The fact that DMN α power reduction extended from the PCC only at S-RS to both the PCC and mPFC at M-RS accentuates the particular DMN vulnerability in PTSD in a sensory-rich environment. In addition, as α oscillations synchronize activity and facilitate coherence across regions, reduced α power in these key DMN hubs could further suggest compromised communication across the network in PTSD. Indeed, connectivity analyses revealed reduced PCC→mPFC α connectivity at M-RS in the PTSD group. This hypoconnectivity between the DMN hubs highlights impaired communication within the core architecture of the DMN. Clinically, DMN α deficits in both local power and interhub connectivity, especially acute in a sensory-rich environment, could contribute to difficulty in maintaining “tranquility” or “rest” (Buckner et al., 2008; Abdallah et al., 2017; Akiki et al., 2018) and avoidance of sensory stimulation in patients with PTSD (Stewart and White, 2008; Engel-Yeger et al., 2013).
