1. Bolte S, Bartl-Pokorny KD, Jonsson U, Berggren S, Zhang D, Kostrzewa E, Falck-Ytter T, Einspieler C, Pokorny FB, Jones EJ, Roeyers H, Charman T, Marschik PB. {{How can clinicians detect and treat autism early? Methodological trends of technology use in research}}. {Acta Paediatr};2015 (Oct 19)
We reviewed original research papers that used quantifiable technology to detect early autism spectrum disorder (ASD) and identified 376 studies from 34 countries from 1965- 2013. Publications have increased significantly since 2000, with most coming from the USA. Electroencephalogram, magnetic resonance imaging and eye-tracking were the most frequently used technologies. Conclusion The use of quantifiable technology to detect early ASD has increased in recent decades, but has had limited impact on early detection and treatment. Further scientific developments are anticipated and we hope that they will increasingly be used in clinical practice for early ASD screening, diagnosis and intervention. This article is protected by copyright. All rights reserved.
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2. Dewinter J, Vermeiren R, Vanwesenbeeck I, Van Nieuwenhuizen C. {{Parental Awareness of Sexual Experience in Adolescent Boys With Autism Spectrum Disorder}}. {J Autism Dev Disord};2015 (Oct 19)
Parent report and adolescent self-report data on lifetime sexual experience in adolescents with ASD were compared in 43 parent-adolescent dyads. Parents tended to underestimate the lifetime sexual experience of their sons, particularly solo sexual experiences such as masturbation and experience with orgasm. Parental underestimation and unawareness of adolescents’ sexual experience may influence communication and education about sex and sexuality in families. These findings have implications for the interpretation of earlier research, based on parent and caregiver reports, on sexuality in adolescents with ASD.
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3. Dougherty CC, Evans DW, Myers SM, Moore GJ, Michael AM. {{A Comparison of Structural Brain Imaging Findings in Autism Spectrum Disorder and Attention-Deficit Hyperactivity Disorder}}. {Neuropsychol Rev};2015 (Oct 19)
ASD and ADHD are regarded as distinct disorders in the current DSM-5. However, recent research and the RDoC initiative are recognizing considerable overlap in the clinical presentation of ASD, ADHD, and other neurodevelopmental disorders. In spite of numerous neuroimaging findings in ASD and ADHD, the extent to which either of the above views are supported remains equivocal. Here we compare structural MRI and DTI literature in ASD and ADHD. Our main findings reveal both distinct and shared neural features. Distinct expressions were in total brain volume (ASD: increased volume, ADHD: decreased volume), amygdala (ASD: overgrowth, ADHD: normal), and internal capsule (ASD: unclear, ADHD: reduced FA in DTI). Considerable overlap was noted in the corpus callosum and cerebellum (lower volume in structural MRI and decreased FA in DTI), and superior longitudinal fasciculus (reduced FA in DTI). In addition, we identify brain regions which have not been studied in depth and require more research. We discuss relationships between brain features and symptomatology. We conclude by addressing limitations of current neuroimaging research and offer approaches that account for clinical heterogeneity to better distinguish brain-behavior relationships.
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4. Durbin A, Sirotich F, Lunsky Y, Durbin J. {{Unmet Needs of Adults in Community Mental Health Care With and Without Intellectual and Developmental Disabilities: A Cross-Sectional Study}}. {Community Ment Health J};2015 (Oct 19)
The cross-sectional study compared the clinical and need profiles for clients with and without intellectual and developmental disabilities (IDD) in seven mental health case management programs in Toronto, Canada on March 31, 2013. Unmet needs in domains within four broad clusters were measured by staff using an internationally utilized tool, the Camberwell Assessment of Need. Among the 2560 clients, 8.3 % had a co-occurring IDD. For most assessed domains rates of unmet need were not different for persons with and without IDD. However, the IDD group had greater unmet needs for adaptive functioning/skills and cognitive needs [self-care (p = 0.023), education (p < 0.001), transportation (p < 0.001), and information on condition (p = 0.038)]. While clients with IDD and psychiatric diagnoses often receive poor quality care, in the case management programs examined their rates of unmet need were similar to individuals without IDD across most assessed domains, including in the areas of addictions and physical health care.
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5. Fairthorne J, de Klerk N, Leonard H. {{Brief Report: Burden of Care in Mothers of Children with Autism Spectrum Disorder or Intellectual Disability}}. {J Autism Dev Disord};2015 (Oct 19)
Compared to other mothers, mothers of children with autism spectrum disorder (ASD) or intellectual disability (ID) have higher rates of treatment episodes for psychiatric disorders. We aimed to estimate the maternal burden of care by comparing the length of hospitalisations for psychiatric disorders and the treatment rates for psychiatric disorders after the birth in mothers of children with ASD/ID and no psychiatric history to that of other mothers with no psychiatric history. Mothers of children with ID of known cause (not Down syndrome) and mothers of children ASD without ID emerged as particularly vulnerable. Mothers of children with Down syndrome were resilient. The development of specialised organisations to provide support to mothers of children with ID of known cause (not Down syndrome) and mothers of children with ASD without ID could assist them to maintain their mental health.
