Literature DB >> 25014561

Structure, integrity, and function of the hypoplastic corpus callosum in spina bifida myelomeningocele.

Jennifer T Crawley1, Khader Hasan, H Julia Hannay, Maureen Dennis, Catherine Jockell, Jack M Fletcher.   

Abstract

Although there are many studies of people with complete or partial hypogenesis of the corpus callosum (CC), little is understood about the hypoplastic CC in which all structures are present but thinned. Spina bifida myelomeningocele (SBM) is a model organism for such studies because many have either a hypogenetic or hypoplastic CC. We used diffusion tensor tractography (DTT) to evaluate the hypoplastic CC in SBM and its relation to interhemispheric functions and intelligence quotient (IQ). Participants were individuals with SBM and an intact or hypoplastic CC (n=28), who were compared to a typically developing comparison group (n=32). Total and regional DTT volume and integrity measures (fractional anisotropy, axial diffusivity, and radial diffusivity) of the CC were related to measures of intelligence (IQ), bimanual motor functioning, and dichotic auditory performance. As predicted, DTT showed variations in volume and integrity that were maximized in the entire CC and the posterior CC. IQ correlated with entire CC volume, anterior and posterior regional CC volumes, and also with measures of integrity. Bimanual motor functioning correlated with the anterior and posterior volumes of the CC but not with any integrity measures. Axial diffusivity in the posterior CC was negatively correlated with right ear dichotic listening performance. The hypoplastic CC is not macrostructurally or microstructurally intact in SBM, even when it appears radiologically intact. Both volume and integrity of the posterior regions were related to reductions in IQ and to interhemispheric processing. These findings may transfer to other disorders characterized by a hypoplastic CC.

Entities:  

Keywords:  cognition; corpus callosum; dichotic listening; diffusion tensor imaging; interhemispheric transfer; spina bifida

Mesh:

Year:  2014        PMID: 25014561      PMCID: PMC4203469          DOI: 10.1089/brain.2014.0237

Source DB:  PubMed          Journal:  Brain Connect        ISSN: 2158-0014


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