Autoimmune
Multiple sclerosis (neurologic pain interpreted as muscular)
Myositis
Mixed connective tissue disease
Lupus erythematosus
Fibromyalgia syndrome
Familial Mediterranean fever
Polyarteritis nodosa
Devics disease
Morphea
Sarcoidosis

Metabolic defect
Carnitine palmitoyltransferase II deficiency
Conns syndrome
Adrenal insufficiency
Hyperthyroidism
Hypothyroidism
Diabetes
Hypogonadism
Postorgasmic illness syndrome

Other
Chronic fatigue syndrome (aka myalgic encephalomyelitis)
Channelopathy
Ehlers Danlos Syndrome
Stickler Syndrome
Hypokalemia
Hypotonia
Exercise intolerance
Mastocytosis
Peripheral neuropathy
Eosinophilia myalgia syndrome
Barcoo Fever
Herpes
Hemochromatosis
Delayed onset muscle soreness
HIV/AIDS
Generalized anxiety disorder
Tumor-induced osteomalacia
Hypovitaminosis D
Infarction

Withdrawal syndrome from certain drugs
Sudden cessation of high-dose corticosteroids, opioids, barbiturates, benzodiazepines, caffeine, or alcohol can induce myalgia. Treatment
When the cause of myalgia is unknown, it should be treated symptomatically. Common treatments include heat, rest, paracetamol, NSAIDs, massage, cryotherapy and muscle relaxants. See also
Arthralgia
Myopathy
Myositis

References


== External links ==
The uncontrolled wave of calcium can be forced out through the cell membrane via the sodium-calcium exchanger, causing an electric current known as a delayed afterdepolarisation. Afterdepolarisations, if large enough, can trigger additional action potentials, premature ventricular contractions, or sustained arrhythmias. Causes
CPVT can be caused by mutations in several genes, all of which are responsible for regulating the concentrations of calcium within cardiac muscle cells. The most commonly identified genetic mutation in CPVT is a mutation in the RYR2 gene that encodes the cardiac ryanodine receptor, responsible for releasing calcium from the sarcoplasmic reticulum. Mutations associated with CPVT have also been identified in the CASQ2 gene which encodes calsequestrin, a protein that binds calcium within the sarcoplasmic reticulum. Other genes associated with rarer, atypical forms of CPVT include TECRL encoding Trans-2,3-enoyl-CoA reductase-like protein, CALM1, CALM2 and CALM3 all encoding Calmodulin, and TRDN encoding Triadin. CPVT1: RYR2 mutations
The most commonly identified genetic mutations in those with CPVT occur in the RYR2 gene which encodes the cardiac ryanodine receptor. Mutations in this gene lead to an autosomal dominant form of typical CPVT known as CPVT1. While the precise effect differs between specific mutations in this gene, many RYR2 mutations cause the ryanodine receptor to open in response to lower concentrations of calcium—the threshold for calcium release is lower. As a result, the sarcoplasmic reticulum spontaneously releases calcium through these abnormal ryanodine receptors when the concentration of calcium within the sarcoplasmic reticulum rises, a process known as store-overload induced calcium release.