Martin Skov

The anti-convulsants lacosamide, lamotrigine and rufinamide reduce myotonia in isolated human and rat skeletal muscle

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INTRODUCTION: In myotonia congenita, loss of ClC-1 Cl(-) -channel function results in skeletal muscle hyperexcitability and myotonia. Anti-myotonic treatment has typically targeted the voltage gated sodium channel in skeletal muscle (Nav1.4). This study explored whether 3 sodium channel modulating anti-epileptics can reduce myotonia in isolated rat and human muscle.

METHODS: Dissected muscles were rendered myotonic by ClC-1 channel inhibition. The ability of the drugs to suppress myotonia was then assessed from sub-clinical to maximal clinical concentrations. Drug synergy was determined using isobole plots.

RESULTS: All drugs were capable of abolishing myotonia in both rat and human muscles. Lamotrigine and rufinamide completely suppressed myotonia at sub-maximal clinical concentrations, while lacosamide had to be raised above the maximal clinical concentration to completely suppress myotonia. A synergistic effect of lamotrigine and rufinamide was observed.

CONCLUSION: These findings suggest that lamotrigine and rufinamide could be considered for anti-myotonic treatment in myotonia congenita. This article is protected by copyright. All rights reserved.

Original languageEnglish
JournalMuscle & Nerve
Pages (from-to)136-142
Publication statusPublished - Jul 2017

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