Alcoholic neuropathy is difficult to separate from nutritional, specifically thiamine-deficient, neuropathy. '92! The
clinical pattern and pathology of axonal degeneration is virtually identical to beriberi. The incidence ranges from 9 to 30 percent among hospitalized alcoholics, y , y and up to 93 percent of ambulatory alcoholics may have electrophysiological evidence of neuropathy. y Victor and associates found signs of polyneuropathy in 82 percent of 230 patients with WKS, '8 and 84 percent of patients, who were able to give a dietary history, reported at least a 20-pound weight loss in the previous year. Alcoholic neuropathy occurs in those patients consuming at least 100 g of alcohol daily for several years. It is potentiated by nutritional deficiency. Men outnumber women, but women may be more susceptible at lower doses than men.y Although it is not known how alcohol injures peripheral nerves, theories include altered membrane lipid permeability'^ and oxidation injury from free radical formation. y How nutritional deficiency may potentiate the toxicity of alcohol awaits further study.
Attempts to control for the influences of alcohol and nutrition have yielded conflicting results. Alcoholics with neuropathy were allowed to continue drinking while receiving a nutritious diet with vitamin supplementation, and all noted improvement in symptoms. y Hallet and co-workers were unable to produce neuropathy in monkeys after 3 to 5 years of a high alcohol diet. '100' However, Behse and Buchthal reported 37 cases of alcoholic neuropathy in patients drinking about 3 L of thiamine and pyridoxine-fortified beer daily, the equivalent of 100 ml of ethanol. y Fourteen of 37 (37 percent) had marked weight loss. All patients had normal serum vitamin levels, except for one with thiamine deficiency and three with folate deficiency. The pattern and severity of the neuropathy did not differ between those with and without adequate nutrition. Similarly, Monforte and colleagues found no relationship between the nutritional status and the incidence of autonomic and peripheral neuropathies in alcoholics.'™! Pathologically, the peripheral nerve undergoes axonal degeneration with loss of large and small myelinated fibers in autonomic, '102' sensory, and motor nerves.y
The neuropathy is often asymptomatic until it is pointed out to the patient. The symptoms begin with paresthesias and burning feet, and later, painful calves, numbness, cramps, weakness, and sensory ataxia may develop. On examination, patients may have sensory loss (vibratory and deep sensation) in the distal legs, motor weakness, areflexia, calf tenderness, and orthostatic hypotension. W The skin of the legs becomes shiny, swollen, and subject to trauma and ulceration. Neuropathic joint degeneration may occur with bony resorption and deep tissue infection. y Other neurological processes including beriberi, inflammation, or metabolic disturbances should be ruled out. Blood studies and neurophysiological studies are useful in evaluating these patients and establishing the diagnosis.
These individuals are best managed by recommending abstinence from alcohol intake and enhancing their diet with vitamin supplements. Supplemental thiamine and pain control may be warranted in selected individuals. The prognosis depends on the severity and duration of symptoms. Behse and Buchthal found no evidence of clinical improvement or regeneration on nerve biopsy in 17 patients studied 2 years later. y The earlier patients abstain and establish regular diets, the more likely they are to recover from the neuropathy. Alcoholics with autonomic neuropathy have a reduced life expectancy. [1p3]
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