DIFFERING PATTERNS OF STRIATAL F-18 DOPA UPTAKE IN PARKINSONS-DISEASE, MULTIPLE SYSTEM ATROPHY, AND PROGRESSIVE SUPRANUCLEAR PALSY

Using positron emission tomography (PET), we studied regional striatal 18F‐dopa uptake in 16 patients with L‐dopa‐responsive Parkinson's disease (PD), 18 patients with multiple system atrophy, and 10 patients with progressive supranuclear palsy. Results were compared with those of 30 age‐matched normal volunteers. The patients with PD showed significantly reduced mean uptake of 18F‐dopa in the caudate and putamen compared to controls, but while function in the posterior part of the putamen was severely impaired (45% of normal), function in the anterior part of the putamen and in the caudate was relatively spared (62% and 84% of normal). Mean 18F‐dopa uptake in the posterior putamen was depressed to similar levels in all patients. Unlike patients with PD, the patients with progressive supranuclear palsy showed equally severe impairment of mean 18F‐dopa uptake in the anterior and posteior putamen. Caudate 18F‐dopa uptake was also significantly lower in patients with progressive supranuclear palsy than in patients with PD, being depressed to the same level as that in the putamen. Mean 18F‐dopa uptake values in the anterior putamen and caudate in patients with multiple system atrophy lay between PD and progressive supranuclear palsy levels. Locomotor disability of individual patients with PD or multiple system atrophy correlated with decline in striatal 18F‐dopa uptake, but this was not the case for the patients with progressive supranuclear palsy. We conclude that patients with PD have selective nigral pathological features with relative preservation of the dopaminergic function in the anterior putamen and caudate, whereas there is progressively more extensive nigral involvement in multiple system atrophy and progressive supranuclear palsy. If an akinetic‐rigid patient has equally depressed 18F‐dopa uptake in the caudate and putamen, that person is likely to have neuropathological changes other than those of idiopathic PD. Copyright © 1990 American Neurological Association