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: 10.28). 08/2013; 37(10). DOI: 10.1016/j.neubiorev.2013.07.018
Source: PubMed

ABSTRACT 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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    • "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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    • "This proposal is in accordance to the Research Domain Criteria (RDoC) initiative of the NIMH [167]. For example, impairment in executive function and processing speed related to abnormal activity in the prefrontal cortex and limbic brain circuit networks are associated with dysfunctional affect deregulation [168] and abnormal biasing of attention to negative cognitions [169] in MDD. This circuit would be a target for multi-modal strategies to prevent and treat cognitive deficits in MDD. "
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    • "This may indicate that altered sgACCinsula connectivity does characterize adolescent MDD, but that the directionality of the functional connections change with brain state (Ho et al., 2014). Cognitive control areas within portions of the PFC, such as the DLPFC and the ventrolateral prefrontal cortex (VLPFC) have been implicated in adult MDD (Rive et al., 2013). It has been suggested that reduced DLPFC recruitment in depressed adults is present only when the amygdala is overactive, indicating that dysfunction in the DLPFC may not the primary mechanism involved in adult MDD but that amygdalar hyperactivity may have a bottom-up influence on the level of activity in DLPFC (Drevets et al., 2008). "
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