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Pain in alcoholic polyneuropathy
Last reviewed: 23.04.2024
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According to modern data, alcoholic polyneuropathy is detected in 49-76% of persons suffering from alcoholism (half of these patients - at a subclinical level). The clinical picture is dominated by vegetative and sensory disorders (severe forms of the disease with paresis and paralysis are rarely observed at present). One of the most frequent manifestations of alcoholic polyneuropathy is pain in the legs. Spontaneous pain, dysesthesia, hyperalgesia and burning sensation in the legs are noted by 70-80% of patients, and these symptoms are often the first manifestations of alcoholic polyneuropathy. Acute and subacute stages of the disease are typical shooting, burning and aching pains, for later stages - mostly aching. The intensity of the pain syndrome decreases as the disease progresses.
The pathogenesis of alcoholic polyneuropathy remains poorly understood. Assume the participation of 2 main factors: the toxic effects of ethanol and its metabolites and malnutrition with a deficiency of B vitamins (especially thiamine). Alcoholic polyneuropathy refers to primary axonopathies, but as the disease progresses, segmental demyelination also develops. Pain in alcoholic polyneuropathy is caused by the defeat of thin sensitive A-sigma fibers, a violation of the function 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 a crossed efaptic transmission of excitation.
The most important in the treatment of alcoholic polyneuropathy is the refusal to drink alcohol and the appointment of B vitamins (thiamine, pyridoxine, cyanocobalamin). Benfotiamine, in comparison with thiamine, has better resorption, significantly greater permeability through the cell membrane and a longer half-life. These features are of great clinical importance, because due to them, benfotiamine in moderate doses has a significantly greater therapeutic effect than thiamine in high doses. Benfotiamin appoint 150 mg 2-3 times a day for 2 weeks, then 150 mg 1-2 times a day for 6-12 weeks. In the pathogenetic therapy of alcoholic polyneuropathy antioxidants (thioctic acid) are also used.
There are no controlled randomized trials of symptomatic pain therapy for alcoholic polyneuropathy. Clinical experience indicates a certain effectiveness of amitriptyline and carbamazepine. Taking into account the data on the increase in activity of protein kinase C in alcoholic polyneuropathy and glutamatergic mediation, the inhibitors of protein kinase C and antagonists of NMDA receptors are promising.
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