1. Armstrong T. {{The healing balm of nature: Understanding and supporting the naturalist intelligence in individuals diagnosed with ASD: Comment on: « Implications of the idea of neurodiversity for understanding the origins of developmental disorders » by Nobuo Masataka}}. {Phys Life Rev};2017 (Jan 12)
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2. Brown HK, Cobigo V, Lunsky Y, Vigod S. {{Postpartum Acute Care Utilization Among Women with Intellectual and Developmental Disabilities}}. {J Womens Health (Larchmt)};2017 (Jan 24)
BACKGROUND: Women with intellectual and developmental disabilities have high rates of pregnancy complications. However, their postpartum health is largely unknown. We compared risks for postpartum hospital admissions and emergency department visits among women with and without intellectual and developmental disabilities. METHODS: We conducted a population-based study using linked Ontario (Canada) health and social services administrative data to identify singleton live births to women with (N = 3,803) and without intellectual and developmental disabilities (N = 378,313) (2002-2012). Outcomes were hospital admissions and emergency department visits in the 42 days following delivery discharge. We classified these as medical or psychiatric depending on the recorded primary discharge diagnosis. RESULTS: Women with intellectual and developmental disabilities, compared to those without, had increased risk for postpartum hospital admissions overall (2.4% vs. 1.2%; adjusted hazard ratios [aHR]: 1.76, 95% confidence interval [CI]: 1.43-2.17) and for psychiatric reasons (0.8% vs. 0.1%; aHR: 10.46, 95% CI: 6.96-15.70), but not for medical reasons. They also had increased risk for postpartum emergency department visits overall (16.6% vs. 7.9%; aHR: 1.85, 95% CI: 1.71-2.01) and for both medical (15.8% vs. 7.8%; aHR: 1.80, 95% CI: 1.66-1.96) and psychiatric reasons (1.3% vs. 0.1%; aHR: 5.66, 95% CI: 4.17-7.69). CONCLUSIONS: High rates of postpartum hospital admissions and emergency department visits among women with intellectual and developmental disabilities demonstrate that this group may be vulnerable to acute complications or inadequate preventive care after childbirth. Providing enhanced health services during the postpartum period, in the form of longer or more frequent visits or specialized supports, could optimize their outcomes following delivery.
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3. Elder JH, Kreider CM, Schaefer NM, de Laosa MB. {{A review of gluten- and casein-free diets for treatment of autism: 2005-2015}}. {Nutr Diet Suppl};2015;7:87-101.
BACKGROUND: The gluten free, casein free (GFCF) diet is heralded by strong anecdotal parental reports to greatly improve and even « cure » symptoms of Autism Spectrum Disorders (ASD). Yet to date, little conclusive empirical evidence exists supporting its use. OBJECTIVE: The purpose of this paper is to provide an overview of the state of the recent evidence regarding use of GFCF diet for treatment of individuals with ASD. METHODS: Five database providers (PubMed, Web of Knowledge, EBSCO, ProQuest, and WorldCat) were used to search 19 databases yielding a total of 491 articles that were published through February 2015. Peer reviewed articles published between 2005 and February 2015 were included for review if study participants were identified as having ASD and investigated the effects of the GFCF diet on ASD behaviors or the relationship between the diet and these behaviors. RESULTS: Evaluation of search results yielded 11 reviews, 7 group experimental studies including 5 randomized controlled trials, 5 case reports, and 4 group observational studies published during the last 10 years. These studies represent a marked increase in number of reported studies as well as increased scientific rigor in investigation of GFCF diets in ASD. CONCLUSIONS: While strong empirical support for the GFCF diet in ASD is currently lacking, studies point to the need for identifying subsets of individuals (e.g., those with documented gastrointestinal abnormalities) who may be the best responders to the GFCF diet. Identifying these subsets is critically needed to enhance rigor in this research area. Until rigorous research supporting use of GFCF diet is reported, clinicians should continue use caution and consider several factors when advising regarding implementation of the GFCF diet for individuals with ASD.
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4. Gwynette MF, Morriss D, Warren N, Truelove J, Warthen J, Ross CP, Mood G, Snook CA, Borckardt J. {{Social Skills Training for Adolescents With Autism Spectrum Disorder Using Facebook (Project Rex Connect): A Survey Study}}. {JMIR Ment Health};2017 (Jan 23);4(1):e4.
