The extended default mode network dysconnectivity in schizophrenia

The default mode network (DMN) extends beyond cortex into subcortical structures, yet how this extended DMN (eDMN) is causally reorganized in schizophrenia (SZ) remains unclear. Here, resting-state fMRI from 74 healthy controls (HC) and 66 SZ patients was analyzed. Subject-specific eDMNs were identified using spatially-constrained independent component analysis, and effective connectivity among 13 regions was estimated with spectral dynamic causal modeling, with group effects assessed using parametric empirical Bayes. Causal centrality--a dynamics-sensitive and causality-based measure of nodal importance--was computed per region, compared between groups, and correlated with MATRICS cognitive scores in patients. Causal centrality rankings were highly similar across groups ({rho} = 0.87), with both favoring subcortical over cortical regions. Group differences were regionally specific: temporal cortex was more causally central in patients, whereas posterior parietal cortex was more causally central in controls. Most connection-level SZ-HC differences originated from ventrolateral prefrontal cortex, prefrontal cortex, basal forebrain, temporal cortex, and thalamus. In patients, temporal causal centrality correlated negatively with reasoning/problem-solving, and ventrolateral prefrontal causal centrality with processing speed and composite cognition. The eDMN's core causal architecture is preserved in schizophrenia, but temporal influence is enhanced and parietal influence attenuated--alterations that are behaviorally meaningful and consistent with pathological reorganization.