Kable Julie A, Coles Claire D
Department of Pediatrics at Emory University School of Medicine, Atlanta, Georgia 30329, USA.
Alcohol Clin Exp Res. 2004 Mar;28(3):489-96. doi: 10.1097/01.alc.0000117837.66107.64.
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.
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.
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.
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.
运用婴儿信息处理技能发育研究的方法,通过评估包括注意力调节和处理速度在内的主要认知过程,可以探索产前酒精暴露对后期长期神经认知影响的早期表现。
在一项关于中度产前酒精暴露和宫内生长迟缓的纵向研究中,118名6个月大的婴儿(18名高危婴儿,100名低危婴儿)在一个以心脏反应为因变量的信息处理范式中,同时接受听觉(400赫兹和1000赫兹纯音)和视觉刺激(白人面孔)。分析前三次习惯化试验,以评估根据母亲饮酒状况分为高危和低危的婴儿对环境事件的神经生理编码。心脏反应的特定指标用于评估婴儿的(1)启动注意力的速度,(2)持续注意力,以及(3)刺激消失后的注意力转移。
根据产前酒精暴露累积风险指数被确定为高危的婴儿对刺激的反应较慢,在三次试验中被评定为唤醒水平显著更高,但在持续减速反应或对刺激消失的反应方面没有差异。
在高危婴儿中观察到神经生理编码效率较低,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反应的注意力系统的基本组成部分。编码环境刺激和启动注意力时神经生理反应较慢以及行为唤醒水平较高,表明这些婴儿在调节唤醒水平与处理环境事件所需的注意力系统之间的相互作用方面可能存在困难。这些结果表明,产前酒精暴露会导致早期注意力调节出现特定损伤,这可能会影响依赖于这些主要认知过程的后续认知发展和行为结果。