Neurological and developmental outcomes of prenatally cocaine-exposed offspring from 12 to 36 months.
Neurological and developmental outcomes of prenatally cocaine-exposed offspring from 12 to 36 months.
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产前接触可卡因的后代 12 至 36 个月的神经学和发育结果。
DOI：
10.1081/ada-120037380
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发表时间：
2004
期刊：
影响因子：
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通讯作者：
Rosen,ToveS
中科院分区：
文献类型：
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作者：
Lewis,MarilynW;Misra,Sonya;Johnson,HelenL;Rosen,ToveS
第二代研究产前可卡因暴露未能发现总赤字后，控制混杂因素。人们仍然担心，接触可能会造成微妙的缺陷。这项前瞻性队列研究评估了可卡因在12、18、24和36个月时对发育的影响。从1991年到1993年，从纽约儿童医院、长老会医疗中心的产前诊所或产房套房招募了361对母婴。根据产前可卡因使用或尿液毒理学阳性的报告，将母亲分配到可卡因组。对照组的母亲从同一诊所登记，年龄和社会经济地位（SES）相匹配。有严重医疗问题的妇女被排除在两组之外。在保留的队列中，12个月时，147名婴儿暴露，89名为未暴露病例对照。这两组人都是在贫困的环境中长大的，几乎没有什么支持。对各组设盲进行发育评价。横断面分析显示，在所有时间段内，可卡因相关的神经系统检查和言语缺陷，尽管体重，身高和头围都有所赶上。使用广义估计方程回归分析评价了发育的总体分析。在控制混杂因素后，贝利精神发育指数[Badj= − 6.5（CI-9.4 − 3.5，p ≤ 0.001）]和心理发育指数[Badj= − 3.9（CI-7.4，− 0.5，p = 0.02）]显示出缺陷。男性在身高、运动发育和情绪调节方面更容易受到可卡因的影响。神经系统检查异常（p趋势< 0.08）、精神发育指数（MDI）（p趋势< 0.001）和精神发育指数（PDI）（p趋势< 0.001）缺陷存在剂量-反应关系。虽然未接触可卡因的儿童表现不佳，但接触可卡因的儿童表现更差。两组儿童在18个月时的智力和心理发育都有所下降，只有未接触过的儿童才有所反弹。总体而言，接触可卡因给弱势儿童的发育增加了额外的风险。暴露于可卡因的儿童对这些多重风险的影响的弹性较低。
Second generation studies of prenatal cocaine exposure failed to find gross deficits after controlling for confounders. Concern remained that exposure could cause subtle deficits. This prospective, cohort study evaluated effects of cocaine on development at 12, 18, 24, and 36 months. From 1991–1993, 361 mother‐infant pairs were recruited from the Children's Hospital of New York, Presbyterian Medical Center's prenatal clinic or delivery room suite. Mothers were assigned to the cocaine group based on report of prenatal cocaine use or positive urine toxicology. Control mothers were enrolled from the same clinic and matched for age and socioeconomic status (SES). Women with serious medical problems were excluded from either group. Of the retained cohort, at 12 months, 147 infants were exposed and 89 were unexposed case controls. Both groups were raised in impoverished environments with few supports. Developmental evaluations were conducted blinded to group. Cross‐sectional analysis revealed cocaine‐related deficits in neurological exams and speech across all time periods, in spite of catch up in weight, length, and head circumference. Overall analysis of development was evaluated using Generalized Estimating Equations regression analysis. Bayley Mental [Badj= − 6.5 (CI—9.4 − 3.5, p ≤ 0.001)] and Psychomotor [Badj= − 3.9 (CI—7.4, − 0.5, p = 0.02)] Developmental Indices showed deficits after controlling for confounders. Males were more vulnerable to cocaine exposure for height, motor development, and emotional regulation. Dose‐response relationships existed for abnormal neurological exams (ptrend< 0.08), Mental Development Index (MDI) (ptrend< 0.001), and Psychomotor Development Index (PDI) (ptrend< 0.001) deficits. Although nonexposed children performed poorly, cocaine‐exposed children showed worse performance. Both groups showed declines at 18 months in mental and psychomotor development from which only nonexposed children rebounded. Overall, cocaine exposure adds an additional risk to disadvantaged children's development. Cocaine‐exposed children are less resilient to effects of these multiple risks.