Affective experience has effects on subjective feelings, physiological indices, entails immediate activity changes in the brain, and even influences brain networks in a protracted manner. However, it is still unclear, how the functional connectivity (FC) interplay between major intrinsic connectivity networks upon affective stimulation depends on affective valence, and whether this is specific for affective experience, i.e., can be distinguished from cognitive task execution. Our study included fMRI scans during and after affective stimulation with sad and neutral movies and a working memory task complemented with measures of cardiovascular activity and mood. Via parcellation of the brain into default mode network (DMN), central executive network (CEN), and dorsal attention network, and application of network-based statistics, we identified subnetworks associated with changing psychological contexts. Specific effects for affective stimulation with negative valence were both reduced heart rate variability and mood, and upregulated FC of inter-CEN-DMN connections while intra-DMN connections were downregulated. Furthermore, results demonstrated a valence-specific dynamic carry-over effect in nodes of the CEN, which temporarily increased their FC strength after affective stimulation with negative valence and exhibited distinct temporal profiles. The reported effects were clearly distinguishable from those of a cognitive task and further elucidate the trajectory of affective experience.
Electroconvulsive therapy (ECT) is one of the most effective treatments for treatment-resistant depression. However, the underlying mechanisms of action are not yet fully understood. The investigation of depression-specific networks using resting-state fMRI and the relation to differential symptom improvement might be an innovative approach providing new insights into the underlying processes. In this naturalistic study, we investigated the relationship between changes in resting-state functional connectivity (rsFC) and symptom improvement after ECT in 21 patients with treatment-resistant depression. We investigated rsFC before and after ECT and focused our analyses on FC changes directly related to symptom reduction and on FC at baseline to identify neural targets that might predict individual clinical responses to ECT. Additional analyses were performed to identify the direct relationship between rsFC change and symptom dimensions such as sadness, negative thoughts, detachment, and neurovegetative symptoms. An increase in rsFC between the left amygdala and left dorsolateral prefrontal cortex (DLPFC) after ECT was related to overall symptom reduction (Bonferroni-corrected p = 0.033) as well as to a reduction in specific symptoms such as sadness (r = 0.524, uncorrected p = 0.014), negative thoughts (r = 0.700, Bonferroni-corrected p = 0.002) and detachment (r = 0.663, p = 0.004), but not in neurovegetative symptoms. Furthermore, high baseline rsFC between the left amygdala and the right frontal pole (FP) predicted treatment outcome (uncorrected p = 0.039). We conclude that changes in FC in regions of the limbic-prefrontal network are associated with symptom improvement, particularly in affective and cognitive dimensions. Frontal-limbic connectivity has the potential to predict symptom improvement after ECT. Further research combining functional imaging biomarkers and a symptom-based approach might be promising.
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