Traumatic Injury to Peripheral Nerves

Shlomo Rotshenker*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

10 Scopus citations

Abstract

Neural-dependent functions are lost when traumatic injury to peripheral nerves severs their axons. Functions recover successfully when axons regenerate rapidly so that prompt reinnervation and restoration of function can follow. Repair fails when regeneration and reinnervation are delayed. The timing of regeneration and reinnervation is affected by the type of injury, the distance of the lesion site from the target tissues, and the nature of cellular and molecular events of Wallerian degeneration that injury induces in the nerve segment situated distal to the lesion site and through which the severed axons regenerate back to their target tissues. Wallerian degeneration is essential to repair because it renders the peripheral nerve tissue permissive to and supportive of axonal regeneration. In this context, innate immunity is central to Wallerian degeneration and repair because innate-immune cells, molecules, and functions control Wallerian degeneration.

Original languageEnglish
Title of host publicationNerves and Nerve Injuries
Subtitle of host publicationPain, Treatment, Injury, Disease and Future Directions: Vol 2
PublisherElsevier
Pages611-628
Number of pages18
Volume2
ISBN (Electronic)9780128026533
ISBN (Print)9780128026953
DOIs
StatePublished - 1 Jan 2015

Bibliographical note

Publisher Copyright:
© 2015 Elsevier Ltd. All rights reserved.

Keywords

  • Axonal regeneration
  • Cytokine
  • Inflammation
  • Innate-immunity cells
  • Macrophage
  • Myelin
  • Phagocytosis
  • Schwann cell
  • Wallerian degeneration

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