Neural Mechanisms Of Individual Difference Of Rumination

Rumination refers to behaviors and thoughts that focus one’s attention on one’s depressive symptoms and on the cause, implications results of these symptoms. People who have higher rumination would more likely to develop depression and endure longer and more severe episodes of major depression. Previous accounts and characterizations of control functioning in rumination include resource depletion account, which maintains that a state of rumination usurps limited executive resources from task-relevant processing, and valence-specific accounts which suggests that a tendency to ruminate is related to difficulty controlling attention to emotionally negative, but not to neutral or positive, information. Whitmer and Gotlib (2012) reviewed and discussed the above accounts and pointed out main deficiencies. Subsequently, they presented an attentional scope model of rumination that posited that a constricted array of thoughts, percepts, and actions that were activated in WM or available for selection from long-term memory affects the control functioning of trait ruminators. The present study first investigated the neural correlates of individual difference in rumination of normal people, and then verified the result from depressive patients.The present research included two parts:Experiment1: To investigate the neural mechanisms of individual difference of rumination in normal people,255nonclinical healthy subjects were studied meanwhile filling in classical rumination, depression scales and resting state and structural MRI. For structural data, we analysis the gray matter volume (GMV) using the method of voxel-based morphometry (VBM) for each subject. Multiple regression analysis was performed to investigate which brain region of GMV was associated with rumination and found that regional GMV of dorsolateral prefrontal cortex (DLPFC) and parahippocampal gyrus were positively correlated with individual difference in rumination. For functional data, multiple regression analysis was also performed to investigate the relation between rumination regional homogeneity (ReHo) and found that inter-difference of rumination were negatively correlated with ReHo of DLPFC, which verified the result of VBM. Then, we conducted mediation analysis to investigate the influence of rGMV on the relationship between rumination and depression and found that increased DLPFC volume have mediating effects on the relationship between rumination and depression.Experiment2:To investigate the neural mechanisms of individual difference of rumination in depressive patients,41moderate to severe depressive patients and52age, education matched control subjects were studied. They were also asked to fill in the same scales. We compared the GMV between patients and normal subjects within the regions identified in experiment1and conducted the relation analysis between rumination and rGMV for each group. Results found that, compared with control group, depressed patients showed significantly decreased rGMV in the DLPFC and parahippocampal gyrus. Moreover, there was a significantly negative correlation between the DLPFC volume and depressive rumination.Combining the results of experiment1and2, we found that DLPFC showed contrary trend in different group. That was, in our sample of healthy individuals, increased DLPFC volume (decreased ReHo of the DLPFC) associated with higher rumination might be inefficient inhibition ("overload state" function of DLPFC), and causing sustained negative vicious cycles to enhance individual’s depressive rumination. However, there was a clear association between the DLPFC atrophy and severity of depressive rumination, and the DLPFC atrophy in depressive disorders might reflect an impaired regulatory mechanism ("paralysis state" function of DLPFC). In addition, we found that DLPFC had a mediate effect on relation between rumination and depression. These interesting findings might provide an early risk biomarker of subtle differences in brain structural alterations associated with depressive rumination when and why healthy individuals would develop sustained negative mood which in turn enhances depressive symptoms.