Neural correlates of dysfunctional emotion regulation in major depressive disorder. A systematic review of neuroimaging studies

Program for Mood Disorders, Department of Psychiatry, Academic Medical Center, University of Amsterdam, PO-Box 22660, 1100 DD Amsterdam, The Netherlands. Electronic address: .
Neuroscience & Biobehavioral Reviews (Impact Factor: 8.8). 08/2013; 37(10). DOI: 10.1016/j.neubiorev.2013.07.018
Source: PubMed


Abnormal emotion processing is a core feature of major depressive disorder (MDD). Since the emergence of functional neuroimaging techniques, many studies have been conducted in MDD subjects to elucidate the underlying abnormalities in the neural systems involved in emotion regulation. In this systematic review, we discuss this research in the context of the neural model of emotion regulation previously described by Phillips et al. (2008). This model differentiates between automatic and voluntary emotion regulation subprocesses. Automatic regulation subprocesses were shown to involve predominantly medial prefrontal cortical structures, in addition to the hippocampus and parahippocampus, while voluntary regulation processes additionally recruited lateral prefrontal cortical regions. In conclusion, although the available data is limited, findings suggest that MDD subjects demonstrate abnormally reduced activity in lateral prefrontal cortices during explicit voluntary control of emotional experience. During early, automatic stages of emotion regulation, on the other hand, MDD subjects appear to achieve successful emotion regulation by recruiting additional lateral prefrontal neural regions, that may be mediated by medial prefrontal, especially rostral/dorsal anterior cingulate gyrus (ACG) functioning. Dysfunctional automatic regulation may impair successful voluntary emotion regulation, and may present a target for novel therapeutic approaches in MDD.

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Available from: Henricus G Ruhé, Jan 04, 2015
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    • "During voluntary control strategies, MDD show reduced neuronal activity in lateral prefrontal cortices, which are implicated in cognitive and executive functions (Rive et al., 2013). Given the nCDSs subjects in the present study are in the early-adulthood years (mean age, 19.05 years), they are still undergoing rapid neurodevelopment. "
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    ABSTRACT: Non-clinical depressive symptoms (nCDSs) are highly prevalent in young adults and may be associated with the risk of developing full-fledged depressive disorders. However, the neural basis underlying nCDSs remains unknown. To explore the alteration of spontaneous brain activity in individuals with nCDSs compared with healthy controls (HCs), we investigated resting-state brain activity using the amplitude of low-frequency fluctuations (ALFF) in subjects with nCDSs (n=17) and HCs (n=20). All subjects were drawn from a sample of 1105 college students participating in a survey assessing depressive symptoms. We determined that nCDSs can lead to reduced ALFF in the right ventral lateral prefrontal cortex (VLPFC) and right dorsolateral prefrontal cortex (DLPFC) and to increased ALFF in the left fusiform, left posterior cerebellum, right cuneus, left inferior parietal lobule, right supramarginal gyrus and bilateral precuneus. In addition, with respect to Beck Depression Inventory (BDI) scores and ALFF values in subjects with nCDSs, a positive correlation was discovered in the right DLPFC, while a negative correlation was identified in left posterior cerebellum and bilateral precuneus after correction. These results indicate that nCDSs are characterized by altered spontaneous activity in several important functional regions. We suggest that altered ALFFs in the right DLPFC, left posterior cerebellum and bilateral precuneus may be biomarkers that are related to the pathophysiology of nCDSs in young adults. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Preview · Article · May 2015 · Psychiatry Research: Neuroimaging
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    • "Whether clinical improvements of obesity and depressive symptoms are associated with structural changes should be subject of future longitudinal neuroimaging studies. Interestingly, there has been growing consensus on the etiopathological relevance and the specificity of medial prefrontal structural abnormalities in recent MDD studies (Rive et al., 2013). Since our structural data show that reduced MPFC gray matter volumes are strongly linked to both conditions, improvement of striatocortical dopamine-function might be a promising approach to support treatment and prevention of obesity in future research (Wang et al., 2009). "
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    ABSTRACT: Obesity is one of the most prevalent somatic comorbidities of major depressive disorder (MDD). Both disorders rank among the leading challenges in public health and have been independently characterized by gray matter alterations in partly overlapping brain structures. Hence, it appears crucial to investigate the possibility of a shared neurostructural correlate of this frequent comorbidity as well as its clinical implications.One hundred and fourty-four patients suffering from acute MDD and 141 healthy control subjects underwent structural MRI. Imaging data were analyzed using voxel-based morphometry (VBM). Body-mass-index (BMI) as well as state and course of disease were assessed.Higher BMI was associated with a highly comparable pattern of gray matter reductions in the medial prefrontal cortex, the orbitofrontal cortex, the caudate nucleus and the thalamus in MDD patients and healthy controls alike. In MDD-patients, BMI was associated with a more chronic course of disease and both BMI and chronicity of disorder were related to similar morphometric anomalies in medial prefrontal areas.In MDD, obese subjects might be characterized by a more chronic course of disease. Moreover, obesity and chronicity of disorder seem to share overlapping neurostructural anomalies in prefrontal areas involved in emotion regulation and impulse control. Hence, our data provide evidence for specific morphological alterations underlying this prevalent comorbidity. It further underlines the clinical importance of preventive measures against obesity accompanying MDD treatment.
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    • "This compensatory recruitment occurs in the medial prefrontal cortex, including the ACC. However, during conscious regulation occurring later in an emotional experience, recruitment of lateral prefrontal cortex is diminished , with less activation in dlPFC and/or vlPFC in individuals with MDD compared with healthy controls (Rive et al., 2013). Differential prefrontal cortical influence on amygdala activation in MDD has been observed during regulation of both negative and positive emotions (Greening et al., 2014), although not all studies have found evidence of altered frontolimbic indicators of regulation in MDD (Dillon and Pizzagalli, 2013). "
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    ABSTRACT: Mood disorders are characterized by impaired emotion regulation abilities, reflected in alterations in frontolimbic brain functioning during regulation. However, little is known about differences in brain function when comparing regulatory strategies. Reappraisal and emotional acceptance are effective in downregulating negative affect, and are components of effective depression psychotherapies. Investigating neural mechanisms of reappraisal versus emotional acceptance in remitted major depressive disorder (rMDD) may yield novel mechanistic insights into depression risk and prevention. Thirty-seven individuals (18 rMDD, 19 controls) were assessed during an fMRI task requiring reappraisal, emotional acceptance, or no explicit regulation while viewing sad images. Lower negative affect was reported following reappraisal than acceptance, and was lower following acceptance than no explicit regulation. In controls, the acceptance > reappraisal contrast revealed greater activation in left insular cortex and right prefrontal gyrus, and less activation in several other prefrontal regions. Compared to controls, the rMDD group had greater paracingulate and right midfrontal gyrus (BA 8) activation during reappraisal relative to acceptance. Compared to reappraisal, acceptance is associated with activation in regions linked to somatic and emotion awareness, though this activation is associated with less reduction in negative affect. Additionally, a history of MDD moderated these effects. © The Author (2015). Published by Oxford University Press. For Permissions, please email:
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