Zaakirah N Sharif, Ben J Harrison, Christopher G Davey, Trevor Steward, Lianne Schmaal, Kim L Felmingham, Lisa J Phillips, Hannah S Savage, Alec J Jamieson
Our findings suggest that SAD is associated with alterations in DMN effective connectivity, with converging evidence implicating the PCC as a dysfunctional hub. This is further highlighted by the association between PCC self-connectivity and social anxiety symptom severity. Future studies should determine whether modulating PCC connectivity could have therapeutic utility for those with SAD.
BACKGROUND: Often emerging in early adolescence, social anxiety disorder (SAD) is a mental health condition characterised by persistent fears of negative evaluation. Neuroimaging studies implicate disruptions in the default mode network (DMN) in SAD, however, it remains unclear whether specific DMN regions are driving broader network alterations during this developmental period.
METHODS: Thirty-six adolescents and young adults (aged 16-25) with SAD and 66 age- and gender-matched controls underwent resting-state functional magnetic resonance imaging. Using spectral dynamic causal modelling, we examined effective connectivity between core DMN nodes, including the medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), and bilateral inferior parietal cortex (IPL). Parametric empirical Bayes modelling was used to investigate between-group differences in these connectivity parameters.
RESULTS: Compared to controls, SAD patients demonstrated increased excitatory connectivity from the PCC to the right IPL as well as excitatory connectivity from the left to right IPL. We also observed reduced PCC and MPFC self-inhibition and increased right IPL self-inhibition within SAD patients. Furthermore, leave-one-out cross-validation revealed that altered PCC self-inhibition was associated with social anxiety severity (r = .18, p = 0.039).
CONCLUSIONS: Our findings suggest that SAD is associated with alterations in DMN effective connectivity, with converging evidence implicating the PCC as a dysfunctional hub. This is further highlighted by the association between PCC self-connectivity and social anxiety symptom severity. Future studies should determine whether modulating PCC connectivity could have therapeutic utility for those with SAD.