Our manipulation of visual stimulation between the two states revealed a direct link between α deficits in the VC and the DMN. Consistent with general DMN susceptibility to salient sensory input, we confirmed a general reduction (in the entire sample) in bidirectional α connectivity between the DMN hubs (PCC→mPFC and mPFC→PC) as visual input increased from the S-RS to the M-RS. Beyond that, in the PTSD (but not control) group, increased visual stimulation (from S-RS to M-RS) further diminished visual cortical α connectivity to both DMN hubs (VC→PCC and VC→mPFC). As mentioned above, α oscillations in the sensory cortex mediate sensory inhibition, such that this VC→DMN α projection would serve to protect the DMN by blocking sensory afferents to the network. This notion is supported by prior work demonstrating a modulatory role of α oscillations in the connectivity within the sensory (visual) cortex and between the VC and DMN hubs (Scheeringa et al., 2012). While this protective inhibitory process withstood the increased visual input at M-RS in the control group, it broke down among patients with PTSD, suggesting impaired gating
