Our source-level group analysis further identified α deficits within and between the VC and the DMN in PTSD. Concerning the VC, α oscillations are known to mediate visual cortical inhibition, and accordingly, α power correlates inversely with visual cortical activity (Klimesch et al., 2007; Palva and Palva, 2007; Jensen and Mazaheri, 2010; Lange et al., 2013). In the PTSD group, reduced α power in the VC was extensive and enduring across states. Without visual stimulation (at S-RS, reflecting intrinsic activity), α deficits spanned a large cluster over the cuneus, precuneus, and superior occipital gyrus, suggesting wide-spread, intrinsic neural disinhibition and hyperactivity across primary and secondary visual cortices in PTSD. This sensory cortical disinhibition aligns with extant electrophysiological evidence of impaired sensory gating and sensory cortical hyperactivity (to simple, neutral stimuli; Morgan and Grillon, 1999; Neylan et al., 1999; Stewart and White, 2008; Javanbakht et al., 2011) and behavioral disturbances in sensory filtering/gating and response in these patients (Stewart and White, 2008; Engel-Yeger et al., 2013). With strong visual input at M-RS, α power reduction was particularly localized to the parietal
