Several prior reports have found that some young children with autism spectrum disorder [ASD; including autism and Asperger's syndrome and pervasive developmental disorder - not otherwise specified (PDD-NOS)] have a significant increase in head size and brain weight. However, the findings from older children and adults with ASD are inconsistent. This may reflect the relatively small sample sizes that were studied, clinical heterogeneity, or age-related brain differences.
Hence, we measured head size (intracranial volume), and the bulk volume of ventricular and peripheral cerebrospinal fluid (CSF), lobar brain, and cerebellum in 114 people with ASD and 60 controls aged between 18 and 58 years. The ASD sample included 80 people with Asperger's syndrome, 28 with autism and six with PDD-NOS.
There was no significant between-group difference in head and/or lobar brain matter volume. However, compared with controls, each ASD subgroup had a significantly smaller cerebellar volume, and a significantly larger volume of peripheral CSF.
Within ASD adults, the bulk volume of cerebellum is reduced irrespective of diagnostic subcategory. Also the significant increase in peripheral CSF may reflect differences in cortical maturation and/or ageing.
") and likely related to cerebellar WM (Allen, 2005; Amaral et al., 2008; Courchesne, Webb, & Schumann, 2012). By adulthood, smaller cerebellar volume has been reported (Hallahan et al., 2009). Numerous imaging studies have reported cerebellar hypoplasia in autism, specifically smaller cerebellar vermal lobules VI and VII (e.g., Allen, 2005; Courchesne et al., 2011, 2012; Courchesne, Yeung-Courchesne, Hesselink, & Jernigan, 1988). "
[Show abstract][Hide abstract] ABSTRACT: The cerebellum has been long known for its importance in motor learning and coordination. Recently, anatomical, clinical, and neuroimaging studies strongly suggest that the cerebellum supports cognitive functions, including language and executive functions, as well as affective regulation. Furthermore, the cerebellum has emerged as one of the key brain regions affected in autism. Here, we discuss our current understanding of the role of the cerebellum in autism, including evidence from genetic, molecular, clinical, behavioral, and neuroimaging studies. Cerebellar findings in autism suggest developmental differences at multiple levels of neural structure and function, indicating that the cerebellum is an important player in the complex neural underpinnings of autism spectrum disorder, with behavioral implications beyond the motor domain.
International Review of Neurobiology 12/2013; 113:1-34. DOI:10.1016/B978-0-12-418700-9.00001-0 · 1.92 Impact Factor
"Numerous studies have reported differences in brain anatomy and function in individuals with ASD (e.g. see Craig et al., 2007; Ecker et al., 2010; Hallahan et al., 2009), but the underlying molecular basis of the condition remains unclear. This has led to a paucity of treatment targets. "
[Show abstract][Hide abstract] ABSTRACT: GABA (gamma-amino-butyric-acid) is the primary inhibitory neurotransmitter in the human brain. It has been proposed that the symptoms of autism spectrum disorders (ASDs) are the result of deficient GABA neurotransmission, possibly including reduced expression of GABA(A) receptors. However, this hypothesis has not been directly tested in living adults with ASD. In this preliminary investigation, we used Positron Emission Tomography (PET) with the benzodiazepine receptor PET ligand [(11)C]Ro15-4513 to measure α1 and α5 subtypes of the GABA(A) receptor levels in the brain of three adult males with well-characterized high-functioning ASD compared with three healthy matched volunteers. We found significantly lower [(11)C]Ro15-4513 binding throughout the brain of participants with ASD (p < 0.0001) compared with controls. Planned region of interest analyses also revealed significant reductions in two limbic brain regions, namely the amygdala and nucleus accumbens bilaterally. Further analysis suggested that these results were driven by lower levels of the GABA(A) α5 subtype. These results provide initial evidence of a GABA(A) α5 deficit in ASD and support further investigations of the GABA system in this disorder. This article is part of a Special Issue entitled 'Neurodevelopment Disorder'.
"For example, the findings by others of both increased (Ben Bashat et al., 2007) and similar FA-values (Sundaram et al., 2008) in frontal circuits of younger people with ASD than we included in the present study, argue against this. The currently available evidence also does not strongly support the second option, as there are no reports of an accelerated decrease of white matter in autistic individuals during adulthood [albeit we have recently reported preliminary evidence for significantly greater age-related loss of cortical grey matter in adults with autism as compared to controls (Hallahan et al., 2009)]. Therefore, the third option seems the most likely, i.e., our results may reflect an earlier peak in white matter maturation and an earlier onset of an age-related decrease in FA in autism. "
[Show abstract][Hide abstract] ABSTRACT: Repetitive behaviour and inhibitory control deficits are core features of autism; and it has been suggested that they result from differences in the anatomy of striatum; and/or the 'connectivity' of subcortical regions to frontal cortex. There are few studies, however, that have measured the micro-structural organisation of white matter tracts connecting striatum and frontal cortex.
To investigate differences in bulk volume of striatum and micro-structural organisation of fronto-striatal white matter in people with autism; and their association with repetitive behaviour and inhibitory control.
We compared the bulk volume of striatum (caudate nucleus, putamen and nucleus accumbens) and white matter organisation of fronto-striatal tracts using (respectively) structural magnetic resonance imaging (sMRI) and tract specific diffusion tensor imaging (DTI) measures in 21 adults with autism and 22 controls. We also assessed performance on a cognitive inhibition (go/nogo) task.
Bulk volume of striatal structures did not differ between groups. However, adults with autism had a significantly smaller total brain white matter volume, lower fractional anisotropy of white matter tracts connecting putamen to frontal cortical areas, higher mean diffusivity of white matter tracts connecting accumbens to frontal cortex and worse performance on the go/nogo task. Also, performance on the go/nogo task was significantly related to anatomical variation when both groups were combined; but not within the autism group alone.
These data suggest that autism may be associated with differences in the anatomy of fronto-striatal white matter tracts.
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