This study was supported in part by National Institute on Alcohol Abuse and Alcoholism Research Grants AA10417 (to E.P.R.) andAA06420 (to the Scripps Alcohol Research Center); by National Institutes of Health Grant 5P50NS22343-O9 (to the Center for Developmental Cognitive Neuroscience); and by funding from the Medical Research Service of the Department of Veterans Affairs (to T.L.J.).
Abnormalities of the Corpus Callosum in Children Prenatally Exposed to Alcohol
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 19, Issue 5, pages 1198–1202, October 1995
How to Cite
Riley, E. P., Mattson, S. N., Sowell, E. R., Jernigan, T. L., Sobel, D. F. and Jones, K. L. (1995), Abnormalities of the Corpus Callosum in Children Prenatally Exposed to Alcohol. Alcoholism: Clinical and Experimental Research, 19: 1198–1202. doi: 10.1111/j.1530-0277.1995.tb01600.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication February 28, 1995; accepted May 10, 1995
- Fetal Alcohol Syndrome;
- Corpus Callosum;
- Prenatal Alcohol Exposure
For 20 years, it has been known that fetal alcohol syndrome (FAS) is associated with abnormal brain development. Early autopsy studies point to the corpus callosum as one area affected by heavy alcohol exposure. Little is known, however, about the integrity of the brain in alcohol-exposed children who survive the perinatal period. This study was designed to assess the corpus callosum in living children exposed to high doses of alcohol prenatally. Thirteen children with histories of significant prenatal alcohol exposure and 12 normal control children were evaluated using magnetic resonance imaging. Using the midsagittal section, images were measured for the area of the corpus callosum using a computer-assisted measurement technique. In addition to the overall area, five equiangular regions were determined for each corpus callosum. Of the 13 alcohol-exposed children assessed, two had agenesis of the corpus callosum. The remaining alcohol-exposed children had significantly smaller overall callosal areas, as well as smaller regional areas of four of the five callosal regions, when compared with the normal control children. Importantly, when corrected for brain size, three of the five callosal regions were still smaller in the alcohol-exposed children, although overall area of the corpus callosum was no longer significantly different. These results suggest that prenatal exposure to high levels of alcohol is associated with abnormalities of the corpus callosum. They verify callosal agenesis in children with FAS, which previously had only been noted in autopsy reports. The current findings further document selective reductions in the area of certain regions of the corpus callosum after in utero alcohol exposure, extending our current understanding of alcohol's teratogenic effects on brain development. There is also some indication that the selective reduction in the area of the corpus callosum is similar to that reported in attention deficit disorder.