"The human data compiled to date has been highly selective and almost biased to worst-case scenarios," Miller said, referring to the .30 blood alcohol concentration. "Our findings suggest that moderate alcohol overexposure causes an increase in the number of axons, whereas high alcohol overexposure causes a breakdown, thus reducing the size of the corpus callosum."
Miller said human clinical studies underway at other institutions may confirm this difference between callosal hypergrowth and hypogrowth.
"One particularly interesting finding in our study was that the alcohol overexposure did not increase the entire corpus callosum but mostly enlarged the rostral portion, the part toward the front of the head," Miller added. "This portion of the corpus callosum communicates information between the frontal and parietal cortexes, the brain areas that participate in movement and touch and in executive functions such as initiating voluntary movements and other higher-order processing."
Several behavioral studies on children with fetal alcohol syndrome show that executive functions of the rostral portion are reduced due to the alcohol exposure.
Miller said that although the primate and human clinical studies differ on the effect alcohol has on corpus callosum size, the studies agree that the part most affected is the rostral portion.
He described his findings as "more provocative than coming up with any solutions." He hopes his study will encourage researchers conducting human studies to study a range of people affected by fetal alcohol syndrome.
"There might also be a way of using the MRI analysis in clinical settings to better see how children are affected," he added. "The findings could possibly help other researchers find ways for these children to learn more effectively."
Miller will next investigate callosal projection neurons to u
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Contact: Becky Soglin
becky-soglin@uiowa.edu
319-335-6660
University of Iowa
21-Sep-1999