Abstract
Persistent neurocognitive symptoms, such as “brain fog”, insomnia, or fatigue, are prevalent in PASC (post-acute sequelae of COVID-19, “Long COVID”), even after mild acute illness. However, evidence for the neural underpinnings of cognitive dysregulation and altered spontaneous neural activity is inadequate. EEG data were acquired during an inhibitory Go/NoGo task and wakeful rest from young, otherwise healthy adults with PASC approximately six months after recovery from mild COVID-19. Neurobehavioral indices were computed for correct and erroneous trials, resting state, and the questionnaire battery, and compared with a matched control (CONT) group of individuals not exposed to COVID-19. The PASC group reported higher cognitive difficulties, anxiety, depression, and sleep problems, consistent with the known symptomatic pattern. Despite intact task performance, neural indices indicated altered engagement of cognitive control in the PASC group on both correct and error trials, which was associated with less efficient responding. Moreover, co-oscillatory synchrony trended toward dysregulation during error commission in the PASC group. Altered neural indices of inhibitory control marginally correlated with spontaneous oscillatory slowing, potentially suggesting shared basic mechanisms. The overall pattern of PASC symptoms, altered neural activity during inhibitory control, and oscillatory slowing, is indicative of the core neural dysfunction characterizing PASC.