Diseases and Disorders

A Synopsis of Alcoholic Neuropathy

Christian Gonzalez


Introduction

In 1787, English physician John Coakley Lettsom observed a patient with leg paralysis and hyperesthesia. The patient that was described by Lettsom was the first description of symptoms of a disease that would later be known as alcoholic neuropathy. Later on, in 1822, neuropathy was described in alcoholics as well. By the late 1800s, the symptoms that these physicians and doctors were observing became to be known clinically as alcoholic neuropathy (Mawdsley & Mayer, 1965). Alcoholic neuropathy is a neurological disorder that causes paresthesia (abnormal tingling) and sensory and motor abnormalities, as a result of axonal degeneration of motor and sensory neurons. This is due to either chronic alcoholism or vitamin deficiency, and is closely associated with Korsakoff’s syndrome and Beriberi. (“Types of Peripheral Neuropathy,” n.d.).

 

Overview and Symptoms

    Alcoholic neuropathy typically manifests itself through two different classes of physical symptoms: sensory symptoms and motor symptoms. Some of the most common sensory symptoms include nerve pain, numbness, heat intolerance, and muscle cramps. Additionally, patients may often experience abnormal tingling sensations known as paresthesia (“Types of Peripheral Neuropathy,” n.d.). The acuteness of sensory symptoms depends substantially upon the severity of the disease in a patient. In alcoholic neuropathy, sensory symptoms are the first physical signs that a patient will typically exhibit; these symptoms  can be used as diagnostic and prognostic indicators and are useful to neurologists. After sensory symptoms are displayed by a patient with alcoholic neuropathy, the individual will usually begin to encounter motor symptoms. In the case of motor symptoms, a patient may experience difficulty urinating, constipation, diarrhea, and muscle cramps. In addition to overall muscle weakness, the patient may also be burdened with a lack of coordination known as ataxia as a result of cerebellar degeneration, in addition to muscle spasms, atrophy, dysphagia (difficulty swallowing), and dysarthria (difficulty speaking) (“Alcoholic neuropathy,” 2015).

 

Causes

    The etiological origin of alcoholic neuropathy is the result of excessive alcohol consumption. With respect to the precise mechanism leading to the symptoms and pathology of the disease, however, the root cause is disputed. The two most likely causes are alcohol’s toxic effect and malnutrition linked to alcohol consumption.  Malnutrition results from the phenomenon by which high alcohol consumption disrupts daily habits and patterns in alcoholics but not normal people. Living an unstructured life can lead to alcoholics eating abnormally, resulting in malnutrition due to irregular eating and loss of appetite. Regardless of the cause of symptoms in alcoholic neuropathy, though, the eventual pathological progression of the disease is the result of damage to peripheral nerves. When nerves are damaged, a patient will have motor and sensory symptoms associated with the progression of alcoholic neuropathy. In addition to alcohol consumption, vitamin deficiencies have also been linked to the development of the disease. Specifically, some of the more common deficiencies linked to alcoholic neuropathy are thiamine, retinol, pantothenic acid, pyridoxine, biotin, cobalamin, folic acid, and niacin (“Alcoholic neuropathy,” 2015).  

 

Diagnosis

    When trying to reach an accurate diagnosis of alcoholic neuropathy, physicians will typically examine a patient’s family history for a background of alcoholism and study their symptoms. Unfortunately, many symptoms of Alcoholic Neuropathy are similar to those displayed in other diseases that result from axonal degeneration. If a patient has both sensory and motor symptoms, along with nutritional and vitamin deficiencies, however, then it is much easier to tell that the patient has alcoholic neuropathy rather than another similar condition. Some of the diseases that alcoholic neuropathy is commonly misdiagnosed as include ALS, Beriberi, CMT, Diabetic Neuropathy, and Guillain Barre (“Alcoholic Neuropathy: Background,” n.d.). Besides nutritional deficiencies, other ways that neurologists differentiate between alcoholic neuropathy and other diseases include the use of EGD, EMG, medical imaging, and nerve conduction studies (“Alcoholic neuropathy,” 2015).

 

Pathophysiology

    The progression of alcoholic neuropathy typically presents itself through nerve damage followed by sensory and motor symptoms that can be useful in diagnosing the disease. As discussed above, excess alcohol consumption and vitamin deficiencies result in axonal degeneration, which makes the beginning stages of alcoholic neuropathy less thoroughly understood compared to other stages during its pathology. When axonal degeneration takes place, a process called demyelination occurs that results in a decrease in the travelling speed of action potentials across neurons from the loss of saltatory conduction. This nerve damage underpins the pain that patients with alcoholic neuropathy experience. Low levels of thiamine contribute to the onset of the disease, as decreased thiamine contributes to neurons being unable to maintain normal levels of adenosine triphosphate (ATP) necessary for usual functioning. Additionally, acetaldehyde can have toxic effects on peripheral nerves leading to damage observed in the disease as well (Mawdsley & Mayer, 1965).
 

