Article

Children surviving preterm birth have a high risk of disability, particularly
cognitive and learning problems. There is extensive clinical and experimental
evidence that disability is now primarily related to dysmaturation of white and
gray matter, defined by failure of oligodendrocyte maturation and neuronal
dendritic arborization, rather than cell death alone. The etiology of this
dysmaturation is multifactorial, with contributions from hypoxia-ischemia,
infection/inflammation and barotrauma. Intriguingly, these factors can interact
to both increase and decrease damage. In this review we summarize preclinical and
clinical evidence that all of these factors trigger secondary or chronic
inflammation and gliosis. Thus, we hypothesize that these shared pathological
features play a key role in a final common pathway that leads to the impaired
neural maturation and connectivity and cognitive/motor impairments that are
commonly observed in infants born preterm. This raises the possibility that
secondary or chronic inflammation may be a viable therapeutic target for delayed
interventions to improve neurodevelopmental outcomes after preterm birth. WHAT
THIS PAPER ADDS: Hypoxia-ischemia, infection/inflammation, and
barotrauma/volutrauma all contribute to preterm brain injury. Multiple different
triggers of preterm brain injury are associated with central nervous system
dysmaturation. Secondary brain inflammation may be a viable target to improve
neurodevelopment after preterm birth.
CI - (c) 2017 Mac Keith Press.

Langue : ANGLAIS