Non-dystrophic myotonias are a heterogeneous set of skeletal, muscular channelopathies, which have been associated with specific point mutations within sodium channel α-subunit (SCN4A) or Cl–channel (CLCN1) genes.1,2 The prevalence of non-dystrophic myotonia has been estimated to be ~1 in 100,000 in the worldwide.   3  Voltage-gated sodium channels are prominent transmembrane proteins in excitable tissues and are responsible for the rising phase of the action potential in the membranes of neurons and most electronically excitable cells.1,4. This evidence concerns the gene SCN4A and Myotonia.