Verified by 
For people with social anxiety, even everyday encounters with others can cause an agonizing degree of apprehension. This problem, affecting over 12% of U.S. adults over their lifetimes, may be related to abnormal signals from part of the brain's front end--the developmentally advanced prefrontal cortex.
These signals normally turn down activity in the primitive amygdala below the brain's surface, a site for threatening memories. But when social anxiety is serious enough to be termed a disorder, they turn it up instead--as if turning up the volume of an audio speaker--according to analysis of brain activity with functional magnetic resonance imagery (fMRI) reported by psychologist Ronald Sladky and others in the journal Cerebral Cortex for April 2015. Ramping up this volume could turn an ordinary meeting or party into an ordeal. The anxiety can be accompanied by a fight-or-flight reaction when the sympathetic nervous system produces physical or somatic responses such as increased heart rate, blood pressure, and pupil size.
Whether successful treatment normalizes the signals between the advanced prefrontal cortex and the primitive amygdala remains to be seen.
Other studies show a trend of emerging research based on advances in therapy and in brain scans. Cognitive behavioral therapy or CBT, which includes re-thinking immediate impressions, was found to be an effective treatment for social anxiety disorder, according to Philip Goldin and his colleagues in JAMA Psychiatry in 2013.
Their study showed that before treatment, prefrontal cortex responses in social anxiety disorder were smaller and more delayed compared to normal responses. The implication is that there was less prefrontal modulation of amygdala-based fear responses in these patients. Then 75 social anxiety patients were randomly assigned to either CBT or a wait-list control group. When patients were then presented with autobiographical descriptions of stressful situations, the treated group reported less anxious responses. They also showed larger and earlier prefrontal cortex activity, and their baseline scans showed more coupling between prefrontal cortex and amygdala. A possible implication is that after treatment there was more effective modulation of amygdala activity.
For another viewpoint, I visited the state-of-the-art UCLA Ahmanson-Lovelace Brain Imaging Center to speak with Katherine Narr, Ph.D., a principal investigator who uses advanced brain imaging to study psychological disorders and their treatment.
“In addition to downstream connections that elicit the fight or flight response,” she said, “the amygdala is in a key location which has strong connections…to the hypothalamus which has connections to the endocrine system…The point being that when you’re feeling anxious you have these somatic experiences that you know aren’t normal but you can’t tell your frontal lobe to control them.” However, “when you do CBT you are teaching people to control things that are usually an autonomic response.”
Even in normal people, the ability to properly evaluate people's expressions can be linked to such signals. Say your coworker thinks her boss's irritated expression is because she bungled an assignment. Let her know that he sprained a back muscle and she immediately recognizes it's his problem, not hers. Her attitude becomes less worried, more relaxed.
This type of mental switch, called cognitive reevaluation, corresponded to lighting up—activation-- of prefrontal areas in scans of normal adults presented with angry or other negative faces after instructions in reevaluation, according to psychologist Brady Nelson and others in Behavioral Brain Research in 2015.
I’m not suggesting that your emotional life can be reduced to neural signals or require an understanding of brain mechanisms. People can brake a car without being able to diagram the braking system—and braking has some similarities to modulating emotional reactions. But these studies provide exciting glimpses of brain activity that may underlie successful treatment of social anxiety and related problems.
References:
Sladky, R. et al. Cerebral Cortex (2015) 25 (4)
Goldin, P. et al. JAMA Psychiatry (2013) 170 (10)
Klumpp, H. et al. Biology of Mood and Anxiety Disorders (2014) 4 (1)
Nelson, B.D. et al. Behavioral Brain Research (2015) 279