BACKGROUND: Adolescents with autism spectrum disorder (ASD) spend more time using electronic screen media than neurotypical peers; preliminary evidence suggests that computer-assisted or Web-based interventions may be beneficial for social skills acquisition. The current generation of adolescents accesses the Internet through computers or phones almost daily, and Facebook is the most frequently used social media platform among teenagers. This is the first research study to explore the use of Facebook as a therapeutic tool for adolescents with ASD. OBJECTIVE: To study the feasibility and clinical impact of using a Web-based social platform in combination with social skills training for adolescents with ASD. METHODS: This pilot study enrolled 6 participants (all males; mean age 14.1 years) in an online social skills training group using Facebook. Data was collected on the participants’ social and behavioral functioning at the start and conclusion of the intervention. Outcome measures included the Social Responsiveness Scale-2, the Social Skills Improvement System Rating Scale, and the Project Rex Parent Survey. Participants were surveyed at the conclusion of the intervention regarding their experience. RESULTS: No statistically significant differences in measurable outcomes were observed. However, the online addition of Facebook was well received by participants and their parents. The Facebook intervention was able to be executed with a careful privacy protocol in place and at minimal safety risk to participants. CONCLUSIONS: The utilization of Facebook to facilitate delivery of social skills training for adolescents with ASD appears to be feasible, although the clinical impact of such an addition is still unclear. It is important to note that social difficulties of participants persisted with the addition of the online platform and participants still required assistance to engage with peers in an online environment. A Web-based intervention such as the one utilized in this study has the potential to reach a mass number of patients with ASD and could address disparities in access to in-person treatment services. However, the complexity and evolving nature of Facebook’s website and privacy settings leads to a number of unique online safety concerns that may limit its clinical utility. Issues encountered in our study support the development of an alternative and closed Web-based social platform designed specifically for the target audience with ASD; this platform could be a safer and more easily moderated setting for aiding in social skills development. Despite a small sample size with no statistically significant improvements of target symptoms, the use of electronic screen media as a therapeutic tool for adolescents with ASD is still a promising area of research warranting further investigation. Our study helps inform future obstacles regarding feasibility and safety.
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5. Landsiedel J, Williams DM, Abbot-Smith K. {{A Meta-Analysis and Critical Review of Prospective Memory in Autism Spectrum Disorder}}. {J Autism Dev Disord};2017 (Jan 23)
Prospective memory (PM) is the ability to remember to carry out a planned intention at an appropriate moment in the future. Research on PM in ASD has produced mixed results. We aimed to establish the extent to which two types of PM (event-based/time-based) are impaired in ASD. In part 1, a meta-analysis of all existing studies indicates a large impairment of time-based, but only a small impairment of event-based PM in ASD. In Part 2, a critical review concludes that time-based PM appears diminished in ASD, in line with the meta-analysis, but that caution should be taken when interpreting event-based PM findings, given potential methodological limitations of several studies. Clinical implications and directions for future research are discussed.
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6. Milosavljevic B, Shephard E, Happe FG, Johnson MH, Charman T. {{Anxiety and Attentional Bias to Threat in Children at Increased Familial Risk for Autism Spectrum Disorder}}. {J Autism Dev Disord};2017 (Jan 23)
Anxiety and threat bias were examined in 6-8-year-old children at familial-risk for Autism Spectrum Disorder (ASD) and low-risk (LR, n = 37) controls. The high-risk (HR) group was divided into those who met diagnostic criteria for ASD (HR-ASD, n = 15) and those who did not (HR-non ASD, n = 24). The HR-ASD group had highest levels of parent-reported anxiety. The HR-non ASD group exhibited increased threat bias on a spatial-cueing task, while the HR-ASD group did not. Anxiety symptoms were associated with both threat bias and ASD severity. These findings suggest that the mechanisms underlying anxiety in HR siblings without ASD are similar to those in non-ASD populations. However, among children with ASD, hypersensitivity to threat may not underlie anxiety symptoms.
