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 paresthesias 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.

Objectives:

• Identify the etiology of alcoholic neuropathy.
• Determine the use of the CAGE questionnaire in the history of alcoholic neuropathy.
• Assess the differential diagnoses in alcoholic neuropathy.
• Communicate the importance of improving care coordination among the interprofessional team members to diagnose correctly and counsel patients on their drinking habits for improved outcomes in patients affected by alcoholic neuropathy.

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 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 exams can help to differentiate this condition from other forms of neuropathy. No specific lab test is available for diagnosis. Treatment should be focused on alcohol sobriety and the replacement of key nutrients.[1][2][3]

Etiology

The long-term, negative outcomes of 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 2 key elements when studied among patients with chronic alcohol use disorder. One study suggested that a quantity of more than 100 g/day over many years was likely to cause peripheral neuropathy.[4][5][6][7]

Epidemiology

Alcohol is 1 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.

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 of 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 by damage by free radicals, the release of inflammatory markers, and oxidative stress.

History and Physical

A thorough history and physical examination are 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 2 most important questions to ask when evaluating for alcohol neuropathy are: (1) How much alcohol do you drink? and (2) What is the length of the abuse? These questions can help differentiate 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 vary, including pain, numbness, and paresthesias. Pain seems consistent in the literature as 1 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 that can cause peripheral neuropathies.
• Diabetes Testing - Diabetic neuropathy can have a similar presentation.
• Thiamine, Folate, and Vitamin B12 Testing are key nutrients in neuronal formation in both the 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 includes positive sharp waves 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 has 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 referrals, 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

Key facts to keep in mind about alcohol neuropathy are as follows:

• Alcohol Neuropathy is a complex disease that results from both direct and indirect effects of alcohol.
• A thorough history and physical examination are important to discern the disease from other neuropathy causes.
• 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 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. 

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References

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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]

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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.