Central figure in light tunes has its arm lifted forcefully by surrounding agencies. Light intensity gradually decreases and saturation fades off away from the center. Red texture used to describe rusty air in the illustrated scene.
Middle school was not fun for me. Alongside the concerns of pre-algebra and waking up at seven o’clock each morning, I was terrified of something that constantly surrounded me. Every corner I turned, every hall I walked down, and every classroom I entered was filled with one of my biggest fears: people. The possibility of conversation with someone or responding to the attendance call in front of a classroom filled with my peers consistently occupied my thoughts. It was not until later that I learned that my fear was actually a clinical condition called social anxiety, or social phobia, and not until more recently that I learned how neuroscience could help explain what was going on in my mind.
The DSM-5, a diagnostic manual used by medical professionals and researchers to classify mental illnesses, defines social phobia as a “marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others” [1]. People with social anxiety may experience symptoms that are physical, such as increased heart rate and difficulty breathing; mental, like preoccupation with social judgement; and behavioral, such as active avoidance of social situations [1]. I experienced all of these symptoms throughout middle school and was fortunate enough to feel validated and relieved when a doctor diagnosed me.
But what exactly was making me so afraid of running into someone I knew, of having conversations with a stranger, or of walking down the sidewalk when I thought people in their cars would stare at me? Neuroscientists measure brain activity using techniques such as functional magnetic resonance imaging (fMRI), which tracks changes in blood flow [2]. Because blood flow is correlated with the areas of the brain that are most active, fMRIs allow for visualization of brain activity [2]. Using this method, scientists have found differences in brain activity between people who experience social phobia and those who do not, even when completing the same task or observing the same stimuli. For example, researchers at Friedrich Schiller University in Germany found that when participants were presented with phobia-related words, such as “eye-contact,” the presence of social phobia symptoms correlated with increased activity in brain regions called the insula, amygdala, and orbitofrontal cortex [3]. Another study found that when looking at faces expressing various emotions, people with social phobia here too showed greater activity in the amygdala and insula compared to the controls (people who did not experience social phobia) [4, 5]. While some studies show conflicting results about the correlation between social phobia symptom severity and brain activity, researchers generally agree that in the presence of social stimuli there is differential (significantly higher or lower) activity in various brain regions in people with social phobia compared to control groups [6-10].
What’s exciting about differential brain activity in these areas—the insula, amygdala and orbitofrontal cortex—is that these regions are known to play a role in perception and behavior. The insula is a region deep within the brain that is linked to a wide range of processes including decision making, emotion, self-recognition, and consciousness [11]. For example, a study conducted on healthy subjects found that the insula is highly active when looking at an image of themselves, which suggests that this area is important for self-recognition [12]. Several additional studies have found that the insula is also involved in processing negative emotions [13-15]. Therefore, increased insular activity in people with social anxiety could suggest that they process self-related information and negative emotional stimuli differently than the average non-anxious person [3]. Similarly, the orbitofrontal cortex is implicated in impulse control, including during social situations [16-18]. Notably, one study found that damage to the orbitofrontal cortex led to more socially inappropriate behaviors, such as speaking when others expect you to be silent [19]. Based on this finding, increased activity in the orbitofrontal cortex could affect how people with social phobia perceive what behaviors are socially appropriate and the extent to which they feel the need to inhibit themselves during conversation. Finally, the amygdala plays a role in fear processing and stress [20-24]. For example, the administration of hormones released during stressful situations impair memory formation, and studies have found that the amygdala plays a crucial role in this memory process [25-27]. Perhaps people with social phobia have altered fear responses, which can affect how they perceive the level of danger in a social situation, how they remember it, and therefore how they anticipate future social situations will go [3, 4].
Illustration of two bodies submerged in turbulent flows adjacent to a cliff. The bottom shows glimmering signs of sharp reef covered by grey-toned waterfall. Body portrayed with pure lightness to portray passiveness.