Treatment

    There is currently no available cure for alcoholic neuropathy. Fortunately, patients have a variety of treatment options to lessen the severity of their symptoms that stem from the pathophysiology of their condition. Difficulty walking and issues with mobility can be aided by physical therapy. Additionally, pain experienced during alcoholic neuropathy can be treated with a number of drugs such as vitamin supplements, amitriptyline, gabapentin, and capsaicin. These drugs alter some of the many physical processes that result in the symptoms of the disease. Managing overall symptoms in the disease is also best done through improving nutrition. Specifically, being alcoholically abstinent can help patients lessen the progression of the disease and prevent many of the symptoms associated with alcoholic neuropathy (“Alcoholic Neuropathy: Background,” n.d.).

 

Key Terms:

Hyperesthesia - Increased physical sensitivity in response to stimuli

Paresthesia - Abnormal tingling sensation from nerve damage

Ataxia - Loss of coordination of voluntary muscle movements

Cerebellar Degeneration - Deterioration of neurons in the cerebellum that results in difficulty with balance and coordination

Dysphagia - Difficulty swallowing

Dysarthria - Condition characterized by difficulty speaking as a result of neurological injury

Thiamine (Vitamin B1) -  Vitamin important for proper heart, muscle, and nerve function

Retinol (Vitamin A)- Vitamin important for proper immune function, development, growth, and vision

Pantothenic Acid (Vitamin B5) - Vitamin important for synthesis and metabolism of carbohydrates, fats, and proteins

Pyridoxine (Vitamin B6) - Vitamin important for glucose and protein metabolism, myelin formation, and the synthesis of the neurotransmitters norepinephrine and serotonin

Biotin (Vitamin H or B7)- Vitamin important for synthesis of fatty acids and glucose

Cobalamin (Vitamin B12)- Vitamin important in formation of red blood cells

Folic Acid - Vitamin used to treat anemia; important for synthesis of nucleic acid

Niacin (Vitamin B3) - Vitamin used to treat high levels of cholesterol and triglyceride, niacin deficiency, and lowers heart attack risk

EGD - Esophagogastroduodenoscopy; a test used to examine the esophagus and stomach lining

Electromyography - Technique for assessing muscle health; also known as EMG

Saltatory Conduction - Action potential propagation along neuronal axons via myelin sheath

Adenosine Triphosphate (ATP) - The energy currency for intracellular energy transfer in cells

Acetaldehyde - Toxic byproduct of alcohol metabolism involved in alcoholic neuropathy

Amitriptyline - Tricyclic antidepressant used to treat alcoholic neuropathy

Gabapentin- Anticonvulsant drug used to treat alcoholic neuropathy and epilepsy

Capsaicin- Active ingredient of chili peppers


References


  1. Types of Peripheral Neuropathy - Toxic/Secondary to Drugs. (n.d.). Retrieved September 10, 2016, from http://peripheralneuropathycenter.uchicago.edu/learnaboutpn/typesofpn/toxic/alcohol.shtml

  2. Mawdsley, C., & Mayer, R. F. (1965). Nerve Conduction In Alcoholic Polyneuropathy. Brain, 88 (2), 335-356. doi:10.1093/brain/88.2.335

  3. Chopra, K., & Tiwari, V. (2012). Alcoholic neuropathy: Possible mechanisms and future treatment possibilities. British Journal of Clinical Pharmacology, 73(3), 348-362. doi:10.1111/j.1365-2125.2011.04111.x

  4. Alcoholic neuropathy: MedlinePlus Medical Encyclopedia. (2015). Retrieved September 10, 2016, from https://medlineplus.gov/ency/article/000714.htm

  5. Alcoholic Neuropathy: Background, Pathophysiology, Epidemiology. (n.d.). Retrieved September 10, 2016, from http://emedicine.medscape.com/article/315159-overview

  6. Alcohol & Peripheral Neuropathy - Pins & Needles, Nerve Damage. (n.d.). Retrieved September 10, 2016, from https://www.foundationforpn.org/what-is-peripheral-neuropathy/causes/alcohol/

Christian Gonzalez

Christian Gonzalez


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