Alcoholic Neuropathy Explained In Simple Terms

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Alcoholic neuropathy is a progressive neurological disorder and one of the most common adverse effects of chronic alcohol consumption (with an incidence of as high as 67.1%).

If you have a history of excessive alcohol use and start experiencing symptoms of tingling, numbness, or burning in your limbs, you might be suffering from alcoholic neuropathy.

Here’s how alcohol abuse can cause neuropathy, its symptoms, and how it’s treated.

How Does Alcoholic Neuropathy Happen?

Alcoholic neuropathy is a primary axonal neuropathy that can result in sensory, motor, and autonomic dysfunction, as well as axonal degeneration of the peripheral nervous system.

The axon is the highway that the electrical signals get sent down through. It’s wrapped in a spiral fashion by a myelin sheath, which acts as an insulator to facilitate impulse conduction in axons, like pulling your hand away on touching a hot object.

Excessive alcohol consumption can damage the myelin sheath and, therefore, affect impulse conduction, possibly resulting in chronic pain, deformities, and altered quality of life.

Symptoms of Alcoholic Neuropathy

The most typical pattern of neuropathy symptoms is:

  • Sensory: Affecting the information from the surrounding environment to the body and the central nervous system.
  • Motor: Affecting signals from the central nervous system to the body.
  • Autonomic: Regulating the body’s involuntary physiological processes.

In the early stages of alcoholic neuropathy, patients complain of a feeling of tingling, numbness, or “pins and needles” in the feet and toes before the hands and fingers (also known as stock-to-glove distribution).

They can also complain of spontaneous burning pain, increased sensitivity, extreme response to pain, and pain due to a stimulus that does not normally provoke it, like a gentle touch of exposure to some types of fabrics.

Later, weakness appears in the extremities. Progressively, the sensory and motor symptoms extend proximally to the arms and legs, and finally, the gait may become impaired, manifesting as difficulty walking or a history of frequent falls.

It’s worth noting that although alcoholic neuropathy usually develops slowly over some time, it can sometimes present in an acute and rapidly progressive manner.

Signs

Alcohol-induced neuropathy signs include:

  • Diminished sensation to vibration or pinprick stimulation.
  • Sensation abnormalities to heat and location.
  • Paresthesia: burning or prickling sensation without moving the limbs.
  • Allodynia: pain due to a stimulus that does not normally provoke pain.
  • Hyperalgesia: an increased sensitivity to feeling pain and an extreme response to pain
  • Knee and ankle reflexes are often reduced or absent.
  • Tenderness and cramping when muscles in the feet and legs are pressed.
  • Muscle weakness and wasting.
  • Gait ataxia: loss of coordination during walking.
  • Bilateral foot drop.

Prolonged alcohol abuse without management will then extend to affect the autonomic nervous system, which controls internal body functions. This can lead to:

  • Urinary and Bowel Control: incontinence, urinary retention, constipation, diarrhea.
  • Genital System: sexual dysfunction, erectile dysfunction, impotence.
  • Heat intolerance.
  • Nausea and vomiting.
  • Dizziness.
  • Impaired speech.
  • Difficulty swallowing.

Causes of Alcoholic Neuropathy

The exact cause of alcoholic neuropathy is undecided. However, there are a few theories supported by several studies.

Direct Toxicity

When ethanol is ingested, it gets metabolized. One of its intermediate end products is acetaldehyde, a highly neurotoxic metabolite with extraordinary reactivity. It has direct toxic effects on peripheral nerves.

Indirect Toxicity

It was long believed that alcoholic peripheral neuropathy was caused by a nutritional deficiency, especially thiamine deficiency (also known as Beriberi neuropathy). Because alcohol impairs thiamine absorption through the gastrointestinal tract and its utilization in tissues, reducing the availability of thiamin’s active form.

However, this once firm belief has been contended against in recent studies suggesting that alcohol-related peripheral neuropathy (ALN) is clinically and pathologically distinct from thiamine-deficiency neuropathy (TDN).

Type of Neuropathy

Onset

Clinical Symptoms

ALN

Slowly progressive

Sensory-dominant/Superficial sensation

TDN

Acutely progressive

Motor-dominant/Superficial and deep sensation

Differences between the two types of neuropathy became apparent when nerve conduction tests and sural nerve biopsy were carried out.

It was also found that excessive drinking and chronic alcohol use cause impaired gastrointestinal absorption, which leads to nutritional deficiencies. Other vitamin deficiencies may also contribute to developing alcoholic neuropathy. Chronic alcoholism can affect the absorption and utilization of various nutrients, most notably nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate, and vitamin E.

Oxidative Stress

Another hypothesis is that ethanol has been shown to increase oxidative stress, leading to free radical damage to peripheral nerves. This is also one of the reasons why alcohol abuse causes an increased risk of cancer.

Insulin/Insulin-like Growth Factor Resistance

Emerging research suggests that alcohol causes impairments in the expression of genes and proteins that mediate intracellular signaling through insulin and insulin-like growth factor receptors, leading to Insulin/IGF resistance and oxidative stress promoting nerve cell damage. This is similar to the effects of ethanol on the liver and brain.

Liver Dysfunction

Some studies have speculated that chronic hepatic dysfunction, most often cirrhosis and neuropathy, are associated. Another research paper even suggested that the severity of polyneuropathy was heavily correlated to liver disease in chronic alcohol users.

