American Journal of Epidemiology Original Contribution Maternal Antenatal Complications and the Risk of Neonatal Cerebral White Matter Damage and Later Cerebral Palsy in Children Born at an Extremely Low Gestational Age

American Journal of Epidemiology Original Contribution Maternal Antenatal Complications and the Risk of Neonatal Cerebral White Matter Damage and Later Cerebral Palsy in Children Born at an Extremely Low Gestational Age
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通讯作者:
T. McElrath;E. Allred;K. Boggess;K. Kuban;T. Michael O 'shea
T. McElrath;E. Allred;K. Boggess;K. Kuban;T. Michael O 'shea
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作者:
T. McElrath;E. Allred;K. Boggess;K. Kuban;T. Michael O 'shea

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在一项2002-2004年的前瞻性队列研究中,作者在14个美国中心对小于28周分娩的婴儿进行了研究,寻找新生儿颅超声扫描中明显的白质损伤(脑室肿大和回声病变)和2岁时脑瘫诊断的前兆。在纳入的1455名婴儿中,母亲产前接受类固醇治疗的婴儿患脑室肿大和泛光性病变的风险低于同龄人(分别为10%对23%,P < 0.001和7%对11%,P < 0.06)。与子痫前期分娩的婴儿相比,早产分娩的婴儿患脑室肥大的风险增加(校正优势比5)。早产(OR¼2.7,95% CI: 1.2, 5.7)和宫内生长迟缓(OR¼3.3,95% CI: 1.2, 9.4)导致新生儿出现透光性病变的风险增加。与早产和早产胎膜早破相关的腹泻风险增加一倍没有统计学意义,与宫颈功能不全相关的四肢瘫风险增加一倍和腹泻风险增加两倍也没有统计学意义。极低胎龄(<28周)出生的婴儿出现新生儿白质损伤和后来的运动、认知和行为障碍的风险增加(1)。对于极低胎龄和脑白质损伤之间的联系,一种解释是,导致早产的疾病也会损害发育中的大脑(2)。有了这个解释,妊娠障碍及其相关因素是潜在的关注焦点(3-6)。当婴儿在重症监护室时,颅骨超声病变明显,可以预测数年后脑瘫的诊断(7)。然而,对白质损伤和脑瘫之间联系的解释不需要援引任何怀孕或产前特征。相反,他们认为表明白质损伤的病变是这种疾病的最早表现,而这种疾病多年后会在临床上表现为运动功能障碍(8,9)。脑室肿大和回声病变被认为是白质损伤不同方面的指标,脑室肿大是弥漫性白质损伤的标志,回声病变是局灶性白质损伤的标志(10)。我们对28周前出生的婴儿进行了大样本研究,使我们能够评估妊娠障碍及其临床相关性如何预测产后早期脑白质损伤以及后来脑瘫诊断为四肢瘫、足瘫和偏瘫。因为这些
In a 2002–2004 prospective cohort study of deliveries of infants at <28 weeks at 14 US centers, the authors sought the antecedents of white matter damage evident in newborn cranial ultrasound scans (ventriculomegaly and an echolucent lesion) and of cerebral palsy diagnoses at age 2 years. Of the 1,455 infants enrolled, those whose mothers received an antenatal steroid tended to have lower risks of ventriculomegaly and an echolucent lesion than their peers (10% vs. 23%, P < 0.001 and 7% vs. 11%, P ¼ 0.06, respectively). Risk of ventriculo-megaly was increased for infants delivered because of preterm labor (adjusted odds ratio5) when compared with infants delivered because of pre-eclampsia. Risk of an echolucent lesion was increased for infants delivered because of preterm labor (OR ¼ 2.7, 95% CI: 1.2, 5.7) and intrauterine growth retardation (OR ¼ 3.3, 95% CI: 1.2, 9.4). The doubling of diparesis risk associated with preterm labor and with preterm premature rupture of fetal membranes did not achieve statistical significance, nor did the doubling of quadriparesis risk and the tripling of diparesis risk associated with cervical insufficiency. Babies born at extremely low gestational ages (<28 weeks) are at increased risk of neonatal white matter damage and later motor, cognitive, and behavioral impairments (1). One explanation for the link between extremely low gestational age and cerebral white matter damage is that the same disorders that lead to preterm birth can also damage the developing brain (2). With this explanation, the pregnancy disorder and its correlates are the potential focus of attention (3–6). Cranial ultrasound lesions evident when the infant is in the intensive care nursery predict cerebral palsy diagnoses years later (7). However, explanations for the link between white matter damage and cerebral palsy need not invoke any pregnancy or prenatal characteristic. Rather, they view lesions indicative of white matter damage as the earliest expression of the very disorder that will become clinically evident years later as movement dysfunctions (8, 9). Ven-triculomegaly and an echolucent lesion are considered indicators for different aspects of white matter damage, with ventriculomegaly a marker of diffuse and echolucent lesion a marker of focal white matter damage (10). Our large sample of infants born before the 28th week enabled us to assess how well pregnancy disorders and their clinical correlates predict early postnatal cerebral white matter damage and the later cerebral palsy diagnoses of quadriparesis, diparesis, and hemiparesis. Because these