Alternatively, deficient α activity could give rise to DMN dysfunctions by failing to sustain long-range synchronization across the DMN and failing to inhibit sensory afferents to the DMN. Aberrant α oscillations have been featured in a “thalamocortical dysrhythmia” model of neuropsychiatric disorders (Llinás et al., 1999; Schulman et al., 2011), which are conceptualized transdiagnostically as oscillopathies (Basar, 2013; Buzsáki et al., 2013). Reduced resting-state α activity has been observed in patients with PTSD [vs healthy controls (HCs) and patients with generalized anxiety disorder (GAD); Clancy et al., 2017] and combat veterans with severe symptoms (Clancy et al., 2020). Given the demonstrated association between α oscillations and DMN activity, we hypothesized that PTSD is associated with deficient α activity in the DMN and deficient inhibition of sensory cortical input to the DMN.
