Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options Current Pathobiology Reports

Acetyl-L-carnitine has been tested in clinical [102] and animal studies [103] for the treatment of chemotherapy-induced peripheral neuropathy. The decreases in nerve conduction velocity were significantly less in groups supplemented with acetyl-L-carnitine. In addition, acetyl-L-carnitine did not interfere with the antitumour effects of the drugs. Izumi et al. [73] also demonstrated that a single day of ethanol exposure in rats on post natal day 7 results in significant apoptotic neuronal damage throughout the forebrain after 24 h of ethanol administration.

alcohol neuropathy stages

Many different stimuli, including growth factors, cytokines, viral infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. There are many studies suggesting the role of MEK/ERK signaling in inflammatory pain in male [60–63] and female rats [64]. The primary axonal damage and secondary demyelination of motor and sensory fibres (especially small diameter fibres) are considered to constitute the morphologic basis of alcoholic alcohol neuropathy stages damage to nerve tissue at present [20]. The demyelination is explained as the result of a slowing down (decceleration) of axoplasmic flow and a degradation of the quality of biological properties of axonal enzymes and proteins. This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration. Ethanol and its toxic degradation metabolites affect neuronal metabolism including the metabolic pathways of nucleus, lysosomes, peroxisomes, endoplasmatic reticulum and cytoplasm [21].


Reprinted with permission from Tozakidou M, et al, Neurology.16 © 2011, American Academy of Neurology. When your pain starts to progress, that’s a sign that your nerves are dying. When your peripheral or diabetic neuropathy reaches stage two, your pain and numbness will be more consistent. Many people brush off the symptoms in the first stage because the pain is only noticeable every once in a while, and it’s usually manageable. It is important to seek medical attention as soon as symptoms appear, as early detection and intervention can help manage the condition and potentially slow its progression.

alcohol neuropathy stages

Alcoholic neuropathy is one of the most common but least recognizable consequences of heavy alcohol use. People with a long history of alcohol misuse might experience loss of balance, pain, tingling, weakness, or numbness after drinking alcohol. Treatment involves reducing or eliminating alcohol intake to prevent further nerve damage and managing symptoms through medications, physical therapy, nutritional supplements, and lifestyle changes like diet and exercise. Preventing alcoholic neuropathy is fundamentally about managing our alcohol intake. It’s about understanding the role alcohol plays in our lives and finding healthier alternatives to cope with stress, socialize, and relax. Recognizing the early signs and seeking prompt treatment can significantly mitigate the condition’s impact, allowing for better treatment outcomes and reducing the risk of permanent damage.

Alcohol Abuse Diagnostic Criteria and Biomarkers

ALN is a potentially significant and debilitating complication of alcoholism. The evidence is accruing that ALN should be reclassified as a toxic, rather than nutritional neuropathy. ALN has clinical and electrophysiological features distinct from but overlapping with neuropathy from pure thia-mine deficiency (beriberi).

The ethanol consumption of these patients was more than 100 g day–1 for more than 10 years. 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. Superficial sensation, especially nociception, was predominantly impaired and painful symptoms were the primary complaint in most patients in this group.