Risk Factors for Developing Alcoholic Neuropathy

Total Lifetime Dose of Ethanol (TLDE)

This is used in studies to measure alcohol abuse and alcohol dependence. It’s calculated by measuring the daily alcohol consumption multiplied by 365 and by the number of years of abuse. Currently, it’s the best-validated risk factor for the development of alcohol-related peripheral neuropathy.

Biological Sex

Women are slightly more affected than men by peripheral neuropathy in chronic alcoholism.

Family History

Studies showed a strong relationship between a parental history of alcoholism and the development of neuropathy.

Age

The elderly are more at risk of developing alcoholic neuropathy due to the natural nerve cell degeneration that occurs with aging. The average age at diagnosis is between 40-60 years old among chronic alcohol abusers.

Type of Alcohol Consumed

Alcoholic beverages differ in calories, nutrients like thiamin, the presence of neurotoxic impurities, the amount consumed, and the time it takes to be eliminated from the body. This impacts how they can affect the central and peripheral nervous systems and cause nerve damage.

How is Alcoholic Neuropathy Diagnosed?

Alcoholic polyneuropathy is almost identical to neuropathic pain, which can be caused by many other neurological disorders and movement disorders. The physician takes an extensive medical history and performs a complete physical exam to confirm the diagnosis. They then typically request lab and imaging studies to rule out other clinical syndromes.

Medical workup most commonly involves:

  • Blood tests: To assess blood glucose level and hemoglobin A1C to rule out diabetic neuropathy, which presents with almost identical peripheral neuropathy.
  • Chemistry profile: Excessive alcohol use may cause an increase in liver enzyme levels. This has a direct toxic effect because the liver eliminates more than 90% of alcohol.
  • Creatinine level: Chronic kidney disease indicated by elevated creatinine levels can cause neuropathy.
  • Thiamine status through blood and urine tests: To detect thiamine deficiency.
  • Vitamin B-12, vitamin E, and folic acid levels: To detect vitamin deficiency.
  • Screen for heavy metal toxicity: Lead and other heavy metal toxicity is an established possible cause of neuropathy.
  • Nerve conduction studies (NCSs): To assess nerve damage. Nerve conduction velocities are generally normal or mildly slow in early presentations and slowed in demyelinating conditions.
  • Nerve biopsy: Through a small incision, a sample of nerve tissue is removed and examined under a microscope to identify how far the nerve is damaged and confirm a specific diagnosis.
  • Vibrometer testing: Useful in detecting early signs of subclinical neuropathic disease.
  • Needle electromyography (EMG): It records the electrical activity in a muscle by inserting a needle electrode directly into that muscle.
  • Esophagogastroduodenoscopy (EGD): to examine the lining of the esophagus, stomach, and first part of the small intestine.

Managing Alcoholic Neuropathy

Quitting Alcohol

The most important thing alcoholic patients can do to manage this condition is to quit alcohol and practice long-term alcohol abstinence. Although there is no known cure for alcoholic polyneuropathy, there are several treatments that can help manage the condition once the alcohol problem has been addressed.

Nutritional Therapy

Treatment goals are to focus on nutritional therapy through a balanced diet supplemented by all essential nutrients with multivitamin injections. Followed by symptomatic treatment and promoting physical independence.

Medications

Symptoms of chronic pain can be treated using gabapentin or amitriptyline with other over-the-counter pain medications.

Using painkillers could induce an altered perception of pain and an increase in the pain threshold. However, they are used only for the management of acute painful symptoms and are ineffective in targeting the underlying reasons involved in alcoholic neuropathy.

Topical application of capsaicin may provide relief from pain in patients suffering from alcoholic neuropathy.

Tricyclic antidepressants such as amitriptyline or carbamazepine are often the first-line drugs to alleviate neuropathic and stabbing pain symptoms as they have central and peripheral sedative effects.

In a study, vitamin E was found to be beneficial in preventing hyperalgesia and allodynia.

Physical and Occupational Therapy

Physical therapy is essential. It includes gait and balance training, range-of-motion exercises and stretching, and strength training to compensate for muscle weakness and nerve damage.

Occupational therapy is beneficial to the rehabilitation process in individuals with alcoholic neuropathy. This includes training in performing activities of daily living (ADL) and compensatory strategies to accommodate weakened limbs.

Mental Health Counseling

Consultation with a psychiatrist can be useful to help patients with chronic alcoholism recover from the physical and emotional withdrawal associated with cessation of alcohol consumption.

Can a Person Fully Recover from Alcoholic Neuropathy?

As with all chronic conditions, a better prognosis or possibly full recovery can be achieved if caught early enough. However, in the case of ongoing alcohol use, vitamin and nutritional supplementation alone might not be enough for improvement in most patients.

It’s also important to set realistic expectations and to understand that nerve damage is permanent and irreversible.

Alcoholic neuropathy presents with considerable morbidity and is a potentially life-threatening condition that can be managed. A treatment plan for alcoholism needs to include counseling and/or substance abuse support group support such as Alcoholics Anonymous (AA).

Prevention of Alcoholic Neuropathy Starts with You Today

You can prevent alcoholic neuropathy if you avoid drinking excessive amounts of alcohol. Seek medical guidance if you have any symptoms of alcoholic neuropathy, and reduce your risk by maintaining a balanced diet and taking vitamin supplements if you have deficiencies.

If you or a loved one need help managing alcohol consumption, book an appointment with Curednation to start your recovery journey today.

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