It is now necessary to conduct similar studies in children to confirm the results obtained in adults. Pediatric cohorts are necessary for studies in children of various ages—and therefore brain maturation—and this implies taking into account a much larger population of subjects.
If these initial conclusions are confirmed, it would make it possible to consider the development of new therapeutic approaches for deficits in social cognition. For example, transcranial magnetic stimulation could be explored because brain connectivity between adjacent areas is located on the surface of the brain. Please sign in to add a comment. Registration is free, and takes less than a minute.
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Home Neuroscience Home Autism spectrum disorders. Credit: CEA. Explore further. More information: Marc-Antoine d'Albis et al. Local structural connectivity is associated with social cognition in autism spectrum disorder, Brain DOI: This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission.
The content is provided for information purposes only. Leukemia drug shows promise for treating a childhood brain cancer Sep 20, Sep 20, Related Stories. Unique patterns of neural communications found in brains of children with autism Oct 25, Sep 05, Dec 04, Variation in brain development seen in infants with autism Feb 22, Feb 27, Jul 14, In this sample, men with ASD did not differ significantly from those in the control group on global volume measures but displayed regionally specific differences in gray matter and white matter volume.
Individuals with ASD showed increased gray matter in the anterior temporal and dorsolateral prefrontal regions but decreased gray matter volume in the occipital and medial parietal regions. In addition, the large-scale gray matter systems associated with ASD in adults comprised the cingulate gyrus, supplementary motor area, basal ganglia, amygdala, inferior parietal lobule, and cerebellum, as well as dorsolateral prefrontal, lateral orbitofrontal, and dorsal and ventral medial prefrontal cortices.
Variation in gray matter volume correlated with specific symptom domains within the ASD group. Furthermore, we found that ASD in adults was accompanied by spatially distributed reductions in regional white matter volume. Our findings support the suggestion that regional neuroanatomic abnormalities in ASD persist into adulthood and are linked to specific autistic symptoms.
We first found that high-functioning individuals with ASD do not have an increase in overall brain volume during adulthood.
Review of neuroimaging in autism spectrum disorders: what have we learned and where we go from here
In typical development, total brain volume plateaus at approximately age 13 years and starts to decrease in early adulthood. Such abnormal brain enlargement is disproportionately accounted for by a relatively larger increase in total white matter than gray matter, 51 with each displaying a differential growth trajectory. Although total gray matter volume reaches a peak before adulthood, white matter continues on a linear upward trend during adolescence.
These results suggest that, in adulthood, global brain measures are unaffected in individuals with ASD without intellectual disability. In contrast to earlier development, when most of the neuroanatomic differences may be related to global differences, most of the differences in ASD in adults appear to be linked to specific neural systems.
Local differences in neuroanatomy were initially investigated with VBM. We found that people with ASD displayed significant differences in the anatomy of a number of brain regions. One region with significantly increased gray matter volume was the anterior temporal lobe overlapping with the superior temporal pole.
Left-hemisphere increases in this region were correlated with increased social, but not repetitive or communicative, symptom severity observed on the ADI-R. Prior studies have detected gray matter differences in this area across childhood, 53 adolescence, 34 and young adulthood. We also observed increased gray matter volume in the dorsolateral prefrontal cortex and the dorsal precentral and postcentral gyrus. Prior research reported that people with ASD have differences in frontal lobe neuronal integrity, 61 function, 62 - 64 anatomy, 22 , 34 , 65 , 66 and connectivity.
Given that there may be delay in frontal lobe maturation, 74 in addition to being implicated in executive dysfunction in autism, such frontal abnormalities may underpin some of the impairments in the repetitive behavior domain. This result agrees with previous neuroimaging studies suggesting that abnormalities in frontostriatal-thalamic circuitry mediating some of the repetitive behaviors typically found in ASD may overlap with mediating symptoms observed in people with obsessive-compulsive disorder. Our results therefore add to increasing evidence that individuals with ASD have abnormalities in frontostriatal systems extending into adulthood and that structural abnormalities in frontal regions are related to the severity of ritualistic repetitive behavior observed in ASD.
Individuals with ASD had a significant decrease in gray matter volume in a large cluster located in the occipital and medial parietal regions. In addition, variation in this cluster was associated with the severity of social and communication symptoms in ASD.
