Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression

By Wayne C. Drevets, Joseph L. Price, Maura L. Furey. Brain Structure and Function, 2008

2,184 citations recorded by the source corpus.

AbstractThe neural networks that putatively modulate aspects of normal emotional behavior have been implicated in the pathophysiology of mood disorders by converging evidence from neuroimaging, neuropathological and lesion analysis studies. These networks involve the medial prefrontal cortex (MPFC) and closely related areas in the medial and caudolateral orbital cortex (medial prefrontal network), amygdala, hippocampus, and ventromedial parts of the basal ganglia, where alterations in grey matter volume and neurophysiological activity are found in cases with recurrent depressive episodes. Such findings hold major implications for models of the neurocircuits that underlie depression. In particular evidence from lesion analysis studies suggests that the MPFC and related limbic and striato-pallido-thalamic structures organize emotional expression. The MPFC is part of a larger “default system” of cortical areas that include the dorsal PFC, mid- and posterior cingulate cortex, anterior temporal cortex, and entorhinal and parahippocampal cortex, which has been implicated in self-referential functions. Dysfunction within and between structures in this circuit may induce disturbances in emotional behavior and other cognitive aspects of depressive syndromes in humans. Further, because the MPFC and related limbic structures provide forebrain modulation over visceral control structures in the hypothalamus and brainstem, their dysfunction can account for the disturbances in autonomic regulation and neuroendocrine responses that are associated with mood disorders. This paper discusses these systems together with the neurochemical systems that impinge on them and form the basis for most pharmacological therapies.

Subfields: Behavioral Neuroscience, Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/3481d060342e009b46b39b8ed9d35cd48d948ad9

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Citations in the corpus

Conjoint activity of anterior insular and anterior cingulate cortex: awareness and response (2010, background): “…suggest that the neurobiological basis of major depression is dysfunction of the normal interactions between limbic and cortical areas (Mayberg 1997; Drevets et al. 2008), although these models implicate widely distributed networks and are not specific to the regions under consideration here.”
Reduced resting-state functional connectivity between amygdala and orbitofrontal cortex in social anxiety disorder (2011, background): “Electrical stimulation of the amygdala has been shown to elicit fear, anxiety and social withdrawal and to increase the stress response via cortisol release (Drevets et al., 2008; Lanteaume et al., 2007).”
Identifying major depression using whole-brain functional connectivity: a multivariate pattern analysis. (2012, background): “Altered connectivity of the thalamus with the prefrontal lobe and the limbic areas may account for the distur- bances in autonomic regulations that are associated with depres- sion (Drevets et al., 2008).”
Dopamine System Dysregulation in Major Depressive Disorders (2017, background): “, 2011) as well as a reduction in the size of neurons and a loss of glia (Drevets et al., 2008).”
Rapid and sustained symptom reduction following psilocybin treatment for anxiety and depression in patients with life-threatening cancer: a randomized controlled trial (2016, background): “The former is significant because depressive symptoms have been associated with increased activity in the medial PFC (Drevets et al., 2008; Farb et al., 2011) and normalization of medial PFC activity has been demonstrated with anti-depressant treatment (Deakin et al., 2008; Holtzheimer and Mayberg, ”
COGNITIVE DEFICITS AND FUNCTIONAL OUTCOMES IN MAJOR DEPRESSIVE DISORDER: DETERMINANTS, SUBSTRATES, AND TREATMENT INTERVENTIONS (2013, background): “, neural circuits) of cognitive function and deficits, overlap with those implicated in other components of MDD.[47] The most replicated volumetric abnormality in MDD is bilateral hippocampal reduction, which is a consequence of loss of neuropil, decreased dendritic density, and reduced neuronal som”
Functional atlas of emotional faces processing: a voxel-based meta-analysis of 105 functional magnetic resonance imaging studies. (2009, neutral): “Thus,(30) fMRI has been exponentially employed to address the neurophysiological substrates of impairments in emotional faces processing under different psychiatric conditions.(177) Although many of the brain regions activated during facial emotional processing in healthy participants are also impli”
Gray matter abnormalities in Major Depressive Disorder: a meta-analysis of voxel based morphometry studies. (2012, background): “Subgenual overactivity has been associated with depressive states and there is some evidence that treatment ameliorates this hyperactivity (Drevets et al., 2008; Mayberg, 1997, 2003; Pizzagalli, 2011).”
Whole Brain Resting-State Analysis Reveals Decreased Functional Connectivity in Major Depression (2010, neutral): “Frontiers in Systems Neuroscience www.frontiersin.org September 2010 | Volume 4 | Article 41 | 1 SYSTEMS NEUROSCIENCE Original research article published: 20 September 2010 doi: 10.3389/fnsys.2010.00041 in this disease (Mayberg, 2003; Drevets et al., 2008).”
The Episodic Memory System: Neurocircuitry and Disorders (2009, positive): “Some neuropsychiatric disorders , including depression (Drevets et al, 2008 # 4760; Neumeister et al, 2005 # 4773), schizophrenia (Drevets et al, 2008; Neumeister et al, 2005), and posttraumatic stress disorder (Shin et al, 2004), seem to affect memory systems (particularly the MTL) in important…”
Adult ADHD and comorbid disorders: clinical implications of a dimensional approach (2017, background): “These circuits integrate higher cognitive functions with visceral information and external environmental conditions to affect mood and emotional states, through reciprocal connections with regions of the cortex that are involved with control of higher cognitive functions as well as regions associate”