Alcoholic Paralysis Health Article

Diagnosis

The diagnosis of alcoholic paralysis depends largely upon the practitioner taking a thorough history and finding characteristic symptoms in patients who abuse alcohol. Other possible causes should be excluded by the appropriate tests, which may include blood chemistry, thyroid function tests, brain MRI or computed tomography (CT) scan, and/or cerebrospinal fluid analysis.

Acute alcoholic myopathy can be diagnosed by finding myoglobin in the urine and increased creatine kinase and other blood enzymes released from injured muscle. The surgical removal of a small piece of muscle for microscopic analysis (muscle biopsy) shows the scattered breakdown and repair of muscle fibers. Doctors must rule out other acquired causes of muscle breakdown, which include the abuse of drugs such as heroin, cocaine, or amphetamines; trauma with crush injury; the depletion of phosphate or potassium; or an underlying defect in the metabolism of carbohydrates or lipids. In chronic alcoholic myopathy, serum creatine kinase often is normal, and muscle biopsy shows atrophy, or loss of muscle fibers. Electromyography (EMG) may show features characteristic of alcoholic myopathy or neuropathy.

Treatment

Acute management of alcohol intoxication, delirium tremens, and withdrawal is primarily supportive, to monitor and treat any cardiovascular or respiratory failure that may develop. In delirium tremens, fever and sweating may necessitate treatment of fluid loss and secondary low blood pressure. Agitation may be treated with benzodiazepines such as chlordiazepoxide, beta-adrenergic antagonists such as atenolol, or alpha 2-adrenergic agonists such as clonidine. Because Wernicke's syndrome is rapidly reversible with thiamine, and because death may intervene if thiamine is not given promptly, all patients admitted for acute complications of alcohol, as well as all patients with unexplained encephalopathy, should be given intravenous thiamine.

Withdrawal seizures typically resolve without specific anti-epileptic drug treatment, although status epilepticus (continual seizures occurring without interruption) should be treated vigorously with injections of phenytoin (Dilantin), diazepam (Valium), or phenobarbital. Acute alcoholic myopathy with myoglobinuria requires monitoring and maintenance of kidney function, and correction of imbalances in blood chemistry including potassium, phosphate, and magnesium levels.

Chronic alcoholic myopathy and other chronic conditions are treated by correcting associated nutritional deficiencies and maintaining a diet adequate in protein and carbohydrate. The key to treating any alcohol-related disease is helping the patient overcome alcohol addiction. Behavioral measures and social supports may be needed in patients who develop broad problems in their thinking abilities (dementia) or remain in a state of confusion and disorientation (delirium). People with walking disturbances may benefit from physical therapy and assistive devices. Doctors may also prescribe drugs to treat the pain associated with peripheral neuropathy.

Prognosis

Complete recovery from Wernicke's syndrome may follow prompt administration of thiamine. However, repeated episodes of encephalopathy or prolonged alcohol abuse may cause persistent dementia or Korsakoff psychosis. Most patients recover fully from acute alcoholic myopathy within days to weeks, but severe cases may be fatal due to acute kidney failure or disturbances in heart rhythm secondary to increased potassium levels. Recovery from chronic alcoholic myopathy may occur over weeks to months of abstinence from alcohol and correction of malnutrition. Cerebellar degeneration and alcoholic neuropathy may also improve to some extent with abstinence and balanced diet, depending on the severity and duration of the condition.

Prevention

Prevention requires abstinence from alcohol. Persons who consume small or moderate amounts of alcohol might theoretically help prevent nutritional complications of alcohol use with dietary supplements including B vitamins. Historically, it is known that the incidence of neurological damage to people afflicted with alcoholism was even greater before bakeries began to enrich bread with vitamins and minerals. However, proper nutrition cannot protect against the direct toxic effect of alcohol or of its breakdown products. Patients with any alcohol-related symptoms or conditions, pregnant women, and patients with liver or neurologic disease should abstain completely. Based upon several recent studies, persons with family history of alcoholism or alcohol-related conditions may be considered at increased risk for both alcoholism and the neurologic complications of alcohol use.