Social anxiety disorder

Neurocircuitry models of SAD are still being developed and implicate dysfunctional connections between the AMYG and areas involved in processing social cues. Structural studies, as well as neutral state functional studies, have shown few differences between SAD patients and healthy volunteers in any brain regions. In symptom provocation paradigms contrasting public versus private speaking conditions and in cognitive activation studies where subjects were exposed to human face stimuli or to these stimuli paired with an aversive stimulus, increased activity was observed in the AMYG and related medial temporal lobe areas (orbitofrontal, cingulate, insular cortices).16

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