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 dorsal VC. In light of the “sentinel hypothesis” implicating the DMN in sustained monitoring of the environment (i.e., sensory vigilance; Buckner et al., 2008; Andrews-Hanna, 2012), we surmise this visual-cortex-DMN α dysrhythmia in PTSD may fuse the impairment in “sentinel” function (of the DMN) and in sensory cortical inhibition (via α oscillations), resulting in a pathologic state hypervigilance.
