It has been reported that cortical and subcortical β-γ PAC occurring at rest is suppressed during movement (8, 12, 15, 17). However, findings from previous studies are inconsistent regarding whether enhanced β-γ PAC in patients with PD remains enhanced or returns to normal during movements. On the one hand, PAC was found to be enhanced during movements in patients with PD. For example, movement-related PAC in patients with PD, derived from LFP recordings in the STN, was higher in off state than in medication on state (12). Also, at the cortical level (ECoG recordings in the sensorimotor areas), persistent enhancement of movement-related PAC in patients with PD was found, as compared with patients with a nonmovement-related neurological disorder (8). Furthermore, DBS-induced acceleration of movements and alleviation of bradykinesia during voluntary movement tasks have been associated with reduced cortical movement-related PAC (13, 15). On the other hand, PAC strength derived from scalp EEG did not differ between patients in the off-medication state and healthy controls during a verbally cued intermittent hand-opening/closing task (14). This inconsistency may reflect differences in the characteristics
