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, suggest- ing that prenatal alcohol exposure may disrupt fundamental components of the attentional system respon- sible 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 regu- lation, which may influence subsequent cognitive development and behavioral outcomes dependent on these primary cognitive processes.
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