Alcoholic Neuropathy StatPearls NCBI Bookshelf

It has previously been considered in relationship to nutritional, especially thiamine, deficiencies seen in alcoholics. Thiamine deficiency is closely related to chronic alcoholism and can induce neuropathy alcohol neuropathy stages in alcoholic patients. Ethanol diminishes thiamine absorption in the intestine, reduces hepatic stores of thiamine and affects the phosphorylation of thiamine, which converts it to its active form [12].

How to prevent alcoholic neuropathy

The damage may be the direct result of long periods where you drank too much alcohol. Nutritional problems linked to alcohol use, such as vitamin deficiency, can also cause nerve damage. Not every person with a current or past history of alcohol use develops serious nerve damage as a result of their drinking.

• In general, it takes years for alcoholic neuropathy to develop, so a long-standing history of heavy alcohol use is typical.
• In a similar study, SSR was used to assess the number of reactive sweat glands (SGN), which turned out to be decreased in alcohol-dependent patients [164].
• Prolonged exposure to heavy alcohol use can damage these nerves, which can result in a number of uncomfortable and potentially-dangerous symptoms.

The role of oxidative stress

Proposed mechanisms include circulatory disturbances in liver cirrhosis, metabolic and neurohormonal (renin-angiotensin-aldosterone system) dysfunctions, excessive nitric oxide production, oxidative stress, and inflammatory mediators [11, 171]. There is a strong correlation between AAN and Child-Pugh scale which suggests that liver cirrhosis progression is related to impairments in ANS [172]. Alcohol-abusing patients with liver cirrhosis and vagus nerve neuropathy are at higher risk of a sudden death compared to patients without impairments within the nervous system [173, 174].

Perfusion and Nerve Dissection

People who struggle with alcoholism should try to eat a healthy and balanced diet, even if they don’t feel hungry. In a 2019 study, researchers showed that quitting alcohol had a positive effect on most people’s mental well-being. Completely avoiding alcohol and eating a balanced diet can help minimize damage.

Besides, the key mechanism of chronic pain includes the long-term potentiation of glutamatergic transmission. The percentage of alcohol-dependent patients affected by ALN is estimated to be 66% [50, 51]. The pathophysiology of ALN involves underlying mechanisms that include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters [52,53,54]. 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]. 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].

• A significant decrease in the activity of anti-oxidant enzymes (superoxide dismutase and catalase) and an increase in lipid peroxidation were observed in sciatic nerves of diabetic rats with established neuropathic pain [40].
• Orthotics using splints and braces should be explored to help with ambulation.
• CDT is an indirect metabolite of ethanol and constitutes either a marker of prolonged, heavy alcohol consumption or a marker of relapse.

• Many people who use alcohol neglect their diet, either eating too much or too little of essential nutrients important to maintaining good health.
• Computed tomography (CT) scans showed that among alcohol-dependent patients, the brain volumes were reduced to increase the volume of cerebrospinal fluid; these changes were induced in females in less time [135, 136].

These studies addressed abstinence from alcohol consumption and administration of vitamins. Nine studies reported EMG findings in alcohol-related peripheral neuropathy patients. 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].

Epidermal nerve fibre density was assessed in two studies, both of which supported decremental nerve fibre density distally in the lower limb, anecdotally supportive of a length-dependent pattern [53, 63]. The sometimes-conflicting findings between biopsy findings may be representative of the complex interplay of pathological factors in alcohol-related peripheral neuropathy and is indicative of the need for further research in this area. Alcoholic neuropathy is a severe condition that can lead to chronic pain, loss of some bodily functions, and permanent disability. However, recognizing the symptoms and seeking medical attention early can minimize the impact of the condition.

Food and water consumption; body mass variation; alcohol intake and its concentration in the blood

According to a 2017 review, muscle myopathy is common in alcohol use disorder. In addition, about 40 to 60 percent of people who experience chronic alcohol misuse also experience alcohol-related myopathy. It is likely to get worse if the person continues to use alcohol or if nutritional problems are not corrected. Alcoholic neuropathy is usually not life threatening, but it can severely affect quality of life.