Neuroanatomical deficits in drug-naïve adult patients with generalized social anxiety disorder: A voxel-based morphometry study

Meng, Yajing; Lui, Su; Qiu, Changjian; Qiu, Lihua; Lama, Sunima; Huang, Xiaoqi; Feng, Yuan; Zhu, Chunyan; Gong, Qiyong; Zhang, Wei

doi:10.1016/j.pscychresns.2013.06.002

Cited by 44 publications

(32 citation statements)

References 57 publications

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“…Consistent with our hypothesis, both SAD and MDD shared similar gray matter deficits, particularly reduced GMV in the bilateral OFC, putamen and thalamus, relative to healthy controls, which had been reported in prior independent studies of MDD patients (Nugent et al, 2013, Peng et al, 2016) and SAD patients (Meng et al, 2013, Talati et al, 2013). Furthermore, a direct comparison between MDD and SAD also showed no differences in these regions.…”

Section: Discussionsupporting

confidence: 91%

Gray Matter Abnormalities in Non-comorbid Medication-naive Patients with Major Depressive Disorder or Social Anxiety Disorder

et al. 2017

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BackgroundAn overlap of clinical symptoms between major depressive disorder (MDD) and social anxiety disorder (SAD) suggests that the two disorders exhibit similar brain mechanisms. However, few studies have directly compared the brain structures of the two disorders. The aim of this study was to assess the gray matter volume (GMV) and cortical thickness alterations between non-comorbid medication-naive MDD patients and SAD patients.MethodsHigh-resolution T1-weighted images were acquired from 37 non-comorbid MDD patients, 24 non-comorbid SAD patients and 41 healthy controls (HCs). Voxel-based morphometry analysis of the GMV (corrected with a false discovery rate of p < 0.001) and vertex-based analysis of cortical thickness (corrected with a clusterwise probability of p < 0.001) were performed, and group differences were compared by ANOVA followed by post hoc tests.OutcomesRelative to the HCs, both the MDD patients and SAD patients showed the following results: GMV reductions in the bilateral orbital frontal cortex (OFC), putamen, and thalamus; cortical thickening in the bilateral medial prefrontal cortex, posterior dorsolateral prefrontal cortex, insular cortex, left temporal pole, and right superior parietal cortex; and cortical thinning in the left lateral OFC and bilateral rostral middle frontal cortex. In addition, MDD patients specifically showed a greater thickness in the left fusiform gyrus and right lateral occipital cortex and a thinner thickness in the bilateral lingual and left cuneus. SAD patients specifically showed a thinner cortical thickness in the right precentral cortex.InterpretationOur results indicate that MDD and SAD share common patterns of gray matter abnormalities in the orbitofrontal-striatal-thalamic circuit, salience network and dorsal attention network. These consistent structural differences in the two patient groups may contribute to the broad spectrum of emotional, cognitive and behavioral disturbances observed in MDD patients and SAD patients. In addition, we found disorder-specific involvement of the visual processing regions in MDD and the precentral cortex in SAD. These findings provide new evidence regarding the shared and specific neuropathological mechanisms that underlie MDD and SAD.

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Section: Discussionsupporting

confidence: 91%

Gray Matter Abnormalities in Non-comorbid Medication-naive Patients with Major Depressive Disorder or Social Anxiety Disorder

et al. 2017

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“…Several studies have shown abnormal structural, functional, and network connectivity of thalamus in gSAD. Meng et al, [21] reported bilateral lower gray matter density (GMD) in drug-naïve patients with gSAD and a significant positive correlation between age of onset and value of the right thalamus GMD. In a treatment study by Talati et al, [22] it was found that 8-week pharmacological treatment with paroxetine in participants with gSAD resulted in a significant reduction in the right thalamus gray matter volume measured by voxel based morphometry (VBM).…”

