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]. The symptoms deteriorate through touch and pressure which intensify pain while standing or walking [124]. 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].

Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis appear to be implicated in this process [92,93,94,95,96,97]. Oxidative stress also leads to the indirect damage of nerve fibers via the release of free radicals and proinflammatory cytokines with protein kinase C and ERK kinase phosphorylation [98,99,100,101]. Besides, ALN is characterized by insulin and insulin-like growth factor (IGF) resistance, which results in impaired trophic factor signaling [102, 103]. The first reports about the possible role of excessive alcohol consumption and induction of ALN were introduced in 1787 [60]. Lettsom has observed that paralysis and hypoesthesia related to ALN presented a higher prevalence rate in lower limbs compared to upper limbs [60]. Hawley et al. followed up 11 patients with alcohol-related neuropathy who were abstinent from alcohol and who had begun to consume a normal diet [67].

Alcoholic Neuropathy

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]. In addition, patients with chronic alcoholism tend to consume smaller amounts of essential nutrients and vitamins and/or exhibit impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol.

Navarro et al. (1993) showed that nearly half of the alcohol-dependent patients without AAN symptoms and any aberrations in electrophysiologic studies presented abnormal SSR results [163]. 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]. Nine studies reported EMG findings in alcohol-related peripheral neuropathy patients.

Total number of myelinated axons from sciatic nerve (Naxons)

Superficial sensation, especially nociception, was predominantly impaired and painful symptoms were the primary complaint in most patients in this group. In contrast, the neuropathic symptoms of nonalcoholic thiamine deficiency neuropathy, considered to be identical to beriberi neuropathy [26], were variable, but typically were motor dominant and acutely progressive, affecting both superficial alcohol neuropathy stages and deep sensation. The histologic features of sural nerve biopsy specimens demonstrated small fibre predominant axonal loss as characteristic of the pure form of alcoholic 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.

• There are several possible causes of neuropathy, and knowing about a person’s alcohol intake can help the doctor to make an accurate diagnosis.
• Multiple research studies indicate that 11% to 66% of people with AUD have alcohol-induced PN.
• Miyoshi et al. [15] found that a significant decrease in the mechanical nociceptive threshold was observed after 5 weeks of chronic ethanol consumption in rats.