Fortschr Neurol Psychiatr 2007; 75(7): 387-396
DOI: 10.1055/s-2006-944314
Übersicht
© Georg Thieme Verlag Stuttgart · New York

Dyskinesien bei Morbus Parkinson - Klinik, Ätiologie, Therapie

Dyskinesia in Parkinson's Disease - Major Clinical Features, Aetiology, TherapyG.  Ellrichmann1 , H.  Russ1 , T.  Müller1
  • 1Neurologische Klinik im St. Josef-Hospital, Ruhr Universität Bochum (Direktor: Professor Dr. R. Gold)
Further Information

Publication History

Publication Date:
17 November 2006 (online)

Zusammenfassung

Morbus Parkinson als langsam fortschreitende, neurodegenerative Erkrankung des Zentralnervensystems, die weltweit etwa 10 Millionen Menschen betrifft, wird zurzeit rein symptomatisch behandelt. Hierbei besteht das Ziel vorwiegend darin, den herabgesetzten Dopaminstoffwechsel in striatalen Neuronen auszugleichen. Eine chronische Einnahme dopaminerger Substanzen, wie z. B. Levodopa, verstärkt auf lange Sicht jedoch das Auftreten motorischer Komplikationen und Dyskinesien. Dyskinesien präsentieren sich am häufigsten als Chorea, Athetose, Dystonie, Stereotypie, Ballismus oder eine Kombination. Häufig basieren diese unwillkürlichen Bewegungen des Gesichts, des Rumpfes und der Extremitäten auf der Gesamtmenge der dopaminergen Substitution. Therapiestrategien basieren daher auf einer Reduktion der Gesamtdosis von Dopamin. Alternativ bzw. ergänzend eingesetzt werden Apomorphin, Amantadin oder Clozapin. Neuere Behandlungsmöglichkeiten entstehen durch Substanzen wie Sarizotan, Istradefylline, Fipampezol oder Talampanel. Trotzdem resultieren Beeinträchtigungen und reduzierte Lebensqualität der Patienten und deren Angehörigen. Diese Übersicht beschreibt die klinischen Hauptmerkmale sowie Ätiologie und Demografie therapieassoziierter Dyskinesien beim Morbus Parkinson.

Abstract

Parkinson's disease (PD), a slowly, progressive degenerative disorder of the central nervous system, which affects about ten million people world-wide, is currently treated symptomatically. Current treatment aim i. e. to balance the decreased dopamine turnover in striatal neurons. Chronic exposure to dopaminergic agents, however, supports onset of motor complications and dyskinesia in the long term. Dyskinesia appear mainly as chorea, athetosis, dystonia, stereotypia, ballism or a combination. Sometimes excessive abnormal facial, body and limb movements depend on the overall dosage of dopaminergic substitution. This is why the main therapy is based on reducing the total dosage of dopaminergic substances. Either alternative or additional well-tried substances like apomorphine, amantadine or clozapine are used. New possibilities in treatment emerge from substances like sarizotan, istradefylline, fipampezol or talampanel. Even so disability and reduced quality of life in PD patients and their caregivers may exist. This survey describes the major clinical features, aetiology and demographics of treatment-associated dyskinesia in PD.

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Gisa Ellrichmann

Neurologische Klinik St. Josef-Hospital, Bochum

Gudrunstraße 56

44791 Bochum

Email: gisa.ellrichmann@rub.de

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