Amygdala excitability to subliminally presented emotional faces distinguishes unipolar and bipolar depression: An fMRI and pattern classification study

Grotegerd, Dominik; Stuhrmann, Anja; Kugel, Harald; Schmidt, Simone; Redlich, Ronny; Zwanzger, Peter; Rauch, Astrid Veronika; Heindel, Walter; Zwitserlood, Pienie; Arolt, Volker; Suslow, Thomas; Dannlowski, Udo

doi:10.1002/hbm.22380

Cited by 101 publications

(85 citation statements)

References 75 publications

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“…In our data sensitivity rates outperformed specificity, a finding that is in accordance with the clinical need for sensitive screening instruments to detect psychiatric comorbidity. Accuracy rates were comparable to those of 80% obtained in a pattern analysis study differentiating unipolar from bipolar disorder (Grotegerd et al, 2014) based on amygdalar activation. Accuracies were numerically decreased when accounting for group differences in age, disease onset, and symptom severity (SIGH-A, PAS).…”

Section: Discussionsupporting

confidence: 69%

Separating depressive comorbidity from panic disorder: A combined functional magnetic resonance imaging and machine learning approach

Lueken

Straube

Yang

et al. 2015

Journal of Affective Disorders

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Section: Discussionsupporting

confidence: 69%

Separating depressive comorbidity from panic disorder: A combined functional magnetic resonance imaging and machine learning approach

Lueken

Straube

Yang

et al. 2015

Journal of Affective Disorders

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“…For example, several functional neuroimaging studies have shown that amygdala dysfunction is a key feature of BD (Almeida and Phillips, 2012;Blond et al, 2012;Fournier et al, 2013;Grotegerd et al, 2013Grotegerd et al, , 2014Lim et al, 2013), SCZ (Pankow et al, 2013;Rauch et al, 2010), and MDD (Dannlowski et al, 2007;Groenewold et al, 2012;Siegle et al, 2007;Stuhrmann et al, 2011Stuhrmann et al, , 2013Suslow et al, 2010). Also structural imaging studies have demonstrated decreased amygdala volumes in BD (Blumberg et (Hajek et al, 2012a, b;Redlich et al, 2014), although the respective literature is less consistent than that for the amygdala (Blumberg et al, 2003;Hartberg et al, 2011).…”

Section: Discussionmentioning

confidence: 91%

NCAN Cross-Disorder Risk Variant Is Associated With Limbic Gray Matter Deficits in Healthy Subjects and Major Depression

Dannlowski

Kugel

Grotegerd

et al. 2015

Neuropsychopharmacol

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Genome-wide association studies have reported an association between NCAN rs1064395 genotype and bipolar disorder. This association was later extended to schizophrenia and major depression. However, the neurobiological underpinnings of these associations are poorly understood. NCAN is implicated in neuronal plasticity and expressed in subcortical brain areas, such as the amygdala and hippocampus, which are critically involved in dysfunctional emotion processing and regulation across diagnostic boundaries. We hypothesized that the NCAN risk variant is associated with reduced gray matter volumes in these areas. Gray matter structure was assessed by voxel-based morphometry on structural MRI data in two independent German samples (healthy subjects, n=512; depressed inpatients, n=171). All participants were genotyped for NCAN rs1064395. Hippocampal and amygdala region-of-interest analyses were performed within each sample. In addition, whole-brain data from the combined sample were analyzed. Risk (A)-allele carriers showed reduced amygdala and hippocampal gray matter volumes in both cohorts with a remarkable spatial overlap. In the combined sample, genotype effects observed for the amygdala and hippocampus survived correction for entire brain volume. Further effects were also observed in the left orbitofrontal cortex and the cerebellum/fusiform gyrus. We conclude that NCAN genotype is associated with limbic gray matter alterations in healthy and depressed subjects in brain areas implicated in emotion perception and regulation. The present data suggest that NCAN forms susceptibility to neurostructural deficits in the amygdala, hippocampus, and prefrontal areas independent of disease, which might lead to disorder onset in the presence of other genetic or environmental risk factors.

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“…Previous neuroimaging studies have already addressed the differentiation of BD and unipolar depression (UD) employing structural (Redlich et al, 2014a;Versace et al, 2010) and functional MRI Benson et al, 2014;Grotegerd et al, 2014). These studies yielded differences in regions that contribute to the dysregulation of emotional and cognitive functions.…”

Section: Introductionmentioning

confidence: 99%

Reward Processing in Unipolar and Bipolar Depression: A Functional MRI Study

Redlich

Dohm

Grotegerd

et al. 2015

Neuropsychopharmacol

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Differentiating bipolar disorders (BD) from unipolar depression (UD) remains a major clinical challenge. The identification of neurobiological markers may help to differentiate these disorders, particularly during depressive episodes. This cross-sectional study, including 33 patients with UD, 33 patients with BD, and 34 healthy controls, is one of the first to directly compare UD and BD with respect to reward processing. A card-guessing paradigm was employed and brain activity associated with reward processing was investigated by means of fMRI. A 3 (group) × 2 (condition: reward4control, loss4control) ANOVA was conducted using the nucleus accumbens (NAcc) as ROI. Furthermore, a whole-brain approach was applied. A functional connectivity analysis was performed to characterize diagnosis-related alterations in the functional coupling between the NAcc and other brain areas. The ANOVA revealed higher activity for healthy controls (HCs) than for BD and UD in the NAcc during reward processing. Moreover, UD showed a higher functional connectivity between the NAcc and the VTA than HC. The patients groups could be differentiated in that BD showed a decreased activation, in the reward condition, of the NAcc, caudate nucleus, thalamus, putamen, insula, and prefrontal areas compared with UD. These results may help to refine the understanding of neural correlates of reward processing in both disorders, and to understand the neural underpinnings of anhedonia, a core symptom of depressive episodes.

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Amygdala excitability to subliminally presented emotional faces distinguishes unipolar and bipolar depression: An fMRI and pattern classification study

Abstract: Distinct amygdala excitability during automatic stages of the processing of emotional faces may reflect differential pathophysiological processes in BD versus MDD depression, potentially representing diagnosis-specific neural markers mostly unaffected by current psychotropic medication.

Cited by 101 publications

References 75 publications

Separating depressive comorbidity from panic disorder: A combined functional magnetic resonance imaging and machine learning approach

Separating depressive comorbidity from panic disorder: A combined functional magnetic resonance imaging and machine learning approach

NCAN Cross-Disorder Risk Variant Is Associated With Limbic Gray Matter Deficits in Healthy Subjects and Major Depression

Reward Processing in Unipolar and Bipolar Depression: A Functional MRI Study

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