Prenatal inflammation is the cause of 40-80% of premature births that correlates with an adverse neurodevelopmental outcome. Prenatal inflammation is histologically classified as chorioamnionitis, which can be associated with FIRS. FIRS correlates with a higher rate of neonatal morbidity and mortality. Chorioamnionitis and FIRS are associated with prenatal brain injury, which is a result of many contributing factors and inflammatory cascade that follows the activation of the fetal immune system. The circulating pro-inflammatory cytokines, lead to the weakening of the blood-brain barrier and induce a neuroinflammatory response through the activation of microglia and astrocytes. Pro-inflammatory cytokines affect a vulnerable cell population of pro-oligodendrocytes disrupting their normal maturation and growth. The most severe injury is detected in preterms between the gestational ages from 24 to 32 weeks, when pre-oligodendrocytes predominate in the white matter, causing the brain to be most vulnerable. The cause of the increased vulnerability is the pre-oligodendrocyte development is disruption and the normal maturation toward the myelinating cells is inhibited, leading to hypomyelination and disorganization of the white matter. The results of the studies are not unanimous and can be contradictory when associating chorioamnionitis and adverse neurodevelopmental outcome, which can be result of study heterogeneity, different diagnostic criteria, use of different tests and confounding variables. Since the studies are focused on the effect of chorioamnionitis on neurodevelopmental outcome, without confirmed FIRS, it is not possible to draw a conclusion on the correlation of prenatal inflammation and adverse neurodevelopmental outcome.