These possible consequences of differential brain activity have been partially explored in behavioral studies, and findings indicate that individuals with social phobia interpret social situations differently from those without social phobia [28-31]. One study demonstrated that when interpreting ambiguous social situations, such as dinner guests leaving sooner than expected, those with social phobia are more likely to report a negative interpretation of the event, namely that they committed some social error [32]. Furthermore, several studies have reported that individuals experiencing social phobia have more difficulty recalling details of past social events [33-35]. One such memory study conducted at the University of British Columbia found that people with social phobia were able to recall less information about someone they had just had a social interaction with in comparison to those without social phobia [35]. Given the amygdala’s role in memory, these behavioral outcomes present an intriguing connection between differential brain activity and the everyday experience of having social phobia.
These possible links between my thoughts, feelings, behavior, and neuroscience helped me make sense of a lot of things going on in my mind. For example, my neighborhood often had parties around the holidays. Upon receiving the invitation, my family became excited, planned their outfits, and finished up chores around the house so that they could fully enjoy their time at the gathering. I, however, dreaded these invites and would immediately begin to plan how I could avoid going. Perhaps my amygdala, insula, and various other regions of my brain reacted uniquely to the stimulus of receiving this invite, causing me to perceive the situation as a threat, while my family saw it simply as a chance to have fun.
Before studying neuroscience, I felt guilty and confused as to why I did not want to spend time with other people. However, neuroscience has empowered me. I no longer feel like I am essentially awkward or fundamentally flawed in some way. Instead, I can look at pictures of brain activity and read credible scientists’ writing about why I might be feeling the way that I do. Neuroscientific explanations never involved me being simply “weird”—my brain and the brains of other people with social phobia are simply different. While the research behind why social phobia might arise is exciting, I am even more enthralled by the research surrounding successful treatments.
Although there is no known cure for social phobia, research tends to focus on three “routes” of treatment for social phobia: cognitive behavioral therapy (CBT), medication, and exposure therapy [36]. CBT involves sessions of talk therapy that address thinking styles that may be detrimental to a patient in social situations [37]. Classes of medications that are currently prescribed for social phobia include selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase (MAO) inhibitors, and benzodiazepines [38]. These medications each act on different neurotransmitters, or chemical messengers in the brain, to influence their relative balance [38]. Lastly, exposure therapy for social phobia typically involves repeatedly placing the individual in situations that provoke social anxiety, such as meeting new people [37]. The idea here is that such repeated exposure will eventually reduce the anxiety surrounding those situations [37].
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Strong separation of foreground and background to show
the feeling of being dragged and pulled. The figure
struggles in multicolor waterbody.
Studies comparing the efficacy of the three treatments have mixed results. However, most findings suggest that some form of treatment is better than none [39-47]. Many professionals recommend trying a combination of several treatment approaches, which seemed to be most effective for me, though some still advocate for one treatment over the other [48]. It’s also important to consider that every patient responds to each treatment differently [48].
While additional research is still needed to understand why certain treatments are more effective in some individuals and not others, current work has uncovered neurological changes in response to each treatment. For example, Kilts et al. found that brain activity in people with social phobia became more similar to that of non-social phobic controls after patients were administered nefazodone, an SSRI [7]. Similarly, patients undergoing CBT had levels of brain activity in the studied regions, such as the amygdala, that were more similar to control subjects than patients not undergoing treatment [49, 50]. Exposure therapy is thought to incite similar changes in the brain, such as suppressing an overactive amygdala [51]. These post-treatment changes are thought to rely on neuroplasticity, namely the brain’s ability to change in response to experience [52]. Essentially, these treatments alter how the brain, and thus the mind, reacts to the outside world, possibly allowing the individual to process social situations in less threatening ways.
Importantly, these changes take time. A person does not feel less socially anxious after their first dose of medication, first exposure, or first CBT session [36]. How can we then ensure that we support individuals with social phobia? Perhaps our society could benefit from some plasticity as well.
While certain disability accommodations take some social anxiety disorder symptoms into account, people who require disability accommodations in academic settings often have to advocate for themselves in order to get those accommodations. Given the socially inhibitory nature of the illness, this task of speaking up for oneself is often immensely challenging for those with social anxiety [1]. Furthermore, many accommodations are not granted unless there is medical documentation, which provides another barrier as obtaining a diagnosis is expensive, is not always covered by insurance, and is often stigmatized [40, 53].
