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. 2014 Feb;123(1):35-48.
doi: 10.1037/a0035834.

Neural substrates of trait ruminations in depression

Darcy Mandell  1 , Greg J Siegle  1 , Luann Shutt  2 , Josh Feldmiller  2 , Michael E Thase  3
Affiliations

Neural substrates of trait ruminations in depression

Darcy Mandell et al. J Abnorm Psychol. 2014 Feb.

Abstract

Rumination in depression is a risk factor for longer, more intense, and harder-to-treat depressions. But there appear to be multiple types of depressive rumination-whether they all share these vulnerability mechanisms, and thus would benefit from the same types of clinical attention is unclear. In the current study, we examined neural correlates of empirically derived dimensions of trait rumination in 35 depressed participants. These individuals and 29 never-depressed controls completed 17 self-report measures of rumination and an alternating emotion-processing/executive-control task during functional MRI (fMRI) assessment. We examined associations of regions of interest--the amygdala and other cortical regions subserving a potential role in deficient cognitive control and elaborative emotion-processing--with trait rumination. Rumination of all types was generally associated with increased sustained amygdala reactivity. When controlling for amygdala reactivity, distinct activity patterns in hippocampus were also associated with specific dimensions of rumination. We discuss the possibly utility of targeting more basic biological substrates of emotional reactivity in depressed patients who frequently ruminate.

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Figures

Figure 1
Figure 1. Mean BOLD % signal change in the bilateral amygdala in response to negative words for depressed participants and a group of healthy controls
Highlighted temporal regions denote a significant group difference at p<.05.
Figure 2
Figure 2
Associations of trait rumination with early and sustained BOLD activity in the left amygdala during alternating emotion processing/cognitive distracter task. Note: Color maps represent correlation matrices for correlations of each rumination measure (Figure 2A) or factor (Figure 2B) with BOLD % signal change across 17 scans (scan 1 = baseline). In Figure 2B, asterisks (*) denote scans at which correlation values were significant at p <. 05 and plusses (+) denote scans significant at p < .1. Scatterplots (C, E, and G) show the relationship between depressed subjects’ rumination factor scores and mean activation at significant temporal windows. Dotted vertical lines denote cutoff scores splitting the sample into thirds, to the left and right of which depressed subjects were classified as low- or high-ruminators on that factor. The graphs on the right (D, F, and G) illustrate BOLD % signal change for high-ruminating depressed (N=12), low-ruminating depressed (N=12), and healthy control subjects (N=29). Vertical yellow bars denote temporal windows in which significant correlations were found. T-tests were performed to test for significant differences between each group’s mean activation during these windows. The text above each yellow window indicates whether groups differed in mean activity. * = trend (p < .1), ** = p < .05. HRD = high-ruminating depressed, LRD = low-ruminating depressed, HC = healthy controls. Statistics for group comparisons can be found in Supplement III.
Figure 3
Figure 3
Graphs as in Figure 2 for other regions including the right amygdala, right and left anatomical dlPFC, hippocampus, insula, posterior cingulate, and BA10 in the medial frontal gyrus.
See this image and copyright information in PMC

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