two specific hypotheses of α deficits in PTSD, including (1) attenuated α power and connectivity in the DMN and (2) a deficit of α inhibition of visual cortical (VC) activity (i.e., attenuated α power) and attenuated directed α-frequency connectivity to the DMN (VC→DMN). Finally, we hypothesized that deficient sensory inhibition could be associated with the PTSD symptom of hypervigilance (characterized by excessive sensory scanning of the environment for threat) and thus examined these clinical associations, linking neuropathology to clinical symptomatology.
