1. {{Therapies for Children With Autism Spectrum Disorders: A Review of the Research for Parents and Caregivers}}. 2005.
This guide describes research about the possible benefits and negative side effects of therapies for children who are between 2 and 12 years old and have an ASD. It was created to help you talk with your doctor, school administrator, social worker, and health insurance representative about programs and therapies.
2. {{Comparative Effectiveness of Therapies for Children With Autism Spectrum Disorders}}. 2007.
What evidence is available regarding the effectiveness, benefits, and harms of therapies used to address the core and associated symptoms seen among children ages 2-12 years with autism spectrum disorders?
3. Brock J, Xu JY, Brooks KR. {{Individual differences in visual search: relationship to autistic traits, discrimination thresholds, and speed of processing}}. {Perception}. 2011; 40(6): 739-42.
Enhanced visual search is widely reported in autism. Here we note a similar advantage for university students self-reporting higher levels of autism-like traits. Contrary to prevailing theories of autism, performance was not associated with perceptual-discrimination thresholds for the same stimuli, but was associated with inspection-time threshold–a measure of speed of perceptual processing. Enhanced visual search in autism may, therefore, at least partially be explained by faster speed of processing.
4. Guo H, Hu Z, Zhao J, Xia K. {{Genetics of autism spectrum disorders}}. {Zhong Nan Da Xue Xue Bao Yi Xue Ban}. 2011; 36(8): 703-11.
Autism is a group of etiology and clinical heterogeneous neurodevelopmental disorders with an onset before 3 years old. It has 3 core characteristics: deficits in verbal communication; impairment of social interaction; restricted interests and repetitive behaviors. The incidence is increasing over time worldwide. Twin and family studies have demonstrated that autism has a high heritability (>90%). Although certain progress of autism genetic study has been made in the last de-cades and several autism susceptibility genes and loci have been identified, there are still about 70%-80% of patients for whom an autism-related genetic change cannot be identified.
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5. Hambly C, Fombonne E. {{The Impact of Bilingual Environments on Language Development in Children with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2011.
The impact of bilingual exposure on language learning has not been systematically studied in children with Autism Spectrum Disorders. This study compared the social abilities and language levels of children (mean age = 56 months) with ASDs from bilingual (n = 45) and monolingual (n = 30) environments. Bilingually-exposed children were subgrouped based on simultaneous bilingual exposure from infancy (SIM, n = 24) versus sequential post-infancy bilingual exposure (SEQ, n = 21). Despite significantly different amounts of bilingual exposure across all groups (p = <0.001) and significantly stronger social interaction scores in the SIM group compared to the SEQ group on the Vineland Adaptive Behavior Scales-II Interpersonal subdomain (p = 0.025), there were no significant group differences in language level. Bilingually-exposed children with ASDs did not experience additional delays in language development.
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6. Morita T, Kosaka H, Saito DN, Ishitobi M, Munesue T, Itakura S, Omori M, Okazawa H, Wada Y, Sadato N. {{Emotional responses associated with self-face processing in individuals with autism spectrum disorders: An fMRI study}}. {Soc Neurosci}. 2011.
Individuals with autism spectrum disorders (ASD) show impaired emotional responses to self-face processing, but the underlying neural bases are unclear. Using functional magnetic resonance imaging, we investigated brain activity when 15 individuals with high-functioning ASD and 15 controls rated the photogenicity of self-face images and photographs of others’ faces. Controls showed a strong correlation between photogenicity ratings and extent of embarrassment evoked by self-face images; this correlation was weaker among ASD individuals, indicating a decoupling between the cognitive evaluation of self-face images and emotional responses. Individuals with ASD demonstrated relatively low self-related activity in the posterior cingulate cortex (PCC), which was related to specific autistic traits. There were significant group differences in the modulation of activity by embarrassment ratings in the right insular (IC) and lateral orbitofrontal cortices. Task-related activity in the right IC was lower in the ASD group. The reduced activity in the right IC for self-face images was associated with weak coupling between cognitive evaluation and emotional responses to self-face images. The PCC is responsible for self-referential processing, and the IC plays a role in emotional experience. Dysfunction in these areas could contribute to the lack of self-conscious behaviors in response to self-reflection in ASD individuals.
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7. Veenstra-Vanderweele J, Blakely RD. {{Networking in Autism: Leveraging Genetic, Biomarker and Model System Findings in the Search for New Treatments}}. {Neuropsychopharmacology}. 2011.
Autism Spectrum Disorder (ASD) is a common neurodevelopmental disorder affecting approximately 1% of children. ASD is defined by core symptoms in two domains: negative symptoms of impairment in social and communication function, and positive symptoms of restricted and repetitive behaviors. Available treatments are inadequate for treating both core symptoms and associated conditions. Twin studies indicate that ASD susceptibility has a large heritable component. Genetic studies have identified promising leads, with converging insights emerging from single-gene disorders that bear ASD features, with particular interest in mammalian target of rapamycin (mTOR)-linked synaptic plasticity mechanisms. Mouse models of these disorders are revealing not only opportunities to model behavioral perturbations across species, but also evidence of postnatal rescue of brain and behavioral phenotypes. An intense search for ASD biomarkers has consistently pointed to elevated platelet serotonin (5-HT) levels and a surge in brain growth in the first 2 years of life. Following a review of the diversity of ASD phenotypes and its genetic origins and biomarkers, we discuss opportunities for translation of these findings into novel ASD treatments, focusing on mTor- and 5-HT-signaling pathways, and their possible intersection. Paralleling the progress made in understanding the root causes of rare genetic syndromes that affect cognitive development, we anticipate progress in models systems using bona fide ASD-associated molecular changes that have the potential to accelerate the development of ASD diagnostics and therapeutics.Neuropsychopharmacology Reviews advance online publication, 21 September 2011; doi:10.1038/npp.2011.185.
