Abstract
From 1983, when dopaminergic structures were visualized for the first time in the human brain by positron emission tomography (PET) and onwards about 120 PET studies on Parkinsons disease have been listed in MEDLINE. With 18F-fluorodopa presynaptic dopamine insufficiency can be demonstrated in PD. By using 11C-nomifensine the dopamine reuptake sites can be visualized with PET. These results indicate that the striatal dopaminergic terminals are relatively preserved in PD as compared to the extreme reductions of dopamine in this region post mortem. Radiolabelled D2-agonists indicate a slight increase in these binding sites in de novo PD and no marked reduction in more advanced disease. 11C-selegiline have been used to demonstrate the intracerebral MAO-B inhibition by therapeutic doses of this drug. 11C-L-dopa and PET have demonstrat the rapid striatal decarboxylation of therapeutic doses of L-dopa also in advanced PD and a rough estimate of the striatal dopamine concentration inducing an "on-response" has been obtained. These contributions of PET to PD research are discussed in the article.