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 ?-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.
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