Conflict of interest statement: No conflicts declared.
Tract-specific analyses of diffusion tensor imaging show widespread white matter compromise in autism spectrum disorder
Article first published online: 12 NOV 2010
© 2010 The Authors. Journal of Child Psychology and Psychiatry © 2010 Association for Child and Adolescent Mental Health
Journal of Child Psychology and Psychiatry
Volume 52, Issue 3, pages 286–295, March 2011
How to Cite
Shukla, D. K., Keehn, B. and Müller, R.-A. (2011), Tract-specific analyses of diffusion tensor imaging show widespread white matter compromise in autism spectrum disorder. Journal of Child Psychology and Psychiatry, 52: 286–295. doi: 10.1111/j.1469-7610.2010.02342.x
- Issue published online: 5 FEB 2011
- Article first published online: 12 NOV 2010
- Manuscript accepted 18 August 2010
- Diffusion tensor imaging;
- autism spectrum disorder;
- brain connectivity;
- fractional anisotropy;
- mean diffusion;
- axial diffusion;
- radial diffusion
Background: Previous diffusion tensor imaging (DTI) studies have shown white matter compromise in children and adults with autism spectrum disorder (ASD), which may relate to reduced connectivity and impaired function of distributed networks. However, tract-specific evidence remains limited in ASD. We applied tract-based spatial statistics (TBSS) for an unbiased whole-brain quantitative estimation of the fractional anisotropy (FA), mean diffusion (MD) and axial and radial diffusion of the white matter tracts in children and adolescents with ASD.
Methods: DTI was performed in 26 ASD and 24 typically developing (TD) participants, aged 9–20 years. Groups were matched for age and IQ. Each participant’s aligned FA, MD and axial and radial diffusion data were projected onto the mean FA skeleton representing the centers of all tracts and the resulting data fed into voxelwise group statistics.
Results: TBSS revealed decreased FA and increased MD and radial diffusion in the ASD group compared to the TD group in the corpus callosum, anterior and posterior limbs of the internal capsule, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, superior longitudinal fasciculus, cingulum, anterior thalamic radiation, and corticospinal tract. No single site with inverse effects (increased FA, reduced MD or radial diffusion in the ASD group) was detected. In clusters of significant group difference, age was positively correlated with FA and negatively correlated with MD and radial diffusion in the TD, but not the ASD group.
Conclusions: Our findings reveal white matter compromise affecting numerous tracts in children and adolescents with ASD. Slightly varying patterns of diffusion abnormalities detected for some tracts may suggest tract-specific patterns of white matter abnormalities associated with ASD. Age-dependent effects further show that maturational changes (increasing FA, decreasing MD and radial diffusion with age) are diminished in ASD from school-age childhood into young adulthood.