Lester Barry M, Bagner Daniel M, Liu Jing, LaGasse Linda L, Seifer Ronald, Bauer Charles R, Shankaran Seetha, Bada Henrietta, Higgins Rosemary D, Das Abhik
Department of Pediatrics, Brown Center for the Study of Children at Risk, Women and Infants' Hospital, Brown University, Providence, Rhode Island 02905, USA.
Pediatrics. 2009 Nov;124(5):1355-62. doi: 10.1542/peds.2008-2898. Epub 2009 Oct 12.
The objective of this study was to test a developmental model of neurobehavioral dysregulation relating prenatal substance exposure to behavior problems at age 7.
The sample included 360 cocaine-exposed and 480 unexposed children from lower to lower middle class families of which 78% were black. Structural equation modeling was used to test models whereby prenatal exposure to cocaine and other substances would result in neurobehavioral dysregulation in infancy, which would predict externalizing and internalizing behavior problems in early childhood. Structural equation models were developed for individual and combined parent and teacher report for externalizing, internalizing, and total problem scores on the Child Behavior Checklist.
The goodness-of-fit statistics indicated that all of the models met criteria for adequate fit with 7 of the 9 models explaining 18% to 60% of the variance in behavior problems at age 7. The paths in the models indicate that there are direct effects of prenatal substance exposure on 7-year behavior problems as well as indirect effects, including neurobehavioral dysregulation.
Prenatal substance exposure affects behavior problems at age 7 through 2 mechanisms. The direct pathway is consistent with a teratogenic effect. Indirect pathways suggest cascading effects whereby prenatal substance exposure results in neurobehavioral dysregulation manifesting as deviations in later behavioral expression. Developmental models provide an understanding of pathways that describe how prenatal substance exposure affects child outcome and have significant implications for early identification and prevention.
本研究的目的是检验一个神经行为失调的发展模型,该模型将产前物质暴露与7岁时的行为问题联系起来。
样本包括360名暴露于可卡因的儿童和480名未暴露的儿童,他们来自中下阶层家庭,其中78%为黑人。采用结构方程模型来检验模型,即产前暴露于可卡因和其他物质会导致婴儿期神经行为失调,这将预测幼儿期的外化和内化行为问题。针对儿童行为清单上外化、内化和总问题得分的个体报告以及家长和教师的综合报告,开发了结构方程模型。
拟合优度统计表明,所有模型均符合充分拟合的标准,9个模型中的7个解释了7岁时行为问题方差的18%至60%。模型中的路径表明,产前物质暴露对7岁时的行为问题有直接影响,也有间接影响,包括神经行为失调。
产前物质暴露通过两种机制影响7岁时的行为问题。直接途径与致畸效应一致。间接途径表明存在级联效应,即产前物质暴露导致神经行为失调,表现为后期行为表达的偏差。发展模型有助于理解产前物质暴露如何影响儿童结局的途径,对早期识别和预防具有重要意义。