Clinicians can presently choose from three main pharmacological strategies to medically treat levodopa-induced dyskinesias (LIDs): prevent the occurrence of the priming phenomenon, which generates dyskinesias; reverse, once primed, the changes that occurred in the basal ganglia to induce dyskinesias; or avoid the expression of dyskinesias in an already primed brain. To prevent, at least partly, priming for dyskinesias can be attempted by delaying the need for levodopa, and/or reducing the cumulative dose of levodopa, using, for example, dopamine D2 agonists at the early stages of treatment. The question of reversibility of dyskinesia priming remains a matter of controversy. Any improvement gained from a drug holiday can be short lived, and the re-introduction of levodopa can re-prime the patient. Reducing the dose of levodopa and using other drugs as an adjunct has proved inconsistent. High-frequency deep brain stimulation of the subthalamic nuclei and mesencephalic embryonic cell grafts have shown potential in small numbers of patients. To avoid the expression of dyskinesias in already primed patients, agents that act on either the dopamine or nondopaminergic receptors have been used. For example, amantadine, given as an adjuvant to levodopa, has been shown to improve dyskinesias, but larger, controlled studies are required.