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.
Objectives:
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.
Methods:
The study was approved by the
Results:
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.
Conclusions:
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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