Large-Scale Dysfunctional White-Matter and Grey Matter Networks in Patients With Social Anxiety Disorder

2022 ◽  
Author(s):  
Keren Wen ◽  
Youjin Zhao ◽  
Feifei Zhang ◽  
Su Lui ◽  
Graham Kemp ◽  
...  
2020 ◽  
Vol 31 ◽  
pp. S51-S52
Author(s):  
E. Roelofs ◽  
J.M. Bas-Hoogendam ◽  
H. Van Ewijk ◽  
R.R.J.M. Vermeiren ◽  
P.M. Westenberg ◽  
...  

2011 ◽  
Vol 45 (10) ◽  
pp. 1366-1372 ◽  
Author(s):  
Volker Baur ◽  
Jürgen Hänggi ◽  
Michael Rufer ◽  
Aba Delsignore ◽  
Lutz Jäncke ◽  
...  

2009 ◽  
Vol 66 (7) ◽  
pp. 691-694 ◽  
Author(s):  
K. Luan Phan ◽  
Anton Orlichenko ◽  
Erin Boyd ◽  
Mike Angstadt ◽  
Emil F. Coccaro ◽  
...  

Sensors ◽  
2021 ◽  
Vol 21 (12) ◽  
pp. 4098
Author(s):  
Abdulhakim Al-Ezzi ◽  
Nidal Kamel ◽  
Ibrahima Faye ◽  
Esther Gunaseli

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.


CNS Spectrums ◽  
2009 ◽  
Vol 14 (S3) ◽  
pp. 24-33 ◽  
Author(s):  
Herman G. M. Westenberg

AbstractThe common occurrence and high level of morbidity and burden associated with social anxiety disorder (SAD) are gaining widespread recognition. Interest in understanding and treating the disorder has also grown in response to large-scale investigations that have demonstrated high levels of efficacy with both pharmacologic and nonpharmacologic treatments. Such trials indicate that many patients with generalized SAD (roughly 40% to 60%) respond (eg, Clinical Global Impressions–Improvement rating 1 or 2) after an adequate treatment trial, despite having suffered with disabling symptoms for most of their adult lives. First-line therapy options include the selective serotonin reuptake inhibitors and the dual-acting serotonin-norepinephrine reuptake inhibitor venlafaxine. Second-line options consist of anticonvulsants (gabapentin, pregabalin, valproic acid) and benzodiazepines (clonazepam). Reversible and irreversible monoamine oxidase inhibitors (moclobemide and phenelzine, respectively), while effective, are not widely used. Nonpharmacologic approaches, such as cognitive-behavioral therapy (CBT), are also effective for SAD. Newer treatment strategies such as levetiracetam, atypical antipsychotics, or D-cycloserine in combination with CBT appear promising but require further investigation. Finding a well-tolerated, safe, and effective treatment for each individual patient is crucial as most will require ongoing treatment in order to maintain benefits, prevent SAD relapse, and to experience optimal outcomes in the long term.


2020 ◽  
Vol 28 ◽  
pp. 102493
Author(s):  
Eline F. Roelofs ◽  
Janna Marie Bas-Hoogendam ◽  
Hanneke van Ewijk ◽  
Habib Ganjgahi ◽  
Steven J.A. van der Werff ◽  
...  

2020 ◽  
Vol 87 (9) ◽  
pp. S248
Author(s):  
Eline Roelofs ◽  
Janna-Marie Bas-Hoogendam ◽  
Hanneke van Ewijk ◽  
Steven J.A. van der Werff ◽  
Robert R.J.M. Vermeiren ◽  
...  

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