El Shahed Amr, Chau Vann, Terry Jefferson, Whitehead Clare, Synnes Anne, Grunau Ruth, Miller Steven P
Department of Pediatrics, the Hospital for Sick Children and the University of Toronto, Toronto, ON, Canada.
Neurosciences and Mental Health Research Institute, Toronto, ON, Canada.
Pediatr Res. 2025 Feb 25. doi: 10.1038/s41390-025-03945-x.
To determine the relationship between presumed preterm birth (PTB) etiology and the incidence of brain injury, and neurodevelopmental outcomes at 3 and 4.5 years.
Prospective cohort study including 222 neonates born at 24-32 weeks' gestation. The presumed PTB etiology was defined by placental histopathology and other clinical features. Outcome measures included brain injury defined on MRI, neurodevelopmental outcomes using the Bayley Scales of Infant and Toddler Development, the Movement Assessment Battery for Children, Wechsler Preschool and Primary Scale of Intelligence, Beery Buktenica Developmental Test of Visual-Motor Integration.
Presumed PTB etiology was inflammatory in 85 (38%), vascular in 57 (25%), multiple gestation in 56 (25%) and idiopathic in 24 (11%) neonates. Cognitive outcome at 3 years was marginally lower in the inflammatory group (Beta = -6.2, P = 0.05) relative to multiple gestation. At 4.5 years, white matter injury was associated with significantly lower motor scores (P = 0.004) and there were no significant associations between PTB etiology and WPPSI-III IQ scales or MABC-2 scores.
The lack of association between presumed PTB etiology (using integrated clinical phenotype and placental pathology) and cognitive/motor outcomes suggests that postnatal morbidities and brain injury are pivotal in the neurodevelopmental trajectory of these infants.
The presumed etiology of preterm birth (PTB), based on placental histopathology and clinical features, does not predict long-term neurodevelopmental outcomes, such as cognitive scores at 4.5 years. Postnatal factors, including neonatal morbidities (e.g., bronchopulmonary dysplasia, retinopathy of prematurity, brain injury), are more significant in determining neurodevelopmental outcomes than the initial PTB cause. Placental histopathology helps identify PTB causes but shows no direct link to brain injury or neurodevelopmental outcomes. Infants with "idiopathic" PTB (no clear cause) have the greatest white matter injury burden, suggesting genetic or unrecognized factors.
确定推测的早产病因与脑损伤发生率以及3岁和4.5岁时神经发育结局之间的关系。
前瞻性队列研究，纳入222例孕24 - 32周出生的新生儿。根据胎盘组织病理学和其他临床特征确定推测的早产病因。结局指标包括MRI定义的脑损伤、使用贝利婴幼儿发展量表、儿童运动评估量表、韦氏学前和小学智力量表、贝利视觉运动整合发育测验评估的神经发育结局。
推测的早产病因中，85例（38%）为炎症性，57例（25%）为血管性，56例（25%）为多胎妊娠，24例（11%）为特发性。与多胎妊娠组相比，炎症组3岁时的认知结局略低（β = -6.2，P = 0.05）。在4.5岁时，白质损伤与运动评分显著降低相关（P = 0.004），早产病因与韦氏学前和小学智力量表III智商量表或儿童运动评估量表 - 2评分之间无显著关联。
推测的早产病因（采用综合临床表型和胎盘病理学）与认知/运动结局之间缺乏关联，提示出生后疾病和脑损伤在这些婴儿的神经发育轨迹中起关键作用。
基于胎盘组织病理学和临床特征推测的早产病因不能预测长期神经发育结局，如4.5岁时的认知评分。出生后因素，包括新生儿疾病（如支气管肺发育不良、早产儿视网膜病变、脑损伤），在决定神经发育结局方面比最初的早产原因更重要。胎盘组织病理学有助于确定早产原因，但与脑损伤或神经发育结局无直接联系。“特发性”早产（无明确原因）的婴儿白质损伤负担最大，提示存在遗传或未被认识的因素。
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