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6. Jeffries T, Crosland K, Miltenberger R. {{Evaluating a tablet application and differential reinforcement to increase eye contact in children with autism}}. {J Appl Behav Anal};2015 (Oct 19)
We tested the effectiveness of a tablet application and differential reinforcement to increase eye contact in 3 children with autism. The application required the child to look at a picture of a person’s face and identify the number displayed in the person’s eyes. Eye contact was assessed immediately after training, 1 hr after training, and in a playroom. The tablet application was not effective; however, differential reinforcement was effective for all participants.
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7. Kadak MT, Cetin I, Tarakcioglu MC, Ozer OF, Kacar S, Cimen B. {{Low Serum Level alpha-Synuclein and Tau Protein in Autism Spectrum Disorder Compared to Controls}}. {Neuropediatrics};2015 (Oct 19)
alpha-Synuclein (alpha-syn) and tau proteins are thought to be related with the synaptic loss and cell death underlying several important neurodegenerative diseases. The aim of our study was to investigate serum alpha-syn and tau levels in autism. Serum levels of alpha-syn and tau were measured, and autism spectrum disorder (ASD) severity was assessed at admission using the Childhood Autism Rating Scale (CARS) total score. The mean CARS score of the autism group on admission was 47.91 points (SD: 5.97). The results indicated that the mean serum alpha-syn and serum tau levels were significantly (p < 0.001) lower in children with ASD as compared with normal cases (33.01 +/- 20.78 and 55.19 +/- 15.34 ng/mL and 241.23 +/- 290.5 and 509.78 +/- 269.25 ng/mL, respectively). There was a significant positive correlation between serum alpha-syn levels and serum levels of tau identified by Pearson correlation analysis (r = 0.922, n = 28, p < 0.001). Synaptic abnormality in autism may result from microglial activity. Furthermore, alpha-syn and tau aggregation may lead to synaptic dysfunction, and this may contribute to either neuronal or synaptic dysfunction or neurodegeneration. Our preliminary study suggests that low levels of serum alpha-syn and tau may be implicated in the relationship between synaptic activity and autism.
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8. Miron O, Ari-Even Roth D, Gabis LV, Henkin Y, Shefer S, Dinstein I, Geva R. {{Prolonged auditory brainstem responses in infants with autism}}. {Autism Res};2015 (Oct 19)
Numerous studies have attempted to identify early physiological abnormalities in infants and toddlers who later develop autism spectrum disorder (ASD). One potential measure of early neurophysiology is the auditory brainstem response (ABR), which has been reported to exhibit prolonged latencies in children with ASD. We examined whether prolonged ABR latencies appear in infancy, before the onset of ASD symptoms, and irrespective of hearing thresholds. To determine how early in development these differences appear, we retrospectively examined clinical ABR recordings of infants who were later diagnosed with ASD. Of the 118 children in the participant pool, 48 were excluded due to elevated ABR thresholds, genetic aberrations, or old testing age, leaving a sample of 70 children: 30 of which were tested at 0-3 months, and 40 were tested at toddlerhood (1.5-3.5 years). In the infant group, the ABR wave-V was significantly prolonged in those who later developed ASD as compared with case-matched controls (n = 30). Classification of infants who later developed ASD and case-matched controls using this measure enabled accurate identification of ASD infants with 80% specificity and 70% sensitivity. In the group of toddlers with ASD, absolute and interpeak latencies were prolonged compared to clinical norms. Findings indicate that ABR latencies are significantly prolonged in infants who are later diagnosed with ASD irrespective of their hearing thresholds; suggesting that abnormal responses might be detected soon after birth. Further research is needed to determine if ABR might be a valid marker for ASD risk. Autism Res 2015. (c) 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research.
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9. Sullivan JM, Badimon A, Schaefer U, Ayata P, Gray J, Chung CW, von Schimmelmann M, Zhang F, Garton N, Smithers N, Lewis H, Tarakhovsky A, Prinjha RK, Schaefer A. {{Autism-like syndrome is induced by pharmacological suppression of BET proteins in young mice}}. {J Exp Med};2015 (Oct 19);212(11):1771-1781.
Studies investigating the causes of autism spectrum disorder (ASD) point to genetic, as well as epigenetic, mechanisms of the disease. Identification of epigenetic processes that contribute to ASD development and progression is of major importance and may lead to the development of novel therapeutic strategies. Here, we identify the bromodomain and extraterminal domain-containing proteins (BETs) as epigenetic regulators of genes involved in ASD-like behaviors in mice. We found that the pharmacological suppression of BET proteins in the brain of young mice, by the novel, highly specific, brain-permeable inhibitor I-BET858 leads to selective suppression of neuronal gene expression followed by the development of an autism-like syndrome. Many of the I-BET858-affected genes have been linked to ASD in humans, thus suggesting the key role of the BET-controlled gene network in the disorder. Our studies suggest that environmental factors controlling BET proteins or their target genes may contribute to the epigenetic mechanism of ASD.
