1 like discharges may be seen in patients with paramyotonia congenita.

2 activation, might be a contributing cause of paramyotonia congenita.

3 d sodium channel deactivation contributes to paramyotonia congenita.

4  including the human cold-sensitive disorder paramyotonia congenita.

5 utation exhibited symptoms characteristic of paramyotonia congenita--a condition usually thought to b

6 nvolvement in other muscle disorders such as paramyotonia congenita and hyperkalemic periodic paralys

7 II decrements of >20% were 100% specific for paramyotonia congenita and myotonia congenita, respectiv

8 ndings have implications for drug therapy of paramyotonia congenita, and also provide an insight into

9 g hyperkalemic periodic paralysis (HyperPP), paramyotonia congenita, and potassium-aggravated myotoni

10            Hyperkalaemic periodic paralysis, paramyotonia congenita, and potassium-aggravated myotoni

11 milies with hyperkalemic periodic paralysis, paramyotonia congenita, and the potassium-aggravated myo

12 function could well explain the onset of the paramyotonia congenita in this family and emphasize the

13                                              Paramyotonia congenita is a temperature-sensitive skelet

14                                              Paramyotonia congenita (PC) is a human hereditary diseas

15                                              Paramyotonia congenita (PC) is a human hereditary disord

16  a new genetic mutation in a family with the paramyotonia congenita phenotype.

17 peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skele

18 thmias but is also found to be effective for paramyotonia congenita, potassium-aggravated myotonia, l

19  mutations found in patients with hereditary paramyotonia congenita (T1313M on the III-IV linker and