In the case of myotonia congenita, the chloride channels that allow Cl− to move across the membrane towards its equilibrium potential are defective, thus K+ is the only ion determining the membrane potential, and as more and more K+ accumulates in the transverse tubular system with each subsequent action potential the fiber depolarizes until the membrane potential comes close enough to the action potential threshold for spontaneous activity to ensue
Spontaneous action potentials can arise for several seconds, leading to the delayed relaxation that is the hallmark of myotonia. Cessation of spontaneous activity is associated with sodium channel  inactivation (Nav1.4). Diagnosis
Types
Two types of myotonia congenita exist, an autosomal dominant form and an autosomal recessive form. Autosomal dominant myotonia congenita (OMIM #160800) is also called Thomsen disease, after Danish/German physician Asmus Julius Thomas Thomsen (1815–1896), who himself had the disease and who wrote the first description of it in the medical literature (in 1876). Autosomal recessive myotonia congenita (OMIM #255700) is also called generalized myotonia, recessive generalized myotonia (RGM), Becker disease, and Becker myotonia, after the German professor Peter Emil Becker, who discovered its recessive nature.The term congenital in its sense of "clinically apparent from birth" applies only to Thomsen disease, as the clinical onset of Becker myotonia may be delayed up to the age of 4 to 6 years.
Dry skin and atopic dermatitis may co-exist. The patches may become more apparent after sun exposure, when the normal surrounding skin is tanned. The role of ultraviolet radiation, bathing or not bathing, low serum copper and Malassezia yeasts is not clear. Diagnosis
Diagnosis is mainly done by clinical examination. Shining a Woods light over the skin may reveal further lesions not obviously visible otherwise. Differential diagnosis
Pityriasis versicolor and leprosy. Treatment
No treatment is required and the patches in time will settle. The redness, scale and itch if present may be managed with simple emollients and sometimes hydrocortisone, a weak steroid, is also used.As the patches of pityriasis alba do not darken normally in sunlight, effective sun protection helps minimise the discrepancy in colouration against the surrounding normal skin. Cosmetic camouflage may be required. Tacrolimus has been reported as speeding resolution.In exceptionally severe cases PUVA therapy may be considered. Prognosis
The patches of pityriasis alba may last from 1 month to about one year, but commonly on the face last a year. However it is possible that the white patches may last for more than 1 year on the face. Epidemiology
It occurs in mainly children and adolescents of all races, particularly people with dark skin. The worldwide prevalence is 5% in children, with boys and girls affected equally. adults can also have this disease.Up to a third of US school children may at some stage have this condition. Single-point prevalence studies from India have shown variable rates from 8.4%
to 31%.