However, four main clinical phenotypes have been traditionally described in patients mutated in SCN4A based on myotonia and paralysis features, including sodium-channel myotonia (SCM) and paramyotonia congenita (PMC) considered as non-dystrophic myotonias (NDM) and characterized by increased skeletal muscle excitability, and Hypokalemic type II (HypoPP2) and Hyperkalemic/Normokalemic PP (HyperPP/NormoPP), instead associated with reduced excitability. Here, SCN4A is linked to paramyotonia congenita of Von Eulenburg.