Heightened neural sensitivity to social pain and social gain in major depressive disorder.

2021 ◽  
Author(s):  
Julia Gillard ◽  
Aliza Werner-Seidler ◽  
Jason Stretton ◽  
Tim Dalgleish

Social rejection represents a proximal risk factor for depression onset that is thought to activate a neuro-cognitive alarm system for social and physical pain. However, emerging evidence suggests that both social pain and social gain share an overlapping neural substrate. This remains unexplored in the context of depression. Eighteen participants with Major Depressive Disorder (MDD) and 21 controls listened to and vividly revisited autobiographical social experiences in an ecologically valid script-driven imagery paradigm using naturalistic memory narratives. An overlapping neural substrate in the dorsal anterior cingulate cortex and anterior insula was activated while revisiting both social-inclusion and -rejection experiences relative to neutral ones. These same regions were more active in MDD compared to controls for both rejection and inclusion narratives. Our findings add to the evidence for an overlapping neural substrate of complex representations for both positive and negative social signals and suggest a heightened neural sensitivity in MDD towards any socially salient information as opposed to selective sensitivity towards negative social experiences.

2021 ◽  
Vol 11 ◽  
Author(s):  
Zhuoying Wu ◽  
Qianyi Luo ◽  
Huawang Wu ◽  
Zhiyao Wu ◽  
Yingjun Zheng ◽  
...  

Major Depressive Disorder (MDD) with childhood trauma is one of the functional subtypes of depression. Frequency-dependent changes in the amplitude of low-frequency fluctuations (ALFF) have been reported in MDD patients. However, there are few studies on ALFF about MDD with childhood trauma. Resting-state functional magnetic resonance imaging was used to measure the ALFF in 69 MDD patients with childhood trauma (28.7 ± 9.6 years) and 30 healthy subjects (28.12 ± 4.41 years). Two frequency bands (slow-5: 0.010–0.027 Hz; slow-4: 0.027–0.073 Hz) were analyzed. Compared with controls, the MDD with childhood trauma had decreased ALFF in left S1 (Primary somatosensory cortex), and increased ALFF in left insula. More importantly, significant group × frequency interactions were found in right dorsal anterior cingulate cortex (dACC). Our finding may provide insights into the pathophysiology of MDD with childhood trauma.


2017 ◽  
Vol 42 (12) ◽  
pp. 2434-2445 ◽  
Author(s):  
Tiffany C Ho ◽  
Matthew D Sacchet ◽  
Colm G Connolly ◽  
Daniel S Margulies ◽  
Olga Tymofiyeva ◽  
...  

2016 ◽  
Vol 22 (1) ◽  
pp. 113-119 ◽  
Author(s):  
J Ernst ◽  
A Hock ◽  
A Henning ◽  
E Seifritz ◽  
H Boeker ◽  
...  

2012 ◽  
Vol 43 (6) ◽  
pp. 1219-1230 ◽  
Author(s):  
N. L. Nixon ◽  
P. F. Liddle ◽  
G. Worwood ◽  
M. Liotti ◽  
E. Nixon

BackgroundRecent models of major depressive disorder (MDD) have proposed the rostral anterior cingulate (rACC) and dorsomedial prefrontal cortex (dmPFC) as nexus sites in the dysfunctional regulation of cognitive-affective state. Limited evidence from remitted-state MDD supports these theories by suggesting that aberrant neural activity proximal to the rACC and the dmPFC may play a role in vulnerability to recurrence/relapse within this disorder. Here we present a targeted analysis assessing functional activity within these two regions of interest (ROIs) for groups with identified vulnerability to MDD: first, remitted, high predicted recurrence-risk patients; and second, patients suffering observed 1-year recurrence.MethodBaseline T2* images sensitive to blood oxygen level-dependent (BOLD) contrast were acquired from patients and controls during a Go/No-Go (GNG) task incorporating negative feedback, with 1-year patient follow-up to identify recurrence. BOLD contrast data for error commission (EC) and visual negative feedback (VNF) were used in an ROI analysis based on rACC and dmPFC coordinates from the literature, comparing patientsversuscontrols and recurrenceversusnon-recurrenceversuscontrol groups.ResultsAnalysis of patients (n = 20)versuscontrols (n = 20) showed significant right dmPFC [Brodmann area (BA) 9] hypoactivity within the patient group, co-localized during EC and VNF, with additional significant rACC (BA 32) hypoactivity during EC. The results from the follow-up analysis were undermined by small groups and potential confounders but suggested persistent right dmPFC (BA 9) hypoactivity associated with 1-year recurrence.ConclusionsConvergent hypoactive right dmPFC (BA 9) processing of VNF and EC, possibly impairing adaptive reappraisal of negative experience, was associated most clearly with clinically predicted vulnerability to MDD.


