This review focuses on some of the known and hypothetical pathophysiological mechanisms underlying the motor symptoms in Parkinson's disease (PD). Current views on these mechanisms have largely been influenced by models of basal ganglia functioning and dysfunctioning. These models have allowed to explain some clinical findings and to predict a number of results of basal ganglia surgery in movement disorders. However, neurophysiological studies as well as neurochemical data have broadened our vision on basal ganglia functioning and dysfunctioning in PD. Moreover, these more fundamental insights in basal ganglia functioning allow new concepts on the development of treatment strategies, and on the prevention of motor fluctuations in PD.