背景:产前物质暴露(PSE)可导致胎儿发育中的各种有害结果,并与许多情绪有关,行为,以及以后生活中的认知困难。因此,检查相关大脑结构的发育与PSE之间的关系对于开发更具体或新的预防方法很重要。
目的:我们的研究的主要目的是检查杏仁核的身体发育之间的关系,海马体,产前饮酒后海马旁,烟草,和处方阿片类药物暴露。
方法:我们进行了青少年大脑和认知发育的横断面分析(ABCD)研究,一项纵向神经成像研究,测量从童年到青春期的大脑形态。数据来自美国22个地点的大约12,000名儿童(9岁和10岁)和父母。产前阿片类药物,烟草,和酒精的使用是通过父母在怀孕期间使用的自我报告来确定的。我们提取了评估杏仁核体积大小(mm3)的变量,海马体,海马旁回以及脑容量,贫困水平,年龄,性别,和种族/民族在我们调整后的模型中进行控制。我们报告了总体样本和患有PSE的儿童的社会人口统计学特征。我们通过物质暴露计算并报告了每个特定大脑区域的平均值。最后,我们构建了多变量回归模型来测量不同PSE与人口统计学特征之间的关联,大脑总体积,和每个大脑结构的体积。
结果:在总样本中,24.6%有产前酒精暴露,13.6%的产前烟草暴露,和1.2%的产前阿片类药物暴露。平均而言,发现那些产前烟草暴露者的海马旁具有统计学意义上的较小。
结论:我们发现产前烟草暴露与海马旁体积较小之间存在显著关联,这可能会对个人的生计产生深远的影响,包括汽车延误,不良的认知和行为结果,和长期健康后果。考虑到与PSE相关的累积神经发育效应,我们建议医疗保健提供者提高筛查率,检测,并转介停止。此外,我们建议医学协会游说政策制定者,以解决有效识别高危孕妇的上游障碍,具体来说,消除或显著减少因涉及产前物质使用的州法律而产生的惩罚性法律后果。
BACKGROUND: Prenatal substance exposure (PSE) can lead to various harmful outcomes for the developing fetus and is linked to many emotional, behavioral, and cognitive difficulties later in life. Therefore, examination of the relationship between the development of associated brain structures and PSE is important for the development of more specific or new preventative methods.
OBJECTIVE: Our study\'s primary objective was to examine the relationship between the physical development of the amygdala, hippocampus, and parahippocampus following prenatal alcohol, tobacco, and prescription opioid exposure.
METHODS: We conducted a cross-sectional analysis of the Adolescent Brain and Cognitive Development (ABCD) Study, a longitudinal neuroimaging study that measures brain morphometry from childhood throughout adolescence. Data were collected from approximately 12,000 children (ages 9 and 10) and parents across 22 sites within the United States. Prenatal opioid, tobacco, and alcohol use was determined through parent self-report of use during pregnancy. We extracted variables assessing the volumetric size (mm3) of the amygdala, hippocampus, and parahippocampal gyrus as well as brain volume, poverty level, age, sex, and race/ethnicity for controls within our adjusted models. We reported sociodemographic characteristics of the sample overall and by children who had PSE. We calculated and reported the means of each of the specific brain regions by substance exposure. Finally, we constructed multivariable regression models to measure the associations between different PSE and the demographic characteristics, total brain volume, and volume of each brain structure.
RESULTS: Among the total sample, 24.6% had prenatal alcohol exposure, 13.6% had prenatal tobacco exposure, and 1.2% had prenatal opioid exposure. On average, those with prenatal tobacco exposure were found to have a statistically significant smaller parahippocampus.
CONCLUSIONS: We found a significant association between prenatal tobacco exposure and smaller parahippocampal volume, which may have profound impacts on the livelihood of individuals including motor delays, poor cognitive and behavioral outcomes, and long-term health consequences. Given the cumulative neurodevelopmental effects associated with PSE, we recommend that healthcare providers increase screening rates, detection, and referrals for cessation. Additionally, we recommend that medical associations lobby policymakers to address upstream barriers to the effective identification of at-risk pregnant individuals, specifically, eliminating or significantly reducing punitive legal consequences stemming from state laws concerning prenatal substance use.