This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Prenatal alcohol exposure causes a wide range of physical and behavioral effects. The most serious of these is the effect such exposure has on the developing central nervous system and thus the cognitive abilities of the offspring. These deficits often impact the areas of attention, learning, and memory. In general, most assessments of children with FAS, or those who have been prenatally exposed to alcohol, have relied on traditional, fairly global, psychological tests. Recently, however, research has begun to focus on more specific neuropsychological and neuroanatomical measures of alcohol's teratogenicity. For example, deficits in verbal learning with relative sparing in retention of learned material was recently reported in children with FAS. In addition, alcohol-exposed children displayed specific deficits on one measure of visuospatial processing. However, the effects of prenatal alcohol exposure on many of the specific areas of cognitive functioning are unclear. For example, although some evidence exists that spatial memory deficits occur in alcohol-exposed children, little is known about alcohol's teratogenic effect on the visuospatial domain.
One aim of this proposal is to evaluate visuospatial functioning in children with histories of heavy prenatal alcohol exposure, using a component-process approach to examine specific aspects of this domain of cognitive functioning. Secondly, recent studies involving magnetic resonance imaging of alcohol-exposed children indicate three brain areas that may be particularly affected. These areas are the basal ganglia, the corpus callosum, and the cerebellar vermis. Behavioral correlates of basal ganglia and corpus callosum abnormalities are currently being assessed but those associated with the cerebellum remain untested in alcohol-exposed children.
A second aim of this proposal is to evaluate motor and attentional functioning, which are behaviors known to be associated with the cerebellum. Finally, the specificity of alcohol-related cognitive deficits has not yet been reported. Thus it is unclear whether these deficits are specific to alcohol exposure or are secondary to general cognitive deficits. To address this aim, in both components of this proposal, children with mental deficiency unrelated to prenatal alcohol exposure will be compared to alcohol-exposed children.
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