Parkinson’s disease (PD) has been associated with alterations in neuronal activity in the basal ganglia-thalamocortical network. The motor cortex (M1) is a key node in this network and likely plays a significant role in the expression of impaired movement in PD. Altered neuronal activity in M1 has been reported and characterized at the single-unit level in PD, however, results are difficult to reconcile under one theoretical model (Doudet et al., 1990; Watts \& Mandir, 1992; Pasquereau et al., 2016). One promising avenue toward a mechanistic understanding of M1 pathophysiology in PD is to investigate the neural population dynamics during the movement. This approach, leveraging the coordinated evolution of neuronal activity, has recently been utilized to offer insights into the role of M1 in motor control (Churchland et al., 2012; Kaufman et al., 2014). In this study, we simultaneously recorded large populations of cells in M1 from two nonhuman primates during a reaching task before and after the induction of parkinsonism using the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Significant bradykinesia (slowness) and variable reaching trajectories were observed in the parkinsonian state. We identified a collective oscillatory mode that emerged in the parkinsonian M1 superimposed on the slow dynamics that were similar to the normal state after temporal scaling. Moreover, this collective oscillatory mode extracted from unit activity was only present during the task, suggesting its distinct functional relevance to the altered kinematics present in the parkinsonian condition. Our results offer novel insights into the pathophysiological basis underlying the altered movement present in the parkinsonian condition. This approach also presents a promising analytical framework for understanding the pathophysiological changes that underlie other neurological disorders.