1. {{Editor(s), Journal of Intellectual & Developmental Disability}}. {J Intellect Dev Disabil};2013 (Mar);38(1):92.
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2. Berry RJ, Crider KS, Yeargin-Allsopp M. {{Periconceptional folic acid and risk of autism spectrum disorders}}. {JAMA};2013 (Feb 13);309(6):611-613.
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3. Ecker C, Ginestet C, Feng Y, Johnston P, Lombardo MV, Lai MC, Suckling J, Palaniyappan L, Daly E, Murphy CM, Williams SC, Bullmore ET, Baron-Cohen S, Brammer M, Murphy DG. {{Brain surface anatomy in adults with autism: the relationship between surface area, cortical thickness, and autistic symptoms}}. {JAMA Psychiatry};2013 (Jan 1);70(1):59-70.
CONTEXT Neuroimaging studies of brain anatomy in autism spectrum disorder (ASD) have mostly been based on measures of cortical volume (CV). However, CV is a product of 2 distinct parameters, cortical thickness (CT) and surface area (SA), that in turn have distinct genetic and developmental origins. OBJECTIVE To investigate regional differences in CV, SA, and CT as well as their relationship in a large and well-characterized sample of men with ASD and matched controls. DESIGN Multicenter case-control design using quantitative magnetic resonance imaging. SETTING Medical Research Council UK Autism Imaging Multicentre Study. PARTICIPANTS A total of 168 men, 84 diagnosed as having ASD and 84 controls who did not differ significantly in mean (SD) age (26 [7] years vs 28 [6] years, respectively) or full-scale IQ (110 [14] vs 114 [12], respectively). MAIN OUTCOME MEASURES Between-group differences in CV, SA, and CT investigated using a spatially unbiased vertex-based approach; the degree of spatial overlap between the differences in CT and SA; and their relative contribution to differences in regional CV. RESULTS Individuals with ASD differed from controls in all 3 parameters. These mainly consisted of significantly increased CT within frontal lobe regions and reduced SA in the orbitofrontal cortex and posterior cingulum. These differences in CT and SA were paralleled by commensurate differences in CV. The spatially distributed patterns for CT and SA were largely nonoverlapping and shared only about 3% of all significantly different locations on the cerebral surface. CONCLUSIONS Individuals with ASD have significant differences in CV, but these may be underpinned by (separable) variations in its 2 components, CT and SA. This is of importance because both measures result from distinct developmental pathways that are likely modulated by different neurobiological mechanisms. This finding may provide novel targets for future studies into the etiology of the condition and a new way to fractionate the disorder.
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4. Flight MH. {{Neurodevelopmental disorders: Lovastatin as fragile X therapy}}. {Nat Rev Neurosci};2013 (Feb 13)
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5. Gika DM, Artemiadis AK, Alexopoulos EC, Darviri C, Chrousos GP, Papanikolaou K. {{Use of a relaxation technique by mothers of children with autism: a case-series study}}. {Psychol Rep};2012 (Dec);111(3):797-804.
Mothers of children with autism are subject to considerable stress by having to adjust to the disorder and to cope with practical and social issues. Evidence on the effects of relaxation training on stress of these mothers is scarce. The purpose of this pilot case-series study was to examine the role of a simple 6-week daily stress management technique on mothers of children with autism. Mothers’ stress measurements and children’s functionality were assessed using validated instruments. Participants were 11 mothers of children with autism seen consecutively in the autism clinic of a children’s hospital. Statistically significant median reductions of perceived and parental stress were noted after the 6-week intervention. Median stress scores were lower by 37.1% and 33% from the baseline values of the perceived stress scale and parental stress index, respectively. Stress was not significantly correlated with children’s functioning. Stress management seems to have benefits for mothers of children with autism.
6. Lemcke S, Juul S, Parner ET, Lauritsen MB, Thorsen P. {{Early Signs of Autism in Toddlers: A Follow-Up Study in the Danish National Birth Cohort}}. {J Autism Dev Disord};2013 (Feb 13)
To identify possible early signs of autism spectrum disorder (ASD) within the Danish National Birth Cohort, we studied prospectively collected interviews from 76,441 mothers about their children’s development and behaviour at 6 and 18 months. In Danish national registries, 720 children with ASD and 231 children with intellectual disability (ID) were identified. At 6 months, associations between early signs and ASD or ID were found only in few areas. At 18 months social, language, and motor skills were delayed, and suspicion of vision and hearing problems were increased for both groups. Signs distinguishing ASD from ID were unclear, and the positive predictive values regarding ASD were below 10 % for individual predictors and aggregated risk scores.
