The question arises of why PAC is elevated at rest and why its magnitude is associated with Parkinsonian motor impairment, as reported in previous literature (10, 13). One possibility would be that PAC at rest, or any state-related PAC, is not mechanistically related to the dynPAC abnormality found during slow tapping. Animal experiments may reveal whether state-related PAC and dynPAC could map onto deficient tonic and phasic dopamine activities (46, 47), respectively, which may be tied to deficits in the invigoration of movements (46, 48). If, however, both PAC phenomena are based on a common mechanism, they could reflect processes of movement preparation. In this scenario, on the one hand, the increase of dynPAC would indicate a preparatory state during movement dynamics, with its reduced attenuation at movement transitions indicating a spillover of the preparatory state into the unfolding movement. On the other hand, enhancement of PAC at rest could reflect the abnormal, or abnormally frequent, generation of brief cortical states resembling preparatory population activity without an intention to move. In this way, both the enhanced resting PAC and the
