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Alcoholic Neuropathy

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Pathogenesis of Neuropathic Pain

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Abstract

Alcoholic neuropathy appears in approximately 25–66% of chronic alcoholics. It is associated with both the duration of alcohol abuse as well as the total lifetime alcohol consumption. Here is a higher prevalence with heavy and continuous alcohol abuse as compared to episodic binging; and there is a higher incidence in females than in males. The neuropathology of alcoholic exposure may manifest itself through supraspinal effects or as a peripheral neuropathy. The supraspinal component includes GABA receptors; calcium channels, excitatory amino acids, dopamine release, and adenosine transport and receptor binding.

The peripheral neuropathic effect of alcohol exposure involves several molecular mechanisms which will be described here and includes activation of microglia and mGlu5 receptors; oxidative stress and cytokine release associated with activation of protein kinase.

Treatment of alcohol neuropathy ranges from hepatic transplantation to a plethora of novel pharmacologic interventions to spinal cord stimulation.

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Authors and Affiliations

  1. Department of Anesthesia, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA

    Adaora Chima

  2. University of Rochester School of Medicine and Dentistry, Department of Anesthesiology, Rochester, NY, USA

    Daryl I. Smith

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  1. Adaora Chima
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  1. School of Medicine, University of Rochester, Rochester, NY, USA

    Daryl I. Smith

  2. School of Medicine, University of Rochester, Rochester, NY, USA

    Hai Tran

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Chima, A., Smith, D.I. (2022). Alcoholic Neuropathy. In: Smith, D.I., Tran, H. (eds) Pathogenesis of Neuropathic Pain. Springer, Cham. https://doi.org/10.1007/978-3-030-91455-4_9

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