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7. Owen ER, Baumgartner HA, Rivera SM. {{Using infrared eye-tracking to explore ordinal numerical processing in toddlers with Fragile X Syndrome}}. {J Neurodev Disord};2013 (Feb 12);5(1):1.
ABSTRACT: BACKGROUND: Fragile X syndrome (FXS) is the most common cause of inherited intellectual disability and non-idiopathic autism. Individuals with FXS present with a behavioral phenotype of specific and selective deficits in an array of cognitive skills. Disruption of number processing and arithmetic abilities in higher-functioning adults and female adolescents with FXS has been well established. Still, both numerical skills and developmentally antecedent cognitive processes have just begun to be investigated in toddlers with FXS. The goal of the current study was to assess how very young children with FXS respond to ordinal relationships among numerical magnitudes. METHODS: Infrared eye-tracking was used to explore infants’ novelty recognition during passive viewing of ordinal numerical sequences; t-tests were used to analyze group differences in looking time. RESULTS: Ordinal recognition of numerical magnitudes is significantly impaired in young toddlers with FXS. CONCLUSIONS: This study is the first to experimentally evaluate early number sense and ordinal recognition in toddlers with FXS, and our findings reveal that ordinal recognition of numerical magnitudes is significantly impaired in young toddlers with FXS, suggesting that later arithmetic impairments associated with FXS may have their origins in a developmental impairment of this more basic aspect of numerical cognition.
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8. Suren P, Roth C, Bresnahan M, Haugen M, Hornig M, Hirtz D, Lie KK, Lipkin WI, Magnus P, Reichborn-Kjennerud T, Schjolberg S, Davey Smith G, Oyen AS, Susser E, Stoltenberg C. {{Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children}}. {JAMA};2013 (Feb 13);309(6):570-577.
IMPORTANCE: Prenatal folic acid supplements reduce the risk of neural tube defects in children, but it has not been determined whether they protect against other neurodevelopmental disorders. OBJECTIVE: To examine the association between maternal use of prenatal folic acid supplements and subsequent risk of autism spectrum disorders (ASDs) (autistic disorder, Asperger syndrome, pervasive developmental disorder-not otherwise specified [PDD-NOS]) in children. DESIGN, SETTING, AND PATIENTS: The study sample of 85,176 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study (MoBa). The children were born in 2002-2008; by the end of follow-up on March 31, 2012, the age range was 3.3 through 10.2 years (mean, 6.4 years). The exposure of primary interest was use of folic acid from 4 weeks before to 8 weeks after the start of pregnancy, defined as the first day of the last menstrual period before conception. Relative risks of ASDs were estimated by odds ratios (ORs) with 95% CIs in a logistic regression analysis. Analyses were adjusted for maternal education level, year of birth, and parity. MAIN OUTCOME MEASURE: Specialist-confirmed diagnosis of ASDs. RESULTS: At the end of follow-up, 270 children in the study sample had been diagnosed with ASDs: 114 with autistic disorder, 56 with Asperger syndrome, and 100 with PDD-NOS. In children whose mothers took folic acid, 0.10% (64/61,042) had autistic disorder, compared with 0.21% (50/24,134) in those unexposed to folic acid. The adjusted OR for autistic disorder in children of folic acid users was 0.61 (95% CI, 0.41-0.90). No association was found with Asperger syndrome or PDD-NOS, but power was limited. Similar analyses for prenatal fish oil supplements showed no such association with autistic disorder, even though fish oil use was associated with the same maternal characteristics as folic acid use. CONCLUSIONS AND RELEVANCE: Use of prenatal folic acid supplements around the time of conception was associated with a lower risk of autistic disorder in the MoBa cohort. Although these findings cannot establish causality, they do support prenatal folic acid supplementation.
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9. Suzuki K, Sugihara G, Ouchi Y, Nakamura K, Futatsubashi M, Takebayashi K, Yoshihara Y, Omata K, Matsumoto K, Tsuchiya KJ, Iwata Y, Tsujii M, Sugiyama T, Mori N. {{Microglial activation in young adults with autism spectrum disorder}}. {JAMA Psychiatry};2013 (Jan 1);70(1):49-58.
