Blushing and gaze avoidance in social anxiety disorder : a structural neuroanatomical investigation

Master Thesis


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University of Cape Town

Background: Social anxiety disorder (SAD) is a common psychiatric condition characterised by fear and avoidance of social situations. Lifetime prevalence is 5-16% and co-morbidity with other mood and substance abuse disorders is common. Symptoms including cognitive, behavioural and physiological components vary between individuals. Of these, blushing and gaze fear and avoidance are regarded as cardinal symptoms. First line treatment of SAD involves SSRIs and cognitive behavioural therapy, while surgery may also be considered for excessive blushing. Blushing and gaze avoidance are thought to have an evolutionary adaptive advantage, promoting the display of submissive behaviour and appeasement in threatening situations. MRI research has demonstrated differences on functional and structural neuroimaging between patients with SAD and healthy controls (HCs). However, little is known about the neurocircuitry underlying gaze fear and avoidance or increased blushing propensity or how the severity of these traits correlate with the neuroimaging differences found in SAD. In this research, I explored the neuroanatomy of blushing propensity and gaze fear and avoidance in the context of SAD. Methods: 18 SAD patients and 18 HCs underwent structural MRI scans and self-report scales were administered to assess their symptom severity, blushing propensity and gaze fear and avoidance. Structural data was analysed using voxel-based morphometry (VBM). Regression and contrast analyses were used to correlate blushing propensity and gaze anxiety and avoidance symptoms with brain volumes, controlling for total grey matter volume, age and level of education. Results: Anxiety, blushing propensity and gaze fear and avoidance symptoms were all significantly higher in SAD patients (p<0.001). Brainstem volumes were increased for higher blushing scores a (p<0.01), while the volumes of left inferior parietal lobe b (p=0.04) and left occipital cortex a (p<0.01) were decreased. With increased gaze fear and avoidance, there were associated decreases in the right posterior cingulate cortex a (p<0.01), right occipital lobe b (p=0.03) and right fusiform gyrus a (p<0.01). Increased blushing and gaze symptom severity considered together, was associated with increased brainstem volume a (p<0.01) and decreased pons/cerebellum b (p=0.001), right cerebellum b (p=0.009), left cerebellum c (p<0.001) and left inferior parietal lobe a (p<0.1), volumes. Contrast analysis of SAD and HC brain volumes revealed a greater grey matter volume in HCs in the regions of left occipital cortex (p<0.01), left anterior cingulate (p<0.01) and right inferior parietal lobe (p<0.01) when compared to SAD patients. Increased symptom severity in SAD was significantly associated with higher volumes in the left premotor cortex (p<0.01), right hippocampus (p<0.01), left orbitofrontal cortex (p<0.01) and right superior temporal cortex (p<0.01). Possible areas for of interest for volume differences between SAD and HCs include total grey matter volume (d =0.83), left and right anterior cingulate cortex (d =0.68 and d =0.65), and left and right dorsolateral prefrontal cortex (d =0.55 and d =0.54), yet these differences were not significantly different. (a uncorrected peak levels b uncorrected cluster level, c corrected cluster level). Conclusion: Differences in brain volumes pertaining to blushing and gaze fear and avoidance in SAD patients may be a contributing factor or a consequence of these core symptoms, and a potential biomarker for SAD. Future studies could build on this preliminary research with increased sample sizes, and determine the possible effects of reduced symptom severity and treatment options on brain structure and function. Most importantly, an investigation of the genetic underpinnings and functional neural correlates of blushing and gaze avoidance behaviour may enhance our understanding of the complex aetiology of these cardinal SAD symptoms, thereby improving our understanding of SAD as a psychiatric disorder and facilitating better patient care and management.

Includes bibliographical references.