Pubmed du 13/10/09

mercredi 14 octobre 2009

1. Coskun MA, Varghese L, Reddoch S, Castillo EM, Pearson DA, Loveland KA, Papanicolaou AC, Sheth BR. Increased response variability in autistic brains ? Neuroreport ;2009 (Oct 8)

One of the key ideas regarding atypical connectivity in autistic brains is the hypothesis of noisier networks. The systems level version of this hypothesis predicts reduced reliability or increased variability in the evoked responses of individuals with autism. Using magnetoencephalography, we examined the response of individuals with autism spectrum disorder versus matched typically developing persons to passive tactile stimulation of the thumb and index finger of the dominant (right) hand. A number of different analyses failed to show higher variability in the evoked response to the thumb or to the index finger in the autism group as compared with typicals. Our results argue against the hypothesis that the brain networks in autism are noisier than normal.

2. Hinton VJ, Cyrulnik SE, Fee RJ, Batchelder A, Kiefel JM, Goldstein EM, Kaufmann P, De Vivo DC. Association of autistic spectrum disorders with dystrophinopathies. Pediatr Neurol ;2009 (Nov) ;41(5):339-346.

Parents of 85 boys with dystrophinopathies and 51 sibling controls completed the Social Communication Questionnaire, describing child behaviors associated with autism spectrum disorders and a rating of parental stress. Twenty-one boys with dystrophinopathies and no siblings received scores above the cut-point for possible autistic spectrum disorders. Mothers of identified children were given detailed interviews using the Autism Diagnostic Interview-Revised, and 16 boys (about 19% of the sample) met the criteria for autism spectrum disorders. Significant qualitative abnormalities in reciprocal social interactions and communication were evident in all, whereas restricted and repetitive behaviors were generally less pronounced in the group. Moreover, parents of boys with dystrophinopathy and autism spectrum disorders demonstrated significantly higher ratings of stress than parents of boys with dystrophinopathy alone. Increased attention to behavioral concerns associated with dystrophinopathies is necessary to ensure the well-being of the whole family.

3. Levy SE, Mandell DS, Schultz RT. Autism. Lancet ;2009 (Oct 9)

Autism spectrum disorders are characterised by severe deficits in socialisation, communication, and repetitive or unusual behaviours. Increases over time in the frequency of these disorders (to present rates of about 60 cases per 10 000 children) might be attributable to factors such as new administrative classifications, policy and practice changes, and increased awareness. Surveillance and screening strategies for early identification could enable early treatment and improved outcomes. Autism spectrum disorders are highly genetic and multifactorial, with many risk factors acting together. Genes that affect synaptic maturation are implicated, resulting in neurobiological theories focusing on connectivity and neural effects of gene expression. Several treatments might address core and comorbid symptoms. However, not all treatments have been adequately studied. Improved strategies for early identification with phenotypic characteristics and biological markers (eg, electrophysiological changes) might hopefully improve effectiveness of treatment. Further knowledge about early identification, neurobiology of autism, effective treatments, and the effect of this disorder on families is needed.

4. Raznahan A, Toro R, Daly E, Robertson D, Murphy C, Deeley Q, Bolton PF, Paus T, Murphy DG. Cortical Anatomy in Autism Spectrum Disorder : An In Vivo MRI Study on the Effect of Age. Cereb Cortex ;2009 (Oct 9)

There is increasing evidence that children with autism spectrum disorder (ASD) have age-related differences from controls in cortical volume (CV). It is less clear, however, if these persist in adulthood and whether these reflect alterations in cortical thickness (CT) or cortical surface area (SA). Hence, we used magnetic resonance imaging to investigate the relationship between age and CV, CT, and SA in 127 males aged 10 through 60 years (76 with ASD and 51 healthy controls). "Regional" analyses (using cortical parcellation) identified significant age-by-group interactions in both CV and CT (but not SA) in the temporal lobes and within these the fusiform and middle temporal gyri. Spatially nonbiased "vertex-based" analysis replicated these results and identified additional "age-by-group" interactions for CT within superior temporal, inferior and medial frontal, and inferior parietal cortices. Here, CV and CT were 1) significantly negatively correlated with age in controls, but not in ASD, and 2) smaller in ASD than controls in childhood but vice versa in adulthood. Our findings suggest that CV dysmaturation in ASD extends beyond childhood, affects brain regions crucial to social cognition and language, and is driven by CT dysmaturation. This may reflect primary abnormalities in cortical plasticity and/or be secondary to disturbed interactions between individuals with ASD and their environment.


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