Abstract

Non-dystrophic myotonic syndromes (NDM) represent a heterogeneous group of inherited skeletal muscle disorders, clinically characterized by myotonia with onset in early childhood. NDM can be distinguished in chloride channel gene (CLCN1) mutations (recessive and dominant myotonia congenita) and sodium channel gene (SCN4A) mutations (paramyotonia congenita, sodium channel myotonia and hyperkalaemic periodic paralysis). Today, treatment for NDM consist of sodium channel blockers, however potential cardiac interactions are reported.

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