International Meeting for Autism Research (London, May 15-17, 2008): Cortical Maturation in Autism Spectrum Disorder

Cortical Maturation in Autism Spectrum Disorder

Saturday, May 17, 2008: 1:15 PM
Mancy (Novotel London West)
A. Raznahan , Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, London, United Kingdom
R. Toro , Brain & Body Centre, University of Nottingham, Nottingham, United Kingdom
E. Daly , Department of Brain Maturation, Institute of Psychiatry, King's College London, London, United Kingdom
P. Bolton , Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, United Kingdom
T. Paus , Brain & Body Centre, University of Nottingham, Nottingham, United Kingdom
D. Murphy , Psychological Medicine and Psychiatry, Section of Brain Maturation, King's College London, Institute of Psychiatry, London, United Kingdom
Background: Structural neuroimaging studies have identified early overgrowth and regional abnormalities of the cerebral cortex in autism spectrum disorders (ASD). However, most reports have only examined differences in cortical volume (CV) - but CV is a product of surface area (SA) and cortical thickness (CT). Because SA and CT differ phylogenetically and ontologically– their study could help us better understand the neurobiological underpinnings of ASD.

Objectives: (1) To differentiate cortical abnormalities in autism according to CV, CT and SA. (2) To examine the age-dependency of group differences in regional cortical anatomy.

Methods: We used FreeSurfer to measure global and regional CV, CT and SA in a large sample of children and adults with ASD (n=76) and healthy controls (n=51).

Results: We found abnormalities in ASD of specific cortical systems known to be involved in language, social cognition and executive function. But, the distribution of GMV, CT and SA differences did not overlap – suggesting that not all ASD-related brain differences come about in the same way. Furthermore, we found preliminary evidence that in some brain regions, differences in cortical CV between subjects with ASD and controls seem to depend on the subject’s age. This effect was most pronounced in the temporal lobes (Age by Group interaction for Bilateral Temporal CV: F=10.95, p=0.001), and was mirrored in age by group interactions for CT (F=6.60, p=0.01), but not for SA (p=0.36). The most prominent age by group interactions for CT was found in the fusiform region - which is known to be involved in face processing and shows functional abnormalities in ASD. 

Conclusions: This is the first evidence to date that abnormal brain maturation in ASD is not limited to early life and is regionally specific. We predict that other areas of the social brain will also show evidence of dysmaturation in ASD.

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