Janet E. Lainhart, MD

Slide of the Week: Janet E. Lainhart, MD

Title: Longitudinal changes in cortical thickness in autism and typical development

Legend: Abnormal age-related cortical thickness trajectories in ASD. Coloured brain regions identify significant group differences in age-related cortical thickness changes. Each scan is represented by a dot and repeated scans are connected by lines. Regions depicted were significant both before and after controlling for full-scale IQ at P50.05 (FDR). ASD = blue; typically developing control (TDC) subjects = red.

Citation: Zielinski BA, Prigge MB, Nielsen JA, Froehlich AL, Abildskov TJ, Anderson JS, Fletcher PT, Zygmunt KM, Travers BG, Lange N, Alexander AL, Bigler ED, Lainhart JE. (2014) Longitudinal changes in cortical thickness in autism and typical development. Brain. 2014 Jun;137(Pt 6):1799-812. doi: 10.1093/brain/awu083. Epub 2014 Apr 22.

Abstract: The natural history of brain growth in autism spectrum disorders remains unclear. Cross-sectional studies have identified regional abnormalities in brain volume and cortical thickness in autism, although substantial discrepancies have been reported. Preliminary longitudinal studies using two time points and small samples have identified specific regional differences in cortical thickness in the disorder. To clarify age-related trajectories of cortical development, we examined longitudinal changes in cortical thickness within a large mixed cross-sectional and longitudinal sample of autistic subjects and age- and gender-matched typically developing controls. Three hundred and forty-five magnetic resonance imaging scans were examined from 97 males with autism (mean age = 16.8 years; range 3-36 years) and 60 males with typical development (mean age = 18 years; range 4-39 years), with an average interscan interval of 2.6 years. FreeSurfer image analysis software was used to parcellate the cortex into 34 regions of interest per hemisphere and to calculate mean cortical thickness for each region. Longitudinal linear mixed effects models were used to further characterize these findings and identify regions with between-group differences in longitudinal age-related trajectories. Using mean age at time of first scan as a reference (15 years), differences were observed in bilateral inferior frontal gyrus, pars opercularis and pars triangularis, right caudal middle frontal and left rostral middle frontal regions, and left frontal pole. However, group differences in cortical thickness varied by developmental stage, and were influenced by IQ. Differences in age-related trajectories emerged in bilateral parietal and occipital regions (postcentral gyrus, cuneus, lingual gyrus, pericalcarine cortex), left frontal regions (pars opercularis, rostral middle frontal and frontal pole), left supramarginal gyrus, and right transverse temporal gyrus, superior parietal lobule, and paracentral, lateral orbitofrontal, and lateral occipital regions. We suggest that abnormal cortical development in autism spectrum disorders undergoes three distinct phases: accelerated expansion in early childhood, accelerated thinning in later childhood and adolescence, and decelerated thinning in early adulthood. Moreover, cortical thickness abnormalities in autism spectrum disorders are region-specific, vary with age, and may remain dynamic well into adulthood.

About the Investigator: Lainhart’s research focuses on understanding brain growth, development, and maturation in autism from the prenatal period into adulthood. She leads a multidisciplinary research team that uses high-resolution brain scanning to determine changes in the brain that are specific to autism and linked to clinical symptoms, course, and outcome. The goal of this research is to identify biomarkers of autism that can be used in determining the causes of autism, the brain mechanisms involved, early diagnosis, preventive interventions, and treatment. Lainhart’s research is funded in part by the National Institutes of Mental Health and the Autism Speaks Foundation.

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