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Intrusive re-experiencing in social anxiety disorder: Does context matter?

Subject Area Personality Psychology, Clinical and Medical Psychology, Methodology
General, Cognitive and Mathematical Psychology
Term from 2017 to 2022
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 391419683
 
A crucial characteristic of social anxiety disorder (SAD) is the pronounced fear of negative evaluation. Distorted negative images of the self in social situations are an important maintenance factor. Content and meaning of these images seem to be related to aversive social experiences (e.g. teasing) that occurred around the onset or a marked aggravation of social anxiety. These distorted images resemble intrusive re-experiencing following traumatic events in posttraumatic stress disorder (PTSD). Recent studies show that patients with SAD are indeed characterized by intrusive re-experiencing in response to aversive social events. Dysfunctional extinction of conditioned fear is supposed to be the mechanism underlying the development and maintenance of intrusive re-experiencing. It is assumed that PTSD patients are not able to use contextual information in order to adequately regulate conditioned fear, probably related to an insufficient integration of the traumatic event into the spatio-temporal context and the autobiographical memory. The hippocampus with its direct and indirect projections to the amygdala plays a key role in context-dependent modulation of conditioned fear. Previous studies show that altered extinction processes as well as hippocampal abnormalities characterize SAD similar to PTSD. However, it is unknown if difficulties in context discrimination and contextual modulation of extinction are also of relevance for SAD. In a functional and structural magnetic resonance imaging study, the neural correlates of context-dependent extinction processes will be investigated in 55 patients with SAD and 55 healthy controls. It is expected that patients with SAD will show enhanced intrusive re-experiencing in response to disorder-relevant events. Furthermore, SAD patients should be characterized by deficits in basic context discrimination as well as a reduced contextual modulation of electrodermal conditioned responses during extinction. These contextual processing deficits should further be associated with the amount of intrusive re-experiencing. On the neural level, this should be reflected in diminished activation of the hippocampus as well as its altered connectivity with further structures of the fear and extinction circuit. The results of this study might contribute to determine the relevance of deficits in hippocampal-dependent contextual discrimination and contextual modulation of conditioned fear in SAD as well as to optimize therapeutic interventions in the long-term.
DFG Programme Research Grants
 
 

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