The orbitofrontal cortex (OFC) has been implicated in the pathophysiology of major depression by evidence obtained using neuroimaging, neuropathologic, and lesion analysis techniques. The abnormalities revealed by these techniques show a regional specificity, and suggest that some OFC regions which appear cytoarchitectonically distinct also are functionally distinct with respect to mood regulation. For example, the severity of depression correlates inversely with physiological activity in parts of the posterior lateral and medial OFC, consistent with evidence that dysfunction of the OFC associated with cerebrovascular lesions increases the vulnerability for developing the major depressive syndrome. The posterior lateral and medial OFC function may also be impaired in individuals who develop primary mood disorders, as these patients show grey-matter volumetric reductions, histopathologic abnormalities, and altered hemodynamic responses to emotionally valenced stimuli, probabilistic reversal learning, and reward processing. In contrast, physiological activity in the anteromedial OFC situated in the ventromedial frontal polar cortex increases during the depressed versus the remitted phases of major depressive disorder to an extent that is positively correlated with the severity of depression. Effective antidepressant treatment is associated with a reduction in activity in this region. Taken together these data are compatible with evidence from studies in experimental animals indicating that some orbitofrontal and medial prefrontal cortex regions function to inhibit, while others function to enhance, emotional expression. Alterations in the functional balance between these regions and the circuits they form with anatomically related areas of the temporal lobe, striatum, thalamus, and brain stem thus may underlie the pathophysiology of mood disorders, such as major depression.
"In the present study, we aimed to investigate baseline as well as post-treatment neural correlates of passive emotional picture processing without additional tasks in patients with MDD by means of whole-head MEG. The measure of event-related magnetic fields in combination with inverse source modeling allows for detecting even rapid, transient, and preconscious cortical activations which may not necessarily result in measurable A c c e p t e d M a n u s c r i p t 6 hemodynamic changes and may become object to hemodynamic masking due to compensatory attempts of attenuating the expression or experience of aversive emotions (Drevets, 2007). Our predictions were that medication-free patients with depression as compared to healthy controls would show an overall decreased sensitivity towards arousing pictures in correlation with a particularly right-sided temporo-parietal hypoactivation and a dysfunctional affective modulation at prefrontal cortex regions. "
", 2011 ) . For example , severity of depression correlates positively with activity in ventromedial polar cortex and amygdala , possibly representing an increased vigilance for potential threats to self - esteem ( Drevets , 2007 ; Murray et al . , 2011 ; Price and Drevets , 2012 ) . "
[Show abstract][Hide abstract] ABSTRACT: Counterfactual reasoning is a hallmark of human thought, enabling the capacity to shift from perceiving the immediate environment to an alternative, imagined perspective. Mental representations of counterfactual possibilities (e.g., imagined past events or future outcomes not yet at hand) provide the basis for learning from past experience, enable planning and prediction, support creativity and insight, and give rise to emotions and social attributions (e.g., regret and blame). Yet remarkably little is known about the psychological and neural foundations of counterfactual reasoning. In this review, we survey recent findings from psychology and neuroscience indicating that counterfactual thought depends on an integrative network of systems for affective processing, mental simulation, and cognitive control. We review evidence to elucidate how these mechanisms are systematically altered through psychiatric illness and neurological disease. We propose that counterfactual thinking depends on the coordination of multiple information processing systems that together enable adaptive behavior and goal-directed decision making and make recommendations for the study of counterfactual inference in health, aging, and disease.
Frontiers in Human Neuroscience 07/2015; 9. DOI:10.3389/fnhum.2015.00420 · 2.99 Impact Factor
"Diagnostic categories have been the basis for neuroimaging and genome-wide association studies (Garvey et al., 1986; Clayton, 1990; Moore and Williams, 2009; Savitz and Drevets, 2009), but disease-specific risk factors identified by extant investigations have been equivocal based on the current categorical system of mood disorder diagnoses (Dolan et al., 1993; Sheline et al., 1999; Ravnkilde et al., 2003; Lange et al., 2004; Drevets, 2007; Hamilton et al., 2008; Surguladze et al., 2008). This has led to the pursuit of intermediate phenotypes, sometimes called endophenotypes . "
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