Alcohol-related peripheral neuropathy: a systematic review and meta-analysis Journal of Neurology

Pain seems consistent in the literature as 1 of the most common complaints and can what causes alcoholic neuropathy be the first clinical indication of the disease. Keeping this disease process high on the differential with the right history is essential. Progression of the disease leads to symmetrical ascending motor and sensory deficits.

• According to many studies, alcohol-induced autonomic neuropathy (AAN) not only leads to potential damage to internal organs but also increases the mortality rate of patients 157, 158.
• In a 2019 article, researchers explain that breaking down alcohol in the body produces a chemical that damages axons.
• Talk with your doctor before consuming alcohol if you have any diagnosis of peripheral neuropathy.
• Protein kinase C (PKC) is a family of protein kinases consisting of approximately 10 isozymes.
• Other coexisting, alcohol-related diseases may induce exacerbation of AAN symptoms.
• In addition, patients with chronic alcoholism tend to consume smaller amounts of essential nutrients and vitamins and/or exhibit impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol.

Conditions That May Mimic Alcoholic Neuropathy

Damage to the nerves leads to unusual sensations in the limbs, reduced mobility, and loss of some bodily functions. Alcoholic neuropathy is nerve damage caused by the toxic effect of alcohol on nerves. The primary risk factor for alcoholic neuropathy is chronic consumption of large amounts of alcohol.

• The pain is described as burning, cramp-like, or itching; also, a common symptom is a subjective feeling of cold in both feet 118,119,120,121,122,123.
• Nerve damage from chronic alcohol consumption can develop over several years.
• Alcohol withdrawal syndrome occurs when someone who has been drinking excessive amounts of alcohol for an extended period of time suddenly stops drinking or reduces their intake.
• Heidi Moawad is a neurologist and expert in the field of brain health and neurological disorders.
• Naik et al. 38 suggested the involvement of oxidative stress in experimentally induced chronic constriction injury of the sciatic nerve model in rats.
• The damage from alcohol neuropathy can affect the nerves that control movement, senses, and organ function.
• Rats with experimentally-induced diabetes for 2 months had a 20% reduction in nerve conduction velocity and 48% reduction in endoneurial blood flow.

Data availability

Regular monitoring and an adherence to treatment plans can speed up recovery times and ensure a better quality of life. The psychological impact of chronic conditions such as alcoholic neuropathy should not be underestimated. Counseling or therapy can help us cope with the emotional and mental challenges of a lengthy recovery process. Alcohol misuse can lead to neurological damage that can affect multiple areas of a person’s health and well-being. The best way to avoid the issue is to limit alcoholic consumption to 2 or fewer drinks per day for males and 1 or fewer for females. But delirium tremens is a medical emergency and requires a hospital stay.

Diagnosis of Alcohol-Related Peripheral Neuropathy

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Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status 5. Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol 6, 13. The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. Some other studies have indicated that chronic alcohol intake can decrease the nociceptive threshold with increased oxidative-nitrosative stress and release of pro-inflammatory cytokines coupled with activation of protein kinase C (Figure 1) 10, 16. Therefore, alcoholic neuropathy may occur by a combination of the direct toxic effects of ethanol or its metabolites and nutritional deficiencies, including thiamine deficiency.