Among individuals born very preterm, perinatal inflammation, particularly if sustained or recurring, is highly likely to contribute to adverse neurodevelopmental outcomes, including cerebral white matter damage, cerebral palsy, cognitive impairment, attention-deficit/hyperactivity disorder, and autism spectrum disorder. Antecedents and correlates of perinatal inflammation include socioeconomic disadvantage, maternal obesity, maternal infections, fetal growth restriction, neonatal sepsis, necrotizing enterocolitis, and prolonged mechanical ventilation. Genetic factors can modify susceptibility to perinatal inflammation and to neurodevelopmental disorders. Preliminary evidence supports a role of epigenetic markers as potential mediators of the presumed effects of preterm birth and/or its consequences on neurodevelopment later in life. Further study is needed of factors such as sex, psychosocial stressors, and environmental exposures that could modify the relationship of early life inflammation to later neurodevelopmental impairments. Also needed are pharmacological and non-pharmacological interventions to attenuate inflammation towards the goal of improving the neurodevelopment of individuals born very preterm.

在早产儿中，围产期炎症，尤其是持续或复发的炎症，很可能导致不良的神经发育结果，包括脑白质损害，脑瘫，认知障碍，注意力缺陷/多动障碍和自闭症谱系障碍。围产期炎症的前因和相关因素包括社会经济劣势，孕产妇肥胖，孕产妇感染，胎儿生长受限，新生儿败血症，坏死性小肠结肠炎和长期机械通气。遗传因素会改变围产期炎症和神经发育障碍的易感性。初步证据支持表观遗传标记作为早产的推测影响和/或其对生命后期神经发育的影响的潜在介质。需要进一步研究诸如性别，社会心理压力源和环境暴露等因素，这些因素可能会改变早期炎症与晚期神经发育障碍的关系。还需要药理学和非药理学干预以减轻炎症，以达到改善早产儿神经发育的目的。