There are many ways to implement everyday accommodations for social phobia in the classroom, workplace, and beyond. For example, teachers could provide alternative assignments in place of those involving speaking in front of the class and collect anonymous feedback on comfort levels from students on practices such as cold-calling and group work. In professional settings, companies could provide more work-from-home positions and consistently receive input from employees on making the work environment more accessible. Given that roughly seven percent of the U.S. population suffers from social phobia, you are likely to interact with people who have social phobia [54]. Therefore you too can help make daily life for people with social phobia more accessible by taking actions such as being understanding when someone comes across as “reserved” or “shy” and not forcing someone to speak or engage.
While neuroscience is often a poorly understood field, it is truly a personal and empowering tool for navigating life. Understanding how changes in brain activity could possibly give rise to social phobia, and how treatments possibly work helped me feel validated and motivated to stick with treatment. Communicating scientific findings to the public can help those with social anxiety understand their own brains, as well as help those without social anxiety understand those of their peers. Neuroscience has given me not only a lifelong fascination with the brain, but a lifelong love of socializing.
Dream-like scene depicts ominous octopus-like creature which grasp human figures with tentacled in an oceanic setting. Cliff composed of naive girls’ heads holds a goldfish bowl. Waves are in red.
References
[1] American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorder, Fifth Edition.
[2] Glover, G. H. (2011). Overview of functional magnetic resonance imaging. Neurosurgery Clinics of North America, 22(2), 133–139. https://doi.org/10.1016/j.nec.2010.11.001
[3] Schmidt, S., Mohr, A., Miltner, W. H. R., & Straube, T. (2010). Task-dependent neural correlates of the processing of verbal threat-related stimuli in social phobia. Biological Psychology, 84(2), 304–312. https://doi.org/10.1016/j.biopsycho.2010.03.005
[4] Lira Yoon, K., Fitzgerald, D. A., Angstadt, M., McCarron, R. A., & Phan, K. L. (2007). Amygdala reactivity to emotional faces at high and low intensity in generalized social phobia: A 4-tesla functional MRI study. Psychiatry Research: Neuroimaging, 154(1), 93–98. https://doi.org/10.1016/j.pscychresns.2006.05.004
[5] Straube, T., Hans-Joachim, M., & Miltner, W. (2005). Common and distinct brain activation to thread and safety signals in social phobia. Neuropsychobiology, 52(1), 163-168. https://doi.org/10.1159/00008798
[6] Blair, K. S., Geraci, M., Korelitz, K., Otero, M., Towbin, K., Ernst, M., Leibenluft, E., Blair, R. J. R., & Pine, D. S. (2011). The pathology of social phobia is independent of developmental changes in face processing. American Journal of Psychiatry, 168(11), 1202–1209. https://doi.org/10.1176/appi.ajp.2011.10121740
[7] Kilts, C. D., Kelsey, J. E., Knight, B., Ely, T. D., Bowman, F. D. B., Gross, R. E., Selvig, A., Gordon, A., Newport, D. J., & Nemeroff, C. B. (2006). The neural correlates of social anxiety disorder and response to pharmacotherapy. Neuropsychopharmacology, 31(10), 2243–2253. https://doi.org/10.1038/sj.npp.1301053
[8] Birbaumer, N., Grodd, W., Diedrich, O., Klose, U., Erb, M., Lotze, M., Schneider, F., Weiss, U., & Flor, H. (1998). FMRI reveals amygdala activation to human faces in social phobics. NeuroReport, 9(6), 1223–1226. https://doi.org/10.1097/00001756-199804200-00048
[9] 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. https://doi.org/10.1016/s0006-3223(02)01396-3
[10] Sareen, J., Campbell, D. W., Leslie, W. D., Malisza, K. L., Stein, M. B., Paulus, M. P., Kravetsky, L. B., Kjernisted, K. D., Walker, J. R., & Reiss, J. P. (2007). Striatal function in generalized social phobia: A functional magnetic resonance imaging study. Biological Psychiatry, 61(3), 396–404. https://doi.org/10.1016/j.biopsych.2006.05.043
