Article

Structural brain abnormalities in adolescents with autism spectrum disorder and patients with attention deficit/hyperactivity disorder

Child Neuropsychology Section, Department of Child and Adolescent Psychiatry, University Hospital Aachen, Germany.
Journal of Child Psychology and Psychiatry (Impact Factor: 5.67). 01/2008; 48(12):1251-8. DOI: 10.1111/j.1469-7610.2007.01799.x
Source: PubMed

ABSTRACT Although autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD) are two distinct neurodevelopmental diseases, they share behavioural, neuropsychological and neurobiological characteristics. For the identification of endophenotypes across diagnostic categories, further investigations of phenotypic overlap between ADHD and autism at the behavioural, neurocognitive, and brain levels are needed.
We examined regional grey matter differences and similarities in children and adolescents with ASD and ADHD in comparison to healthy controls using structural magnetic resonance imaging (MRI) and voxel-based morphometry.
With regard to clinical criteria, the clinical groups did not differ with respect to ADHD symptoms; however, only patients with ASD showed deficits in social communication and interaction, according to parental rating. Structural abnormalities across both clinical groups compared to controls became evident as grey matter reductions in the left medial temporal lobe and as higher grey matter volumes in the left inferior parietal cortex. In addition, autism-specific brain abnormalities were found as increased grey matter volume in the right supramarginal gyrus.
While the shared structural deviations in the medial temporal lobe might be attributed to an unspecific delay in brain development and might be associated with memory deficits, the structural abnormalities in the inferior parietal lobe may correspond to attentional deficits observed in both ASD and ADHD. By contrast, the autism-specific grey matter abnormalities near the right temporo-parietal junction may be associated with impaired 'theory of mind' abilities. These findings shed some light on both similarities and differences in the neurocognitive profiles of ADHD and ASD patients.

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    • "Specifically, greater EC abilities are associated with larger volumes of the left orbitofrontal cortex in healthy early adolescents (Whittle et al., 2008). Furthermore, adolescents with ADHD exhibit increased gray matter (GM) volumes in the left inferior parietal lobule (Brieber et al., 2007). Adults with deficits in attention (e.g., ADHD) exhibit decreased cortical thicknesses in the prefrontal, lateral IPL, and cingulate cortices (Rommelse et al., 2011). "
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    • "shows unique structural deviations [Brieber et al., 2007] and abnormal activity in ASD. For example, the fusiform gyrus exhibits dramatically reduced activity when people with ASD process faces of strangers [Pierce, Müller, Ambrose, Allen, & Courchesne, 2001], whereas familiarity with social partners may result in a more neuro-typical response in the temporal area of the " social brain " [Pierce et al., 2004]. "
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    • "Specifically, twin (Lichtenstein, Carlstrom, Rastam, Gillberg, & Anckarsater, 2010; Nijmeijer et al., 2009; Reiersen et al., 2007; Reiersen, Constantino, Grimmer et al., 2008; Reiersen, Constantino, & Todd, 2008; Rommelse , Franke, Geurts, Hartman, & Buitelaar, 2010; Ronald, Simonoff, Kuntsi, Asherson, & Plomin, 2008; Smalley, 1997) and small, family-based studies (Mulligan et al., 2009; van Steijn et al., 2013) have suggested shared genetic overlap, while genome wide association studies have identified both unique and overlapping candidate regions (Bakker et al., 2003; Rommelse et al., 2010; Smalley, 1997; Weiss, 2009). Furthermore, ADHD and ASD have yielded some overlapping findings in regard to brain (MRI) and cognitive correlates (Brieber et al., 2007; Nyden et al., 2010; Rommelse, Geurts, Franke, Buitelaar, & Hartman, 2011). A critical test of shared etiology has classically been shared familial transmission (Cantwell, 1988); yet no large, population-based studies of the familial transmission of these disorders from mothers to offspring have been conducted. "
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