Alcoholic myopathy (AM) affects one-third to more than half of alcohol abusers. It is relieved by withdrawal from alcohol consumption and exacerbated by continued misuse. In acute stages, myopathy presents as rhabdomyolysis. Alcoholic myopathy usually refers to the chronic form and mainly affects the skeletal muscle.
Acute high dose intake of alcohol may lead to rhabdomyolysis. Most literature, when describing alcoholic myopathy (AM) suggests the chronic condition, that is precipitated by chronic alcohol abuse and is characterized by varying degrees of muscle weakness and atrophy, prominent in proximal muscle groups. It is a common cause of myopathy .
AM is progressive, and its severity is determined by the amount of alcohol consumed, as well as the duration of abuse  . Furthermore, those who suffer from liver cirrhosis are more prone to the ailment . In Western countries, it is thought to be the most widely encountered type of myopathy  . Although abstinence is advised, some muscle dysfunction is permanent, thus the theory that there are multiple factors at play in the pathogenesis, such as nutrient deficiency, particularly vitamin B    is also suggested. The presence of the latter makes the clinical picture more obscure and impedes the treatment.
Acute myopathy may result in death due to renal failure and electrolyte imbalance. Rhabdomyolysis may be seen in more severe cases, while milder cases may witness a rise in creatinine kinase. Necrosis of muscle tissue, as well as weakness and pain, are also recognized.
Chronic AM has a more insidious onset, symptoms include gait disturbances, muscle weakness, and wasting. Recovery is slower than in the acute form. Muscle pain may or may not be present, moreover, neuropathy can occur simultaneously but should be treated as a separate medical entity.
Diagnosis is made by combining the clinical picture, histological and laboratory findings. Muscle atrophy as a result of impaired synthesis as well as apoptosis may be evaluated microscopically, and type II fibers are most affected  . Type I muscle fibers are usually normal .
In high magnification studies, acute alcohol intake also produces histological evidence of cell injury where damage to cell organelles such as the mitochondria, sarcoplasmic reticulum is visualized, together with the failure of fat and glycogen storage regulatory mechanisms and cell edema. The histological picture is similar to that of alcoholic liver disease . Further tests, conducted routinely when presented with a patient suffering from a myopathy, include: