Contributions of the default mode and central executive networks during posterior cingulate cortex-targeted fMRI neurofeedback in PTSD

INTRODUCTION: Functional magnetic resonance imaging-based neurofeedback (fMRI-NFB) enables individuals to regulate brain activity implicated in psychopathology, including post-traumatic stress disorder (PTSD). While most fMRI-NFB studies in PTSD target the amygdala, which engages the central executive network (CEN) for top-down regulation, the posterior cingulate cortex (PCC), a core node of the default mode network (DMN), has recently emerged as a promising therapeutic target. However, the relative contributions of intra-network DMN mechanisms versus inter-network CEN engagement during PCC downregulation remain unclear.

METHODS: We used independent component analysis (ICA) to examine DMN and CEN functional connectivity during PCC-targeted fMRI-NFB in individuals with PTSD (n = 14) and healthy controls (n = 15) while viewing trauma-related/distressing words. Mixed-design repeated measures ANOVAs assessed within- and between-group connectivity changes, and clinical correlations were explored.

RESULTS: During PCC downregulation, PTSD participants exhibited greater DMN connectivity than controls with trauma-related regions, including the precentral gyrus and anterior insula, which correlated with PTSD severity and emotion regulation difficulties. Conversely, CEN connectivity decreased in both groups, with PTSD participants showing progressively reduced connectivity across training. Direct comparisons revealed that DMN connectivity exceeded CEN connectivity with several brain regions, particularly among PTSD participants.

CONCLUSION: These findings highlight the predominant role of DMN mechanisms in PCC downregulation in PTSD. The reliance on intra-network DMN processes over CEN-driven regulation underscores distinct network dynamics that may be unique to PCC-targeted fMRI-NFB. These neural mechanistic insights may inform targeted fMRI-NFB protocols to recalibrate altered DMN connectivity and enhance emotion regulation in PTSD.