ORIGINAL PAPER Grey matter abnormalities in social anxiety disorder: a pilot study Supriya Syal & Coenraad J. Hattingh & Jean-Paul Fouché & Bruce Spottiswoode & Paul D. Carey & Christine Lochner & Dan J. Stein Received: 16 January 2012 / Accepted: 22 March 2012 # Springer Science+Business Media, LLC 2012 Abstract While a number of studies have explored the functional neuroanatomy of social anxiety disorder (SAD), data on grey matter integrity are lacking. We conducted structural MRI scans to examine the cortical thickness of grey matter in individuals with SAD. 13 unmedicated adult patients with a primary diagnosis of generalized social anx- iety disorder and 13 demographically (age, gender and education) matched healthy controls underwent 3T structur- al magnetic resonance imaging. Cortical thickness and sub- cortical volumes were estimated using an automated algorithm (Freesurfer Version 4.5). Compared to controls, social anxiety disorder patients showed significant bilateral cortical thinning in the fusiform and post central regions. Additionally, right hemisphere specific thinning was found in the frontal, temporal, parietal and insular cortices of individuals with social anxiety disorder. Although uncor- rected cortical grey matter volumes were significantly lower in individuals with SAD, we did not detect volumetric differences in corrected amygdala, hippocampal or cortical grey matter volumes across study groups. Structural differ- ences in grey matter thickness between SAD patients and controls highlight the diffuse neuroanatomical networks involved in both social anxiety and social behavior. Addi- tional work is needed to investigate the causal mechanisms involved in such structural abnormalities in SAD. Keywords Social anxiety disorder . MRI . Structural abnormalities . Cortical thickness . Social behaviour Introduction Social anxiety disorder (SAD) involves an intense and irratio- nal fear of social situations including a particular fear of social embarrassment that commonly leads to avoidance of social situations (Bandelow and Stein 2004; Stein 2008). Although it is one of the most commonly occurring anxiety disorders on the DSM-IV (APA 2000), a relatively small body of research has addressed the neurobiology of this condition. Individuals with elevated fears of most social or performance situations are considered to have the generalized form of SAD, which is characterized by greater impairment, higher heritability, and more underlying neurocircuitry dysfunction than the specific or situation bound type of SAD (Stein 2008). Compared to healthy controls, individuals with SAD show aberrant activity in multiple brain regions involved in the processing of negative social affect, including in- creased amygdala activation in response to pictures of angry and contemptuous faces (Stein et al. 2002), increased ante- rior cingulate activation during the processing of disgust faces (Amir et al. 2005) and hyperactivation of Brodmann’ s area 10, 46, and 38 in response to fearful (relative to neutral) faces (Blair et al. 2008). Studies have also found increased activation of the insula (Straube et al. 2004; Lorberbaum et al. 2004) in the context of social tasks (emotional face perception or public speaking) in SAD patients. Notably, this effect is reversed in the context of a task that does not S. Syal (*) : C. J. Hattingh : D. J. Stein Department of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa e-mail: supriya.syal@uct.ac.za P. D. Carey : C. Lochner : D. J. Stein MRC Unit on Anxiety & Stress Disorders, Department of Psychiatry, University of Stellenbosch, Cape Town, South Africa J.-P. Fouché : B. Spottiswoode MRC/UCT Medical Imaging Research Unit, Department of Human Biology, University of Cape Town, Cape Town, South Africa Metab Brain Dis DOI 10.1007/s11011-012-9299-5