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Alcoholic Neuropathy

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Last Update: December 30, 2022.

Continuing Education Activity

Alcoholic neuropathy is one of the most common adverse effects of chronic alcohol consumption. There is damage to the nerves due to the direct toxic effect of alcohol and the malnutrition induced by it. Patients present with pain, ataxia and parasthesias in the lower extremities. This activity describes the evaluation and management of alcoholic neuropathy and reviews the role of the interprofessional team in improving care for patients with this condition.


  • Identify the etiology of alcoholic neuropathy.
  • Describe the use of the CAGE questionaire in the history of alcoholic neuropathy.
  • Summarize the differential diagnoses in alcoholic neuropathy.
  • Explain the importance of improving care coordination among the interprofessional team members to correctly diagnose and counsel patients on their drinking habits for improved outcomes in patients affected by alcoholic neuropathy.
Access free multiple choice questions on this topic.


Chronic alcohol consumption can have deleterious effects on the central and peripheral nervous systems. One of the most common adverse effects seen in patients with chronic alcohol use disorder is alcohol neuropathy. This commonly presents with pain, paresthesias, and ataxia in the distal lower extremities. The exact number of people affected by this condition is not known, but studies have shown that up to 66% of patients with chronic alcohol use disorder may have some form of the disease. The cause is multifactorial, from both nutritional deficiencies and alcohol metabolism's direct toxic effects on neurons. History and physical exam can help to differential this condition from other forms of neuropathy. No specific lab test is available for diagnosis. Treatment should be focused on alcohol sobriety and replacement of key nutrients.[1][2][3]


The long-term, negative outcomes from alcohol consumption have been well-studied and identified, but the specific causes for these outcomes are not well understood. Multiple components are responsible for the development of alcoholic neuropathy. The duration of alcohol abuse and the lifetime quantity of alcohol consumed are two key elements when studied among patients with chronic alcohol use disorder. One study suggested that a quantity more than 100 g/day over a number of years was likely to cause peripheral neuropathy.[4][5][6][7]


Alcohol is one of the most commonly used substances in the world. Among patients with chronic alcohol use disorder, neuropathy is the most common harmful sequelae. It is estimated that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy; however, the true incidence in the general population is unknown. The majority of patients were middle-class, working men and continuous drinkers were more affected than episodic drinkers. Parental family history is a risk factor for developing this condition. Women are more likely to develop alcohol polyneuropathy and suffer from a more rapid onset and greater severity.


Alcohol causes neuropathy via multifactorial processes, many of which are still under investigation. Alcohol enters the bloodstream from the digestive system within 5 minutes of consumption, and peak absorption is seen within 30 to 90 minutes. One of the many inhibitory effects of chronic alcohol use is malnutrition. Patients who abuse alcohol tend to consume fewer calories and have poor absorption of nutrients in the gastrointestinal tract. There are also direct toxic effects of alcohol and its metabolites on neurons affecting cellular cytoskeletons and demyelination of neurons.

One of the key nutrients inhibited by alcohol is thiamine, vitamin-B1. Thiamine serves as an important coenzyme in carbohydrate metabolism and neuron development. The lack of thiamine in the nervous system affects the cellular structure and can cause cell membrane damage and irregular ectopic cells. Other vitamin deficiencies seen with alcohol abuse include, but are not limited to, B-vitamins, folic acid, and vitamin-E. Poor absorption and low intake of these vitamins have clinical features of dermatitis, neuropathy, and anorexia.

Other studies have shown a direct, negative effect from alcohol and its many metabolites on the nervous system. Axonal degeneration and demyelination of neurons were seen in both humans and lab mice receiving alcohol. The cause is a diverse multifactorial process caused from damage by free radicals, the release of inflammatory markers, and oxidative stress.

History and Physical

A thorough history and physical is key when evaluating patients with alcohol use disorder. Screening patients for alcohol abuse and alcohol consumption is very important. Many patients may not mention alcohol consumption when interviewed and may present with neuropathy complaints only. Additional nutritional and diet questions should be investigated. The National Institute on Alcohol Abuse and Alcoholism recommends using the CAGE questionnaire to help identify a patient's potential problem with alcohol. CAGE questions include: 

  • Have you ever felt you should Cut Down on your drinking? 
  • Have people Annoyed you by criticizing your drinking? 
  • Have you ever felt bad or Guilty about your drinking? 
  • Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover (Eye opener)?

The two most important questions to ask when evaluating for alcohol neuropathy: (1) How much alcohol do you drink? and (2) What is the length of the abuse? These questions can help differential alcohol neuropathy from other forms of neuropathy. Screening for other disease processes that may cause neuropathy, such as diabetes, is also important. 

Most patients with alcohol neuropathy initially present with symmetrical polyneuropathies in the lower distal extremities, however; heavier abuse can progress to distal upper extremity symptoms. The most common findings are sensory related and are varied to include pain, numbness, and paresthesias. Pain seems to be consistent through the literature to be one of the most common complaints and can 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.

A complete neurological exam is imperative. Physical exam findings include diminished sensation to vibration, pain, dysfunctional thermo-proprioception, weakness in the ankle and toes with flexion and extension, atrophy of foot muscles, gait ataxia, and diminished deep tendon reflexes.


No specific tests diagnose this condition. History and physical are key to making the diagnosis. Some studies that may help rule in or out this condition include:

  • Chemistry Panel - Assess electrolytes which can cause peripheral neuropathies.
  • Diabetes Testing - Diabetic neuropathy can have a similar presentation.
  • Thiamine, Folate, and Vitamin-B12 Testing - Key nutrients in neuronal formation in both peripheral and central nervous systems.
  • Heavy Metal Toxicities - Can commonly cause neuropathy in the extremities. 
  • HIV and Syphilis - Both diseases can have neuropathy in advanced presentations. 
  • Nerve Conduction Tests - Nerve conduction velocities are generally normal or mildly slow in early presentations and slowed in demyelinating conditions.
  • Needle Electromyography (EMG) - Commonly seen with alcohol neuropathy and include positive sharp waves and/or fibrillation potentials and complex repetitive discharges.

