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帕金森病中的肌张力障碍:临床和药理学特征

Dystonia in Parkinson's disease: clinical and pharmacological features.

作者信息

Poewe W H, Lees A J, Stern G M

机构信息

University Clinic for Neurology, Innsbruck, Austria.

出版信息

Ann Neurol. 1988 Jan;23(1):73-8. doi: 10.1002/ana.410230112.

Abstract

We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L-dopa. Dystonia was seen as an initial symptom in patients with both early- and late-onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L-dopa-induced dystonia was seen as an off-period, biphasic, or peak-dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off-period dystonia is genuinely induced by L-dopa and best relieved by antiparkinsonian agents.

摘要

我们研究了9例未经治疗的特发性帕金森病患者和56例接受左旋多巴持续治疗患者的肌张力障碍特征。肌张力障碍在早发型和晚发型帕金森病患者中均可见为初始症状,包括肢体动作性肌张力障碍和颅肌张力障碍。虽然帕金森综合征和肌张力障碍并存提示存在共同的病理生理学,但抗帕金森病药物对肌张力障碍性痉挛的影响并不一致。左旋多巴诱发的肌张力障碍表现为关期、双相或峰剂量现象。每种类型都显示出肌张力障碍性痉挛的独特定位模式,这可能反映了基底节躯体定位的神经化学方面。对12例患者进行的神经药理学研究表明,关期肌张力障碍确实由左旋多巴诱发,抗帕金森病药物能最好地缓解。

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