Striatal glucose metabolism and [18F]fluorodopa uptake in a patient with tumor-induced hemiparkinsonism.

We studied a patient with a falx meningioma in the right supplementary motor area and a left-sided hemiparkinsonism that resolved after the tumor was removed. Because there was no evidence of distortion of the basal ganglia and midbrain by the tumor on neuroradiological examination, the possible mechanism of parkinsonism is an impairment of the basal ganglia output to the supplementary motor area. Positron emission tomography scans with 2-[18F]fluoro-2-doxy-D-glucose and 6-L-[18F]fluorodopa were performed to measure regional cerebral glucose metabolism and striatal dopamine metabolism, respectively. Regional cerebral glucose metabolism was decreased in the striatum of the side of the lesion, although dopamine metabolism was normal. These data suggest that the tumor may have impaired synaptic function of the striatum as a whole, giving rise to contralateral hemiparkinsonism without an impairment of the presynaptic dopaminergic nerve terminals in the striatum.