing in MDD, circuit-level abnormalities remain largely unexplored. Furthermore, whereas studies contrasting experimental conditions from incentive tasks have revealed important information about reward processing, temporal difference modeling of reward-related prediction error (PE) signals might give a more accurate representation of the reward system. We used a monetary incentive delay task during functional MRI scanning to explore PE-related striatal and ventral tegmental area (VTA) activation in response to anticipation and delivery of monetary rewards in 24 individuals with MDD versus 24 healthy controls (HCs). Furthermore, we investigated group differences in temporal difference related connectivity with a generalized psychophysiological interaction (gPPI) analysis with the VTA, ventral striatum (VS) and dorsal striatum (DS) as seeds during reward versus neutral, both in anticipation and delivery. Relative to HCs, MDD patients displayed a trend-level (p = 0.052) decrease in temporal difference-related activation in the VS during reward anticipation and delivery combined. Moreover, gPPI analyses revealed that during reward anticipation, MDD patients exhibited decreased functional connectivity between the VS and anterior cingulate cortex / medial prefrontal cortex, anterior cingulate gyrus, angular/middle orbital gyrus, left insula, superior/middle frontal gyrus (SFG/MFG) and precuneus/superior occipital gyrus/cerebellum compared to HC. Moreover, MDD patients showed decreased functional connectivity between the VTA and left insula compared to HC during reward anticipation. Exploratory analysis separating medication free patients from patients using antidepressant revealed that these decreased functional connectivity patterns were mainly apparent in the MDD group that used antidepressants. These results suggest that MDD is characterized by alterations in reward circuit connectivity rather than isolated activation impairments. These findings represent an important extension of the existing literature since improved understanding of neural pathways underlying depression-related reward dysfunctions, may help currently unmet diagnostic and therapeutic efforts