We found that PAC decreased around movement onset in both patients and controls. This reduction of PAC during movement is in line with studies where PAC was derived from oscillatory ECoG signals in M1 (8, 15, 17). It has long been known that voluntary motor activity is also accompanied by event-related β-power desynchronization in the cortex (38–41). In the present study, we found movement-related β power and PAC to be similarly modulated in the slow tapping and pressing tasks. This suggests that the movement-related power and PAC changes were related to a certain degree. Indeed, the suppression of β power could affect the computation of PAC by influencing the estimation of phases. However, the correlation between PAC change and power change among different movement transitions was not always present. Importantly, the magnitude of PAC was not correlated with the absolute β power in previous resting state studies (9, 10, 14) and in the movement states of our study. Furthermore, it has been suggested that cortical PAC is more specifically related to the pathophysiology of PD than is cortical β power.
