Regional Homogeneity Changes in Patients with Social Anxiety Disorders after Cognitive Behavioral Therapy

Objective To examine the altered spontaneous brain activity in patients with social anxiety disorders (SAD) before and after cognitive behavior therapy (CBT), and determine the neuromechanism of formation, treatment and recovery of SAD. Methods Fifteen SAD patients were treated with an eight-week group CBT. The patients underwent functional magnetic resonance imaging (fMRI) at resting state before and after the treatments. Eighteen healthy controls (HC) were recruited and underwent a baseline fMRI scan. The regional homogeneity (ReHo) of the patients was compared with the healthy controls. Before the baseline scanning, all participants were assessed with the Liebowitz Social Anxiety Scale（LSAS）, the Hamilton Anxiety Rating Scale (HAMA) and the Hamilton Depression Rating Scale (HAMD). Results All participants were right-handed. 10 males and 4 females were in the patient group, with mean age of （27.07±8.11） years. 13 males and 5 females were in the HC group, with mean age of （26.28±2.42） years. There was no difference for gender and age while significant differences were found in LSAS，HAMA，HAMD between patients and controls （P<0.01）. After 8 weeks of group CBT, clinical assessments significantly decreased （P<0.05） in patients group. Compared with HC, the pre-treatment SAD patients showed significantly increased ReHo in right cerebellum lobe at baseline 〔(P<0.05, with Gaussian random field (GRF) correction〕; but the difference became insignificant after the group CBT. The post-treatment patients showed increased ReHo in left putamen and right caudate compared with their pre-treatment conditions (P<0.05，with GRF correction). Pre-post ReHo change in right cerebellum posterior in patients was positively correlated with pre-post change of LSAS-fear scores （r=0.62, P=0.015）. Conclusion The activity of cerebellum might be one of the potential biomakers to modulate the treatment effect of CBT in SAD, which provides a basis for further investigation into the pathophysiology of SAD.