This core visual-cortex-DMN system of α dysrhythmia was reinforced by the specificity of α deficit sources. Despite the use of whole-brain analyses, group differences in α power and clinical associations between α power and hypervigilance were localized to the VC and the DMN only (except for the associative auditory cortex and insula as discussed below). While DMN hypoactivity is known to be associated with PTSD symptom severity (Sripada et al., 2012; Miller et al., 2017a,b; Akiki et al., 2018), the clinical association in the VC highlights an additional pathway linking visual cortical disinhibition to PTSD symptoms. Notably, the associations with hypervigilance implicate not only both the dorsal (i.e., the parietal cortex) and ventral visual cortices (i.e., the inferior temporal gyrus) but also the higher-order regions with strong interactions with limbic and frontal regions. As the ventral VC underpins visual object perception, its involvement here aligns with the fact that hypervigilance in PTSD is associated with hyperactivity and hypersensitivity to (threat and neutral) sensory cues (Ehlers and Clark, 2000; Hayes et al., 2012), in addition to excessive spatial scanning engaging the
