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Since the time amyotrophic lateral sclerosis (ALS) claimed Lou Gehrig’s life, there has been remarkable progress in preclinical research suggesting that the pathogenesis of ALS involves free radical toxicity, mitochondrial dysfunction, glutamate excitotoxicity, intermediate filament aggregation, and apoptotic pathways. However, this basic science progress has yet to be translated into practical clinical applications. A decade since it was introduced,1 riluzole remains the only Food and Drug Administration (FDA)–approved medication for ALS. Although survival was the outcome measure in the riluzole trials, its use is problematic because it requires a large sample size and relatively long study duration. In search of a surrogate, ALS researchers have turned to alternative outcome measures such as the slope of muscle strength decline, which was used in the trial of topiramate reported by Cudkowicz et al. in this issue of Neurology.2
The 296 study participants received up to 800 mg daily of topiramate or placebo for 12 months. Whereas …
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