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].

Factors Influencing Recovery

• Medical News Today publishes that medical procedures and therapies, medications, and adjunctive and alternative therapies are commonly used to treat alcoholic polyneuropathy.
• People who drink heavily on a regular basis are at risk of developing this condition.
• The decreases in nerve conduction velocity were significantly less in groups supplemented with acetyl-L-carnitine.
• Utilize adaptive aids, such as compression garments or braces, to keep affected limbs comfortable and relieve pressure on your axons.

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. These patients were divided into two groups based on thiamine status. 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.

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

The percentage of alcohol-dependent patients affected by ALN is estimated to be 66% [50, 51]. 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]. It is estimated that consumption of more than 100 ml of ethyl alcohol per day significantly increases the risk of ALN [56]. 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.

• Alcohol can have toxic effects on the body, especially in excessive amounts and over a long period of time.
• Joseph & Levine [71] suggested that activity in signaling pathways that ultimately lead to apoptosis plays a critical role in the generation of neuropathic pain, before death of sensory neurones becomes apparent.
• Untreated alcoholic neuropathy continues to worsen over time, and the effects can be permanent.
• The recovery time for alcoholic neuropathy varies significantly among individuals and is influenced by the severity of the neuropathy and the individual’s history of alcohol consumption.
• Depletion of glutathione increases the susceptibility of neurones to oxidative stress and hyperalgesia [43, 44].

Clinical Examination

Ongoing therapy and counseling can address the psychological aspects of addiction and help develop strategies for coping with the challenges of neuropathy. Not every person with a current or past history of alcohol alcohol neuropathy stages use develops serious nerve damage as a result of their drinking. There are certain factors some people may possess or be at risk for that can make them more likely to develop alcohol-related neuropathy.

Methylcobalamin for the treatment of peripheral neuropathy

• The most important strategy against alcoholic neuropathy lies in preventing the symptoms from getting worse by decreasing alcohol consumption as soon as possible.
• 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.
• However, neuropathy is generally an exclusion criterion for transplantation.

It was observed that abstinence may lead to the regression of several symptoms of AAN [159]. If you have a diagnosis of alcoholic neuropathy, abstinence from alcohol is the primary treatment to restore nerve function. Drinking alcohol with any neuropathy could cause further damage to nerves. Talk with your doctor before consuming alcohol if you have any diagnosis of peripheral neuropathy.

A wide range of support networks and medical treatments are available. Alcoholic neuropathy is a severe condition that can lead to pain, loss of some bodily functions, and loss of mobility. However, recognizing the symptoms and seeking medical attention early may minimize the impact of the condition. A doctor may suggest an inpatient detox when a person’s alcohol use disorder is very severe. They may also recommend other options, such as medications for alcohol reduction or cessation maintenance, support groups, and psychotherapy. The psychological impact of chronic conditions such as alcoholic neuropathy should not be underestimated.

Poor absorption and low intake of these vitamins have clinical features of dermatitis, neuropathy, and anorexia. Studies on this condition have estimated that up to 66 percent of chronic alcoholics develop permanent nerve damage as a result of their drinking. Long-term alcohol use can wreak havoc on several vital organs and essential functions in the body. As yet there is no effective therapeutic intervention available for relieving the neuropathic pain due to chronic alcohol consumption. Accumulating evidence suggests a pivotal role for metabotropic glutamate receptors (mGluRs) in nociceptive processing, inflammatory pain and hyperalgesia [74, 75].

The role of inflammation

Enhancing Healthcare Team Outcomes