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Alcoholic polyneuropathy
Last reviewed: 04.07.2025

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Alcoholic polyneuropathy is the most common neurological complication of chronic alcoholism, which develops in most people who have suffered from chronic alcoholism for a long time.
Clinical signs of alcoholic polyneuropathy were first described in the second half of the 18th century by Lettsom (1787).
Causes alcoholic polyneuropathy
The disease is primarily caused by axonal degeneration. The myelin sheath is affected to a lesser extent. Axonal degeneration is caused by the direct effect of toxic alcohol metabolites on the nerve fiber and a deficiency of B vitamins (primarily thiamine). The latter is caused by the patient's poor and monotonous diet, as well as impaired resorption of vitamin B due to gastroenteritis. In addition, other factors may also be involved, including genetic, autoimmune, age-related, etc.
Symptoms alcoholic polyneuropathy
Alcoholic polyneuropathy is a symmetrical sensorimotor neuropathy. The first signs may be moderate muscle wasting in the legs, decreased and lost Achilles and knee reflexes. Later, paresthesia, hyperesthesia with elements of hyperpathy, numbness, pain in the feet, painful spasms of the calf muscles join in. Some patients experience allodynia. Paresis of the extensors of the fingers and feet usually develops gradually. Weakness in the feet leads to changes in gait such as "steppage". Gradually, these symptoms spread to the proximal parts of the lower extremities, in severe cases - to the distal parts of the arms and lower parts of the body. The disease slowly progresses over many months and years.
Diagnostics alcoholic polyneuropathy
On examination, muscle wasting of the shins and feet is revealed, as well as decreased pain and temperature sensitivity in the distal parts of the extremities (like "gloves" and "socks"). Other types of sensory disorders are often found. Most patients have decreased or absent Achilles reflexes, half of the patients have weakened or absent knee reflexes, and less often - reflexes from the upper extremities. Pain is often detected during palpation of nerve trunks and muscles. Autonomic disorders are noted in the form of distal hyperhidrosis, trophic disorders of the skin and nails, edema and hyperpigmentation, and changes in skin color. Changes in pupillary reactions, orthostatic hypotension, urination disorders, impotence, and gastrointestinal dysfunction are possible.
Instrumental methods
In the subclinical course of alcoholic polyneuropathy, needle electroneuromyography is indicated. Histologically, signs of distal axonal degeneration and secondary myelinopathy are revealed.
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Treatment alcoholic polyneuropathy
It is recommended to give up alcohol, have a complete, balanced diet, administer thiamine in combination with other B vitamins, and drugs that improve microcirculation and have a metabolic effect. It is advisable to begin treatment of alcoholic polyneuropathy with parenteral administration of thiamine (2-4 ml of a 5% solution intramuscularly).
After improvement is achieved, switch to taking 100 mg 2-3 times a day. In case of concomitant liver damage, alpha-lipoic acid (espolipon) is prescribed parenterally (600 mg intravenously by drip daily or every other day 20 injections), and then orally 600 mg for 1-2 months. Physical exercises are recommended to prevent contractures and strengthen muscles.