[11] Craig, A. D. (2009). How do you feel — now? the anterior insula and human awareness. Nature Reviews Neuroscience, 10(1), 59–70. https://doi.org/10.1038/nrn2555
[12] Deuve, C., Collette, F., Balteau, E., Degueldre, C., Luxen, A., Maquet, P., & Brédart, S. (2007). Here I am: The cortical correlates of visual self-recognition. Brain Research, 1143, 169–182. https://doi.org/10.1016/j.brainres.2007.01.055
[13] Dilger, S., Straube, T., Mentzel, H., FItzek, C., Reichenbach, J., Hecht, H., Kreischel, S., Gutberlet, I., Miltner, W. (2003). Brain activation of phobia-related pictures in spider phobic humans: an event-related functional magnetic resonance imaging study. Neuroscience Letters, 348(1), 29-32. doi:10.1016/S0304-3940(03)00647-5
[14] Wright, C., Martis, B., McMullin, K., Shin, L., & Raunch, S. (2003). Amygdala and insular responses to emotionally valenced human faces in small animal specific phobia. Biological Psychiatry, 54(10), 1067-76. https://doi.org/ 10.1016/s0006-3223(03)00548-1.
[15] Berntson, G., Norman, G., Bechara, A., Bruss, J., Tranel, D., & Cacioppo, J. (2011). The insula and evaluative processes. Psychological Science, 22(1), 80-86.https://doi.org/10.1177/0956797610391097
[16] Rolls, E. T., Hornak, J., Wade, D., & McGrath, J. (1994). Emotion-related learning in patients with social and emotional changes associated with frontal lobe damage. Journal of Neurology, Neurosurgery & Psychiatry, 57(12), 1518–1524. https://doi.org/10.1136/jnnp.57.12.1518
[17] Kaczmarek, B. L. J. (1984). Neurolinguistic analysis of verbal utterances in patients with focal lesions of frontal lobes. Brain and Language, 21(1), 52–58. https://doi.org/10.1016/0093-934x(84)90035-x
[18] Beer, J. S., Heerey, E. A., Keltner, D., Scabini, D., & Knight, R. T. (2003). The regulatory function of self-conscious emotion: Insights from patients with orbitofrontal damage. Journal of Personality and Social Psychology, 85(4), 594–604. https://doi.org/10.1037/0022-3514.85.4.594
[19] Beer, J. S., John, O. P., Scabini, D., & Knight, R. T. (2006). Orbitofrontal Cortex and social behavior: Integrating self-monitoring and emotion-cognition interactions. Journal of Cognitive Neuroscience, 18(6), 871–879. https://doi.org/10.1162/jocn.2006.18.6.871
[20] McGaugh, J. L., & Roozendaal, B. (2002). Role of adrenal stress hormones in forming lasting memories in the brain. Current Opinion in Neurobiology, 12(2), 205–210. https://doi.org/10.1016/s0959-4388(02)00306-9
[21] Clayton, E. C., & Williams, C. L. (2000). Adrenergic activation of the nucleus tractus solitarius potentiates amygdala norepinephrine release and enhances retention performance in emotionally arousing and spatial memory tasks. Behavioural Brain Research, 112(1-2), 151–158. https://doi.org/10.1016/s0166-4328(00)00178-9
[22] Buchanan, T. W. (2006). Impaired memory retrieval correlates with individual differences in cortisol response but not autonomic response. Learning & Memory, 13(3), 382–387. https://doi.org/10.1101/lm.206306
[23] de Quervain, D. J.-F., Aerni, A., & Roozendaal, B. (2007). Preventive effect of β-adrenoceptor blockade on glucocorticoid-induced memory retrieval deficits. American Journal of Psychiatry, 164(6), 967–969. https://doi.org/10.1176/ajp.2007.164.6.967
[24] Roozendaal, B., McEwen, B. S., & Chattarji, S. (2009). Stress, memory and the amygdala. Nature Reviews Neuroscience, 10(6), 423–433. https://doi.org/10.1038/nrn2651
[25] Davis, M., Rainnie, D., Cassel, M. (1994). Neurotransmission in the rat amygdala related to fear and anxiety. Trends in Neuroscience, 17(5), 208-214. https://doi.org/10.1016/0166-2236(94)90106-6
[26] Roozendaal, B, & McGaugh, J. (1997). Basolateral amygdala lesions block the memory-enhancing effect of glucocorticoid administration in the dorsal hippocampus of rats. European Journal of Neuroscience, 9(1), 76-83. https://doi.org/10.1111/j.1460-9568.1997.tb01355.x.
