The impact of prenatal alcohal exposure on neurophysiological encoding of environmental events at six months
The impact of prenatal alcohal exposure on neurophysiological encoding of environmental events at six months
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DOI：
10.1097/01.alc.0000117837.66107.64
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发表时间：
2004-03-01
影响因子：
3.2
通讯作者：
Coles, CD
中科院分区：
文献类型：
--
作者：
Kable, JA;Coles, CD
背景资料：使用来自婴儿信息处理技能的发展研究的方法，可以通过评估初级认知过程（包括注意力调节和处理速度）来探索产前酒精暴露对后期长期神经认知影响的早期表现。方法：118名6个月大的婴儿（18高风险，100低风险）的纵向研究，中度产前酒精暴露和胎儿生长迟缓，提出了两个听觉（400和1000赫兹纯音）和视觉刺激（彩色高加索人的脸）在信息处理范式与心脏反应作为因变量。前三个习惯性试验进行了分析，以评估神经生理编码的环境事件在婴儿分类为高风险和低风险的基础上，母亲饮酒的状态。心脏反应的具体指标用于评估婴儿的（1），启动注意的速度，（2）持续注意，（3）刺激抵消后转移注意。根据产前酒精暴露的累积风险指数确定为高风险的婴儿对刺激的反应更慢，并且在三项试验中被评为唤醒水平显着较高，但没有显示出差异结论：低效率的神经生理编码中观察到高风险的婴儿，这表明产前酒精暴露可能会破坏负责调节身体对环境事件的反应的注意力系统的基本组成部分。参与编码环境刺激和启动注意力的较慢的神经生理反应和较高水平的行为唤醒表明，这些婴儿可能难以调节唤醒水平和注意力系统之间的相互作用，以提供处理环境事件的最佳效率。这些结果表明，产前酒精暴露导致早期注意力调节的特定损伤，这可能会影响随后的认知发育和依赖于这些主要认知过程的行为结果。
Background: Using methodologies from developmental studies on infant information-processing skills, early manifestations of later long-term neurocognitive effects of prenatal alcohol exposure can be explored by assessing primary cognitive processes, including attentional regulation and processing speed.Methods: One hundred eighteen 6-month-old infants (18 high risk, 100 low risk) from a longitudinal study of moderate prenatal alcohol exposure and intrauterine growth retardation were presented with both auditory (400 and 1000 Hz pure tones) and visual stimuli (chromatic Caucasian faces) in an information-processing paradigm with cardiac response as the dependent variable. The first three habituation trials were analyzed to assess neurophysiological encoding of environmental events in infants categorized as high and low risk based on status of maternal drinking. Specific indexes of the cardiac response were used to assess the infant's (1), speed of initiating attention, (2) sustained attention, and (3) shifting attention after stimulus offset.Results: Infants identified as high risk based on a cumulative risk index for prenatal alcohol exposure responded more slowly to stimuli and were rated as significantly higher in arousal level across the three trials but did not display differences in their sustained deceleration responses or responses to stimulus-offset.Conclusions: Less efficient neurophysiological encoding was observed among high-risk infants, suggesting that prenatal alcohol exposure may disrupt fundamental components of the attentional system responsible for regulating the body's responses to environmental events. Slower neurophysiological responses involved in encoding environmental stimuli and initiating attention and higher levels of behavioral arousal suggest that these infants may have had difficulties with regulating the interactions between arousal level and the attentional system needed to provide optimal efficiency in processing environmental events. These outcomes suggest that prenatal alcohol exposure results in specific impairments in early attentional regulation, which may influence subsequent cognitive development and behavioral outcomes dependent on these primary cognitive processes.