Levodopa has become established as the treatment of choice in Parkinson's disease. It is adsorbed by an active mechanism from the small bowel. Its pharmacological activity depends upon the formation of dopamine and possibly other metabolites. Its beneficial effect in Parkinson's disease probably depends upon temporarily restoring the ability of degenerating nigro-striatal cells to release dopamine. Its main side effect, that of dyskinesia, may reflect a direct action of dopamine on striatal receptors. Peripheral decarboxylase inhibitors reduce the incidence of levodopa-induced nausea, probably by lowering the concentration of dopamine in the area postrema. The introduction of levodopa in the treatment of Parkinson's disease is generally regarded as one of the uncommon examples in medicine where effective therapy has resulted from systematic research rather than seredipity. As our knowledge of the pharmacology of levodopa grows, we may be forced to admit that perhaps the right drug was chosen for the wrong reasons.