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Peripheral systems: neuropathy.
Handb Clin Neurol. 2014; 125:513-25.HC

Abstract

Long-term, excessive consumption of alcoholic beverages produces a peripheral neuropathy with symptoms of decreased superficial sensation, hyperalgesia, and weakness. Alcoholic neuropathy is characterized by axonal degeneration with reduced density of both small and large fibers and axonal sprouting. Electrophysiologic studies reveal a marked reduction in the amplitude of sensory potentials and moderate slowing of nerve conduction, mainly in the lower extremities. Dietary deficiency of vitamins, which are often associated with chronic alcoholism, can contribute to the pathogenesis. Recent studies using animal models have identified several mechanisms by which ethanol impacts peripheral nerve function. Ethanol can exert direct neurotoxic effects on peripheral nerves via its metabolite acetaldehyde and by enhancing oxidative stress. Ethanol activation of protein kinase Cε signaling in primary afferent nociceptors plays an important role in lowering nociceptive threshold. Further, ethanol causes cytoskeletal dysfunction and inhibits both anterograde and retrograde axonal transport. Alcoholic neuropathy is potentially reversible and treatments include abstinence from alcoholic beverages and consumption of a nutritionally balanced diet supplemented with B vitamins. However, response to these treatment strategies can be variable, which underscores the need for novel therapeutic strategies. In this review, we provide an overview of the clinical findings and insights on molecular mechanisms from animal models.

Authors+Show Affiliations

College of Pharmacy, University of Texas, Austin, TX, USA.College of Pharmacy, University of Texas, Austin, TX, USA. Electronic address: romessing@austin.utexas.edu.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25307593

Citation

Maiya, Rajani P., and Robert O. Messing. "Peripheral Systems: Neuropathy." Handbook of Clinical Neurology, vol. 125, 2014, pp. 513-25.
Maiya RP, Messing RO. Peripheral systems: neuropathy. Handb Clin Neurol. 2014;125:513-25.
Maiya, R. P., & Messing, R. O. (2014). Peripheral systems: neuropathy. Handbook of Clinical Neurology, 125, 513-25. https://doi.org/10.1016/B978-0-444-62619-6.00029-X
Maiya RP, Messing RO. Peripheral Systems: Neuropathy. Handb Clin Neurol. 2014;125:513-25. PubMed PMID: 25307593.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peripheral systems: neuropathy. AU - Maiya,Rajani P, AU - Messing,Robert O, PY - 2014/10/14/entrez PY - 2014/10/14/pubmed PY - 2016/7/29/medline KW - acetaldehyde KW - alcohol use disorder KW - axonal transport KW - cytoskeleton KW - ethanol KW - folate KW - neuropathy KW - oxidative stress KW - pain KW - protein kinase C epsilon KW - thiamine SP - 513 EP - 25 JF - Handbook of clinical neurology JO - Handb Clin Neurol VL - 125 N2 - Long-term, excessive consumption of alcoholic beverages produces a peripheral neuropathy with symptoms of decreased superficial sensation, hyperalgesia, and weakness. Alcoholic neuropathy is characterized by axonal degeneration with reduced density of both small and large fibers and axonal sprouting. Electrophysiologic studies reveal a marked reduction in the amplitude of sensory potentials and moderate slowing of nerve conduction, mainly in the lower extremities. Dietary deficiency of vitamins, which are often associated with chronic alcoholism, can contribute to the pathogenesis. Recent studies using animal models have identified several mechanisms by which ethanol impacts peripheral nerve function. Ethanol can exert direct neurotoxic effects on peripheral nerves via its metabolite acetaldehyde and by enhancing oxidative stress. Ethanol activation of protein kinase Cε signaling in primary afferent nociceptors plays an important role in lowering nociceptive threshold. Further, ethanol causes cytoskeletal dysfunction and inhibits both anterograde and retrograde axonal transport. Alcoholic neuropathy is potentially reversible and treatments include abstinence from alcoholic beverages and consumption of a nutritionally balanced diet supplemented with B vitamins. However, response to these treatment strategies can be variable, which underscores the need for novel therapeutic strategies. In this review, we provide an overview of the clinical findings and insights on molecular mechanisms from animal models. SN - 0072-9752 UR - https://www.unboundmedicine.com/medline/citation/25307593/Peripheral_systems:_neuropathy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/B978-0-444-62619-6.00029-X DB - PRIME DP - Unbound Medicine ER -