A Preliminary Longitudinal Magnetic Resonance Imaging Study of Brain Volume and Cortical Thickness in Autism

Department of Psychiatry and Behavioral Sciences, Stanford University, California 94305, USA.
Biological psychiatry (Impact Factor: 10.26). 07/2009; 66(4):320-6. DOI: 10.1016/j.biopsych.2009.04.024
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Autism is a developmental neurobiologic disorder associated with structural and functional abnormalities in several brain regions including the cerebral cortex. This longitudinal study examined developmental changes in brain volume and cortical thickness (CT) using magnetic resonance imaging (MRI) in children with autism.
MRI scans and behavioral measures were obtained at baseline and after a 30-month interval in a sample of male subjects with autism (n = 18) and healthy age-, and sex-matched control subjects (n = 16) between ages 8 and 12 years at baseline.
No differences in brain volumes were observed between the autism and control subjects at baseline or follow-up. However, differences in total gray matter volumes were observed over time with significantly greater decreases in the autism group compared with control subjects. Differences in CT were observed over time with greater decreases in the autism group compared with control subjects in several brain regions including the frontal lobe. When accounting for multiple comparisons, differences between the two groups became nonsignificant except for changes in occipital CT. Furthermore, associations were observed between several clinical features and changes in CT with greater thinning of the cortex being correlated with more severe symptomatology.
Findings from this study provide preliminary evidence for age-related changes in gray matter volume and CT in children with autism that are associated with symptoms severity. Future longitudinal studies of larger sample sizes are needed to evaluate developmental changes and examine the relationships between structural abnormalities and clinical expressions of the disorder.

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    • " controls from childhood to adulthood , Zielinski et al . [ 2014 ] found a trajectory of early accelerated growth in childhood followed by accelerated thinning in adolescence and decelerated thinning in early adulthood . Some previous work has found significant relation - ships between GM volume and autistic symptomology and severity in children [ Hardan et al . , 2009 ; Pierce & Courchesne , 2001 ] ; however , others have found no rela - tionships [ Langen , Durston , Staal , Palmen , & van Enge - land , 2007 ; Webb et al . , 2009 ] . In studies including adults , significant relationships between general autism symptomology and GM volume have been found in the left dorsolateral frontal cluster , fro"
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    ABSTRACT: Although it is widely accepted that autism spectrum disorder (ASD) involves neuroanatomical abnormalities and atypical neurodevelopmental patterns, there is little consensus regarding the precise pattern of neuroanatomical differences or how these differences relate to autism symptomology. Furthermore, there is limited research related to neuroanatomical correlates of autism symptomology in individuals with ASD and the studies that do exist primarily include small samples. This study was the first to investigate gray matter (GM) changes throughout the ASD lifespan, using voxel-based morphometry to determine whether significant differences exist in the GM volumes of a large sample of individuals with ASD compared to age- and IQ-matched typical controls. We examined GM volume across the lifespan in 531 individuals diagnosed with ASD and 571 neurotypical controls, aged 7–64. We compared groups and correlated GM with age and autism severity in the ASD group. Findings suggest bilateral decreased GM volume for individuals with ASD in regions extending from the thalamus to the cerebellum, anterior medial temporal lobes, and orbitofrontal regions. Higher autism severity was associated with decreased GM volumes in prefrontal cortex, inferior parietal and temporal regions, and temporal poles. Similar relationships were found between GM volume and age. ASD diagnosis and severity were not associated with increased GM volumes in any region. Autism Res 2015. © 2015 International Society for Autism Research, Wiley Periodicals, Inc.
    Autism Research 01/2015; 8(4). DOI:10.1002/aur.1453 · 4.33 Impact Factor
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    • "Changes of cortical thickness are often credited to normal cognitive development during adolescence such as shifts in intelligence quotient (IQ) over 6–22 years, which were related to rates of cortical thinning mainly in frontal regions (Burgaleta et al., 2014), and thinner parietal cortex, which predicted better neuropsychological performance in early adolescents at 12–14 years (Squeglia et al., 2013). Longitudinal cortical thickness trajectories have differed during adolescence with pathology where less thinning has been observed in cortical regions of early onset schizophrenia (Bakalar et al., 2009), fetal alcohol spectrum disorders (Treit et al., 2014) and attention deficit hyperactivity disorder (Shaw et al., 2013), while greater thinning has been reported in autism (Hardan et al., 2009) and 22q11.2 deletion syndrome (Schaer et al., 2009). "
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    • "The first is a difference in cortical thickness at any age, i.e. either thicker or thinner in ASD (Chung et al., 2005; Hadjikhani et al., 2006; Hardan et al., 2006; Dziobek et al., 2010; Hyde et al., 2010; Wallace et al., 2010; Scheel et al., 2011; Misaki et al., 2012). The second is a difference in age-related change in cortical thickness, represented by age  diagnosis interactions (Chung et al., 2005; Hardan et al., 2009; Raznahan et al., 2010; Wallace et al., 2010; Scheel et al., 2011; Mak-Fan et al., 2012; Misaki et al., 2012). However, age-related changes in cortical thickness in ASD are predominantly drawn from cross-sectional data, which can only infer developmental trends from changes across individuals (Kraemer et al., 2000). "
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    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.
    Brain 04/2014; 137(6). DOI:10.1093/brain/awu083 · 9.20 Impact Factor
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