Section: Discussionmentioning

confidence: 99%

Aberrant pulvinar effective connectivity in generalized social anxiety disorder

Tadayonnejad¹,

Klumpp²,

Ajilore³

et al. 2016

Medicine

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Recent neuroimaging findings in general social anxiety disorder (gSAD) have extended our understanding of the neural mechanisms of gSAD beyond an amygdala-centric fear-based hyperactivity model to include other brain regions and networks relevant to salient cues. In particular, higher order areas compromising visual networks that process emotional and social information have been implicated. The pulvinar anchors this network and is a key regulatory node that mediates complex sensory inputs and the integration between limbic and frontal brain systems. However, the role of the pulvinar and specifically alteration of its effective connectivity with the rest of the brain has not been examined in the pathophysiology of gSAD, a disorder characterized by aberrant socio-emotional processing. The main aim of this study was to examine the pulvinar network effective connectivity in gSAD. In this study, we recruited 21 individuals with gSAD and 19 demographically matched healthy controls (HC), who performed an emotional face processing task while brain activity was recorded using functional magnetic resonance imaging (fMRI). To examine pulvinar-based network dynamics, Granger causality (GC) based effective connectivity (EC) analysis was applied on fMRI data to compare gSAD and HC. The EC analysis revealed heightened casual influential dynamics between pulvinar in higher order visual and frontal regions in gSAD. In conclusion, these preliminary data suggest a novel network-based cortico-pulvino-cortical neural mechanism in the pathophysiology of gSAD.

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“…Overall, 14 studies addressed structural changes in SAD. Seven studies focused on grey matter changes using whole-brain analyses (Syal et al, 2012, Talati et al, 2013, Frick et al, 2013a, Meng et al, 2013, Bruhl et al, 2014, two others did only region of interest (ROI)-based analyses (Irle et al, 2010, Machado-de-Sousa et al, 2014. One of the studies reported on two independent samples, which we here present as two studies (Talati et al, 2013).…”

Section: Literature Search and Selectionmentioning

confidence: 99%

“…Seven studies investigated white matter alterations in SAD. Of these, two measured only white matter volume (Machado- de-Sousa et al, 2014, Meng et al, 2013. Three studies used ROI-based approaches (Baur et al, 2011, Baur et al, 2013a.…”

Section: Literature Search and Selectionmentioning

confidence: 99%

Neuroimaging in social anxiety disorder—A meta-analytic review resulting in a new neurofunctional model

Brühl

Delsignore

Komossa

et al. 2014

Neuroscience & Biobehavioral Reviews

384

289

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Social anxiety disorder (SAD) is one of the most frequent anxiety disorders. The landmark meta-analysis of functional neuroimaging studies by Etkin and Wager (2007) revealed primarily the typical fear circuit as overactive in SAD. Since then, new methodological developments such as functional connectivity and more standardized structural analyses of grey and white matter have been developed. We provide a comprehensive update and a meta-analysis of neuroimaging studies in SAD since 2007 and present a new model of the neurobiology of SAD. We confirmed the hyperactivation of the fear circuit (amygdala, insula, anterior cingulate and prefrontal cortex) in SAD. In addition, task-related functional studies revealed hyperactivation of medial parietal and occipital regions (posterior cingulate, precuneus, cuneus) in SAD and a reduced connectivity between parietal and limbic and executive network regions. Based on the result of this meta-analysis and review, we present an updated model of SAD adopting a network-based perspective. The disconnection of the medial parietal hub in SAD extends current frameworks for future research in anxiety disorders.

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Neuroanatomical deficits in drug-naïve adult patients with generalized social anxiety disorder: A voxel-based morphometry study

Cited by 44 publications

References 57 publications

Gray Matter Abnormalities in Non-comorbid Medication-naive Patients with Major Depressive Disorder or Social Anxiety Disorder

Gray Matter Abnormalities in Non-comorbid Medication-naive Patients with Major Depressive Disorder or Social Anxiety Disorder

Aberrant pulvinar effective connectivity in generalized social anxiety disorder

Neuroimaging in social anxiety disorder—A meta-analytic review resulting in a new neurofunctional model

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