Parkinson’s disease (PD) is the second most common neurodegenerative disorder in the world. It is associated with progressive motor, postural, and gait abnormalities, and presently has no known cause or cure. While the behavioral symptomatology has been well-characterized, the neurophysiological underpinnings of these symptoms are only vaguely understood. Previous invasive studies using local field potentials and scalp electroencephalography have shown pathological beta synchronization during rest throughout the cortical-basal ganglia motor network in patients with severe PD. In healthy humans, there is a specific pattern of beta desynchronization and resynchronization in the motor cortices that is necessary for the proper execution of movement. Thus, it is possible that the pathological beta synchronization observed in patients with PD may directly or indirectly perturb the healthy pattern of cortical desynchronization/resynchronization, and in turn generate motor-related symptoms. For my Master’s thesis, we used magnetoencephalography (MEG) to investigate whether these oscillatory beta responses were abnormal during hand movements in patients with PD relative to matched controls. MEG is a noninvasive neurophysiological imaging technique with exceptional temporal resolution and good spatial accuracy, which permits recording of population-level oscillatory activity during movement planning, execution, and termination. My thesis showed that patients with PD have significantly diminished beta desynchronization compared with controls prior to and during movement, which likely indicates abnormalities in motor planning and movement selection. Patients also exhibited marginally significant reductions in the post-movement beta rebound, indicative of motor plan termination deficits. In my Ph.D. Dissertation project, we followed-up these findings by using MEG and three novel motor sequence planning/termination tasks to evaluate the nature of these deficits in un-medicated patients with PD and a matched group of healthy adults. In the first task, the Motor Time experiment, participants executed finger-tapping sequences, while we manipulated the amount of available time they had to plan the movement prior to motor execution. We found that patients with PD performed comparatively to controls, despite having reduced beta ERD amplitude throughout the motor cortical network. In the second task, the Motor Complexity task, the complexity of the to-be-executed motor plan was manipulated. In this experiment, patients with PD exhibited significantly different patterns of beta activity compared to healthy controls while performing Simple relative to Complex sequences, and also performed significantly worse than healthy controls across conditions. In the third task, the Motor Termination task, we manipulated when participants were forced to terminate a specific motor command. Patients with PD terminated movement at a significantly slower velocity than healthy controls, despite exhibiting largely comparable post-movement beta activity. Taken together, these data suggest that beta aberrations in PD are specific to distinct components and parameters of the motor control process, and may help direct future development of new treatment avenues and physiological biomarkers of disease progression and treatment efficacy.