Alcoholic Neuropathy


Article Author:
Adam Sadowski


Article Editor:
Richard Houck



Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
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Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
1/24/2019 2:30:33 PM

Introduction

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 alcoholism 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 alcoholism 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]

Etiology

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 alcoholism. 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]

Epidemiology

Alcohol is one of the most commonly used substances in the world. Among patients with chronic alcoholism, 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.

Pathophysiology

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 alcoholism. 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.

Evaluation

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 alcoholism. 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 alcoholism. 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 alcoholism.
  • 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 alcoholism 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 alcoholism 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 a multidisciplinary team. The management of alcoholic neuropathy is not satisfactory. The treatment rests of abstinence from alcohol and replacement of key nutrients. Unfortunately, patient compliance is poor and the condition often progresses leading to a poor quality of life. Even in patients who quit alcohol, residual neuropathy is common. (Level V)

 

 

 


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Alcoholic Neuropathy - Questions

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How does peripheral neuropathy in a chronic alcoholic patient usually present?



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A 45-year-old male who drinks 12 beers a day for the past 3 years presents with pain in his feet. He describes the pain as sharp and constant. It extends from his toes to his ankles bilaterally. He denies any trauma. On exam, he has decreased vibratory sensation at the distal feet and decreased 2 point discrimination. There is no presence of muscle atrophy, rashes, or skin lesions. What question or questions are most important to help differentiate the cause of this patient's neuropathy?



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What is the best treatment for alcohol neuropathy?



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A 55-year-old female presents to the emergency department with bilateral foot pain. She denies any trauma. She reports this has been a slow process that has been getting worse over the last several months. She does not have a primary care provider. She denies any significant past medical or surgical history. Her vitals are all within normal limits. She mentions she drinks about 12 beers a day since her father passed away 8 months ago. From what vitamin deficiency is this patient most likely suffering?



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A 65-year-old man presents with gait ataxia and paresthesias in his feet. He has a long history of alcohol use for at least 25 years. He recently stopped drinking alcohol and has entered counseling. He was diagnosed with alcoholic neuropathy. He presents to ask about prognosis. What is the prognosis of the disease?



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A 40-year-old female with a history of chronic alcohol use presents with decreased bilateral sensation in her feet that has developed over the past month. She also has lower extremity muscle weakness but no upper extremity weakness or sensory deficits. What is a typical neurological finding?



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Alcoholic Neuropathy - References

References

Julian T,Glascow N,Syeed R,Zis P, Alcohol-related peripheral neuropathy: a systematic review and meta-analysis. Journal of neurology. 2018 Nov 22;     [PubMed]
Hammoud N,Jimenez-Shahed J, Chronic Neurologic Effects of Alcohol. Clinics in liver disease. 2019 Feb;     [PubMed]
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 : international journal of phytotherapy and phytopharmacology. 2018 Sep 15;     [PubMed]
Pakdel F,Sanjari MS,Naderi A,Pirmarzdashti N,Haghighi A,Kashkouli MB, Erythropoietin in Treatment of Methanol Optic Neuropathy. Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society. 2018 Jun;     [PubMed]
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. Clinical and molecular hepatology. 2018 Dec;     [PubMed]
Neary J,Goodwin SE,Cohen LB,Neuman MG, Alcohol Misuse Link to POEMS Syndrome in a Patient. Cancers. 2017 Sep 23;     [PubMed]
Hamel J,Logigian EL, Acute nutritional axonal neuropathy. Muscle     [PubMed]
Dervaux A,Laqueille X, [Thiamine (vitamin B1) treatment in patients with alcohol dependence]. Presse medicale (Paris, France : 1983). 2017 Mar;     [PubMed]
Zeng L,Alongkronrusmee D,van Rijn RM, An integrated perspective on diabetic, alcoholic, and drug-induced neuropathy, etiology, and treatment in the US. Journal of pain research. 2017;     [PubMed]
Di Ciaula A,Grattagliano I,Portincasa P, Chronic alcoholics retain dyspeptic symptoms, pan-enteric dysmotility, and autonomic neuropathy before and after abstinence. Journal of digestive diseases. 2016 Nov;     [PubMed]

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