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Published on: July 13, 2014
Relation of prenatal alcohol exposure to cognitive processing speed and efficiency in childhood
Matthew J Burden1, Sandra W Jacobson, Joseph L Jacobson
1Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan 48207, USA. mburden@wayne.edu
Insights
Prenatal alcohol exposure slows processing speed and efficiency in children, particularly in complex cognitive tasks. This deficit partially explains alcohol-related working memory impairments.
Area of Science:
- Neuroscience
- Developmental Psychology
- Cognitive Science
Background:
- Prenatal alcohol exposure is linked to cognitive deficits.
- Studies indicate impaired processing speed in infancy and childhood.
Purpose of the Study:
- To examine prenatal alcohol-related deficits in processing speed and efficiency.
- Investigate effects across four cognitive domains.
Main Methods:
- Assessed 337 Black children (age 7.5) using Sternberg paradigm tasks.
- Used hierarchical linear modeling to analyze reaction time (RT) and processing efficiency.
- Compared effortful vs. automatic processing tasks and used path analysis for mediation.
Main Results:
- Prenatal alcohol exposure correlated with slower processing speed on Sternberg tasks.
- A specific deficit in processing efficiency was observed in the number comparison task.
- Slower processing speed partially mediated the relationship between prenatal alcohol exposure and working memory.
Conclusions:
- Confirms prenatal alcohol exposure slows processing speed in complex cognition, not automatic tasks.
- Reduced processing speed partially explains alcohol-related working memory deficits.
- Number comparison processing efficiency was uniquely affected, suggesting a specific prenatal alcohol impact.
Background:
Prenatal alcohol exposure has been linked to deficits in processing speed in both infancy and later in childhood. This study was designed to examine prenatal alcohol-related deficits in both processing speed and processing efficiency in four domains of cognitive function.
Methods:
Black children (n=337; age, 7.5 years), prospectively recruited to over-represent prenatal alcohol exposure at moderate-to-heavy levels, were assessed on four processing speed tasks, using a Sternberg paradigm. Hierarchical linear modeling was used to contrast overall processing speed, indicated by reaction time (RT) differences at the intercept, with processing efficiency, indicated by the slope of RT changes across increasing levels of task difficulty. Performance on these tasks within an effortful cognitive framework was compared with RT on a task involving relatively more automatic processing. Path analysis was used to examine the degree to which the effect of prenatal alcohol exposure on working memory was mediated by slower RT.
Results:
Prenatal alcohol exposure was associated with slower processing speed on several of the Sternberg tasks, and the number comparison task showed a specific deficit in processing efficiency. These effects on tasks involving effortful processing contrasted with the lack of performance differences on the more automatic RT measure. The relation of prenatal alcohol exposure to working memory was mediated, in part, by an associated reduction in processing speed.
Conclusions:
These data confirm reports by other investigators linking prenatal alcohol exposure to slower processing speed and show that this RT deficit is found within the context of complex cognition but not where automatic processing is involved. The reduction in RT accounts, in part, for the previously reported alcohol-related effects on working memory. The number comparison slope was the only specific component of information processing affected, confirming previous reports of a distinctive prenatal alcohol effect on number processing.
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