Inflammation in white matter: Clinical and pathophysiological aspects

David E Pleasure, Athena Soulika, Sunit K. Singh, Vittorio Gallo, Peter Bannerman

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

While the central nervous system (CNS) is generally thought of as an immunopriviledged site, immune-mediated CNS white matter damage can occur in both the perinatal period and in adults, and can result in severe and persistent neurological deficits. Periventricular leukomalacia (PVL) is an inflammatory white matter disease of premature infants that frequently results in cerebral palsy (CP). Clinical and experimental studies show that both hypoxic/ischemic and innate immune mechanisms contribute to the destruction of immature oligodendroglia and of axons in the deep cerebral white matter in PVL. No data are yet available as to whether there is any genetic predisposition to PVL or to its neurological sequelae. Multiple sclerosis (MS) is an inflammatory white matter disease that often begins in young adulthood, causes multifocal destruction of mature oligodendroglia and of axons, and eventually leads to substantial cumulative neurological disability. Certain genetic polymorphisms contribute to susceptibility to MS, and adaptive immune responses to myelin-associated self antigens, or to exogenous antigens that mimic these self antigens, play a central role in the pathophysiology of this disease.

Original languageEnglish (US)
Pages (from-to)141-146
Number of pages6
JournalMental Retardation and Developmental Disabilities Research Reviews
Volume12
Issue number2
DOIs
StatePublished - 2006

Keywords

  • Axonal disruption
  • Inflammation
  • Multiple sclerosis
  • Oligodendroglia
  • Periventricular leukomalacia

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Neuropsychology and Physiological Psychology
  • Genetics(clinical)

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