[27] Liang, K. C., Juler, R. G., & McGaugh, J. L. (1986). Modulating effects of posttraining epinephrine on memory: Involvement of the amygdala noradrenergic system. Brain Research, 368(1), 125–133. https://doi.org/10.1016/0006-8993(86)91049-8
[28] Rapee, R., & Heimberg, R. (1997). A cognitive model of anxiety in social phobia. Behavioral Research and Therapy, 35(8), 741-56. https://doi.org/10.1016/s0005-7967(97)00022-3
[29] Amin, N., Foa, E. B., & Coles, M. E. (1997). Negative interpretation bias in social phobia. Behaviour Research and Therapy, 36(10), 945–957. https://doi.org/10.1016/s0005-7967(98)00060-6
[30] Hirsch, C. R., Clark, D. M., Mathews, A., & Williams, R. (2002). Self-images play a causal role in social phobia. Behaviour Research and Therapy, 41(8), 909–921. https://doi.org/10.1016/s0005-7967(02)00103-1
[31] Moscovitch, D. A., Rodebaugh, T. L., & Hesch, B. D. (2012). How awkward! social anxiety and the perceived consequences of social blunders. Behaviour Research and Therapy, 50(2), 142–149. https://doi.org/10.1016/j.brat.2011.11.002
[32] Stopa, L., & Clark, D. M. (1998). Social phobia and interpretation of social events. Behaviour Research and Therapy, 38(3), 273–283. https://doi.org/10.1016/s0005-7967(99)00043-1
[33] Kimble, C. E., & Zehr, H. D. (1982). Self-consciousness, information load, self-presentation, and memory in a social situation. The Journal of Social Psychology, 118(1), 39–46. https://doi.org/10.1080/00224545.1982.9924416
[34] Hope, D. A., Heimberg, R. G., & Klein, J. F. (1990). Social anxiety and the recall of interpersonal information. Journal of Cognitive Psychotherapy, 4(2), 185–195. https://doi.org/10.1891/0889-8391.4.2.185
[35] Mellings, T. M. B., & Alden, L. E. (2000). Cognitive processes in social anxiety: The effects of self-focus, rumination and anticipatory processing. Behaviour Research and Therapy, 38(3), 243–257. https://doi.org/10.1016/s0005-7967(99)00040-6
[36] Rodebaugh, T. L., Holaway, R. M., & Heimberg, R. G. (2004). The treatment of Social Anxiety Disorder. Clinical Psychology Review, 24(7), 883–908. https://doi.org/10.1016/j.cpr.2004.07.007
[37] American Psychological Association. (2017). What is cognitive behavior therapy?
