NEURAL MECHANISMS OF DYSTONIA - EVIDENCE FROM A 2-DEOXYGLUCOSE UPTAKE STUDY IN A PRIMATE MODEL OF DOPAMINE AGONIST-INDUCED DYSTONIA

被引:84
作者
MITCHELL, IJ [1 ]
LUQUIN, R [1 ]
BOYCE, S [1 ]
CLARKE, CE [1 ]
ROBERTSON, RG [1 ]
SAMBROOK, MA [1 ]
CROSSMAN, AR [1 ]
机构
[1] UNIV MANCHESTER,SCH BIOL SCI,DEPT CELL & STRUCT BIOL,EXPTL NEUROL GRP,OXFORD RD,MANCHESTER M13 9PT,LANCS,ENGLAND
关键词
2‐Deoxyglucose uptake; Dopamine agonist; Dystonia; Primate model;
D O I
10.1002/mds.870050113
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The neural mechanisms that mediate dystonia were investigated in a novel experimental primate model of dopamine agonist‐induced dystonia. This condition was produced by long‐term (15 months) dopamine agonist therapy of a macaque monkey that had been rendered hemiparkinsonian by unilateral infusion of 1–methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine into the right common carotid artery. The 2–deoxyglucose (2–DG) metabolic mapping technique was applied to the animal during the expression of active unilateral dystonia, and regional brain uptake of 2–DG was assessed autoradiographically. The results demonstrate that dystonia is associated with marked increases in 2–DG uptake in the constituent nuclei of the basal ganglia (caudate nucleus, putamen, medial and lateral segments of the globus pallidus) and in the subthalamic nucleus, but decreased uptake in the structures that receive output of the basal ganglia (ventral anterior/ventral lateral thalamic complex and lateral habenula). Based on these findings it is suggested that dystonia is characterized by increased activity in the putaminopallidal and pallidosubthalamic pathways, and decreased activity in the subthalamopallidal and pallidothalamic pathways. Copyright © 1990 Movement Disorder Society
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页码:49 / 54
页数:6
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