Abstinence from alcohol as a part of the treatment plan will help provide the best outcome to enhance the patient’s quality of life. Nerve degeneration progresses from sensory symptoms to include motor function problems of the lower and upper extremities. Patients may stand and walk with a wide base of support to maintain balance.

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. Thus, it is quite possible that chronic alcohol consumption is responsible for inducing neuropathy by activation of the caspase cascade and may be an important target for the treatment of alcoholic neuropathy. Spinal cord glial cells are implicated in the exaggerated pain state created by diverse manipulations such as subcutaneous inflammation, neuropathy and spinal immune activation [65, 66]. It has been recognized that spinal cord glial cells, astrocytes and microglia are activated by neuropathic pain or peripheral inflammation [42]. 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].

Direct toxic effects of ethanol or its metabolites (direct toxicity)

Once alcohol use has been addressed, your doctor can focus on the neuropathy itself. Nerve damage can also make it difficult for you to carry out the functions of daily life. The total number of axons was estimated directly with the physical fractionator method (Gundersen, 1986, Mayhew and Olsen, 1991). This method consists of distribution from counting fields which are systematically and evenly displaced (in a SURS way) on the whole nerve cross-section.

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. The aim of this systematic review is to characterise the presentation of alcohol-related peripheral https://ecosoberhouse.com/ neuropathy, to determine the typical ancillary test results, to establish the importance of various risk factors and to explore the likely pathogenetic mechanisms. Due to the breadth of the literature surrounding this topic, this review shall focus exclusively upon peripheral neuropathy, without discussing autonomic neuropathy.

Peripheral neuropathy

However, some people notice an improvement in symptoms a few months after discontinuing alcohol intake. Both the toxicity of alcohol and nutritional deficiencies in those who drink heavily have been linked with nerve pain in alcoholic neuropathy. 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. In a study by Mellion et al. (2013) with three different strains of rats, they investigated the effects of alcohol exposure on nerves and muscles. 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.

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].

Increased Pain and Hypersensitivity

It was proposed that ALN pathogenesis, besides thiamine deficiency itself, could be due to its inappropriate use in the organism or transketolase deficiency [150]. Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153]. ALN is characterized by spontaneous burning pain, hyperalgesia, and allodynia.

• 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 damage to nerve tissue at present [20].
• In addition, 32 patients with nonalcoholic thiamine deficiency neuropathy were also evaluated for comparison.
• Has been contributing to medical fields including mental health and addiction since she retired from medicine; with over 19 years of practicing clinical experience.
• Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol [6, 13].

Chronic and excessive alcohol consumption is the primary cause of peripheral neuropathy. It is worth noting that peripheral neuropathy has no reliable treatment due to the poor understanding of its pathology. The available data addressing the role of hepatic dysfunction is presently inconclusive. It is possible that hepatic dysfunction alcohol neuropathy 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.