Longitudinal Cortical Development During Adolescence and Young Adulthood in Autism Spectrum Disorders: Increased Cortical Thinning but Comparable Surface Area

Background: Autism spectrum disorders (ASD) are associated with atypical early brain development, with many reports of excessive brain growth during the preschool years.  Recent cross-sectional studies suggest that later cortical development during adolescence and young adulthood may also be aberrant (Hadjikhani et al., 2006; Wallace et al., 2010), though longitudinal designs are required to evaluate atypical growth trajectories.  In order to address this question, we provide the first longitudinal study investigating highly localized differences in cortical development, examining both cortical thickness and surface area, among adolescents and young adults with high functioning ASD.

Objectives: The purpose of the current study is to compare longitudinal changes in cortical thickness and surface area among adolescents and young adults with ASD versus typically developing (TD) youth.

Methods: 17 youth with ASD (diagnosed using DSM-IV criteria and the ADI/ADOS) and 18 TD youth provided two high-resolution 3 Tesla anatomic magnetic resonance imaging scans which were obtained, on average, approximately two years apart.  Groups were matched on age (ASD scan 1 mean=17.37+/- 2.41, scan 2 mean=19.12 +/- 2.51; TD scan 1=17.46 +/- 1.45, scan 2=19.60 +/- 1.61), IQ (ASD mean=116.59 +/- 13.05; TD mean=116.17 +/- 9.54), sex ratio (male:female – ASD=15:2; TD=17:1), and duration between scans (ASD mean=1.72 +/- 0.83; TD mean=2.10 +/- 0.95).  The FreeSurfer image analysis suite (version 5.1) was used to derive vertex-level cortical thickness and surface area values and to complete longitudinal analyses.

Results: There was widespread accelerated cortical thinning for the ASD group as compared to the TD group.  Most prominently, two areas in the left hemisphere, the posterior region of the fusiform gyrus and superior parietal cortex demonstrated greater thinning in the ASD group (cluster corrected p<.01).  Group comparisons at time point one indicated comparable cortical thickness, while time point two (~19 years) was characterized by thinner cortex in the ASD group, particularly in the aforementioned left hemisphere regions.  In contrast, longitudinal changes in surface area did not differ between groups after cluster correction for multiple comparisons.

Conclusions: The present longitudinal study complements and builds upon prior cross-sectional research by demonstrating extended cortical thinning in ASD during adolescence and into young adulthood.  Specifically, in portions of the temporal and parietal lobes, the cortex appears to have ceased thinning by 19 years of age (i.e., time two of this study) among TD individuals, while thinning continues to occur in these regions in ASD individuals.  On the other hand, surface area, another component of brain volume, appears to exhibit comparable growth rates for TD and ASD individuals during this developmental window.  These findings provide further evidence for a second period of atypical cortical development in ASD marked by increased cortical thinning in late adolescence/young adulthood.