Recent brain imaging findings by using different methods (e.g., fMRI and PET) have suggested that social anxiety disorder (SAD) is correlated with alterations in regional or network-level brain function. However, due to many limitations associated with these methods, such as poor temporal resolution and limited number of samples per second, neuroscientists could not quantify the fast dynamic connectivity of causal information networks in SAD. In this study, SAD-related changes in brain connections within the default mode network (DMN) were investigated using eight electroencephalographic (EEG) regions of interest. Partial directed coherence (PDC) was used to assess the causal influences of DMN regions on each other and indicate the changes in the DMN effective network related to SAD severity. The DMN is a large-scale brain network basically composed of the mesial prefrontal cortex (mPFC), posterior cingulate cortex (PCC)/precuneus, and lateral parietal cortex (LPC). The EEG data were collected from 88 subjects (22 control, 22 mild, 22 moderate, 22 severe) and used to estimate the effective connectivity between DMN regions at different frequency bands: delta (1-3 Hz), theta (4-8 Hz), alpha (8-12 Hz), low beta (13-21 Hz), and high beta (22-30 Hz). Among the healthy control (HC) and the three considered levels of severity of SAD, the results indicated a higher level of causal interactions for the mild and moderate SAD groups than for the severe and HC groups. Between the control and the severe SAD groups, the results indicated a higher level of causal connections for the control throughout all the DMN regions. We found significant increases in the mean PDC in the delta (p = 0.009) and alpha (p = 0.001) bands between the SAD groups. Among the DMN regions, the precuneus exhibited a higher level of causal influence than other regions. Therefore, it was suggested to be a major source hub that contributes to the mental exploration and emotional content of SAD. In contrast to the severe group, HC exhibited higher resting-state connectivity at the mPFC, providing evidence for mPFC dysfunction in the severe SAD group. Furthermore, the total Social Interaction Anxiety Scale (SIAS) was positively correlated with the mean values of the PDC of the severe SAD group, r (22) = 0.576, p = 0.006 and negatively correlated with those of the HC group, r (22) = -0.689, p = 0.001. The reported results may facilitate greater comprehension of the underlying potential SAD neural biomarkers and can be used to characterize possible targets for further medication.
Social anxiety disorder (SAD) is characterized by a fear of negative evaluation, negative self-belief and extreme avoidance of social situations. These recurrent symptoms are thought to maintain the severity and substantial impairment in social and cognitive thoughts. SAD is associated with a disruption in neuronal networks implicated in emotional regulation, perceptual stimulus functions, and emotion processing, suggesting a network system to delineate the electrocortical endophenotypes of SAD. This paper seeks to provide a comprehensive review of the most frequently studied electroencephalographic (EEG) spectral coupling, event-related potential (ERP), visual-event potential (VEP), and other connectivity estimators in social anxiety during rest, anticipation, stimulus processing, and recovery states. A search on Web of Science provided 97 studies that document electrocortical biomarkers and relevant constructs pertaining to individuals with SAD. This study aims to identify SAD neuronal biomarkers and provide insight into the differences in these biomarkers based on EEG, ERPs, VEP, and brain connectivity networks in SAD patients and healthy controls (HC). Furthermore, we proposed recommendations to improve methods of delineating the electrocortical endophenotypes of SAD, e.g., a fusion of EEG with other modalities such as functional magnetic resonance imaging (fMRI) and magnetoencephalograms (MEG), to realize better effectiveness than EEG alone, in order to ultimately evolve the treatment selection process, and to review the possibility of using electrocortical measures in the early diagnosis and endophenotype examination of SAD.