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), visualevent 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.

Neuroimaging investigations have proven that social anxiety disorder (SAD) is associated with aberrations in the connectivity of human brain functions.The assessment of the effective connectivity (EC) of the brain and its impact on the detection and medication of neurodegenerative pathophysiology is hence a crucial concern that needs to be addressed. Nevertheless, there are no clinically certain diagnostic biomarkers that can be linked to SAD. Therefore, investigating neural connectivity biomarkers of SAD based on deep learning models (DL) has a promising approach with its recent underlined potential results. In this study, an electroencephalography (EEG)-based detection model for SAD is constructed through directed causal influences combined with a deep convolutional neural network (CNN) and the long shortterm memory (LSTM). The EEG data were classified by applying three different DL models, namely, CNN, LSTM, and CNN+LSTM to discriminate the severity of SAD (severe, moderate, mild) and healthy controls (HC) at different frequency bands (delta, theta, alpha, low beta, and high beta) in the default mode network (DMN) under resting-state condition. The DL model uses the EC features as input, which are derived from the cortical correlation within different EEG rhythms for certain cortical areas that are more susceptible to SAD. Experimental results revealed that the proposed model (CNN+LSTM) outperforms the other models in SAD recognition. For our dataset, the highest recognition accuracies of 92.86%, 92.86%, 96.43%, and 89.29%, specificities of 95.24%, 95.24%, 100%, and 90.91%, and sensitivities of 85.71%, 85.71%, 87.50%, and 83.33% were achieved by using CNN+LSTM model for severe, moderate, mild, and HC, respectively. The fundamental contribution of this analysis is the characterization of neural brain features using different DL models to categorize the severity of SAD, which can represent a potential biomarker for SAD.INDEX TERMS Effective connectivity network, convolutional neural networks (CNNs), social anxiety disorder (SAD), default mode network (DMN), deep learning models, partial directed coherence (PDC), Electroencephalogram (EEG), human brain mapping.

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.

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The diagnosis of social anxiety disorder (SAD) is of great consequence not only due to its impacts on the individual and society but also the expenditures to the national health systems. There is yet a deficiency of objective neurophysiological information to assist the present clinical SAD diagnosis. The main objective of this study is to analyze the electroencephalogram (EEG) complexity of 88 SAD subjects, subdivided into 4 balanced groups (22 severe, 22 moderate, 22 mild, and 22 healthy controls (HCs) using Fuzzy Entropy measure (FE) and machine learning algorithms. In addition, this study aimed at designing a computer-aided diagnosis system to identify the severity of SAD (severe, moderate, mild, and HC) in different EEG frequency bands (delta, theta, alpha, and beta). The experimental results showed that among the HC and the three considered levels of SAD, SAD patients in fast-waves exhibited significantly less FE values in resting-state compared with HCs (p ≤ 0.05). The EEG complexity analysis showed a discriminatory neuronal activity over the frontoparietal and occipital regions between SAD patients and HCs. Additionally, the FE values measured in the resting-state were positively correlated with Social Interaction Anxiety Scale (SIAS) scores in fast-waves (beta and alpha), indicating that the regional FE measures are putative biomarkers in assessing the clinical symptoms of SAD. Also, the classification results demonstrated that the proposed method outperformed the state of the art methods with an accuracy of 86.93 %, sensitivity of 92.46%, and specificity of 95.32% with the Naive Bayes (NB) classifier. This study emphasizes the viability of quantitative FE measures and the specific combinations involving the chosen classifiers could be considered as an alternative biomarker for future clinical SAD recognition.