A clinical trial of dextromethorphan in amyotrophic lateral sclerosis

Introduction ‐ Although the cause of amyotrophic lateral sclerosis (ALS) is unknown, excitotoxicity mediated by glutamate has been implicated. Dextromethorphan is a NMDA‐glutamate receptor antagonist with neuroprotective properties. Material and methods ‐ The effect of treatment with dextromethorpha...

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Published inActa neurologica Scandinavica Vol. 96; no. 1; pp. 8 - 13
Main Authors Gredal, O., Werdelin, L., Bak, S., Christensen, P. B., Boysen, G., Kristensen, M. Ø., Jespersen, J. H., Regeur, L., Hinge, H. H., Jensen, T. S.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.07.1997
Blackwell
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Summary:Introduction ‐ Although the cause of amyotrophic lateral sclerosis (ALS) is unknown, excitotoxicity mediated by glutamate has been implicated. Dextromethorphan is a NMDA‐glutamate receptor antagonist with neuroprotective properties. Material and methods ‐ The effect of treatment with dextromethorphan (150 mg daily) in ALS patients was evaluated in a randomized, double‐blind, placebo‐controlled study. Forty‐five patients were included in the analysis. Results ‐ At the end of the treatment period, 12 months after randomization, 15 patients (65%) in the placebo group and 12 patients (55%) in the dextromethorphan group were still alive (log rank test, P=0.49). Rates of disease progression, as expressed by rates of decline in pulmonary function and in functional disability, were similar in both groups except for a significantly less pronounced rate of decline in the ability scores for the lower extremities in the dextromethorphan group. Conclusion ‐ Treatment with a relatively low dose of dextromethorphan did not result in an improvement in 12‐month survival in ALS.
Bibliography:istex:892BDB29EB5929C76BED7EE21C363F9F8ADB7F4C
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ISSN:0001-6314
1600-0404
DOI:10.1111/j.1600-0404.1997.tb00231.x