Think of the last time you had to speak up in a large group of people you didn’t know well. Was it at a conference where you had to give a presentation to a room full of experts in your field? Was it when your teacher asked everyone to go around and say something interesting about themselves on the first day of class? Or was it when you tried to make a joke during your first dinner with your partner’s friends? In any case, you might remember feeling a bit anxious – that odd feeling in the pit of your stomach, your palms sweating, your heart racing.
Many individuals experience such mild anxiety in social situations, especially when it involves people they don’t know. Social anxiety disorder (SAD) is diagnosed only when this anxiety is so out of proportion to the actual situation that it becomes disabling to the person who is experiencing it. In fact, according to the DSM-5 (American Psychiatric Association, 2013), to be diagnosed with SAD, one must suffer “significant distress or impairment that interferes with his or her ordinary routine in social settings, at work or school, or during other everyday activities”. So if you pissed off your adviser because you didn’t even apply to speak at that conference, got a bad grade because you called in sick the first day of class even though attendance was required, or got broken up with because your partner had enough of your skipping events with her friends, and this level of anxiety has been typical for a while in your daily life, you might consider seeking some help.
You might also wonder, “Why do I feel this way? What is going on in my head?” Scientists in many disciplines such as clinical psychology, psychiatry, social psychology, cognitive psychology, and neuroscience have been trying to figure out exactly that for a while now. In this blog post, I will delve into this topic taking a neuroscientific approach and explore what scientists have discovered about what goes on in the brains of those with SAD.
The vast majority of studies conducted in this field investigate functional differences in the brains of those with SAD, compared to individuals without the disorder – the so-called “healthy controls” (HCs). In most of these studies, participants are shown stimuli relevant to social anxiety while scientists measure blood flow to certain areas of their brain as an indirect measure of brain activity. They often do this by using functional magnetic resonance imaging (fMRI) or positron emission tomography (PET). Investigating these activation patterns not only helps scientists understand the reasons behind the disorder, but it also helps them target certain processes for more successful treatment.
Many studies to date have shed light on this issue. In a recent fMRI study published in Biological Psychology, for example, Klumpp and colleagues (2012) had 29 generalized SAD (gSAD) patients and 26 HCs complete a modified Emotional Face Matching Task in which participants were shown a set of emotional faces and were asked to match a target face to the face in the set that expressed the same emotion. The researchers then compared activation in response to fearful (versus happy) faces between gSAD patients and HCs, and found more activation in the amygdala, insula, and the dorsal medial prefrontal cortex (DMPFC) of patients with gSAD.
Similar results have been found with different socially relevant stimuli as well. In another recent fMRI study published in Psychiatry Research, Blair and colleagues (2011) investigated the differences in brain function between those who had gSAD and HCs in response to self-referential comments. More specifically, the 15 participants with SAD and the 15 HCs were shown positive, neutral, or negative comments that were either from first-person viewpoints (e.g. “I am beautiful”) or second-person viewpoints (e.g. “You are beautiful”). Importantly, they were told that the comments were always about them, and that they just varied dependent upon whether they concerned another person’s point of view or their self-view. Interestingly, when they looked at the effects of simply hearing comments about the self, regardless of the point of view in which they were presented, they found more activation in the amygdala, DMPFC, and the lateral middle frontal cortex for those with SAD.
Using yet another different set of socially-relevant stimuli, and this time utilizing PET technology rather than fMRI, Tillfors and colleagues (2002) also examined the functional alterations in the brains of those with SAD. This time, instead of comparing patients with SAD to HCs, they compared the activation of brain areas within a group of 18 socially anxious individuals in two different experimental conditions. All participants were told that they would speak about a travel experience or vacation, both in front of an audience and alone. However, some participants spoke alone first (and thus anticipated the public speaking task), while others spoke in front of an audience first. Those in the anticipatory group indicated higher levels of anxiety as measured by heart rate and self-report. The results also indicated higher activation in the amygdaloid-hippocampal region, the dorsolateral prefrontal cortex, as well as the inferior temporal cortex as a function of anticipation of public speaking.
So, what do all these fancy names for brain parts mean? What is the take-home message here? Overall, these three studies, as well as others not cited here (see meta-analysis by Bruhl, Delsignore, Komossa, & Weidt, 2014), seem to converge on similar functional differences. Almost all relevant studies indicate an overactive amygdala, which is a region associated with arousal and negatively-valenced emotions. On the other hand, the prefrontal regions, which are often associated with emotion regulation, also seem active in most studies. Could it be possible that patients try to regulate their emotions by using prefrontal regions, but that this regulatory effect somehow does not reach the overactive amygdala (Bruhl et al., 2014)? Could it be that although patients are using their prefrontal cortex for emotion regulation, they are picking strategies such as emotional suppression that are unsuccessful at actually regulating their emotions, instead of picking more successful strategies such as reappraisal (Bruhl et al., 2014)? And beyond these questions about the basic neurobiology of SAD, what are some things that actually explain these differences? More on this soon.
 American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.
 Blair, K. S., Geraci, M., Otero, M., Majestic, C., Odenheimer, S., Jacobs, M., et al. (2011). Atypical modulation of medial prefrontal cortex to self-referential comments in generalized social phobia. Psychiatry Research: Neuroimaging, 193, 38-45.
 Bruhl, A. B., Delsignore, A., Komossa, K., & Weidt, S. (2014). Neuroimaging in social anxiety disorder: A meta-analytic review resulting in a new neurofunctional model. Neuroscience and Biobehavioral Reviews, 47, 260-280.
 Klumpp, H., Andstadt, M., & Phan, K. L. (2012). Insula reactivity and connectivity to anterior cingulate cortex when processing threat in generalized social anxiety disorder. Biological Pschology, 89, 273-276.
 Tillfors, M., Furmark, T., Marteinsdottir, I., & Fredrikson, M. (2002). Cerebral blood flow during anticipation of public speaking in social phobia: A PET study. Biological Psychiatry, 52(11), 1113-1119.
[Social anxiety comic]. Retrieved October 10, 2014, from: http://www.picturesinboxes.com/comics/2014-02-08-anxiety.jpg
[Prefrontal cortex and the amygdala]. Retrieved October 10, 2014, from: http://www.dana.org/uploadedImages/Images/Spotlight_Images/DanaGuide_CH14C31_P427_spot.jpg