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

Pain from peripheral neuropathy is usually the most disruptive symptom, but medications or other treatments may help. Autonomic symptoms are among the most serious because they involve your body’s vital functions. When those don’t work correctly, it Drug rehabilitation can have very severe — and sometimes dangerous — effects. Peripheral neuropathy can affect anyone, regardless of age, sex, race or ethnicity, personal circumstances, medical history, etc. However, some people are at greater risk for specific types of peripheral neuropathy (see below under Causes and Symptoms for more about this).

• The primary treatment for alcoholic neuropathy is seeking help for alcohol use disorder.
• Alcoholic neuropathy damages the nerves due to prolonged and excessive alcohol consumption.
• Symptoms include burning pain in the body, hyperalgesia (increased sensitivity to pain), and allodynia (a condition in which normal stimulus, like a soft touch, produces pain).
• A mechanism of cisplatin chemotherapy-induced peripheral neuropathy was elucidated in an in vitro mouse model.
• 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.

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• Hypoglycemia can have serious, even life-threatening, consequences, because adequate blood sugar levels are needed to ensure brain functioning.
• The first step in treating alcoholic neuropathy includes stopping alcohol use altogether.
• The first function, which involves most of the pancreatic cells, is the production of digestive enzymes.
• Among their many functions, insulin and glucagon regulate the conversion of fat molecules (i.e., fatty acids) into larger molecules (i.e., triglycerides), which are stored in the fat tissue.
• In another small Russian study, 14 chronic alcoholic men with polyneuropathy were given 450 mg benfotiamine daily for 2 weeks, followed by 300 mg daily for an additional 4 weeks.
• Future research should involve large, controlled trials to clarify erythropoietin’s role and establish it as a standard treatment.

Additionally, 21 cases exhibited a reduction in retinal nerve fiber layer thickness, with one showing a reduction towards the normal range. We systematically searched English and Persian databases including PubMed, Scopus, Embase, Web of Science, and Scientific Information Database (SID) as of July 2024. Two independent authors screened the articles based on their titles, abstracts, and full texts to finalize the included articles in this study. The selected articles underwent quality assessments via the Joanna Briggs Institute (JBI) checklists. Many impotent diabetic men also have lower than normal levels of the sex hormone testosterone in their blood.

What Is Alcoholic Neuropathy?

These are some other questions people often ask about alcoholic neuropathy. In a 2019 article, researchers explain that breaking down alcohol in the body produces a chemical that damages axons. Axons are the groups of nerve fibers that carry impulses between the brain and the nervous system. The only way to prevent alcoholic neuropathy is not to drink excessive amounts of alcohol. Medicines may be needed to treat pain or uncomfortable sensations due to nerve damage.

Alcoholic Neuropathy Treatment

The main goal of a treatment program for alcoholic polyneuropathy is to improve quality of life and offer relief from symptoms. Alcohol-related neuropathy is a condition caused by consuming large amounts of alcohol over a long period. The toxic effects of alcohol may damage your peripheral nerves, which play a role in movement and sensation.

Increased Pain and Hypersensitivity

Recent studies show contradictory information about the role of malnutrition and micronutrients (thiamine) deficiency in the pathogenesis of ALN; however, it is assumed that these might induce the progression of ataxia or movement disorders 55, 57. 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.

Diabetes and alcohol consumption are the two most common underlying causes of peripheral neuropathy. Among diabetics, the prevalence of neuropathy with obvious symptoms (i.e., symptomatic neuropathy) increases with increasing disease duration. That increase in prevalence was most apparent in patients with a disease duration of less than 4 years.

• The data, however, is conflicting as to the role which malnutrition plays.
• Despite various therapeutic attempts, an approved treatment for Methanol-induced optic neuropathy (MION), a sight-threatening disorder, is still lacking.
• The main goal of a treatment program for alcoholic polyneuropathy is to improve quality of life and offer relief from symptoms.
• Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy.
• It’s not completely clear why some people are more prone to this complication than others.

In three patients, those changes did not reverse, even after months or years. The two other patients died as a result of complications indirectly related to their hypoglycemia-induced neurological changes. Therefore, to avoid alcohol-related hypoglycemia and its consequences, diabetics should consume alcohol only with or shortly after meals. A qualified and trained healthcare provider can diagnose it, but the diagnosis process almost always involves some form of diagnostic, imaging or laboratory testing. You may suspect you have peripheral neuropathy based on the symptoms you experience, but you should see a healthcare provider to be sure. Motor and sensory symptoms can also greatly disrupt your ability to work and go about your daily activities.

Uniquely, Vittadini and colleagues found a relationship between the type neuropathy alcohol risk of alcohol consumed and neuropathy. Specifically, the study demonstrated worse NCS study dysfunction amongst wine drinkers, than those who drank beer or spirits alone 6. The authors point out that this could be an anomaly due to the wine drinkers consuming more ethanol than other alcohol abusers but offer an alternative explanation that wine may contain more toxic impurities than other beverages.

• The action of these abnormal proteins is explained by competition with normal proteins causing the damage to function and metabolism of the cell 22.
• Alcohol enters the bloodstream from the digestive system within 5 minutes of consumption, and peak absorption is seen within 30 to 90 minutes.
• In fact, some studies have indicated that isolated episodes of drinking with a meal may have a beneficial effect by slightly lowering blood sugar levels that tend to rise too high in diabetics (Swade and Emanuele 1997).
• Peripheral neuropathy refers to damage or disease of the nerves that carry messages to and from the brain or spinal column and the rest of the body.

Peripheral neuropathy may be reversible in some cases, but many factors influence whether or not this is possible. Because there are so many factors involved, your healthcare provider should be the one to answer this question for you. The information they provide will be the most accurate and relevant for your specific case and circumstances.

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Reduced recruitment pattern of motor units was a frequently reported outcome 16, 28, 67, 70. Active denervation (presence of positive waves and fibrillations) was also present in the majority of patients. The prevalence of denervation findings on EMG ranged from muscle to muscle, with the highest being in the muscles of the lower limbs suggesting a length-dependent pattern 35, 45, 52, 59.