2012 ◽  
Vol 42 (10) ◽  
pp. 2071-2081 ◽  
Author(s):  
C. G. Davey ◽  
B. J. Harrison ◽  
M. Yücel ◽  
N. B. Allen

BackgroundDepression has been associated with functional alterations in several areas of the cingulate cortex. In this study we have taken a systematic approach to examining how alterations in functional connectivity vary across the functionally diverse subregions of the rostral cingulate cortex.MethodEighteen patients with major depressive disorder, aged 15 to 24 years, were matched with 20 healthy control participants. Using resting-state functional connectivity magnetic resonance imaging (fcMRI), we systematically investigated the functional connectivity of four subregions of the rostral cingulate cortex. Voxelwise statistical maps of each subregion's connectivity with other brain areas were compared between the patient and control groups.ResultsThe depressed participants showed altered patterns of connectivity with ventral cingulate subregions. They showed increased connectivity between subgenual anterior cingulate cortex (ACC) and dorsomedial frontal cortex, with connectivity strength showing positive correlation with illness severity. Depressed participants also showed increased connectivity between pregenual ACC and left dorsolateral frontal cortex, and decreased connectivity between pregenual ACC and the caudate nucleus bilaterally.ConclusionsThe results reinforce the importance of subgenual ACC for depression, and show a close link between brain regions that support self-related processes and affective visceromotor function. The pregenual ACC also has an important role, with its increased connectivity with dorsolateral frontal cortex suggesting heightened cognitive regulation of affect; and reduced connectivity with the caudate nucleus potentially underlying symptoms such as anhedonia, reduced motivation and psychomotor dysfunction.


2019 ◽  
Vol 50 (10) ◽  
pp. 1653-1662 ◽  
Author(s):  
Mathew A. Harris ◽  
Xueyi Shen ◽  
Simon R. Cox ◽  
Jude Gibson ◽  
Mark J. Adams ◽  
...  

AbstractBackgroundSubstantial clinical heterogeneity of major depressive disorder (MDD) suggests it may group together individuals with diverse aetiologies. Identifying distinct subtypes should lead to more effective diagnosis and treatment, while providing more useful targets for further research. Genetic and clinical overlap between MDD and schizophrenia (SCZ) suggests an MDD subtype may share underlying mechanisms with SCZ.MethodsThe present study investigated whether a neurobiologically distinct subtype of MDD could be identified by SCZ polygenic risk score (PRS). We explored interactive effects between SCZ PRS and MDD case/control status on a range of cortical, subcortical and white matter metrics among 2370 male and 2574 female UK Biobank participants.ResultsThere was a significant SCZ PRS by MDD interaction for rostral anterior cingulate cortex (RACC) thickness (β = 0.191, q = 0.043). This was driven by a positive association between SCZ PRS and RACC thickness among MDD cases (β = 0.098, p = 0.026), compared to a negative association among controls (β = −0.087, p = 0.002). MDD cases with low SCZ PRS showed thinner RACC, although the opposite difference for high-SCZ-PRS cases was not significant. There were nominal interactions for other brain metrics, but none remained significant after correcting for multiple comparisons.ConclusionsOur significant results indicate that MDD case-control differences in RACC thickness vary as a function of SCZ PRS. Although this was not the case for most other brain measures assessed, our specific findings still provide some further evidence that MDD in the presence of high genetic risk for SCZ is subtly neurobiologically distinct from MDD in general.


