摘要：Preterm newborns represent a high-risk population for brain damage, primarily affecting the
white matter, and for related neurodevelopmental disabilities. Determinants of brain damage have been
extensively investigated, but there are still many controversies on how these factors can influence the developing
brain and provoke damage. The concept of etiological pathway, instead of a single determinant, appears to better
explain pathogenetic mechanisms: the brain damage may represent the final outcome of exposure to several
combinations of risk factors in the same pathway or in different pathways and can change according to the
gestational age. The aim of this article is to review the current knowledge on the pathogenesis of brain damage
in preterm infants, within the frame of two main theoretical models, the ischemic and the inflammatory
pathway. The relationship between the two pathways and the contribution of genetic susceptibility to ischemic
and/or inflammatory insult, in modulating the extent and severity of brain damage, is also discussed.
