International Meeting for Autism Research (May 7 - 9, 2009): Differences in Cortical Thickness in Autism Spectrum Disorders and Relation to Everyday Executive Function

Differences in Cortical Thickness in Autism Spectrum Disorders and Relation to Everyday Executive Function

Thursday, May 7, 2009
Northwest Hall (Chicago Hilton)
10:00 AM
K. M. Mak-Fan , Psychology, University of Toronto, Toronto, ON, Canada
M. J. Taylor , Diagnostic Imaging, Hospital for Sick Children, Toronto, ON, Canada
M. K. Malone , Diagnostic Imaging, Hospital for Sick Children, Toronto, ON, Canada
W. Roberts , Department of Pediatrics, Hospital for Sick Children & Bloorview Kids Rehab, University of Toronto, Toronto, ON, Canada
J. P. Lerch , Mouse Imaging Centre, The Hospital for Sick Children, Toronto, ON, Canada
Background: Recent research has suggested that cortical growth follows an abnormal developmental trajectory in children with autism spectrum disorders (ASD), resulting in regional abnormalities in brain volume (e.g., Carper and Courchesne, 2005). These findings may be due to abnormalities in cortical thickness, but only a few published studies have examined this question. In addition, the relation between structural abnormalities and behavioural symptoms of ASD, such as executive function impairment, has also been largely unexplored.

Objectives: To examine differences in cortical thickness between a group of typically developing children and a group of children with ASD, and to explore correlations between cortical thickness and a measure of everyday executive function (the Behaviour Rating of Executive Function (BRIEF), Gioia et al., 2000), skills known to be impaired in children with ASD.

Methods: Participants were 32 typically developing children (mean age 10.2 years, SD= 2.47) and 21 high-functioning children with ASD (mean age 9.72 years, SD = 2.40). T1-weighted MR images were obtained for all subjects on a 1.5 Tesla GE scanner. Cortical thickness maps were derived from these MRI data for each subject as described elsewhere (Lerch and Evans, 2005), and between-group statistical analyses were then performed with mean cortical thickness covaried. We corrected for multiple comparisons were corrected for using the False Discovery Rate (Genovese et al., 2002). Ethical approval for the study was obtained in accordance with the Hospital for Sick Children (Toronto, ON) guidelines.

Results: Mean cortical thickness was greater in the ASD cohort, although this did not reach significance. Between-group analyses revealed thicker cortex for the children with ASD in the posterior cingulate gyrus (0.23±0.05mm, t=4.3, q=0.07) and the parieto-occipital junction (0.26±0.07mm, t=3.9, q=0.08) for the ASD children. These patterns were fairly bilateral, but more pronounced in the right hemisphere. 

In children with ASD, preliminary analyses using overall composite scores on the BRIEF suggest that these measures are correlated with differences in cortical thickness in the cingulate gyrus and parieto-occipital junction, dorsolateral prefrontal cortex (DLPFC), temporal pole and premotor cortex. This pattern of correlation, although weaker, was also found for t-scores on BRIEF subscales such as Emotional Control and Shift.

Conclusions: Regional differences in cortical thickness were observed in children with ASD compared to typically developing children between 7-13 years of age, primarily in the cingulate and parieto-occipital areas. There were also trends for cortical thickness in regions important for executive function (e.g. cingulate, DLPFC) to correlate with scores on a behavioural measure of everyday executive function (BRIEF). This relation between structural abnormalities and behavioural symptoms may contribute to the growing understanding of the neurodevelopmental basis of ASD symptoms.

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