Alcoholic neuropathy: possible mechanisms and future treatment possibilities

The evidence of positive dynamics at peripheral and segmental nerve system level was supported by neurophysiological data. Benfotiamine was found to be beneficial in patients with alcoholic polyneuropathy 98. Chronic alcohol consumption can have deleterious effects on the central and peripheral nervous systems. One of the most common adverse effects seen in patients with chronic alcohol use disorder is alcohol neuropathy.

A connection between MEK/ERK signaling and alcoholic neuropathy

Primarily, thiamine deficiency is the crucial risk factor of ALN since it induces the progression of Korsakoff’s syndrome and beriberi 144, 145. Due to similar histologic and electrophysiological symptoms, it was believed that ALN may make up a subtype of beriberi 146. 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 alcoholic neuropathy the amount of vitamin B1 in the serum; further, patients who were involved in the study have received an unrefined form of the supplement.

• A common adverse effect of chronic alcohol consumption is alcohol neuropathy.
• There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine.
• A person can improve their outlook by significantly reducing or stopping their alcohol intake and ensuring that they are receiving the right balance of nutrients.
• In total, 585 papers did not meet the inclusion/exclusion criteria and were excluded.

Synthesis of results

The mouse 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.

Understanding and treating alcoholic neuropathy

When this message is interrupted due to damaged nerves, the muscles cannot function as they normally would. During the initial stages of ALN, the disease may appear asymptomatic and demonstrable only on electroneurographic investigation 71, 111, 112. Because ALN is a length-dependent axonopathy, it manifests mainly in a “stocking-glove” form, affecting the lower extremities at the beginning 28, 113. The main symptoms of ALN include dysesthesia, paresthesia, numbness, and pain in the lower extremities which progressively reach higher parts of the body 114,115,116,117. The pain is described as burning, cramp-like, or itching; also, a common symptom is a subjective feeling of cold in both feet 118,119,120,121,122,123.

What Are the Symptoms of Alcoholic Neuropathy?

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. Alcohol can have significant negative effects on the central nervoussystem (CNS). Drinking alcohol can also have negative effects on the peripheral nervous system (PNS). 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.

• Ethanol and its toxic metabolites affect neural metabolism including metabolic activities in the nucleus, lysosomes, peroxisomes, endoplasmic reticulum, and cytoplasm 104.
• For the most part this review consists of non-interventional studies for which generally accepted tools to evaluate risk of bias are not available.
• So, the nerve damage of alcoholic neuropathy is generally permanent and likely to worsen if the person does not stop drinking.
• It has been recognized that spinal cord glial cells, astrocytes and microglia are activated by neuropathic pain or peripheral inflammation 42.
• We do not know precisely how many people are affected by alcohol neuropathy, but research has shown that at least 66% of chronic alcohol abusers may have some form of neuropathy.

Depending on your individual insurance plan, treatment at a specific facility may or may not be covered. Use the free online insurance coverage checker tool below to find out if your health insurance provides coverage for addiction rehab  and other rehabilitation treatment plans for substance abuse recovery. If you are ready to learn more about addiction treatment, American Addiction Centers (AAC) is ready to help. AAC is a leading provider of evidence-based addiction treatment with facilities across the U.S.

What are symptoms of alcoholic neuropathy?

It is possible Sober living house that hepatic dysfunction and alcoholic toxicity each cause neuropathy independently, and that there is frequently overlap between the two. It may also be that comorbid hepatic dysfunction is a risk factor for alcohol-related peripheral neuropathy. Further studies are required to develop a greater understanding of the interaction these entities.

• Referral to a behavioral health addiction facility may be required to treat alcohol addiction.
• 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.

Alcoholic neuropathy has many of the same symptoms as peripheral neuropathy. For most, this includes a tingling, burning, or painful feeling in their legs, feet, arms, and hands. They may not feel strong sensations in these areas, either, due to the damage to the nerves. They may notice a weakness in their hands or that they have lost some of their coordination. Their balance can be affected due to the nerve damage in the legs and feet. The available data addressing the role of hepatic dysfunction is presently inconclusive.

Amongst those who did not respond to thiamine, two patients with grade I neuropathy and one with grade II responded with the correction https://ecosoberhouse.com/ of low circulating nicotinic acid. One patient with grade I neuropathy responded with the correction of low pantothenic acid. One patient with grade III neuropathy responded with the correction of low circulating vitamin B6.

These findings support the idea that the increased number of membrane-bound mGluR5 following chronic ethanol consumption may lead to a long lasting activation of neuronal protein kinase C in the dorsal horn of the spinal cord. This phenomenon may be responsible for the induction of the neuropathic pain like behaviour following chronic ethanol consumption. Not only mGluRs but ionotropic glutamate (NMDA) receptors are also involved in alcoholic-induced neuropathic pain.