Progression of symptoms is usually gradual, continuing over months or years [2, 4]. Electrophysiologic and pathologic findings mainly indicate axonal neuropathy with reduced nerve fibre densities. Densities of small myelinated fibres and unmyelinated fibres were more severely reduced than the density of large myelinated fibres, except in patients with a long history of neuropathic symptoms and marked axonal sprouting [2]. Subperineurial oedema is more prominent in thiamine deficient neuropathy, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier is more frequent in alcoholic neuropathy [3]. The neurotoxic effects of alcohol cause damage to the axon through demyelination of sensory and motor fibers, primarily from the presence of acetaldehyde.

It is important to supplement the diet with vitamins, including thiamine and folic acid. Your health care provider will perform a physical exam and ask alcoholic neuropathy recovery time about symptoms. Changes in muscle strength or sensation usually occur on both sides of the body and are more common in the legs than in the arms.

Natural history

Diabetic neuropathy typically occurs 10 to 20 years after you are diagnosed with diabetes. If you are a diabetic and do not have your blood sugar levels well-controlled, you have an increased risk for diabetic neuropathy. Dr. Mary Vo is an Assistant Professor of Neurology and Assistant Attending Neurologist at New York Presbyterian/Weill Cornell Medical College. She received her medical degree from SUNY Stony Brook School of Medicine in 2008 after graduating with honors from St. John’s University, where she earned her bachelor and doctoral degrees in Pharmacy. She completed internship, neurology residency and neurophysiology fellowship training at NewYork-Presbyterian/Weill Cornell Medical Center.

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• Medication can help in reducing some of the symptoms of alcoholic neuropathy.
• The main symptoms of ALN include dysesthesia, paresthesia, numbness, and pain in the lower extremities which progressively reach higher parts of the body [114,115,116,117].
• Dr. Raja is a board-certified internal medicine physician, certified by both the American Board of Internal Medicine and the American Society of Addiction Medicine.
• Obtaining a degree in Registered Nursing from Saddleback College, Mr. Collier has held a Registered Nursing License since the early1980’s.

Although benfotiamine therapy was superior to Milgamma-N or placebo for all parameters, results reached statistical significance only for motor function, paralysis and overall neuropathy score. The reason for better results in the benfotiamine alone group than in the Milgamma-N group, despite the fact that the benfotiamine dosage was equivalent, is not completely understood. The authors hypothesized that vitamins B6 and B12 might have competed with the effects of vitamin B1 in the Milgamma-N group [97]. In another small Russian study, 14 chronic alcoholic men with polyneuropathy were given 450 mg benfotiamine daily for 2 weeks, followed by 300 mg daily for an additional 4 weeks.

Symptoms

Alcohol abuse affects the peripheral and the central nervous system adversely. A common adverse effect of chronic alcohol consumption is alcohol neuropathy. We do not know precisely how many people are affected by alcohol neuropathy, but research has shown that at least 66% of chronic alcohol abusers may have some form of neuropathy. Neuropathy has multifactorial causes, ranging from nutritional deficiencies to the toxic effects that alcohol has on neurons. Because of the many effects that alcohol has on the organism, it is important that patients with alcoholic neuropathy be managed by a team of inter-professionals in the health industry.