[38] Blanco, C., Bragdon, L., Schneier, F., & Liebowitz, M. (2013). The evidence-based pharmacotherapy of social anxiety disorder. International Journal of Neuropsychopharmacology, 16(1), 235-49. https://doi.org/10.1017/S1461145712000119
[39] Rowa, K., & Antony, M. (2005). Psychological treatments for social phobia. Canadian Journal of Psychiatry, 50(1), 308-16. https://doi.org/10.1177/070674370505000603
[40] McAleavey, A. A., Castonguay, L. G., & Goldfried, M. R. (2014). Clinical experiences in conducting cognitive-behavioral therapy for social phobia. Behavior Therapy, 45(1), 21–35. https://doi.org/10.1016/j.beth.2013.09.008
[41] Gould, R. A., Buckminster, S., Pollack, M. H., Otto, M. W., & Yap, L. (1997). Cognitive-behavioral and pharmacological treatment for social phobia: A meta-analysis. Clinical Psychology: Science and Practice, 4(4), 291–306. https://doi.org/10.1111/j.1468-2850.1997.tb00123.x
[42] Feske, U., & Chambless, D. L. (1995). Cognitive behavioral versus exposure only treatment for social phobia: A meta-analysis. Behavior Therapy, 26(4), 695–720. https://doi.org/10.1016/s0005-7894(05)80040-1
[43] Mattick, R. P., Peters, L., & Clarke, J. C. (1989). Exposure and cognitive restructuring for social phobia: A controlled study. Behavior Therapy, 20(1), 3–23. https://doi.org/10.1016/s0005-7894(89)80115-7
[44] Taylor, S. (1996). Meta-analysis of cognitive-behavioral treatments for social phobia. Journal of Behavior Therapy and Experimental Psychiatry, 27(1), 1–9. https://doi.org/10.1016/0005-7916(95)00058-5
[45] Ginzburg, D., Bohn, C., Höfling, V., Weck, F., Clark, D., & Strangier, U. (2012). Treatment specific competence predicts outcome in cognitive therapy for social anxiety disorder. Behavioral Research and Therapy, 50(12), 747-752. https://doi.org/ 10.1016/j.brat.2012.09.001
[46] Abbott, M., & Rapee, R. (2004). Post-event rumination and negative self-appraisal in social phobia before and after treatment. Journal of Abnormal Psychology, 113(1), 136-144. https:// 10.1037/0021-843X.113.1.136
[47] Clark, D. M., Ehlers, A., Hackmann, A., McManus, F., Fennell, M., Grey, N., Waddington, L., & Wild, J. (2006). Cognitive therapy versus exposure and applied relaxation in social phobia: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 74(3), 568–578. https://doi.org/10.1037/0022-006x.74.3.568
[48] Blomhoff, S., Haug, T. T., Hellström, K., Holme, I., Humble, M., Madsbu, H. P., & Wold, J. E. (2001). Randomised controlled general practice trial of sertraline, exposure therapy and combined treatment in generalised social phobia. British Journal of Psychiatry, 179(1), 23–30. https://doi.org/10.1192/bjp.179.1.23
[49] Goldin, P. R., Ziv, M., Jazaieri, H., Hahn, K., Heimberg, R., & Gross, J. J. (2013). Impact of cognitive behavioral therapy for Social Anxiety Disorder on the neural dynamics of cognitive reappraisal of negative self-beliefs. JAMA Psychiatry, 70(10), 1048. https://doi.org/10.1001/jamapsychiatry.2013.234
[50] Furmark, T., Tillfors, M., Marteinsdottir, I., Fischer, H., Pissiota, A., Långström, B., & Fredrikson, M. (2002). Common changes in cerebral blood flow in patients with social phobia treated with citalopram or cognitive-behavioral therapy. Archives of General Psychiatry, 59(5), 425. https://doi.org/10.1001/archpsyc.59.5.425
[51] McNally, R. J. (2007). Mechanisms of exposure therapy: How neuroscience can improve psychological treatments for anxiety disorders. Clinical Psychology Review, 27(6), 750–759. https://doi.org/10.1016/j.cpr.2007.01.003
[52] Kolb, B., & Gibb, R. (2011). Brain plasticity and behaviour in the developing brain. Journal of the Canadian Academy of Child and Adolescent Psychiatry = Journal de l'Academie canadienne de psychiatrie de l'enfant et de l'adolescent, 20(4), 265–276.
[53] Shim, R., Kho, C., & Murray-García, J. (2018). Psychiatric Annals, 48(3), 138-42. https://doi.org/10.3928/00485713-20180213-01
[54] National Institute of Health. (2021). Social Anxiety Disorder: More than Just Shyness
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