Examining Social Phobia Through Aversive Emotional Triggers
Schneider et al.’s experiment on subcortical correlation with aversive emotional cues detailed the profound impact that social phobia has on mental processing of emotion and stress. A cohort of 12 “healthy” controls and 12 individuals diagnosed with Social Anxiety Disorder (SAD) were introduced to a classical conditioned test to identify differences in neurological functioning of the Amygdala and Hippocampus. This powerful study bridges the gap between a foundational psychological study design (Classical Conditioning) and modern neuroscience research. In addition, the experiment’s conclusion offers strong implications that treatment for social anxiety should be unique between patients diagnosed with SAD and those not diagnosed. The results that spurred this conclusion highlight that individuals with SAD spent more time emotionally processing stimuli as opposed to the control patients. Such differences are important to unveil as they usher the need for unique, enduring interventions for socially anxious people. Furthermore, the study challenges stigmas about dismissing anxiety disorder as legitimate medical conditions to a simple overreaction or habit. As a result, I felt that selecting Schneider et al.’s research article, discussing the profound results, and shedding light on a neglected issue of social anxiety eclipsed other potential articles I reviewed. Moreover, this experiment hinges on Classical Conditioning, a study design rooted in psychology’s history, this psychology class and is known to provide reliable results on psychological studies. Schneider et al. utilizes this study design to activate neural transmission in the hippocampus and amygdala: regions of the brain discussed in length in this class. For this classical conditioned study, the conditioned stimulus (CS) was neutral facial expressions that subjects were introduced to, while the presence of a negative order served as the aversive unconditioned stimulus (US). Eventually this warranted a conditioned response (CR) from both the control and test group. Then, Magnetic Resonance Imaging (fMRI) scans contrasted the differing responses to these facial expressions.
Outside the realm of psychology this specific study brings forth many avenues of improvements in a multitude of aspects of life. Primarily, the result can be extracted to interventions in medicine. The conclusion from the article by Schneider et al. displayed different regions of the brain being illuminated for differing amounts of time between the two groups after being exposed to the same facial expression. These results imply that the individuals diagnosed with social anxiety handle uncomfortable situations for a greater amount of time, which in turn opens the door to personalized treatment regarding social stress. These conclusions prompt awareness for social anxiety issues through public campaigns, new policies that promote a more comfortable environment for diagnosed individuals, and a greater stress on mental health within education. These benefits stretch beyond awareness as the methodology of the article enables strides in both social and technological dynamics. Professional environment can utilize the content within this article to foster a more inviting and comfortable environment for those struggling with social anxiety. In addition, professional, social, and other settings could gain insight into the capabilities of the technology utilized to support this study as technological advancements in fMRI scans become more adept and successful.
To achieve such successful fMRI scan-based conclusions, Schneider et al. first had to develop their hypothesis and construct a fitting test. Their initial hypothesis centered around the notion that individuals with social phobias exhibited distinct neural responses. As previously mentioned, this independent samples test was conducted via a classical conditioned examination. In this research study, two groups (control and experimental) were introduced to neutral facial expressions, for example, a blank stare. However, a negative odor (diluted rotten yeast) was also introduced through a small tube in the test room for that specific stare. The negative odor was present with the same specific neutral facial expression for both groups (CR). After the acquisition phase, examiners would compare fMRI scans of a neutral expression without the odor, to the CR within each group, as well as the fMRI scans of the CR between both groups. When examining the fMRI scans Schneider et al. focused on the activation of different regions of the brain and signal change within the scans to determine the effects of both the non-aversive and aversive stimulus.
After receiving promising fMRI scans, Schneider et al. needed to summarize then to draw a conclusion. What was noticeable about these scans was the higher activation of the Amygdala when managing the aversive-stimulus as opposed to the non-aversive stimulus, with a mean difference of 0.4% signal change for both groups. Furthermore, the findings suggest that other regions of the brain such as the Thalamus, Prefrontal Cortex and Medial Temporal Cortex all played significant roles in processing the non-aversive stimulus. The Thalamus highlighted the usage of sensory relay of the aversive stimulus, the Prefrontal Cortex indicated cognitive regulation of these sensory relays, while the Medial Temporal Cortex held a significant role with emotional memory due to the sensory relays. Both groups highlighted similar responses to the aversive odor and had higher activation in the subcortical region of the brain with less involvement from other areas. These statistics were helpful for deciphering the basic mechanisms that took place in the face of an aversive stimulus, but did not offer many conclusions for the differences between the two groups. What did arise from these findings was a delayed acquisition of the US from the group with SAD as well as a prolonged extinction from the social anxiety group. Furthermore, the study found that there was a significant decrease in activity of the Amygdala over time in the healthy group, while there was a persistent and prolonged activity of the Amygdala in the test group. This indicates that socially anxious individuals developed a much more emotional response to the negative odor, and kept this response for much longer periods of time. Patterns within the Hippocampus supported these findings as patients had a greater difficulty in decreasing emotional regulation to the aversive stimulus even during the extinction portion of the study. Overall, the study found an increased and prolonged activation of the Amygdala and Hippocampus region of the brain for the SAD patients, suggesting that they had greater difficulty in regulation and processing negative emotions to the aversive stimulus during the acquisition and extinction phases of this study.
This study was conducted to investigate the underlying emotional learning, through classical conditioning, between healthy control groups and patients facing social anxiety. Despite Schneider et al.’s initial hypothesis of different biological processing for the same aversive stimulus, what they found was a differing period of time between the two groups. The SAD patient group had a much greater difficulty with reducing emotional influence on the US. The finding suggests that there was heightened subcortical activity within the test group opposed to the control for the entire duration of the experiment. This research result is important because it enhances our understanding of the neural basis of emotional learning and details that heightened subcortical activity in individuals with social phobia contributes to their exaggerated emotional responses. It also sheds light on potential neural targets for therapeutic interventions aimed at treating anxiety disorders by addressing maladaptive emotional processing.
One future study for this research topic would be to explore different types of conditioned stimulus. More specifically, focusing on positive non-aversive conditioned stimulus. This could be personalized to each patient which can then help with interventions to reduce anxiety levels for individuals with SAD. Moreover, if a specific stimulus is found to have the same time frame of acquisition and extinction as compared to the control, then it could be implemented in treatment options as well as implemented in a multitude of social groups, namely work environments to help reduce stress levels of patients. Another crucial aspect to focus on is different regions of the brain when taking fMRI scans. Schneider et al. states that their fMRI scans often neglected other regions of the brain besides the subcortical region due to the prolonged period of time and extended need for resources to analyze other regions. This restricts the study to only being able to assess the neurological processing for this specific region. Focusing on other parts of the brain could provide a clarity to the overall neural mechanisms when processing negative stimuli. From the summary of the findings, it appears that similar interventions to healthy patients may work for socially anxious patients, but the length of time spent on intervention should be longer. Although this initial test proved to be profound and meaningful the sample size of this study hinders the extrapolation of this data to a greater population. The sample size was only 12 individuals in each group, the study was not randomized, and female participants were excluded. Consequently, it is difficult to set these results as facts due to potential confounding factors, lack of randomization and exclusion of characteristics. Despite this, these results present the foundation for future research in social anxiety that stresses the need for more attentive and long-lasting care for social anxiousindividuals as opposed to different treatment in general.
References:
Schneider, Frank, et al. (1999). Subcortical correlates of differential classical conditioning of aversive emotional reactions in social phobia. Biological psychiatry, 45.7, 863-871. https://www.sciencedirect.com/science/article/pii/S0006322398002698