2019 ◽  
Vol 4 (12) ◽  
pp. 1049-1058 ◽  
Author(s):  
Lejla Colic ◽  
Felicia von Düring ◽  
Dominik Denzel ◽  
Liliana Ramona Demenescu ◽  
Anton R. Lord ◽  
...  

2019 ◽  
Vol 45 (4) ◽  
pp. 703-712 ◽  
Author(s):  
Qian Li ◽  
Youjin Zhao ◽  
Ziqi Chen ◽  
Jingyi Long ◽  
Jing Dai ◽  
...  

Abstract Alterations in cortical thickness have been identified in major depressive disorder (MDD), but findings have been variable and inconsistent. To date, no reliable tools have been available for the meta-analysis of surface-based morphometric (SBM) studies to effectively characterize what has been learned in previous studies, and drug treatments may have differentially impacted findings. We conducted a comprehensive meta-analysis of magnetic resonance imaging (MRI) studies that explored cortical thickness in medication-free patients with MDD, using a newly developed meta-analytic mask compatible with seed-based d mapping (SDM) meta-analytic software. We performed the meta-regression to explore the effects of demographics and clinical characteristics on variation in cortical thickness in MDD. Fifteen studies describing 529 patients and 586 healthy controls (HCs) were included. Medication-free patients with MDD, relative to HCs, showed a complex pattern of increased cortical thickness in some areas (posterior cingulate cortex, ventromedial prefrontal cortex, and anterior cingulate cortex) and decreased cortical thickness in others (gyrus rectus, orbital segment of the superior frontal gyrus, and middle temporal gyrus). Most findings in the whole sample analysis were confirmed in a meta-analysis of studies recruiting medication-naive patients. Using the new mask specifically developed for SBM studies, this SDM meta-analysis provides evidence for regional cortical thickness alterations in MDD, mainly involving increased cortical thickness in the default mode network and decreased cortical thickness in the orbitofrontal and temporal cortex.


2014 ◽  
Vol 44 (14) ◽  
pp. 2927-2937 ◽  
Author(s):  
Y.-J. Zhao ◽  
M.-Y. Du ◽  
X.-Q. Huang ◽  
S. Lui ◽  
Z.-Q. Chen ◽  
...  

BackgroundBecause cerebral morphological abnormalities in major depressive disorder (MDD) may be modulated by antidepressant treatment, inclusion of medicated patients may have biased previous meta-analyses of voxel-based morphometry (VBM) studies. A meta-analysis of VBM studies on medication-free MDD patients should be able to distinguish the morphological features of the disease itself from those of treatment.MethodA systematic search was conducted for the relevant studies. Effect-size signed differential mapping was applied to analyse the grey matter differences between all medication-free MDD patients and healthy controls. Meta-regression was used to explore the effects of demographics and clinical characteristics.ResultsA total of 14 datasets comprising 400 medication-free MDD patients and 424 healthy controls met the inclusion criteria. The pooled meta-analysis and subgroup meta-analyses showed robustly reduced grey matter in prefrontal and limbic regions in MDD. Increased right thalamus volume was only seen in first-episode medication-naive patients, and increased grey matter in the bilateral anterior cingulate cortex only in medication wash-out patients. In meta-regression analyses the percentage of female patients in each study was negatively correlated with reduced grey matter in the right hippocampus.ConclusionsBy excluding interference from medication effects, the present study identified grey matter reduction in the prefrontal–limbic network in MDD. The subgroup meta-analysis results suggest that an increased right thalamus volume might be a trait directly related to MDD, while an increased anterior cingulate cortex volume might be an effect of medication. The meta-regression results perhaps reveal the structural underpinning of the sex differences in epidemiological and clinical aspects of MDD.


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