The Neurobiology of Social Anxiety Disorderby Divya Mathur, PhD | April 22, 2010
Shyness is a unique trait and all of us experience it in various degrees when faced with performance situations or new social surroundings. However, many people go through life dreading such encounters and exposure to the feared social situation provokes anxiety, or possibly a panic attack. Social anxiety disorder (SAD) or social phobia is a common anxiety disorder in which individuals shun all forms of interpersonal contact or undergo extreme physical or mental discomfort in social settings. Until recently, this condition was dismissed as ascribing pathology to a normal variant of human personality in order to sell treatments. However, most psychiatrists now believe that social phobia is not a pathological label for shyness. Shyness neither is a prerequisite for nor can be considered as synonymous with social anxiety disorder.
Patients with SAD crave for company but fear social interactions because they are afraid of being ridiculed and perceived as unlikable, stupid or boring. They suffer from low self esteem and SAD is also associated with an increased risk of comorbid conditions such as depression, bipolar disorder and substance abuse.
Clinically it is not difficult to diagnose SAD but its causes are not yet clearly understood. The cortico-limbic and cortico-striatal circuits are composed of the temporal brain structures such as the amygdala, prefrontal cortex, hippocampus, and striatum. They are responsible for a range of cognitive and affective processes regarding attention, memory, judgment and interpretation about self and others. It is believed that in people suffering from SAD, these circuits send distorted assumptions in response to random images of human faces, suggesting a system sensitive not only to harmful stimuli but also to stimuli that are considered affectively neutral. At a molecular level, patients with SAD exhibit increased glutamate content in the anterior cingulate cortex region of the brain along with some striatal dopamine and serotonin abnormalities when compared to healthy controls.
A number of family, twin and high risk studies have shown a pattern of family aggregation for SAD. The risk for first degree relatives of people suffering from generalized SAD is ten times more than for the general population. Several candidate genes have been associated with traits for social phobia such as the serotonin transporter gene and a functional variant of ß-adrenergic receptor (ADRB1) gene. Association analysis has also implicated the gene encoding regulator of G protein signaling 2 (RGS2), although a clear loci has so far eluded scientists.
Presently, the treatment options for SAD include either psychotherapy, medication, or both. Cognitive behavior therapy that aims at changing the thought patterns and physical reactions to anxiety-inducing situations is found to be effective in treating social phobia. The medications mostly prescribed include antidepressants such as selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and monoamine oxidase inhibitors (MAOIs), beta-blockers and benzodiazepines.
SAD has been described as an “illness of lost opportunities.” Few people with social anxiety disorder seek professional help. For most patients suffering in silence, it remains a pervasive disabling condition that prevents them from leading a fuller, richer life.
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Smoller, J., Paulus, M., Fagerness, J., Purcell, S., Yamaki, L., Hirshfeld-Becker, D., Biederman, J., Rosenbaum, J., Gelernter, J., & Stein, M. (2008). Influence of RGS2 on Anxiety-Related Temperament, Personality, and Brain Function Archives of General Psychiatry, 65 (3), 298-308 DOI: 10.1001/archgenpsychiatry.2007.48
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