Alcoholic Neuropathy StatPearls NCBI Bookshelf


July 2020

In an animal model, Kaur et al. (2017) showed that curcumin and sildenafil administrated alone or in combination represent a therapeutic advantage in alcohol-induced neuropathic pain [176]. An analysis of lab data may correlate with the patient’s neuropathic syndrome and systemic symptoms. Elevated levels of the liver enzymes gamma-glutamyl transpeptidase, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase may indicate long-standing heavy alcohol consumption and its effects on hepatic function. Decreasing albumin, increasing bilirubin, and prolonged clotting factors may indicate hepatic decompensation.

Recently, extended release gabapentin relieved symptoms of painful polyneuropathy [120]. Lamotrigine was effective in relieving central post stroke pain [121] and painful diabetic polyneuropathy [122], but recent larger studies have failed to show a pain relieving effect in mixed neuropathic pain [123] and painful polyneuropathy [124]. Valproate demonstrated varying effects in different studies of neuropathic pain, with three studies from one group reporting high efficacy [125–127] and others failing to find an effect [128, 129].

Direct toxic effects of ethanol or its metabolites (direct toxicity)

Other botanical or nutrient therapies include myo-inositol, vitamin E, topical capsaicin, and N-acetylcysteine. The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. 87 articles were included in this review, 29 case–control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7– 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy. The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed.

alcohol neuropathy

It is worth noting that peripheral neuropathy has no reliable treatment due to the poor understanding of its pathology. A skin biopsy of the sural nerve may be conducted and will initially show small fiber neuropathy, which results from injury to nerve fibers that may be myelinated or unmyelinated. Allodynia—when pain is experienced by a stimulus that wouldn’t normally cause pain—may be present in small fiber neuropathy. For example, a patient experiences pain or other dysesthesias when putting on socks. Patients with small fiber neuropathy commonly report burning pain and may tell you, “My feet burn.” Patients may be hypersensitive to a stimulus (hyperesthesia). Patients may also experience numbness, restless legs syndrome, dry eyes and mouth, increased sweating, stomach problems, bladder control issues, skin discoloration, and cardiovascular symptoms.

How soon does alcoholism cause neuropathy?

Alcoholic neuropathy is also caused by nutritional deficiency, as well as toxins that build up in the body. Alcohol decreases the absorption of nutrients, such as protein and vitamin B12, causing significant deficits that affect many areas of the body, including the nerves. In general, it takes years for alcoholic neuropathy to develop, so a long-standing history of heavy alcohol use is typical.

  • Axonal degeneration and demyelination of neurons were seen in both humans and lab mice receiving alcohol.
  • During the treatment the regression of neuropathy symptoms, other sensor and movement disorders were observed.
  • An essential risk factor regarding the etiology of ALN is the amount of alcohol consumed throughout the years since alcohol displays direct toxicity on nerve fibers [55].

Worth mentioning, bottles were tested for leakage, an issue that could hinder precise measurement of the solutions. The leakage was negligible, hence, not affecting the calculations of consumption. Also, levels of alcohol in the blood higher than 60 mg/dL confirmed the consistency of this protocol and were compatible with other studies (Bell et al., 2006, Simms et al., 2008a, Simms et al., 2008b). According to Simms et al., 2008a, Simms et al., 2008b, using similar protocol of intermittent alcohol (20%; v/v) ingestion, the alcohol concentration in the blood ranged from 4 to 93 mg / dL in Wistar rats submitted to 20 ingestion sessions. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), acute intoxication in alcohol consumption (binge drinking) corresponds to a blood concentration of 80 mg / dL or higher, and a pattern of heavy drinking to a concentration of 60 mg / dL or higher.

History and Physical

There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy. Dina et al. [16] maintained rats on a diet to simulate chronic alcohol consumption in humans and found mechanical hyperalgesia by the fourth week which was maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present with decreased mechanical threshold of C-fibres. The hyperalgesia was acutely attenuated by intradermal injection of nonselective PKC or selective PKCε inhibitors injected at the site of nociceptive testing. Western immunoblot analysis indicated a higher level of PKCε in dorsal root ganglia from alcohol-fed rats, supporting a role for enhanced PKCε second messenger signalling in nociceptors contributing to alcohol-induced hyperalgesia [16].

Further progression of ALN leads to the weakening of tendon reflexes or total areflexia and disturbed proprioception, which additionally impair the ability to walk [28, 113]. ALN further manifests as weakness and atrophy of muscles due to the damage of greater motor fibers and impaired neuromuscular transmission. The mechanism of direct damage of nerve fibers due to alcohol intoxication remains unclear. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis appear to be implicated in this process [92,93,94,95,96,97]. Oxidative stress also leads to the indirect damage of nerve fibers via the release of free radicals and proinflammatory cytokines with protein kinase C and ERK kinase phosphorylation [98,99,100,101]. Besides, ALN is characterized by insulin and insulin-like growth factor (IGF) resistance, which results in impaired trophic factor signaling [102, 103].

Nerve damage can also make it difficult for you to carry out the functions of daily life. It is important to share any history of alcohol use with your doctor to get an accurate diagnosis. Peripheral neuropathy can result from traumatic injuries, infections, metabolic problems, inherited causes and exposure to toxins. The total number of axons was estimated directly with the physical fractionator method (Gundersen, 1986, Mayhew and Olsen, 1991). This method consists of distribution from counting fields which are systematically and evenly displaced (in a SURS way) on the whole nerve cross-section.

Treatment options include steps to quit alcohol use and managing symptoms of the disease. This condition is typically not life-threatening, but the nerve damage from alcoholic neuropathy is usually permanent. If it affects two or more nerves in different areas, it’s called multiple mononeuropathy, and if it affects many nerves, it’s called polyneuropathy. In order to diagnose ALN, usually, several tests are needed to be performed to provide a complete and reliable diagnosis. Besides blood chemistry test and complete blood count (CBC), esophagogastroduodenoscopy is needed when a patient vomits and has nausea for an unknown reason; X-rays of the gastrointestinal tract can also be performed. Electromyography and nerve conduction tests are performed in order to reveal signs of ALN.

Red blood cells (RBCs) tend to be larger than normal (macrocytosis) and reduced in number from a deficiency in vitamin B9 or B12 or GI bleeding. There may be an increase in erythrocyte macrocytic volume because alcohol interferes with the development of normal RBCs. Glucose fluctuation, hyponatremia, hypokalemia, and hypomagnesemia are common features. An elevated carbohydrate-deficient transferrin level is a sensitive indicator of chronic heavy alcohol consumption. Transferrin is a serum protein that facilitates iron transport under the control of glycosyltransferase, which is a carbohydrate chain. Alcohol-induced peripheral neuropathy (PN) is a chronic and painful condition in which the neurotoxic effects of alcohol and nutritional deficiencies cause a pathologic response in nerve function.

PKC is involved in receptor desensitization, modulating membrane structure events, regulating transcription, mediating immune responses, regulating cell growth and in learning and memory. These functions are achieved by PKC mediated phosphorylation of other proteins [16]. Apart from above function, over-activation of epsilon form of protein kinase C (PKCε) is known to be involved in mediating neuropathic pain, such as pain induced by cancer chemotherapy (vincristine) [56] and diabetes [57]. PKC and protein kinase A (PKA) are both known to be important in nociceptor function [57–59].

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