CONTEXT A growing body of evidence suggests that aberrant immunologic systems underlie the pathophysiologic characteristics of autism spectrum disorder (ASD). However, to our knowledge, no information is available on the patterns of distribution of microglial activation in the brain in ASD. OBJECTIVES To identify brain regions associated with excessively activated microglia in the whole brain, and to examine similarities in the pattern of distribution of activated microglia in subjects with ASD and control subjects. DESIGN Case-control study using positron emission tomography and a radiotracer for microglia-[11C](R)-(1-[2-chrorophynyl]- N-methyl- N-[1-methylpropyl]-3 isoquinoline carboxamide) ([11C](R)-PK11195). SETTING Subjects recruited from the community. PARTICIPANTS Twenty men with ASD (age range, 18-31 years; mean [SD] IQ, 95.9 [16.7]) and 20 age- and IQ-matched healthy men as controls. Diagnosis of ASD was made in accordance with the Autism Diagnostic Observation Schedule and the Autism Diagnostic Interview-Revised. MAIN OUTCOME MEASURES Regional brain [11C](R)-PK11195 binding potential as a representative measure of microglial activation. RESULTS The [11C](R)-PK11195 binding potential values were significantly higher in multiple brain regions in young adults with ASD compared with those of controls (P < .05, corrected). Brain regions with increased binding potentials included the cerebellum, midbrain, pons, fusiform gyri, and the anterior cingulate and orbitofrontal cortices. The most prominent increase was observed in the cerebellum. The pattern of distribution of [11C](R)-PK11195 binding potential values in these brain regions of ASD and control subjects was similar, whereas the magnitude of the [11C](R)-PK11195 binding potential in the ASD group was greater than that of controls in all regions. CONCLUSIONS Our results indicate excessive microglial activation in multiple brain regions in young adult subjects with ASD. The similar distribution pattern of regional microglial activity in the ASD and control groups may indicate augmented but not altered microglial activation in the brain in the subjects with ASD.
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10. Thompson T. {{Autism research and services for young children: history, progress and challenges}}. {J Appl Res Intellect Disabil};2013 (Mar);26(2):81-107.
For three decades after Leo Kanner’s first clinical description, research progress in understanding and treating autism was minimal but since the late 1960s the growth of autism discoveries has been exponential, with a remarkable number of new findings published over the past two decades, in particular. These advances were made possible first by the discovery and dissemination of early intensive behavioural intervention (EIBI) for young children with autism that created the impetus for earlier accurate diagnosis. Other factors influencing the rapid growth in autism research were the first accepted diagnostic test for autism, the Autism Diagnostic Interview and Observation Schedule (ADI and ADOS). Developments in brain imaging and genetic technology combined to create a fuller understanding of the heterogeneity of autism, its multiple aetiologies, very early onset and course, and strategies for treatment. For a significant proportion of children with autism, it appears EIBI may be capable of promoting brain connectivity in specific cerebral areas, which is one of autism’s underlying challenges. Disagreements about the most appropriate early intervention approach between developmental and behavioural psychologists have been unproductive and not contributed to advancing the field. Naturalistic behavioural and structured discrete trial methods are being integrated with developmental strategies with promising outcomes. Over these past 30 years, young people with autism have gone from receiving essentially no proactive treatment, resulting in lives languishing in institutions, to today, when half of children receiving EIBI treatment subsequently participate in regular classrooms alongside their peers. The future has entirely changed for young people with autism. Autism has become an eminently treatable condition. The time is overdue to set aside philosophical quarrels regarding theories of child development and apply what we know for the benefit of children with autism and their families.
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11. Volk HE, Lurmann F, Penfold B, Hertz-Picciotto I, McConnell R. {{Traffic-related air pollution, particulate matter, and autism}}. {JAMA Psychiatry};2013 (Jan 1);70(1):71-77.
CONTEXT Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments. OBJECTIVE To examine the relationship between traffic-related air pollution, air quality, and autism. DESIGN This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother’s address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency’s Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development. SETTING Case-control study from California. PARTICIPANTS A total of 279 children with autism and a total of 245 control children with typical development. MAIN OUTCOME MEASURES Crude and multivariable adjusted odds ratios (AORs) for autism. RESULTS Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 mum in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates. CONCLUSIONS Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.