Treatment / Management

Treatment should be focused on therapy to stop alcohol abuse. The overall prognosis is favorable. Abstinence for several months up to a few years have shown both clinical examination and electroneurographic improvements, with most patients showing complete regain of function. Additional treatment includes replacing nutrients such as thiamine, vitamin-B12, and folic acid. Psychiatry referral, alcohol abstinence abuse programs, and support groups have shown favorable ways to help patients recover from alcohol use disorder. Physical therapy and occupational therapy can play a role in supporting the patient as they regain movement and perform everyday functions.[8][9][10]

Differential Diagnosis

Many differential diagnoses are seen in other forms of neuropathies and chronic alcohol use disorder. These include but are not limited to the following:

  • Beriberi
  • Diabetic Neuropathy
  • Wernicke-Korsakoff Syndrome
  • Amyotrophic Lateral Sclerosis
  • Folate Deficiency
  • Vitamin B12 Deficiency
  • Guillain-Barre Syndrome
  • Lead Poisoning
  • Mercury Poisoning 
  • Human Immunodeficiency Virus (HIV)
  • Syphilis
  • Hyponatremia
  • Hypocalcemia

Pearls and Other Issues

  • Alcohol Neuropathy is a complex disease that results from both direct and indirect effects of alcohol.
  • A thorough history and physical is important to discern the disease from other causes of neuropathy.
  • Two key factors are the duration of alcohol abuse and the lifetime quantity of alcohol consumed when studied among patients with chronic alcohol use disorder.
  • Treatment should focus on stopping the alcohol abuse and replacing important nutrients such as thiamine and other B-vitamins.

Enhancing Healthcare Team Outcomes

Chronic alcohol consumption can have deleterious effects on the central and peripheral nervous systems. One of the most common adverse effects seen in patients with chronic alcohol use disorder is alcohol neuropathy. This commonly presents with pain, paresthesias, and ataxia in the distal lower extremities. The exact number of people affected by this condition is not known, but studies have shown that up to 66% of patients with chronic alcohol use disorder may have some form of the disease. The cause is multifactorial, from both nutritional deficiencies and alcohol metabolism's direct toxic effects on neurons. Because of the diverse effects of alcohol on the body, these patients should be managed by an interprofessional team. The management of alcoholic neuropathy is not satisfactory. The treatment rests on abstinence from alcohol and the replacement of key nutrients. Unfortunately, patient compliance is poor and the condition often progresses leading to poor quality of life. Even in patients who quit alcohol, residual neuropathy is common. (Level V)

Review Questions


Julian T, Glascow N, Syeed R, Zis P. Alcohol-related peripheral neuropathy: a systematic review and meta-analysis. J Neurol. 2019 Dec;266(12):2907-2919. [PMC free article: PMC6851213] [PubMed: 30467601]
Hammoud N, Jimenez-Shahed J. Chronic Neurologic Effects of Alcohol. Clin Liver Dis. 2019 Feb;23(1):141-155. [PubMed: 30454828]
Sun J, Chen F, Braun C, Zhou YQ, Rittner H, Tian YK, Cai XY, Ye DW. Role of curcumin in the management of pathological pain. Phytomedicine. 2018 Sep 15;48:129-140. [PubMed: 30195871]
Pakdel F, Sanjari MS, Naderi A, Pirmarzdashti N, Haghighi A, Kashkouli MB. Erythropoietin in Treatment of Methanol Optic Neuropathy. J Neuroophthalmol. 2018 Jun;38(2):167-171. [PubMed: 29300238]
Humbertjean-Selton L, Selton J, Riou-Comte N, Lacour JC, Mione G, Richard S. Bilateral optic neuropathy related to severe anemia in a patient with alcoholic cirrhosis: a case report and review of the literature. Clin Mol Hepatol. 2018 Dec;24(4):417-423. [PMC free article: PMC6313028] [PubMed: 29065678]
Neary J, Goodwin SE, Cohen LB, Neuman MG. Alcohol Misuse Link to POEMS Syndrome in a Patient. Cancers (Basel). 2017 Sep 23;9(10) [PMC free article: PMC5664068] [PubMed: 28946631]
Hamel J, Logigian EL. Acute nutritional axonal neuropathy. Muscle Nerve. 2018 Jan;57(1):33-39. [PubMed: 28556429]
Dervaux A, Laqueille X. [Thiamine (vitamin B1) treatment in patients with alcohol dependence]. Presse Med. 2017 Mar;46(2 Pt 1):165-171. [PubMed: 27818067]
Zeng L, Alongkronrusmee D, van Rijn RM. An integrated perspective on diabetic, alcoholic, and drug-induced neuropathy, etiology, and treatment in the US. J Pain Res. 2017;10:219-228. [PMC free article: PMC5268333] [PubMed: 28176937]
Di Ciaula A, Grattagliano I, Portincasa P. Chronic alcoholics retain dyspeptic symptoms, pan-enteric dysmotility, and autonomic neuropathy before and after abstinence. J Dig Dis. 2016 Nov;17(11):735-746. [PubMed: 27684550]

Disclosure: Adam Sadowski declares no relevant financial relationships with ineligible companies.

Disclosure: Richard Houck declares no relevant financial relationships with ineligible companies.

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Bookshelf ID: NBK499856PMID: 29763031


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