Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol. Behse & Buchthal [31] compared 37 Danish patients with alcoholic neuropathy with six patients with nonalcoholic post gastrectomy polyneuropathy. The authors noted that Danish beer at the time of the study contained thiamine and vitamin B6. Thus, deficiency of these vitamins was felt to be unlikely in Danish beer drinkers at that time and, indeed, measured vitamin concentrations were mostly normal.

Without treatment, alcohol-induced effects can cause permanent damage and severely affect the quality of life. 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. alcohol neuropathy 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.

How does alcohol cause neuropathy?

Changes in muscle strength or sensation usually occur on both sides of the body and are more common in the legs than in the arms. Completely avoiding alcohol and eating a balanced diet can help minimize damage. Your chances for recovery depend on how early the disease is diagnosed and how much damage has already occurred. Up to 46 percent of people with alcohol-related myopathy showed noticeable reductions in strength compared with people without the condition. It usually develops as symptoms of Wernicke’s encephalopathy go away.

The abnormalities were usually of reduced amplitude, in keeping with axonal loss [2, 3, 5, 11, 12, 16, 21, 27, 37–39, 47, 51, 53, 54, 56, 63–68]. H and F wave latencies were not routinely reported but were found to be prolonged in those with alcohol-related peripheral neuropathy in studies that did [4, 67]. Particular attention was paid to radial SNAPs, tibial CMAPs, and sural SNAPs due to them being spared in entrapment neuropathies unlike the median, ulnar, and peroneal nerves.

Alcohol-related peripheral neuropathy: a systematic review and meta-analysis

Alcohol enters the blood as early as 5 min after ingestion and its absorption peaks after 30–90 min. 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.

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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. The primary axonal damage and secondary demyelination of motor and sensory fibres (especially small diameter fibres) are considered to constitute the morphologic basis of alcoholic damage to nerve tissue at present [20]. The demyelination is explained as the result of a slowing down (decceleration) of axoplasmic flow and a degradation of the quality of biological properties of axonal enzymes and proteins. This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration. Ethanol and its toxic degradation metabolites affect neuronal metabolism including the metabolic pathways of nucleus, lysosomes, peroxisomes, endoplasmatic reticulum and cytoplasm [21].

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Malnutrition has been implicated in the pathology of alcohol-related neuropathy by several authors. The data, however, is conflicting as to the role which malnutrition plays. The majority of studies which investigate the relationship between malnutrition and neuropathy focus on thiamine deficiency as an aetiological factor, drawing upon existing knowledge of Beri Beri.

what is alcohol neuropathy

A wide range of support networks and medical treatments are available. A doctor may also want to test the functioning of the kidneys, liver, and thyroid. In addition, they may order blood tests to check for vitamin and nutrient deficiencies.

There was not however, complete resolution of symmetric neuropathy with persistent mild loss of vibration sense or pinprick sensation in the feet or loss of ankle tendon reflexes. To better understand the neurological effects of alcohol, it helps to explore some of the more well-known pathologies, disorders, and diseases. The following sections provide a brief overview of several neurologic conditions related to alcohol consumption. There are no medications that can help improve loss of sensation, strengthen muscle weakness, or assist with the coordination and balance problems caused by alcoholic neuropathy.

what is alcohol neuropathy

However, some people notice an improvement in symptoms a few months after discontinuing alcohol intake. 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. Alcoholic neuropathy is one of the most common but least recognizable consequences of heavy alcohol use. People with a long history of alcohol misuse might experience loss of balance, pain, tingling, weakness, or numbness after drinking alcohol.

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