STRIATAL GLUCOSE-METABOLISM AND [18F]FLUORODOPA UPTAKE IN A PATIENT WITH TUMOR-INDUCED HEMIPARKINSONISM

Citation
Y. Miyagi et al., STRIATAL GLUCOSE-METABOLISM AND [18F]FLUORODOPA UPTAKE IN A PATIENT WITH TUMOR-INDUCED HEMIPARKINSONISM, Neurosurgery, 32(5), 1993, pp. 838-841
Citations number
24
Categorie Soggetti
Surgery,Neurosciences
Journal title
ISSN journal
0148396X
Volume
32
Issue
5
Year of publication
1993
Pages
838 - 841
Database
ISI
SICI code
0148-396X(1993)32:5<838:SGA[UI>2.0.ZU;2-4
Abstract
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 examinati on, the possible mechanism of parkinsonism is an impairment of the bas al ganglia output to the supplementary motor area. Positron emission t omography scans with 2-[18F]fluoro-2-deoxy-D-glucose and 6-L-[18F]fluo rodopa were performed to measure regional cerebral glucose metabolism and striatal dopamine metabolism, respectively. Regional cerebral gluc ose 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 o f the presynaptic dopaminergic nerve terminals in the striatum.