Some studies 90 , 91 have also suggested that neuroanatomic abnormalities in the visual cortex may at least partially contribute to some of the characteristic social abnormalities in ASD. Poor processing of eye gaze and facial expression, for instance, relies heavily on primary visual processes, which, if impaired, may have significant detrimental effects on the ability to communicate socially. Autistic spectrum disorder is a highly heterogeneous disorder with multifactorial etiologic characteristics. Partial least-squares analysis revealed a spatially distributed network of regions where gray matter volume was highly correlated with ASD.
This pattern included regions detected by the voxelwise approach but also identified an additional set of network components such, as the cerebellum; and dorsolateral, orbital, and ventral medial prefrontal cortex, and limbic regions, such as the cingulate cortex and amygdala. All these network components have been reported, 13 , 22 , 34 , 97 and some have been related to symptoms. For example, differences in limbic regions have been linked to impairments in socioemotional processing and face processing 98 - ; the medial prefrontal cortex is critical for typically developing social cognition and empathy , and has also been linked to atypical mentalizing or theory of mind , and self-referential cognition in ASD.
Notably, PLS analysis identified networks of positive and negative associations with group membership, often in close spatial proximity eg, within the cerebellum. This further supports the notion that our results do not reflect global differences in neuroanatomy but indicate subtle and spatially distinct networks of regions implicated in adults with ASD. Given the composition of the sample, these neural systems likely reflect the end result of atypical cortical development of gray matter rather than represent the primary neuropathologic characteristics of the condition, which is best investigated in younger age groups.
Large longitudinal studies are therefore required to disentangle the effects of pathologic factors and brain maturation in ASD, as well as to isolate which neuroanatomic changes are primary and which are secondary to the condition eg, via compensatory mechanisms.
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The neuroanatomic differences observed for gray matter were accompanied by spatially distributed reductions in white matter volume. White matter abnormalities have been reported in individuals with ASD. For example, studies found that people with ASD have significant differences in white matter volume 17 , 23 , and microstructural integrity as measured by diffusion tensor MRI. Such prior reports mostly highlight significant increases in white matter during early childhood, which may precede the abnormal pattern of growth in gray matter.
There is also evidence that anatomic underconnectivity between frontal and parietal areas affects executive functioning and is accompanied by abnormalities in connecting fibers, including the corpus callosum, 94 and differences in the neurodevelopmental trajectory of white matter in ASD on the global and regional level. Thus, although it is difficult to link specific cognitive functions to white matter deficits, altered brain connectivity, together with the structural alterations within specific gray matter regions, may explain some of the behavioral features observed in ASD.
Our study raises a number of methodologic issues. First, we investigated neuroanatomy in a sample of high-functioning men, using the ADI-R as a diagnostic tool, which is not representative of all individuals on the autism spectrum. Our sample therefore represents a subpopulation of the autistic phenotype, and results should be interpreted in light of this. In addition, we did not distinguish between putative subtypes of ASD eg, high-functioning autism and Asperger syndrome.
Evidence suggests that, by adulthood, these groups are largely indistinguishable clinically or cognitively. However, the extent to which these groups differ at the level of brain anatomy is unknown and requires investigation. Second, a multicenter design was used for MRI data acquisition to overcome single-site recruitment limitations. A recently developed acquisition protocol that standardizes structural MRI data across multiple platforms and acquisition parameters was used.
In addition, intersite effects were accounted for in the statistical model. Finally, the voxelwise analysis has inherent limitations. For instance, cortical volume comprises 2 subcomponents cortical thickness and surface area , which in turn have different cellular components and developmental determinants. In summary, our results suggest that adults with ASD do not have a significant increase in overall brain volume, but they do have regional differences in brain anatomy, which are correlated with specific autistic symptoms.
Submitted for Publication: January 14, ; final revision received June 3, ; accepted July 15, Daly; Sean C. Murphy, MD; Declan G.
Brain Imaging Studies in Autism Spectrum Disorders
Williams, PhD. We are grateful to the individuals who agreed to undergo MRI and who gave their time so generously to this study. All Rights Reserved. View Large Download. Table 1. Participant Demographics.
What does autism look like in the brain?
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Overly persistent brain connections
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