33 Neuroendocrinological aspects of social anxiety and aggression related disorders Neuroendocrinology of social anxiety disorder Social anxiety disorder (SAD) is associated with deviations in the neuroendocrine brain circuits underlying social motivational behavior. Unfortunately, evidence is inconsistent, and may be due to relatively small sample sizes (averaging 12 patients per group) and differences in methods and analyses. Nevertheless, several meta-analytic studies have consistently shown a hyperactive amygdala in response to social threat, probably reflecting enhanced processing of and attention to threat (Brühl, Delsignore, Komossa, & Weidt, 2014; Cremers & Roelofs, 2016; Fouche, van Der Wee, Roelofs, & Stein, 2013). In addition, prefrontal structures are also more active than in healthy controls; however, prefrontal–amygdala connectivity seems to be reduced (Brühl et al., 2014; Cremers & Roelofs, 2016; Fouche et al., 2013), indicating an inability to regulate subcortical regions. Interestingly, pharmaco- and psychotherapy seem to “normalize” deviating activation patterns in SAD (Fouche et al., 2013; Freitas-Ferrari et al., 2010). Studies also show alterations in striatal functioning in SAD, but findings are mixed (Freitas-Ferrari et al., 2010). A recent fMRI study in patients with SAD (n = 20) compared to healthy controls (n = 20) reported reduced striatal activity in anticipation of social reward and relative increased striatal activity for avoiding social punishment (Cremers, Veer, Spinhoven, Rombouts, & Roelofs, 2015). These findings suggest that patients with SAD show a reduced motivation to obtain social reward and relative increased motivation to avoid social punishment compared to healthy controls. In addition, patients with SAD showed a reduced pattern of fronto-striatal connectivity during reward and punishment anticipation, relative to healthy controls. Patients with SAD (n = 18) show an increased cortisol response to social stress, compared to healthy participants (n = 22) and patients with Post-Traumatic Stress Disorder (PTSD; n = 17; small to medium effect sizes), and this response was associated with social avoidance behavior (large effect sizes) (Roelofs, van Peer, et al., 2009b). Studies combining cortisol administration with electroencephalography (EEG) in patients with SAD confirmed a causal relationship between cortisol and increased early processing of emotional faces during social avoidance (van Peer et al., 2009, n = 21, large effect size), and modulation of early threat processing depending on motivational context and symptom severity (van Peer, Spinhoven, & Roelofs, 2010, n = 18). In addition, both higher baseline levels of cortisol and exogenous cortisol are associated with EEG wave activity patterns related to anxiety and behavioral inhibition (Schutter & Van Honk, 2005, n = 28; van Peer, Roelofs, & Spinhoven, 2008, n = 40), whereas testosterone has an opposite effect (Schutter & van Honk, 2004, n = 16). Studies on testosterone in SAD are scarce, and although previous results on the relation between SAD and baseline testosterone levels show no differences (Gerra et al., 2
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