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. This is evident in DBS and dopamine therapies that improve the motor symptoms of PD by suppressing excessive cortical PAC rather than altering cortical β power (13–15). Therefore, the dynamic modulation of β-γ PAC during repetitive voluntary movements may still encode an essential component of the motor command that is related to the motor impairment of patients with PD. At the same time, it may be distinct from the mechanism underlying event-related desynchronization, even though we cannot exclude some influence of β power on the evaluation of PAC modulation.
