In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a delay of mu rhythm movement-related desynchronisation, suggesting hypoactivation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in the amplitude of beta rhythm movement-related synchronisation was observed over the same region. This decrease--not seen in control subjects--was thus thought to be related to an impairment in cortical deactivation. By monitoring movement-related (de)synchronisation, we aimed (i) to extend to advanced PD the observations made in less-advanced situations and (ii) to test the effect of acute L-Dopa on these abnormalities. The United Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% following acute L-Dopa administration, and we observed the following concurrent changes: a marked increase in mu desynchronisation pre-movement latency (thus reduced delay) during movement preparation over contralateral, central regions; an increase in mu desynchronisation during movement execution over bilateral central regions; a decrease in mu desynchronisation latency over bilateral frontocentral regions, and a significant increase in beta synchronisation over contralateral, central regions after movement. Changes of mu and beta rhythm parameters seemed to be inversely correlated with bradykinesia. Mu rhythm desynchronisation latency and beta synchronisation amplitude further decreased in advanced PD compared to earlier stages of the disease, suggesting greater impairment of cortical activation/deactivation as the disease progresses. L-Dopa partially restored the abnormal mu and beta rhythm cortical (de)synchronisation patterns over the PSM cortex.