Corpus Callosum Volume In Autism and Its Extended Phenotype

Background:  Several lines of research have converged to suggest the corpus callosum (CC) may be central to understanding the pathophysiology of autism spectrum condition (ASC).  As the largest white matter tract in the brain, the CC mediates the interhemispheric communication underpinning higher cognitive functioning.  Subsections of the callosum have been shown to vary dramatically in quantitative characteristics of axon density, size, and degree of myelination (LaMantia and Rakic, 1990) and one of the most replicated findings in autism research has been decreases in CC size (Hardan et al., 2000).  Discrepancies remain, however, as to which subregions of the CC are affected in autism (Brambilla et al., 2003) paving the way for further research in this area. 

Objectives:  To investigate possible differences in corpus callosum size and asymmetry.

Methods:  High-resolution structural magnetic resonance images (MRI) of the brain have been obtained on adolescent subjects with ASC (n=40), their unaffected siblings (n=40), and unrelated typically developing controls (n=40). 

Results:  Structural neuroimaging data will be presented from the three groups and will include midsaggital and parasaggital corpus callosum size measurements.  The CC has been partitioned into the seven functional subregions according to the Witelson method (Witelson, 1989).

Conclusions:  This work seeks to extend previous research from our group employing the same partition methodology wherein fetal testosterone was found to be a primary mechanism for asymmetric callosal size and the isthmus emerged as a subregion of particular interest (Chura et al., 2010).  Differences in CC subregion size and symmetry may have implications for understanding lateralization of the brain, task performance, and relevant cognitive deficits associated with ASC.  Moreover, to date siblings of individuals on the autistic spectrum have been the subject of very little neuroimaging research, and this study aims to shed light on the extended phenotype of ASC.