Grewen Karen, Burchinal Margaret, Vachet Clement, Gouttard Sylvain, Gilmore John H, Lin Weili, Johns Josephine, Elam Mala, Gerig Guido
University of North Carolina, Department of Psychiatry, Chapel Hill, NC 27599, USA.
University of North Carolina, Frank Porter Graham Child Development Institute, Chapel Hill, NC 27599, USA.
Neuroimage. 2014 Nov 1;101:114-23. doi: 10.1016/j.neuroimage.2014.06.070. Epub 2014 Jul 3.
Prenatal cocaine exposure (PCE) is related to subtle deficits in cognitive and behavioral function in infancy, childhood and adolescence. Very little is known about the effects of in utero PCE on early brain development that may contribute to these impairments. The purpose of this study was to examine brain structural differences in infants with and without PCE. We conducted MRI scans of newborns (mean age = 5 weeks) to determine cocaine's impact on early brain structural development. Subjects were three groups of infants: 33 with PCE co-morbid with other drugs, 46 drug-free controls and 40 with prenatal exposure to other drugs (nicotine, alcohol, marijuana, opiates, SSRIs) but without cocaine. Infants with PCE exhibited lesser total gray matter (GM) volume and greater total cerebral spinal fluid (CSF) volume compared with controls and infants with non-cocaine drug exposure. Analysis of regional volumes revealed that whole brain GM differences were driven primarily by lesser GM in prefrontal and frontal brain regions in infants with PCE, while more posterior regions (parietal, occipital) did not differ across groups. Greater CSF volumes in PCE infants were present in prefrontal, frontal and parietal but not occipital regions. Greatest differences (GM reduction, CSF enlargement) in PCE infants were observed in dorsal prefrontal cortex. Results suggest that PCE is associated with structural deficits in neonatal cortical gray matter, specifically in prefrontal and frontal regions involved in executive function and inhibitory control. Longitudinal study is required to determine whether these early differences persist and contribute to deficits in cognitive functions and enhanced risk for drug abuse seen at school age and in later life.
产前可卡因暴露(PCE)与婴儿期、儿童期和青少年期认知及行为功能的细微缺陷有关。关于子宫内PCE对早期大脑发育的影响,我们知之甚少,而这种影响可能导致这些损伤。本研究的目的是检查有或无PCE的婴儿的脑结构差异。我们对新生儿(平均年龄 = 5周)进行了磁共振成像扫描,以确定可卡因对早期脑结构发育的影响。研究对象为三组婴儿:33名PCE合并其他药物使用的婴儿、46名无药物使用的对照组婴儿以及40名产前暴露于其他药物(尼古丁、酒精、大麻、阿片类药物、选择性5-羟色胺再摄取抑制剂)但未接触可卡因的婴儿。与对照组和非可卡因药物暴露的婴儿相比,PCE婴儿的总灰质(GM)体积较小,而总脑脊液(CSF)体积较大。区域体积分析显示,全脑GM差异主要是由PCE婴儿前额叶和额叶脑区GM较少所致,而后部区域(顶叶、枕叶)在各组之间并无差异。PCE婴儿CSF体积增加主要出现在前额叶、额叶和顶叶区域,而枕叶区域没有变化。在背侧前额叶皮质观察到PCE婴儿存在最大差异(GM减少、CSF增大)。结果表明,PCE与新生儿皮质灰质结构缺陷有关,特别是与涉及执行功能和抑制控制的前额叶和额叶区域有关。需要进行纵向研究来确定这些早期差异是否持续存在,并导致学龄期及以后出现认知功能缺陷和药物滥用风险增加。