International Meeting for Autism Research: Anterior and Posterior Cortical Folding In Autism

Anterior and Posterior Cortical Folding In Autism

Friday, May 13, 2011
Elizabeth Ballroom E-F and Lirenta Foyer Level 2 (Manchester Grand Hyatt)
10:00 AM
G. Fung1, C. Cheung2, M. E. King3, L. Ling3, V. Cheung4, K. S. Tai5, P. Leung6, S. F. Hung7, T. P. Ho1, C. C. Lee7, C. P. Tang7, S. E. Chua8,9 and G. M. McAlonan1,9, (1)Psychiatry, University of Hong Kong, Hong Kong, Hong Kong, (2)Psychiatry, The University of Hong Kong, Pokfulam, Hong Kong, (3)Education, University of Hong Kong, Hong Kong, Hong Kong, (4)Rehabilitation Sciences, Polytechnic University, Hong Kong, Hong Kong, (5)Hospital Authority, Hong Kong, Hong Kong, (6)Psychology, Chinese University of Hong Kong, Hong Kong, Hong Kong, (7)Psychiatry, Kwai Chung Hospital, Hong Kong, Hong Kong, (8)Psychiatry, University of Hong Kong, Pokfulam, Hong Kong, (9)State Key Laboratory for Brain and Cognitive Sciences, Hong Kong, Hong Kong

Cortical gyrification is a useful summary marker of cortical folding. The gyrification index (GI) is calculated as the external cortical circumference divided by the total cortical contour. Preliminary evidence suggests an increase in folding in frontal regions of the brain in children with autism (Hardan et al., 2004), implying aberrant development of frontal regions. However, it is unknown whether folding differences involve the whole brain and whether they are specific to autism or a more general consequence of neurodevelopmental disorder.


The present study aimed to examine both anterior and posterior brain GI in a sizeable number of intellectually able children with autism (ASD) and typically developing controls. In addition, we included a neurodevelopmental control group of children with attention-deficit-hyperactivity disorder (ADHD) to assess whether differences are indeed specific to autism.


The study was approved by the University of Hong Kong/ Hospital Authority Research Ethics Committee. Informed consent was obtained from participants’ parents prior to MRI scanning. T1 images were acquired from 6 – 16 year old children with ASD (n=34), ADHD (n=19), and typically developing controls (n=65). There were no differences in age and verbal IQ. The GI was measured using a conventional manual tracing technique (Jou et. al., 2010). One coronal slice anterior and one posterior to the corpus callosum were selected for measurement. Both hemispheres were divided into superior and inferior portions. The outer and total contours were traced for each quadrant.


Contrary to prior study, we observed significantly lower mean GI in the left anterior and right anterior-inferior frontal regions in ASD compared to both controls and children with ADHD. Despite lower GI in the left anterior-inferior region in the ASD (mean GI=2.07) when compared to controls (mean GI=2.14), correlation analysis revealed a significant positive correlation of GI with age in the ASD group but not in the control groups. Further exploration indicated that children with autism younger than 12.5years have lower frontal GI than controls while those older than 12.5 years have higher GI than controls. No significant differences emerged in the posterior brain across all three groups.


These findings provide preliminary evidence for age-related differences in the cortical folding pattern in children with ASD. The childhood group in the study by Harden et al 2004 was older than ours and this may explain our opposite findings. The trajectory of cortical development therefore appears quite distinct in autism making issues of age-matching in studies of autism critical to address. These findings, which appear relatively restricted to frontal regions and specific to ASD, may provide clues to timing and aetiology of pathogenic mechanisms in autism.

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