What is Alcoholic Neuropathy? Causes, symptoms, & treatment

Alcoholic neuropathy can result in hypersensitivity to touch and even resting pain. Light touch can feel exaggerated and painful, particularly in the fingers and toes. People who drink too much may start to feel pain and tingling in their limbs. Seeking immediate help, eating a healthy diet, taking vitamin supplements and not being afraid to ask for specialized https://ecosoberhouse.com/ help can help the person return to normal life and deal with dry drunk traits before permanent nerve damage incurs. Chronic alcohol abuse can exhaust the pool of liver proteins, which are crucial in energy production. Once alcohol enters the organism, it is degraded by ethanol dehydrogenase into acetaldehyde and then into acetate which is metabolized.

  • Alcoholic neuropathy can result in hypersensitivity to touch and even resting pain.
  • This test is a widely used and safe test that consists of a cold object (ice stick at −20 °C) applied to the center of the pelvic limbs (paw pads) of the animals five times, in a five-minute interval, to avoid desensitization.
  • However, more severe cases may be intractable, even with abstinence, and lead to lifelong impairment.

The key role in the degradation of ethanol is played by ethanol dehydrogenase and acetaldehyde dehydrogenase-two step enzymatic systems by which ethanol is converted to acetate which is further metabolized in humans. Acetaldehyde dehydrogenase is a mitochondrial enzyme which undergoes a single amino acid substitution (mutation) in about 50% of the Asian population in a way similar to the genetic changes in sickle cell anaemia [21]. Thus, in alcoholics with the mutated dehydrogenase enzyme, acetaldehyde concentrations may reach values about 20 times higher than in individuals without the mutation. A certain amount of acetaldehyde is not metabolized by the usual pathways (Figure 2) and binds irreversibly to proteins which results in the creation of cytotoxic proteins which adversely affect the function of nervous system cells. These abnormal proteins influence other cell populations especially the hepatocytes where the damage to hepatic mitochondria results in hepatic cirrhosis with reduction of energetic substrates in the liver. The action of these abnormal proteins is explained by competition with normal proteins causing the damage to function and metabolism of the cell [22].

Manage underlying conditions

The doctor might also suggest an inpatient detox or outpatient rehab in an alcohol treatment center if the patient’s alcohol disorder is severe. In alcohol neuropathy, the nerves that send information between the brain and the body’s extremities become damaged due to excessive alcohol use. Early alcoholic neuropathy, usually presenting as sensory symptoms in the extremities, is reversible if the patient stops drinking and establishes proper nutrition. However, more severe cases may be intractable, even with abstinence, and lead to lifelong impairment. Alcoholic neuropathy is progressive damage to peripheral nerves and, in extreme cases, the autonomic nervous system, through chronic, heavy alcohol use. Alcohol Use Disorder (AUD) is a chronic and progressive condition involving young people and adults worldwide (Diagnostic and Statistical Manual of Mental Disorders-5; World Health Organization, 2018).

Symptoms of AAN are non-specific; in the sympathetic division, these include impairments in perspiration, orthostatic hypotension, whereas in parasympathetic hoarseness, swallowing difficulties, or cardiac arrhythmias [111, 166]. Gastrointestinal symptoms include delayed stomach emptying and intestinal transit, dyspepsia, and faster emptying of the gallbladder [165]. Besides, approximately 55% of men with AAN develop erectile dysfunctions [167].

Signs and symptoms of alcoholic neuropathy

Once alcohol use has been addressed, your doctor can focus on the neuropathy itself. Nerve damage can also make it difficult for you to carry out the functions of daily life. The most important thing you can do to treat this condition is to stop drinking. Others may be able to stop drinking with outpatient therapy or social support. These abnormal proteins deteriorate the hepatic mitochondria leading to hepatic cirrhosis and also affect the nervous system, which does not have any protective barrier, leading to neuropathy. People who struggle with alcoholism should try to eat a healthy and balanced diet, even if they don’t feel hungry.

Nevertheless, heavy alcohol drinkers are usually significantly malnourished because of the improperly balanced diet and impaired absorption of the essential nutrients and elements [58, 59]. Benfotiamine (S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine (vitamin B1). A deficiency of vitamin B1 in chronic alcoholics can be due to inadequate dietary intake, reduced capacity for hepatic storage, inhibition of intestinal transport and absorption or decreased formation of the active coenzyme form. In an animal study, it has been found that chronic alcohol consumption in rats resulted in a significant depletion in thiamine diphosphate (TDP), the active coenzyme form of thiamine. Supplementation with benfotiamine significantly increased concentrations of TDP and total thiamine compared with supplementation with thiamine HCl [96]. An 8 week, randomized, multicentre, placebo-controlled, double-blind study compared the effect of benfotiamine alone with a benfotiamine complex (Milgamma-N) or placebo in 84 alcoholic patients.

