Gregor K Wenning1. 1. Department of Neurology, Innsbruck Medical University, Austria. gregor.wenning@uibk.ac.at
Abstract
OBJECTIVE:Multiple-system atrophy (MSA) often presents as atypical parkinsonian syndrome with rapid progression and poor response to levodopa. Reports on the open-label use of amantadine in MSA suggest variable antiparkinsonian efficacy. The authors therefore conducted a double-blind, placebo-controlled crossover trial of amantadine in MSA patients. METHODS:Eight patients were enrolled in this study. They received either amantadine 200 mg twice daily or placebo for 3 weeks, followed by a 1-week washout and the alternate treatment of 3 weeks. Antiparkinsonian effects were evaluated using the Unified Parkinson's Disease Rating Scale part II (UPDRS-II, activities of daily living) and UPDRS-III (motor examination) before and at the end of each treatment phase. Timed tests were also performed according to the CAPIT protocol. RESULTS: There was a trend toward reduction of UPDRS-III scores during amantadine treatment (P = 0.058). Delta values of the treatment arm were higher than those of the placebo arm. However, this difference (-2.25 pt; 95% CI, -6.7-2.2) failed to reach significance. Reduction of UPDRS-III subscores for akinesia, rigidity, tremor, postural instability, and gait disorder failed to reach significance too. The hand-arm movement test revealed nonsignificant improvement in the amantadine arm. CONCLUSION: This study suggests that amantadine fails to provide clinically significant antiparkinsonian benefit to patients with MSA. The authors cannot exclude mild effects due to the limited sample size.
RCT Entities:
OBJECTIVE:Multiple-system atrophy (MSA) often presents as atypical parkinsonian syndrome with rapid progression and poor response to levodopa. Reports on the open-label use of amantadine in MSA suggest variable antiparkinsonian efficacy. The authors therefore conducted a double-blind, placebo-controlled crossover trial of amantadine in MSA patients. METHODS: Eight patients were enrolled in this study. They received either amantadine 200 mg twice daily or placebo for 3 weeks, followed by a 1-week washout and the alternate treatment of 3 weeks. Antiparkinsonian effects were evaluated using the Unified Parkinson's Disease Rating Scale part II (UPDRS-II, activities of daily living) and UPDRS-III (motor examination) before and at the end of each treatment phase. Timed tests were also performed according to the CAPIT protocol. RESULTS: There was a trend toward reduction of UPDRS-III scores during amantadine treatment (P = 0.058). Delta values of the treatment arm were higher than those of the placebo arm. However, this difference (-2.25 pt; 95% CI, -6.7-2.2) failed to reach significance. Reduction of UPDRS-III subscores for akinesia, rigidity, tremor, postural instability, and gait disorder failed to reach significance too. The hand-arm movement test revealed nonsignificant improvement in the amantadine arm. CONCLUSION: This study suggests that amantadine fails to provide clinically significant antiparkinsonian benefit to patients with MSA. The authors cannot exclude mild effects due to the limited sample size.
Authors: Phillip A Low; David Robertson; Sid Gilman; Horacio Kaufmann; Wolfgang Singer; Italo Biaggioni; Roy Freeman; Susan Perlman; Robert A Hauser; William Cheshire; Stephanie Lessig; Steven Vernino; Jay Mandrekar; William D Dupont; Thomas Chelimsky; Wendy R Galpern Journal: Lancet Neurol Date: 2014-02-05 Impact factor: 44.182