Alcoholic Neuropathy: Symptoms, Causes, Treatments

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]. 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]. The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. 87 articles were included in this review, 29 case–control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies.

Symptoms Of Alcoholic Neuropathy

Further research has confirmed the role of thiamine in the pathogenesis of ALN—the well-balanced diet and vitamin B1 supplementation significantly decreased the severity of ALN symptoms [147, 148]. However, the limitations of those studies include the lack of the possibility to measure the amount of vitamin B1 in the serum; further, patients who were involved in the study have received an unrefined form of the supplement. Later, the results have been supported by Victor and Adams (1961)—among 12 patients with ALN, neuropathic symptoms were alleviated just after thiamine supplementation, even though the alcohol consumption was previously completely reduced [149]. Koike et al. (2003) compared clinical and histological differences between ALN with and without thiamine deficiency [65].

Role of caspases in alcoholic neuropathy

A healthcare professional can offer support for people with alcohol use disorder. A doctor may also recommend treatments to manage neurological symptoms, such as pain relief medications, physical therapy, and mobility aids. Alcoholic neuropathy refers to nerve damage resulting from chronic heavy alcohol use.

• They may also recommend other options, such as medications for alcohol reduction or cessation maintenance, support groups, and psychotherapy.
• For instance, this condition can disrupt the body’s ability to sense temperature changes, making a person more likely to suffer heat stroke or burns.
• The most effective way to treat alcoholic polyneuropathy is to seek professional help from a medical doctor.
• Specifically, the study demonstrated worse NCS study dysfunction amongst wine drinkers, than those who drank beer or spirits alone [6].
• Based on these studies, it can be determined that there is a high rate of peripheral neuropathy amongst chronic alcohol abusers.
• It also appears that the addition of NCS may improve the identification of alcohol-related peripheral neuropathy.

Topical Collection on The Pathobiology of Alcohol Consumption

This phenomenon varied according to different susceptibility of genetic patterns, suggesting that nerve injury is influenced by individual genetic characteristics, in addition to chronicity and ingested volume of alcohol (Goldman et al., 2005, Mellion et al., 2013). No significant difference between groups was observed in food and water consumption as well as in body mass gain at the end of the treatment, as demonstrated in our previous work (Conte et al., 2019a, Conte et al., 2019b) that used the same animals. 1 shows the intake profile of alcohol solution and water by the animals of the two groups. It includes more than 30 independent observation parameters, which are grouped into domains.

Perfusion and Nerve Dissection

• Because ALN is a length-dependent axonopathy, it manifests mainly in a “stocking-glove” form, affecting the lower extremities at the beginning [28, 113].
• Physical therapy and orthopedic appliances (such as splints) may be needed to maintain muscle function and limb position.
• Symptoms of alcohol-related nerve damage develop gradually over time, and can become worse without treatment.
• Due to similar histologic and electrophysiological symptoms, it was believed that ALN may make up a subtype of beriberi [146].
• However, the limitations of those studies include the lack of the possibility to measure the amount of vitamin B1 in the serum; further, patients who were involved in the study have received an unrefined form of the supplement.

The diagnosis of alcoholic neuropathy involves a combination of medical history, physical examination, and possibly blood tests or nerve tests such as electromyography (EMG) and nerve conduction studies (NCV). 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. Both the toxicity of alcohol and nutritional deficiencies have been linked with alcoholic neuropathy, which is one of the most common but least recognizable consequences of heavy alcohol use.

• A mechanism of cisplatin chemotherapy-induced peripheral neuropathy was elucidated in an in vitro mouse model.
• Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy.
• It is likely to get worse if the person continues to use alcohol or if nutritional problems are not corrected.
• Ethanol and its toxic metabolites affect neural metabolism including metabolic activities in the nucleus, lysosomes, peroxisomes, endoplasmic reticulum, and cytoplasm [104].
• Alcoholic neuropathy is nerve damage that results from the toxic effect of alcohol on nerves.
• However, it is most common among people with a history of heavy, long-term alcohol use.

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. Sometimes alcohol causes such severe damage to the body that a liver transplant may be necessary. In this case, there may be some improvement in the symptoms of alcoholic neuropathy after the liver transplant, but the neuropathy may also be so advanced that there may be little, if any, improvement, even after a transplant. Alcoholic neuropathy is caused by nutritional deficiency, as well as toxins that build up in the body.

Progressed disease

Further progression of ALN leads to the weakening of tendon reflexes or total areflexia and disturbed proprioception, which additionally impair the ability to walk [28, 113]. ALN further manifests as weakness and atrophy alcohol neuropathy stages of muscles due to the damage of greater motor fibers and impaired neuromuscular transmission. The first reports about the possible role of excessive alcohol consumption and induction of ALN were introduced in 1787 [60].

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Regarding the autonomic domain, we evaluated lacrimation, pupil size, palpebral closure, salivation, piloerection, and breathing parameters. The behavioral domain was assessed by observation of spontaneous activity (hyperactivity), affective response (reactivity to catching and handling, defecation, and urination), and sensorial responses (touch response and tail-pinch response). On test day, the reactivity of each animal was examined by manipulation and stimuli while they were still in their cages or when placed in the arena of the open field test. It is important to supplement the diet with vitamins, including thiamine and folic acid. Autonomic nerves are concerned with muscular functions which are reflexive, such as breathing, heartbeats and peristalsis (rhythmic movements of the intestines). Based upon these results, vitamin supplementation appears to exert a positive therapeutic effect in alcohol-related neuropathy.

Alcoholic Neuropathy Clinical Presentation

Furthermore, females tend to be more vulnerable to the brain damage and neurotoxic effects of alcohol [134]. 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]. Ammendola et al. (2000) showed an inverse correlation of the sensory-evoked potential (SEP) amplitude of the sural nerve which informs about sensory dysfunctions and is altered even in asymptomatic patients throughout the course alcohol dependence [137]. The mouse https://ecosoberhouse.com/article/alcohol-vs-drugs-comparison-of-addictions/ model of the injection of β-estradiol in males resulted in higher activity of cytosolic alcohol dehydrogenase (ADH), microsomal aniline hydroxylase (ANH), and aldehyde dehydrogenase (ALDH) which are crucial in ethanol metabolism [138]. Female mouse with injected testosterone showed the decreased activity of cytosolic isoform of ALDH which implies that those enzymes are sensitive to estrogen and testosterone and alcohol metabolism is greater in females. In one clinical study, aimed at studying distinct clinicopathologic features of alcoholic neuropathy, 64 patients were assessed.