Neuroimaging of dyskinesia

Dyskinesias are observed in the majority of Parkinson's disease (PD) patien ts who have been chronically exposed to levodopa, and these may result from supersensitivity of postsynaptic striatal dopamine D-1 and D-2 receptors f ollowing loss of nigral dopaminergic projections. Dyskinetic and nondyskine tic PD patients were studied using C-11-SCH23390 and C-11-raclopride positr on emission tomography (PET). No difference in mean putamen or caudate D-1 or D-2 receptor binding between the two patient subgroups was found, sugges ting that dyskinesias are unlikely to arise from a primary disturbance of d opamine receptor availability. When dyskinetic and nondyskinetic patients w ere studied with C-11-diprenorphine PET, the former showed a significant re duction (p < 0.05) in striatal and thalamic opioid site availability, compa tible with the presence of raised levels of endogenous opioid peptides. (H2 O)-O-15 PET activation studies of patients with focal limb dyskinesias show ed that resting levels of regional cerebral blood now after oral levodopa w ere increased during dyskinesias in lentiform nuclei, motor, premotor and d orsal prefrontal cortex. These results suggest that dyskinesias are associa ted with derangement of basal ganglia opioid transmission, resulting in ove ractivity of basal ganglia-frontal projections.