Alcoholic myopathies

Alcoholic myopathies are common and are more frequently observed in men due to a higher incidence of alcohol consumption among males. However, women are at risk of developing these myopathies at half the alcohol dosage compared to men, due to a less efficient alcohol metabolism in females.

Pathophysiology

The mechanisms behind these myopathies are not yet fully understood.

Generally, it is believed that there is a direct toxicity of alcohol and its metabolites on mitochondrial function, electrolyte disturbances, oxidative stress, and rhabdomyolysis (due to alcohol-induced seizures or limb compressions during stupor episodes).

Acute myopathy episodes frequently involve triggering factors such as seizures, hypokalemia, food deprivation, delirium tremens, prolonged limb compression, or an intercurrent infection, among others.

Histologically, chronic myopathies are characterized by predominant atrophy of type IIb muscle fibers (fast-twitch fibers). In acute myopathies, areas of necrosis (sometimes with an inflammatory component) and regeneration are observed, with predominant atrophy of type I fibers (slow-twitch fibers).

Although various deficiencies have long been suspected, it has been shown that the occurrence of alcoholic myopathies is not related to a state of malnutrition.

It should be noted that alcoholic cardiomyopathies discussed here constitute a different entity from Beriberi cardiomyopathies (usually caused by vitamin B1 deficiency), which occur in malnourished alcoholic patients.

Clinical Presentation

Several clinical forms are distinguished, often overlapping:

• Cardiomyopathies:
  • Chronic: Typically manifest as slowly progressing dilated cardiomyopathies with chronic heart failure.
  • Acute: May occur as an acute decompensation of chronic heart failure or appear abruptly in an acute manner.

• Skeletal Myopathies:
  • Subacute or Chronic:
    • Often asymptomatic or with few symptoms, presenting as weakness in the shoulder and hip girdles, sometimes with atrophy, and non-painful muscles.
    • Affects 50% to 60% of alcoholics.
  • Acute:
    • Severe weakness and painful edema of muscles.
    • May coexist with involvement of swallowing muscles (dysphagia, which significantly increases mortality).
    • Risk of renal failure (role of myoglobinuria?) and severe electrolyte disturbances.
    • Generally reversible within a few days to a few months if alcohol abstinence is maintained.

The distinction between these forms is theoretical. The coexistence of cardiomyopathies and skeletal myopathies is common. Acute episodes usually occur in the context of pre-existing chronic myopathy. Chronic forms are much more frequent than acute forms.

Additionally, they generally coexist with other complications of alcoholism.

Additional Tests

The diagnosis is usually evident based on clinical presentation, and additional tests are of limited value except to exclude differential diagnoses or detect complications. Biological tests may show elevated CK, CK-MB, and myoglobinuria in acute myopathies. In chronic forms, CK elevation is inconsistent, and myoglobinuria is absent.

Echocardiography is essential to assess any potential cardiac involvement.

Management

There is no specific treatment.

• Symptomatic management and treatment of complications (special attention to electrolyte disturbances and renal failure in acute myopathies, management of heart failure, swallowing disorders, etc.).
• Systematic vitamin supplementation (high doses IV in acute myopathies).
• Alcohol abstinence.

With early intervention, total or partial recovery is the rule in acute forms for survivors.

In chronic forms, abstinence is rarely achieved. However, if abstinence is maintained, symptoms often improve, although less dramatically than in acute forms.

Bibliography

Charness ME, Overview of the chronic neurologic complications of alcohol, Uptodate, 2024

EMC, Neurologie, Elsevier, 2018

Goetz CG, Textbook of Clinical Neurology, 3th ed., Saunders, 2007

Rafie IM et al., Alcohol-induced cardiomyopathy, Uptodate, 2024