Involvement of the sympatho-adrenal and hypothalamo-pituitary-adrenal (HPA) axis in alcoholic peripheral neuropathy

Since nutritional deficiencies are partly to blame for alcoholic neuropathy, supplementation with vitamin B12, folate, vitamin E, and thiamine may be recommended. Alcoholic neuropathy is also caused by nutritional deficiency, as well as toxins that build up in the body. Alcohol decreases the absorption of nutrients, alcohol neuropathy such as protein and vitamin B12, causing significant deficits that affect many areas of the body, including the nerves. Alcoholic neuropathy damages sensory nerves, resulting in a decreased sensation in the hands and feet. If the sensation is decreased enough, you may feel actual numbness after drinking alcohol.

  • People diagnosed with alcohol neuropathy can alleviate the current symptoms and also prevent future nerve deterioration by stopping drinking.
  • The most important thing you can do to treat this condition is to stop drinking.
  • There is no alcoholic neuropathy cure, but the first step to do is to stop drinking.
  • This phenomenon may be responsible for the induction of the neuropathic pain like behaviour following chronic ethanol consumption.
  • The disease manifests itself through a tingling sensation in the limbs, caused by nerve and brain damage from alcohol consumption.
  • The true incidence of alcoholic neuropathy in the general population is unknown, and figures vary widely depending on the definition of chronic alcoholism and the criteria used to detect and classify neuropathy.

In 47 of these patients sural nerve biopsy was performed, with discrimination in terms of their thiamine status [3]. The ethanol consumption of these patients was more than 100 g day–1 for more than 10 years. The subgroup without thiamine deficiency consisted of 36 patients, while the subgroup with thiamine deficiency consisted of 28 patients. In addition, 32 patients with nonalcoholic thiamine deficiency neuropathy were also evaluated for comparison. The subgroup without thiamine deficiency, considered to be a pure form of alcoholic neuropathy, uniformly showed slowly progressive, sensory dominant symptoms.

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]. Lacosamide, a new anticonvulsant drug, had a small but significant pain relieving effect on painful diabetic neuropathy [130], while subsequent trials have failed to find an effect, except for the efficacy of a 400 mg dose in subgroup analyses [131, 132]. N-acetylcysteine, an amino acid, is a potent antioxidant and helps to enhance glutathione concentrations. N-acetylcysteine may have application in the prevention or treatment of neuropathy.

Spinal cord glial cells are implicated in the exaggerated pain state created by diverse manipulations such as subcutaneous inflammation, neuropathy and spinal immune activation [65, 66]. It has been recognized that spinal cord glial cells, astrocytes and microglia are activated by neuropathic pain or peripheral inflammation [42]. Furthermore, astrocytes and microglia are activated by such pain relevant substances as substance P, calcitonin-gene related peptide (CGRP), ATP and excitatory amino acids from primary afferent terminals, in addition to viruses and bacteria [67, 68]. Many different stimuli, including growth factors, cytokines, viral infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. There are many studies suggesting the role of MEK/ERK signaling in inflammatory pain in male [60–63] and female rats [64].

Chronic alcoholism can alter the intake, absorption and utilization of various nutrients (nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate or vitamin E). Deficiencies of B vitamins other than thiamine also may contribute to variation in clinical features, but characteristic symptoms of multiple vitamin deficiency were not seen in patients with thiamine deficiency neuropathies due to gastrectomy and dietary imbalance [26]. Thus, these vitamin deficiencies were not considered to be major causal factors of neuropathy [26].

  • 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.
  • In a 2019 study, researchers showed that quitting alcohol had a positive effect on most people’s mental well-being.
  • Because ALN is a length-dependent axonopathy, it manifests mainly in a “stocking-glove” form, affecting the lower extremities at the beginning [28, 113].

Alcoholic neuropathy can affect both sensory and motor nerves, causing pain, hypersensitivity, numbness, muscle weakness, and lack of coordination and fine motor controls, largely in the extremities. Alcohol abuse contributes to peripheral neuropathy development involving both somatic and autonomic nerves [154, 155]. However, impairments of autonomic functions are scarcer and less intensified, and, usually, clinical symptoms are delayed [156]. According to many studies, alcohol-induced autonomic neuropathy (AAN) not only leads to potential damage to internal organs but also increases the mortality rate of patients [157, 158]. It was observed that abstinence may lead to the regression of several symptoms of AAN [159].