By scanning the reference lists of included studies, an additional 4 papers were identified. This study is reported in accordance with the preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines [7]. Statistical calculation of pooled proportions was conducted in R language, using the default settings of the “meta” package and the “metaprop” function with a random effects model [8]. When significantly limiting or stopping alcohol consumption, receiving ongoing support is essential.
- A review of the human literature implicates nutritional deficiencies, most often thiamine deficiency, that are common in alcoholic patients, as commonly accompanying complicating factors in the development of this neuropathy.
- American Addiction Centers (AAC) is committed to delivering original, truthful, accurate, unbiased, and medically current information.
- Alcoholic neuropathy, also called alcohol-induced peripheral neuropathy, is nerve damage in the body caused by the toxic effects of alcohol.
- ALN is characterized by spontaneous burning pain, hyperalgesia, and allodynia.
Prevalence of alcoholic neuropathy
No amount of alcohol is safe to drink while pregnant, according to the CDC. However, experts still do not have a full understanding of how alcoholic neuropathy happens, which can make treatment challenging. It is important to supplement the diet with vitamins, including thiamine and folic acid.
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Thus, treatment with TCAs may provide symptomatic relief in patients with alcoholic neuropathy. Therefore, topical application with capsaicin may provide symptomatic relief from neuropathic pain in patients suffering from alcoholic neuropathy. Hawley et al. followed up 11 patients with alcohol-related neuropathy who were abstinent from alcohol and who had begun to consume a normal diet [67]. This identified improvement in sensory symptoms within a few days and a clinical improvement in strength over a period of weeks to months, but in up to 2 years in the most severe cases. 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. Alcoholic neuropathy is a severe condition caused by excessive alcohol use.
Review Date 4/29/2023
Thus, it is quite possible that chronic alcohol consumption is responsible for inducing neuropathy by activation of the caspase cascade and may be an important target for the treatment of alcoholic neuropathy. Oxidative stress is known to play a very important role in experimental animal models of neuropathic pain. Lee et al. [36] suggested that reactive oxygen species are importantly involved in the development and maintenance of capsaicin-induced pain, particularly in the process of central sensitization in the spinal cord in rats. Naik et al. [38] suggested the involvement of oxidative stress in experimentally induced chronic constriction injury of the sciatic nerve model in rats.
- Sometimes symptoms get better, especially if caused by a condition that can be treated.
- However, alternative therapies do not have side effect and tackle nutritional deficiencies and oxidative stress.
- The best way to avoid the issue is to limit alcoholic consumption to 2 or fewer drinks per day for males and 1 or fewer for females.
- One of the other important issues in alcoholic individuals is the source of their calorie intake.
Long-term alcohol consumption is toxic to many areas of the body, including the nervous system. Drinking heavily is also connected to malnutrition, leading to nutritional deficiency and vitamin deficiencies. Other coexisting, alcohol-related diseases may induce exacerbation of AAN symptoms.
- The evidence points toward alcohol-related peripheral neuropathy being a form of toxic neuropathy, rather than nutritional neuropathy.
- The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.
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- It also appears that the addition of NCS may improve the identification of alcohol-related peripheral neuropathy.
Indirect effects are mainly induced by vitamin deficiencies (B1, B2, B3, B5, B6, B7, B9, and B12) [84, 88]. A review of the human literature implicates nutritional deficiencies, most often thiamine deficiency, that are common in alcoholic patients, as commonly accompanying complicating factors in the development of this neuropathy. Persons with alcoholism may consume smaller amounts of essential nutrients and vitamins and/or exhibit impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol. Malnutrition has been implicated in the pathology of alcohol-related neuropathy by several authors. 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.
This damage prevents the nerves from communicating information from one body area to another. Our muscles need to receive a message from nearby nerves in order to function. When this message is interrupted due to damaged nerves, the muscles cannot function as they normally would.
Motor function of the tibial nerve was the next common [3, 11, 51, 54, 59, 63]. Finally, one study examined the strength-duration time constant (SDTC) and rheobase in median nerves of those with alcoholic peripheral alcohol neuropathy stages neuropathy [69]. The SDTC was normal compared to controls, but the rheobase was significantly different suggesting that APN may affect internodal channels other than nodal channels or the Na+ –K+ ATP pump.