INDUCTION OF CHOREA AND DYSTONIA IN PARKINSONIAN PRIMATES

被引：61

作者：

BOYCE, S ^{[1
]}

CLARKE, CE ^{[1
]}

LUQUIN, R ^{[1
]}

PEGGS, D ^{[1
]}

ROBERTSON, RG ^{[1
]}

MITCHELL, IJ ^{[1
]}

SAMBROOK, MA ^{[1
]}

CROSSMAN, AR ^{[1
]}

机构：

[1] UNIV MANCHESTER,DEPT CELL & STRUCT BIOL,EXPTL NEUROL GRP,STOPFORD BLDG,MANCHESTER M13 9PL,LANCS,ENGLAND

来源：

MOVEMENT DISORDERS | 1990年 / 5卷 / 01期

关键词：

Chorea; Dystonia; Levodopa; MPTP; Primate;

D O I：

10.1002/mds.870050103

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Administration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine in primates induced a parkinsonian syndrome that could be reversed by levodopa treatment. Animals quickly developed an apparent restlessness (“akathisia”) of the lower limbs after as little as five doses. After 4–10 weeks of regular levodopa therapy, animals developed “peak dose” choreiform movements in the lower limbs that spread, with time, to involve the upper limbs and orofacial musculature. With further treatment (5–21 months), animals developed “peak dose” dystonia that variably involved the limbs and orofacial musculature. These conditions represent novel models of levodopa‐induced chorea and dystonia in humans. They depend on the same underlying neuropathology and treatment regimen as their human counterparts. It is to be anticipated that these models of dyskinesia will be useful in determining the mechanisms underlying chorea and dystonia in humans and are ideally suited for experimental evaluation of new treatment strategies. Copyright © 1990 Movement Disorder Society

引用

页码：3 / 7

页数：5

共 18 条

[1] Fahn S., ‘On‐of’ phenomenon with L‐DOPA therapy in parkinsonism, Neurology, 24, pp. 431-441, (1974)
[2] Marsden CD, Parkes JD, ‘On‐off’ effects in patients with Parkinson's disease on chronic L‐DOPA therapy, Lancet, 1, pp. 292-296, (1976)
[3] Marsden CD, Parkes JD, Success and problems of long‐term L‐DOPA therapy in Parkinson's disease, Lancet, 1, pp. 345-349, (1977)
[4] Langston JW, Ballard P, Tetrud JW, Irwin I., Chronic parkinsonism in humans due to a product of meperidine‐analog synthesis, Science, 219, pp. 979-980, (1983)
[5] Burns RS, Chieuh CC, Markey SP, Ebert MH, Jacobowitz DM, Kopin IJ, A primate model of parkinsonism: selective of dopaminergic neurons in the pars compacta of the substantia nigra by N‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine, Proc Natl Acad Sci USA, 80, pp. 4546-4550, (1983)
[6] Langston JW, Forno LS, Rebert CS, Irwin IJ, Selective nigral toxicity after systemic administration of 1‐methyl‐4 phenyl‐1,2,3,6‐tetrahydropyridine, Science, 225, pp. 1480-1482, (1984)
[7] Clarke CE, Sambrook MA, Mitchell IJ, Crossman AR, Levodopa‐induced dyskinesia and response fluctuations in primates rendered parkinsonian with 1‐methyl‐4‐phenyl 1,2,3,6‐tetrahydropyridine (MPTP), J Neurol Sci, 78, pp. 273-280, (1987)
[8] Hoehn NM, Yahr MD, Parkinsonism: onset, progression and mortality, Neurology, 17, pp. 427-442, (1967)
[9] Bankiewicz KS, Oldfield EH, Chieu CC, Doppman JL, Jacobwitz DM, Kopin IJ, Hemiparkinsonism in monkeys after unilateral internal carotid artery infusion of MPTP, Life Sci, 39, pp. 7-16, (1986)
[10] Clarke CE, Boyce S, Robertson RG, Sambrook MA, Crossman AR, Drug‐induced dyskinesia in primates rendered hemiparkinsonian by the intracarotid administration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP), J Neurol Sci, 90, pp. 307-314, (1989)

← 1 2 →