Alcoholic polyneuropathy pain

According to modern data, alcoholic polyneuropathy is detected in 49-76% of people suffering from alcoholism (in half of these patients - at the subclinical level). The clinical picture is dominated by vegetative and sensory disorders (severe forms of the disease with paresis and paralysis are currently rarely observed). One of the most common manifestations of alcoholic polyneuropathy is pain syndrome in the legs. Spontaneous pain, dysesthesia, hyperalgesia and a burning sensation in the legs are noted by 70-80% of patients, and these symptoms are often the first manifestations of alcoholic polyneuropathy. Shooting, burning and aching pains are typical for the acute and subacute stages of the disease, while aching pains are predominantly typical for later stages. The intensity of the pain syndrome decreases as the disease progresses.

The pathogenesis of alcoholic polyneuropathy remains poorly understood. It is assumed that two main factors are involved: the toxic effect of ethanol and its metabolites and malnutrition with a deficiency of B vitamins (especially thiamine). Alcoholic polyneuropathy is a primary axonopathy, but as the disease progresses, segmental demyelination also develops. Pain in alcoholic polyneuropathy is caused by damage to thin sensitive A-sigma fibers, dysfunction of nociceptors, and the development of central sensitization. In addition, experimental studies confirm the presence of spontaneous ectopic activity in damaged nerve fibers, which leads to the formation of cross-ephaptic transmission of excitation.

Of utmost importance in the treatment of alcoholic polyneuropathy is the abstinence from alcohol and the administration of B vitamins (thiamine, pyridoxine, cyanocobalamin). Benfotiamine, compared to thiamine, has better resorption, significantly greater permeability through the cell membrane and a longer half-life. These features are of great clinical importance, since due to them, benfotiamine in moderate doses has a significantly greater therapeutic effect than thiamine in high doses. Benfotiamine is prescribed at 150 mg 2-3 times a day for 2 weeks, then 150 mg 1-2 times a day for 6-12 weeks. Antioxidants (thioctic acid) are also used in the pathogenetic therapy of alcoholic polyneuropathy.

There are no controlled randomized trials of symptomatic therapy for pain in alcoholic polyneuropathy. Clinical experience indicates a certain effectiveness of amitriptyline and carbamazepine. Taking into account the data on the increase in protein kinase C activity and glutamatergic mediation in alcoholic polyneuropathy, protein kinase C inhibitors and NMDA receptor antagonists are promising.

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