Facial emotion processing in patients with social anxiety disorder and Williams–Beuren syndrome: an fMRI study

Binelli, C.; Muñiz, Armando; Subirà, Susana; Navinés, Ricard; Blanco‐Hinojo, Laura; Pérez-García, D.; Crippa, José Alexandre de Souza; Farré, Magı́; Pérez-Jurado, Luís A.; Pujol, Jesús; Martín‐Santos, Rocío

doi:10.1503/jpn.140384

Cited by 21 publications

(15 citation statements)

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“…Although the vmPFC is also a key node in emotion regulation, it has mainly been implicated in the inhibition and extinction of fear and anxiety responses [ 74 , 77 ]. In previous neuroimaging studies, dysfunction in the vmPFC has been related to the generation of negative emotions, including anxiety and fear [ 78 , 79 ], while SAD patients demonstrated hyperactivity in (para)limbic regions, including the amygdala, insula, and hippocampus, in the face of negative, especially socially aversive stimuli and participation in socioemotional events [80] , [81] , [82] . Interestingly, greater vmPFC responses to unintentional (embarrassment-mediated) situations were also observed in SAD patients [83] , and regarded as a potential endophenotype of SAD [84] .…”

Section: Discussionmentioning

confidence: 99%

Dissociations in cortical thickness and surface area in non-comorbid never-treated patients with social anxiety disorder

et al. 2020

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Background Abnormalities of functional activation and cortical volume in brain regions involved in the neurobiology of fear and anxiety have been implicated in the pathophysiology of social anxiety disorder (SAD). However, few studies have performed separate measurements of cortical thickness (CT) and cortical surface area (CSA) which reflect different neurobiological processes. Thus, we aimed to explore the cortical morphological anomaly separately in SAD using FreeSurfer. Methods High-resolution structural magnetic resonance images were obtained from 32 non-comorbid never-treated adult SAD patients and 32 demography-matched healthy controls. Cortical morphometry indices including CT and CSA were separately determined by FreeSurfer and compared between the two groups via whole-brain vertex-wise analysis, while partial correlation analysis using age and gender as covariates were conducted. Findings The patients with SAD showed decreased CT but increased CSA near-symmetrically in the bilateral prefrontal cortex (PFC) of the dorsolateral, dorsomedial, and ventromedial subdivisions, as well as the right lateral orbitofrontal cortex; increased CSA in the left superior temporal gyrus (STG) was also observed in SAD. The CSA in the left PFC was negatively correlated with the disease duration. Interpretation As the balloon model hypothesis suggests that the tangentially stretched cortex may cause dissociations in cortical morphometry and affect the cortical capacity for information processing, our findings of dissociated morphological alterations in the PFC and cortical expansion in the STG may reflect the morphological alterations of the functional reorganization in those regions, and highlight the important role of those structures in the pathophysiology and neurobiology of SAD. Funding This study was funded by the (Grant Nos. 31700964, 31800963, 81621003, and 81820108018).

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Section: Discussionmentioning

confidence: 99%

Dissociations in cortical thickness and surface area in non-comorbid never-treated patients with social anxiety disorder

et al. 2020

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“…A total of 1297 publications were retrieved from initial search, among which 37 studies met the inclusion criteria (654 participants in the SAD groups and 594 participants in the control groups). There were 15 studies that adopted emotional faces as task stimuli [ 6 , 10 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ], 8 that presented specific situations as task stimuli [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ], and the other 14 employed other types of tasks [ 7 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 ]. In total, the coordinates where SAD groups performed significantly better or significantly worse than control groups were 335 and 115 respectively (see specific characteristics in Table 1 ).…”

Section: Resultsmentioning

confidence: 99%

“…Gentili et al studied the face perception ability of patients with SAD and found that the face stimulation task led to increased activations of the amygdala, globus pallidus, superior temporal sulcus, visual cortex, and prefrontal cortex of patients with SAD [ 5 ]. Binelli et al found abnormal activation of the limbic system in patients with SAD [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Cognitive Neural Mechanism of Social Anxiety Disorder: A Meta-Analysis Based on fMRI Studies

