Brain rhythms at distinct frequencies interact with each other, enabling neuronal ensembles to flexibly bind together across different temporal and spatial scales. Although coupling among neural oscillations in different frequency bands may have functional significance for normal behavior (1–4), abnormal coupling has been associated with a variety of neurological disorders (5–7). It is widely held that exaggerated cross-frequency coupling between the phase of β oscillations and the amplitude of γ oscillations (β-γ PAC), as detected in cortical (8–10) or subcortical (11) resting state recordings of patients with Parkinson’s disease (PD), is closely involved in the pathophysiology of Parkinsonian motor impairment. Importantly, interventions that alleviate Parkinsonian motor impairment, such as deep brain stimulation (DBS) of the subthalamic nucleus (STN) or globus pallidus internus (GPi), and dopamine replacement therapy, also decrease enhanced resting state β-γ PAC in STN (12) and motor cortex (13–15). Increased resting β-γ PAC and β power have been found in subcortical nuclei of patients with PD (8, 11). However, at the cortical level, enhanced β-γ PAC at rest was more pronounced than enhanced β power (9, 13, 15).
