Examining the Role of the Mirror Neuron System in Social Anxiety Disorder and Borderline Personality Disorder: Pathophysiological Insights and Treatment Perspectives
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საკვანძო სიტყვები

Social Anxiety Disorder (SAD)
Borderline Personality Disorder (BPD)
Mirror Neuron System (MNS)
Social Cognition
Neuroscience informed Interventions

როგორ უნდა ციტირება

Roy, G. P., Slee, E., Nupur, N., Majid, M., & Hafeez, S. (2025). Examining the Role of the Mirror Neuron System in Social Anxiety Disorder and Borderline Personality Disorder: Pathophysiological Insights and Treatment Perspectives. ახალგაზრდა მკვლევარები, 3(5), 76–92. https://doi.org/10.52340/jr.2025.03.05.08

ანოტაცია

Social Anxiety Disorder (SAD) and Borderline Personality Disorder (BPD) both involve serious social and emotional impairments, though their origins and clinical features differ. SAD is characterized by a persistent fear of social judgment, while BPD stems from early relational trauma and is marked by emotional instability and impulsivity. Both disorders show disrupted social cognition and hypersensitivity to rejection. Emerging evidence points to dysfunction in the mirror neuron system (MNS), This network that we possess allows us to interpret the actions, intentions, and feelings of other people by reflecting them in our brain. Research shows people with SAD often have reduced activity in core MNS areas like the inferior frontal gyrus and inferior parietal lobule, especially during tasks involving emotional recognition or social observation. These deficits may explain common SAD symptoms such as the like for social withdrawal, fear of evaluation, and trouble learning from social interactions. In BPD, the picture is less clear. Some studies suggest disrupted MNS function, but inconsistent methods and limited comparative data make it hard to draw solid conclusions. Still, both disorders involve altered brain connectivity in regions tied to emotional regulation and social processing, like the amygdala and prefrontal cortex. That matters, especially during adolescence when the MNS is still developing and social vulnerability peaks. Promising treatments are now starting to emerge, like neurofeedback, transcranial magnetic stimulation, and action observation therapy all show early signs of boosting MNS activity and improving social functioning. These tools, combined with cognitive or dialectical behavior therapies, could lead to a more tailored, neuroscience-informed care. Even better, spotting MNS problems early might help prevent full-blown disorders later. And in short, the MNS may be a key player in both SAD and BPD. But to unlock its full potential, we need better methods, more diverse samples, and long-term studies that track how these brain patterns change over time and how we can use them to heal.

https://doi.org/10.52340/jr.2025.03.05.08
PDF (English)

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