Ruan

Yawen

et al. 2021

IJERPH

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Objective: The present meta-analysis aimed to explore the cognitive and neural mechanism of social anxiety disorder (SAD) from a whole-brain view, and compare the differences in brain activations under different task paradigms. Methods: We searched Web of Science Core Collection and other databases with the keywords related to social anxiety, social phobia, and functional magnetic resonance imaging (fMRI) for comparing persons with SAD to healthy controls and used the activation likelihood estimation method. Thirty-seven papers met the inclusion criteria, including 15 with emotional faces as stimuli, 8 presenting specific situations as stimuli, and 14 using other types of tasks as stimuli. Among these papers, 654 participants were in the SAD group and 594 participants were in the control group with 335 activation increase points and 115 activation decrease points. Results: Whole-brain analysis showed that compared with healthy controls, persons with SAD showed significantly lower activation of the left anterior cingulate gyrus (MNI coordinate: x = −6, y = 22, z = 38; p < 0.001). Sub-group analysis based on task indicated that when performing tasks with emotional faces as stimuli, persons with SAD showed significantly lower activation of the left cerebellar slope and fusiform gyrus (MNI coordinate: x = −26, y = −68, z = −12; p < 0.001), and significantly higher activation of the right supramarginal gyrus and angular gyrus, than healthy controls (MNI coordinate: x = 58, y = −52, z = 30; p < 0.001). Conclusion: Individuals with social anxiety disorder show abnormal activation in the cingulate gyrus, which is responsible for the process of attention control, and task type can influence the activation pattern.

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“…The copyright holder for this preprint (which this version posted April 7, 2021. ; https://doi.org/10.1101/2021.04.07.438774 doi: bioRxiv preprint Previous fMRI studies have shown that, during face perception, less activity can be observed in patients with WS than in neurotypical participants in areas specialized in early processing of face parts 54 . Our data are consistent with these results and suggest that the FFA-driven process of combining parts of the face into a holistic representation may be specifically impaired in WS.…”

Section: Discussionmentioning

confidence: 99%

Dissociation of early and late face-related processes in Autism Spectrum Disorder and Williams syndrome

Gomez

Lio

Costa

et al. 2021

Preprint

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Autistic Spectrum Disorder (ASD) and Williams syndrome (WS) are characterized by atypical social interaction and face processing, with opposite profiles. Evoked activity in the superior temporal sulcus (STS) occurring at 260ms is an eyes-sensitive neuronal marker. Here, we tested whether a double dissociation between these two syndromes is also observed at the cerebral level within faces processing network. Forty-two participants divided into three groups (diagnosed with WS, ASD or without neurodevelopmental disorders) performed a face perception task during a high-density EEG recording. In each trial, a particular area of the face was flashed under the participants fovea. First, using the predefined filter STS at 260ms, we found that the cortical sensitivity of STS to facial features, observed in neurotypical participants1, extended to patients with WS as opposed to patients with ASD. Again, this activity was eyes sensitive. Next, we used spatial regressor of the face cue map and computed, at each time point (without spatial a priori), to what extent the multichannel EEG signal could decode this regressor. We showed that, in contrast to patients with ASD, WS patients and young adults, produce a late (260ms) STS evoked response that is sensitive to socially relevant facial features (such as the eye and mouth). We also showed that the early (170ms) evoked response can be predicted by socially relevant facial features in patients with ASD and controls, but not in WS patients. In patients with WS, the decoding peak occurred only in the late component (at 260 ms) of the EEG, while, for patients with ASD, it occurred preferentially in the early component (at 170 ms). The present study confirms the previous results reported by Lio et al. and extend these findings by dissociating the time course of neural processes involved in face perception in WS and ASD patients. It reveals a dissociation among these two patients groups and suggest that although both syndromes are associated with social disturbances, their impairment at the neural level may have a different origin. These results provide essential evidence for understanding what, where and when neurocomputations are performed in our brain.

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Facial emotion processing in patients with social anxiety disorder and Williams–Beuren syndrome: an fMRI study

Cited by 21 publications

References 69 publications

Dissociations in cortical thickness and surface area in non-comorbid never-treated patients with social anxiety disorder

Dissociations in cortical thickness and surface area in non-comorbid never-treated patients with social anxiety disorder

Cognitive Neural Mechanism of Social Anxiety Disorder: A Meta-Analysis Based on fMRI Studies

Dissociation of early and late face-related processes in Autism Spectrum Disorder and Williams syndrome

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