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Volume 60, Issue 3, Pages 218-225 (1 August 2006)


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Mapping Corpus Callosum Deficits in Autism: An Index of Aberrant Cortical Connectivity

Christine N. Vidala, Rob Nicolsonbc, Timothy J. DeVitoa, Kiralee M. Hayashia, Jennifer A. Geagaa, Dick J. Drostc, Peter C. Williamsonbc, Nagalingam Rajakumarb, Yihong Suia, Rebecca A. Duttona, Arthur W. Togaa, Paul M. ThompsonaCorresponding Author Informationemail address

Received 4 February 2005; received in revised form 1 November 2005; accepted 3 November 2005. published online 06 February 2006.

Background

Volumetric studies have reported reductions in the size of the corpus callosum (CC) in autism, but the callosal regions contributing to this deficit have differed among studies. In this study, a computational method was used to detect and map the spatial pattern of CC abnormalities in male patients with autism.

Methods

Twenty-four boys with autism (aged 10.0 ± 3.3 years) and 26 control boys (aged 11.0 ± 2.5 years) underwent a magnetic resonance imaging (MRI) scan at 3 Tesla. Total and regional areas of the CC were determined using traditional morphometric methods. Three-dimensional (3D) surface models of the CC were also created from the MRI scans. Statistical maps were created to visualize morphologic variability of the CC and to localize regions of callosal thinning in autism.

Results

Traditional morphometric methods detected a significant reduction in the total callosal area and in the anterior third of the CC in patients with autism; however, 3D maps revealed significant reductions in both the splenium and genu of the CC in patients.

Conclusions

Statistical maps of the CC revealed callosal deficits in autism with greater precision than traditional morphometric methods. These abnormalities suggest aberrant connections between cortical regions, which is consistent with the hypothesis of abnormal cortical connectivity in autism.

a Laboratory of Neuro Imaging, Brain Mapping Division, Department of Neurology, UCLA School of Medicine, Los Angeles, California

b Department of Psychiatry, University of Western Ontario, London, Ontario, Canada

c Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada

Corresponding Author InformationAddress reprint requests to Dr. Paul Thompson, Laboratory of Neuro Imaging, Department of Neurology, UCLA School of Medicine, 635 Charles E. Young Drive South, Suite 225E, Los Angeles, CA 90095-7332

PII: S0006-3223(05)01424-1

doi:10.1016/j.biopsych.2005.11.011


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