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7. Reis VN, Kitajima JP, Tahira AC, Feio-Dos-Santos AC, Fock RA, Lisboa BC, Simoes SN, Krepischi AC, Rosenberg C, Lourenco NC, Passos-Bueno MR, Brentani H. {{Integrative Variation Analysis Reveals that a Complex Genotype May Specify Phenotype in Siblings with Syndromic Autism Spectrum Disorder}}. {PLoS One};2017;12(1):e0170386.
It has been proposed that copy number variations (CNVs) are associated with increased risk of autism spectrum disorder (ASD) and, in conjunction with other genetic changes, contribute to the heterogeneity of ASD phenotypes. Array comparative genomic hybridization (aCGH) and exome sequencing, together with systems genetics and network analyses, are being used as tools for the study of complex disorders of unknown etiology, especially those characterized by significant genetic and phenotypic heterogeneity. Therefore, to characterize the complex genotype-phenotype relationship, we performed aCGH and sequenced the exomes of two affected siblings with ASD symptoms, dysmorphic features, and intellectual disability, searching for de novo CNVs, as well as for de novo and rare inherited point variations-single nucleotide variants (SNVs) or small insertions and deletions (indels)-with probable functional impacts. With aCGH, we identified, in both siblings, a duplication in the 4p16.3 region and a deletion at 8p23.3, inherited by a paternal balanced translocation, t(4, 8) (p16; p23). Exome variant analysis found a total of 316 variants, of which 102 were shared by both siblings, 128 were in the male sibling exome data, and 86 were in the female exome data. Our integrative network analysis showed that the siblings’ shared translocation could explain their similar syndromic phenotype, including overgrowth, macrocephaly, and intellectual disability. However, exome data aggregate genes to those already connected from their translocation, which are important to the robustness of the network and contribute to the understanding of the broader spectrum of psychiatric symptoms. This study shows the importance of using an integrative approach to explore genotype-phenotype variability.
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8. Schaafsma SM, Gagnidze K, Reyes A, Norstedt N, Mansson K, Francis K, Pfaff DW. {{Sex-specific gene-environment interactions underlying ASD-like behaviors}}. {Proc Natl Acad Sci U S A};2017 (Jan 23)
The male bias in the incidence of autism spectrum disorders (ASDs) is one of the most notable characteristics of this group of neurodevelopmental disorders. The etiology of this sex bias is far from known, but pivotal for understanding the etiology of ASDs in general. Here we investigate whether a « three-hit » (genetic load x environmental factor x sex) theory of autism may help explain the male predominance. We found that LPS-induced maternal immune activation caused male-specific deficits in certain social responses in the contactin-associated protein-like 2 (Cntnap2) mouse model for ASD. The three « hits » had cumulative effects on ultrasonic vocalizations at postnatal day 3. Hits synergistically affected social recognition in adulthood: only mice exposed to all three hits showed deficits in this aspect of social behavior. In brains of the same mice we found a significant three-way interaction on corticotropin-releasing hormone receptor-1 (Crhr1) gene expression, in the left hippocampus specifically, which co-occurred with epigenetic alterations in histone H3 N-terminal lysine 4 trimethylation (H3K4me3) over the Crhr1 promoter. Although it is highly likely that multiple (synergistic) interactions may be at work, change in the expression of genes in the hypothalamic-pituitary-adrenal/stress system (e.g., Crhr1) is one of them. The data provide proof-of-principle that genetic and environmental factors interact to cause sex-specific effects that may help explain the male bias in ASD incidence.
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9. Towle PO, Patrick PA. {{Autism Spectrum Disorder Screening Instruments for Very Young Children: A Systematic Review}}. {Autism Res Treat};2016;2016:4624829.
Research on ASD in infancy has provided a rationale for developing screening instruments for children from the first year of life to age of 18 months. A comprehensive literature search identified candidate screening tools. Using methodological probe questions adapted from the Quality Assessment of Diagnostic Accuracy Studies (QUADAS), two Level 1 and three Level 2 screening instruments were reviewed in detail. Research evidence conclusions were that instrument development was in beginning phases, is not yet strong, and requires further development. Clinical recommendations were to continue vigilant developmental and autism surveillance from the first year on but to use the screening instruments per se only for high-risk children rather than for population screening, with considerations regarding feasibility for individual settings, informing caregivers about strengths and weaknesses of the tool, and monitoring new research.
