Alcoholic Neuropathy: Causes, Symptoms, & Treatments

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.

Peripheral neuropathy

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].

• In general, it takes years for alcoholic neuropathy to develop, so a long-standing history of heavy alcohol use is typical.
• In this study, we observed that Wistar rats that consumed alcoholic solution (20%; v/v) for eight weeks showed initial signs of demyelinating lesions in the peripheral nervous system.
• This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration.

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• Progression of the disease leads to symmetrical ascending motor and sensory deficits.
• Many people who use alcohol neglect their diet, either eating too much or too little of essential nutrients important to maintaining good health.
• Peth on the other hand is a direct alcohol metabolite that can be measured to monitor alcohol consumption as well as for the identification of early signs of alcohol-related clinical manifestations.
• 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].

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.

The Aftereffects of Alcoholism: Alcoholic Neuropathy

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].

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 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].

• There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy.
• Another prominent effect of alcoholic neuropathy involves painful and uncomfortable sensations.
• Furthermore, astrocytes and microglia are activated by such pain relevant substances as substance P, calcitonin-gene related peptide (CGRP), ATP and excitatory amino acids from primary afferent terminals, in addition to viruses and bacteria [67, 68].
• Each slice was fixed in buffered 2.5% glutaraldehyde and stored in the same fixative for subsequent dehydration and embedding in Epon resin 812.

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.

Benfotiamine for the treatment of alcohol related peripheral neuropathy

Alcoholic neuropathy is one of the most common adverse effects of chronic alcohol consumption. There is damage to the nerves due to the direct toxic effect of alcohol and the malnutrition induced by it. Patients present with pain, ataxia and parasthesias in the lower extremities. This activity describes the evaluation and management of alcoholic neuropathy and reviews the role of the interprofessional team in improving care for patients with this condition. Chronic alcohol consumption leads to malnutrition with dysfunctions in protein and lipid metabolism which affect the metabolic pathways and progression of ALN symptoms within the central and peripheral nervous systems [89].

Selected systemic effects of heavy alcohol consumption

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 alcohol neuropathy stages 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].