Cited by 244Alcoholism and Thiamine DeficiencyPain Mechanisms and TreatmentsAlcohol Consumption and Health Effects

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

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Chopra, Kanwaljit, Tiwari, Vinod·2012·British Journal of Clinical Pharmacology

Abstract

Chronic alcohol consumption produces painful peripheral neuropathy for which there is no reliable successful therapy, mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy involves coasting caused by damage to nerves that results from long term excessive drinking of alcohol and is characterized by spontaneous burning pain, hyperalgesia and allodynia. The mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. These include activation of spinal cord microglia after chronic alcohol consumption, oxidative stress leading to free radical damage to nerves, activation of mGlu5 receptors in the spinal cord and activation of the sympathoadrenal and hypothalamo‐pituitary‐adrenal (HPA) axis. Nutritional deficiency (especially thiamine deficiency) and/or the direct toxic effect of alcohol or both have also been implicated in alcohol‐induced neuropathic pain. Treatment is directed towards halting further damage to the peripheral nerves and restoring their normal functioning. This can be achieved by alcohol abstinence and a nutritionally balanced diet supplemented by all B vitamins. However, in the setting of ongoing alcohol use, vitamin supplementation alone has not been convincingly shown to be sufficient for improvement in most patients. The present review is focused around the multiple pathways involved in the development of peripheral neuropathy associated with chronic alcohol intake and the different therapeutic agents which may find a place in the therapeutic armamentarium for both prevention and management of alcoholic neuropathy.

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  1. Ludin HP, Tackman W. Polyneuropathien. Stuttgart, New York: Georg Thieme Verlag, 1984; 250-55.
  2. Young MR, Fleetwood-Walker SM, Dickinson T, Blackburn-Munro G, Sparrow H, Birch PJ, Bountra C. Behavioural and electrophysiological evidence supporting a role for group I metabotropic glutamate receptors in the mediation of nociceptive inputs to the rat spinal cord. Brain Res 1997; 777: 161-9.
  3. Jia H, Rustioni A, Valtschanoff JG. Metabotropic glutamate receptors in superficial laminae of the rat dorsal horn. J Comp Neurol 1999; 410: 627-42.

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Authors
Chopra, K., & Tiwari, V.
Affiliations
Panjab University (IN)
Corresponding author
Chopra, Kanwaljit
Venue
British Journal of Clinical Pharmacology
Publisher
Wiley
Published
2012-02-13
Volume
73
Issue
3
Pages
348-362
ISSN
  • 0306-5251 (ISSN-L)
  • 1365-2125
OpenAlex
W1572142321
Cited by
244
References
133
Citations by year
2026: 10 · 2025: 22 · 2024: 25 · 2023: 26 · 2022: 23 · 2021: 17 · 2020: 20 · 2019: 23 · 2018: 15 · 2017: 13 · 2016: 9 · 2015: 9 · 2014: 17 · 2013: 14
FWCI
1.27
Type
journal article
Language
en
Open access
Locations
  • British Journal of Clinical Pharmacology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Alcoholism and Thiamine Deficiency
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Keywords
alcoholic neuropathy, chronic alcohol consumption, peripheral neuropathy, neuropathic pain, hyperalgesia, allodynia, oxidative stress, mGlu5 receptor, sympathoadrenal system, hypothalamic-pituitary-adrenal axis, thiamine deficiency, vitamin B12 supplementation, alcohol abstinence, neuropathic pain treatment
MeSH terms
Alcohol Drinking, Ethanol, Alcoholism, Humans, Hyperalgesia, Pain, Peripheral Nerves, Thiamine Deficiency, Time Factors, Pain Threshold, Alcoholic Neuropathy

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