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10. Wilson J, Wright B, Jost S, Smith R, Pearce H, Richardson S. {{Can urinary indolylacroylglycine levels be used to determine whether children with autism will benefit from dietary intervention?}}. {Pediatr Res};2017 (Jan 25)
BACKGROUND: An increase in urinary indolyl-3-acryloylglycine (IAG) has been reported in children with autism spectrum disorders (ASD) who suffer with bowel problems in comparison to ASD children without gastrointestinal (GI) problems. The case for dietary intervention for ASD children with GI symptoms might be strengthened were such a difference to be autism-specific. METHODS: Quantitative analysis of urinary IAG levels was performed for 53 children on the autism spectrum and 146 age-matched controls. The parents of each child were asked to provide information on bowel symptoms experienced by the child and their eating habits over a period of 2 wk. RESULTS: We find no significant difference in urinary IAG levels between the ASD children with GI problems and ASD children without GI problems. Although we see some difference between ASD children with GI problems and controls in mainstream schools with GI problems, the difference between non-autistic children with other developmental disorders and controls in mainstream schools is more significant so that any difference is not autism-specific. We find a strong correlation between bowel symptoms and diet problems in ASD children, especially idiosyncratic feeding behavior and we show that ASD children suffering from multiple bowel symptoms tend to be those who also have dietary problems. CONCLUSION: We found no evidence to support the hypothesis that children with ASD who suffer with bowel problems have increased levels of urinary IAG in comparison to children with ASD who do not have gastrointestinal problems.Pediatric Research (2017); doi:10.1038/pr.2016.256.
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11. Yang YJ, Sukhodolsky DG, Lei J, Dayan E, Pelphrey KA, Ventola P. {{Distinct neural bases of disruptive behavior and autism symptom severity in boys with autism spectrum disorder}}. {J Neurodev Disord};2017;9:1.
BACKGROUND: Disruptive behavior in autism spectrum disorder (ASD) is an important clinical problem, but its neural basis remains poorly understood. The current research aims to better understand the neural underpinnings of disruptive behavior in ASD, while addressing whether the neural basis is shared with or separable from that of core ASD symptoms. METHODS: Participants consisted of 48 male children and adolescents: 31 ASD (7 had high disruptive behavior) and 17 typically developing (TD) controls, well-matched on sex, age, and IQ. For ASD participants, autism symptom severity, disruptive behavior, anxiety symptoms, and ADHD symptoms were measured. All participants were scanned while viewing biological motion (BIO) and scrambled motion (SCR). Two fMRI contrasts were analyzed: social perception (BIO > SCR) and Default Mode Network (DMN) deactivation (fixation > BIO). Age and IQ were included as covariates of no interest in all analyses. RESULTS: First, the between-group analyses on BIO > SCR showed that ASD is characterized by hypoactivation in the social perception circuitry, and ASD with high or low disruptive behavior exhibited similar patterns of hypoactivation. Second, the between-group analyses on fixation > BIO showed that ASD with high disruptive behavior exhibited more restricted and less DMN deactivation, when compared to ASD with low disruptive behavior or TD. Third, the within-ASD analyses showed that (a) autism symptom severity (but not disruptive behavior) was uniquely associated with less activation in the social perception regions including the posterior superior temporal sulcus and inferior frontal gyrus; (b) disruptive behavior (but not autism symptom severity) was uniquely associated with less DMN deactivation in the medial prefrontal cortex (MPFC) and lateral parietal cortex; and (c) anxiety symptoms mediated the link between disruptive behavior and less DMN deactivation in both anterior cingulate cortex (ACC) and MPFC, while ADHD symptoms mediated the link primarily in ACC. CONCLUSIONS: In boys with ASD, disruptive behavior has a neural basis in reduced DMN deactivation, which is distinct and separable from that of core ASD symptoms, with the latter characterized by hypoactivation in the social perception circuitry. These differential neurobiological markers may potentially serve as neural targets or predictors for interventions when treating disruptive behavior vs. core symptoms in ASD.
