Demyelination in multiple sclerosis

Handb Clin Neurol. 2014;122:89-99. doi: 10.1016/B978-0-444-52001-2.00004-2.


This review, focused on demyelination in multiple sclerosis, is divided in two parts. The first part addresses the many and not exclusive mechanisms leading to demyelination in the central nervous system. Although the hypothesis that a primary oligodendrocyte or myelin injury induces a secondary immune response in the central nervous system is still a matter of debate, most recent advances underline the influence of a primary immune response against myelin antigen(s), with a diversity of potential targets. Whereas multiple sclerosis was long considered as a T cell-mediated disease, the role of B lymphocytes is now increasingly recognized, and the influence of antibodies on tissue damage actively investigated. The second part of the review describes the axonal consequences of demyelination. Segmental demyelination results in conduction block or slowing of conduction through adaptative responses, notably related to modifications in the distribution of voltage gated sodium channels along the denuded axon. If demyelination persists, these changes, as well as the loss of trophic and metabolic support, will lead to irreversible axonal damage and loss. In this respect, favouring early myelin repair, during a window of time when axonal damage is still reversible, might pave the way for neuroprotection.

Keywords: adaptive immunity; antibodies; antigens; autoimmunity; cytokines; inflammation; injury; innate immunity; mechanisms; myelin proteins; neuronal damage; oligodendrocytes.

Publication types

  • Review

MeSH terms

  • Animals
  • Axons / immunology
  • Axons / metabolism
  • Axons / pathology
  • Demyelinating Diseases / immunology*
  • Demyelinating Diseases / metabolism
  • Humans
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / metabolism*
  • Myelin Sheath / immunology
  • Myelin Sheath / pathology*
  • Oligodendroglia / cytology
  • Sodium Channels / metabolism


  • Sodium Channels