LEVODOPA-INDUCED DYSKINESIAS IN PARKINSONS-DISEASE - CLINICAL AND PHARMACOLOGICAL CLASSIFICATION

被引:193
作者
LUQUIN, MR
SCIPIONI, O
VAAMONDE, J
GERSHANIK, O
OBESO, JA
机构
[1] UNIV NAVARRA,CLIN UNIV,DEPT NEUROL,MOVEMENT DISORDERS UNIT,APARTADO 192,E-31080 PAMPLONA,SPAIN
[2] HOSP FRANCES RIOSA,DEPT NEUROL,EXTRAPYRAMIDAL DIS SECT,BUENOS AIRES,ARGENTINA
关键词
L; DOPA-INDUCED DYSKINESIAS; PARKINSONS DISEASE;
D O I
10.1002/mds.870070204
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Levodopa-induced dyskinesias (LID) in Parkinson's disease (PD) may be classified into three main categories: "On" dyskinesias, diphasic dyskinesias (DD), and "off" periods. The study of 168 parkinsonian patients showed that about half (n = 84) showed one pattern of LID only. A combination of two was present in 68, and 16 had the three presentation patterns. A fairly good correlation between type of dyskinesia and presentation pattern was established. Chorea, myoclonus, and dystonic movements occurred during the "on" period. Dystonic postures, particularly affecting the feet, were mainly present in the "off" period, but a few patients had a diphasic presentation. Repetitive stereotyped movements of the lower limbs always corresponded to DD. Acute pharmacological tests using dopamine agonists (subcutaneous apomorphine 3-8 mg; intravenous lisuride 0.1-0.15 mg) and dopamine antagonists (intravenous sulpiride 200-400 mg and intravenous chlorpromazine 25 mg) were performed in 40 patients. Dopamine agonists enhanced "on" dyskinesias and markedly reduced or abolished "off" period dystonia and DD. Dopamine antagonists reduced all types of LID but usually aggravated parkinsonism. These clinical and pharmacological results indicate that LID in PD are a heterogeneous phenomenon difficult to explain on the basis of a single pathophysiological mechanism.
引用
收藏
页码:117 / 124
页数:8
相关论文
共 29 条
[21]  
Mouradian MM, Heuser JJF, Baronti F, Fabbrini G, Juncos JL, Chase TN., Pathogenesis of dyskinesias in Parkinson's disease, Ann Neurol, 25, pp. 523-526, (1989)
[22]  
Boyce S, Rupniak NMJ, Steventon MJ, Iversen SD., Differential effects of D‐1 and D‐2 agonists in MPTP‐treated primates: functional implications for Parkinson's disease, Neurology, 40, pp. 927-933, (1990)
[23]  
Luquin MR, Herrero T, Tubia M, Obeso JA., Drugs with selective D‐1 or D‐2 receptor activity exhibit similar antiparkinsonian potency in the MPTP‐treated monkey, Neurology, 40, (1990)
[24]  
Penny JB, Young AB., Strital inhomogeneities and basal ganglia function, Movement Disorders, 1, pp. 3-15, (1986)
[25]  
Crossman AR., A hypothesis on the pathophysiological mechanisms that underlie levodopa or dopamine agonist induced dyskinesia in Parkinson's disease: implications for future strategies in treatment, Movement Disorders, 5, pp. 100-108, (1990)
[26]  
Crossman AR, Sambrook MA, Jackson A., Experimental hemichorea/hemibalismus in the monkey, Brain, 107, pp. 579-596, (1984)
[27]  
Crossman AR, Mitchell IJ, Sambrook MA, Jackson A., Chorea and myoclonus in the monkey induced by Gammaaminobutiric acid antagonist in the lentiform complex, Brain, 111, pp. 1211-1233, (1988)
[28]  
Mitchell IJ, Jackson A, Sambrook MA, Crossman AR., The role of the subthalamic nucleus in experimental chorea, Brain, 112, pp. 1533-1548, (1989)
[29]  
Quinn N, Chritchley P, Marsden CD., Young onset Parkinson's disease, Movement Disorders, 2, pp. 73-92, (1987)