1. Ameis SH, Fan J, Rockel C, Soorya L, Wang AT, Anagnostou E. {{Altered cingulum bundle microstructure in autism spectrum disorder}}. {Acta Neuropsychiatr};2013 (Oct);25(5):275-282.
OBJECTIVE: Here, we examined the cingulum bundle, a long-range white matter tract mediating dorsal limbic connectivity, using diffusion tensor imaging (DTI) tractography, in children and adolescents with autism spectrum disorder (ASD) versus controls. We hypothesised that cingulum bundle microstructure would be altered in ASD, based on evidence implicating abnormal white matter connectivity in this disorder. METHODS: DTI data were acquired for 19 ASD participants (IQ 70; 7-18 years; mean = 12.4 +/- 3.1) and 16 age-matched controls (7-18 years; mean = 12.3 +/- 3.6) on a 3 T magnetic resonance imaging system. Deterministic tractography was used to isolate the cingulum bundle. Left and right cingulum bundles were examined for differences in several DTI metrics in ASD children/adolescents versus controls, including: fractional anisotropy (FA), mean, axial, and radial diffusivity. RESULTS: Significant age x group interaction effects were found for all DTI metrics (mean diffusivity: F 1,28 = 9.5, p = 0.005, radial diffusivity: F 1,28 = 7.8, p = 0.009, axial diffusivity: F 1,28 = 5.2, p = 0.03, FA: F 1,28 = 4.4, p = 0.04). Interaction effects were driven by increases in cingulum bundle diffusivity (mean, radial, and axial diffusivity), and decreased FA, in younger ASD participants within our sample versus controls. CONCLUSION: Our results point to immature microstructural organisation of the cingulum bundle in ASD, particularly during the early years of life, with implications for limbic network synchronisation and complex socio-emotional performance.
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2. Arnett MT, Herman DH, McGee AW. {{Deficits in tactile learning in a mouse model of fragile x syndrome}}. {PLoS One};2014;9(10):e109116.
The fragile X mental retardation 1 mutant mouse (Fmr1 KO) recapitulates several of the neurologic deficits associated with Fragile X syndrome (FXS). As tactile hypersensitivity is a hallmark of FXS, we examined the sensory representation of individual whiskers in somatosensory barrel cortex of Fmr1 KO and wild-type (WT) mice and compared their performance in a whisker-dependent learning paradigm, the gap cross assay. Fmr1 KO mice exhibited elevated responses to stimulation of individual whiskers as measured by optical imaging of intrinsic signals. In the gap cross task, initial performance of Fmr1 KO mice was indistinguishable from WT controls. However, while WT mice improved significantly with experience at all gap distances, Fmr1 KO mice displayed significant and specific deficits in improvement at longer distances which rely solely on tactile information from whiskers. Thus, Fmr1 KO mice possess altered cortical responses to sensory input that correlates with a deficit in tactile learning.
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3. Bone D, Goodwin MS, Black MP, Lee CC, Audhkhasi K, Narayanan S. {{Applying Machine Learning to Facilitate Autism Diagnostics: Pitfalls and Promises}}. {J Autism Dev Disord};2014 (Oct 8)
Machine learning has immense potential to enhance diagnostic and intervention research in the behavioral sciences, and may be especially useful in investigations involving the highly prevalent and heterogeneous syndrome of autism spectrum disorder. However, use of machine learning in the absence of clinical domain expertise can be tenuous and lead to misinformed conclusions. To illustrate this concern, the current paper critically evaluates and attempts to reproduce results from two studies (Wall et al. in Transl Psychiatry 2(4):e100, 2012a; PloS One 7(8), 2012b) that claim to drastically reduce time to diagnose autism using machine learning. Our failure to generate comparable findings to those reported by Wall and colleagues using larger and more balanced data underscores several conceptual and methodological problems associated with these studies. We conclude with proposed best-practices when using machine learning in autism research, and highlight some especially promising areas for collaborative work at the intersection of computational and behavioral science.
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4. Busch de Ahumada LC, Ahumada JL. {{Contacting a 19 month-old mute autistic girl: A clinical narrative}}. {Int J Psychoanal};2014 (Oct 8)
Conveying that psychoanalysis offers rich opportunities for the very early treatment of autistic spectrum disorders, this clinical communication unfolds the clinical process of a 19 month-old ‘shell-type’ encapsulated mute autistic girl. It details how, in a four-weekly-sessions schedule, infant Lila evolved within two years from being emotionally out-of-contact to the affective aliveness of oedipal involvement. Following Frances Tustin’s emphasis on the analyst’s ‘quality of attention’ and Justin Call’s advice that in baby-mother interaction the infant is the initiator and the mother is the follower, it is described how the analyst must, amid excruciating non-response, even-mindedly sustain her attention in order to meet the child half-way at those infrequent points where flickers of initiative on her side are adumbrated. This helps attain evanescent ‘moments of contact’ which coalesce later into ‘moments of sharing’, eventually leading to acknowledgment of the analyst’s humanness and a receptiveness for to-and-fro communication. Thus the ‘primal dialogue’ (Spitz) is reawakened and, by experiencing herself in the mirror of the analyst, the child’s sense of I-ness is reinstated. As evinced by the literature, the mainstream stance rests on systematic early interpretation of the transference, which has in our view strongly deterred progress in the psychoanalytic treatment of autistic spectrum disorders.
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5. Chantiluke K, Barrett N, Giampietro V, Brammer M, Simmons A, Rubia K. {{Disorder-dissociated effects of fluoxetine on brain function of working memory in attention deficit hyperactivity disorder and autism spectrum disorder}}. {Psychol Med};2014 (Oct 8):1-11.
Background. Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are often co-morbid and share performance and brain dysfunctions during working memory (WM). Serotonin agonists modulate WM and there is evidence of positive behavioural effects in both disorders. We therefore used functional magnetic resonance imaging (fMRI) to investigate shared and disorder-specific brain dysfunctions of WM in these disorders, and the effects of a single dose of the selective serotonin reuptake inhibitor (SSRI) fluoxetine. Method. Age-matched boys with ADHD (n = 17), ASD (n = 17) and controls (n = 22) were compared using fMRI during an N-back WM task. Patients were scanned twice, under either an acute dose of fluoxetine or placebo in a double-blind, placebo-controlled randomized design. Repeated-measures analyses within patients assessed drug effects on performance and brain function. To test for normalization effects of brain dysfunctions, patients under each drug condition were compared to controls. Results. Under placebo, relative to controls, both ADHD and ASD boys shared underactivation in the right dorsolateral prefrontal cortex (DLPFC). Fluoxetine significantly normalized the DLPFC underactivation in ASD relative to controls whereas it increased posterior cingulate cortex (PCC) deactivation in ADHD relative to control boys. Within-patient analyses showed inverse effects of fluoxetine on PCC deactivation, which it enhanced in ADHD and decreased in ASD. Conclusions. The findings show that fluoxetine modulates brain activation during WM in a disorder-specific manner by normalizing task-positive DLPFC dysfunction in ASD boys and enhancing task-negative default mode network (DMN) deactivation in ADHD.
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6. Dillenburger K, Jordan JA, McKerr L, Keenan M. {{The Millennium child with autism: Early childhood trajectories for health, education and economic wellbeing}}. {Dev Neurorehabil};2014 (Oct 7):1-10.
Abstract Objective: Most of what we know about children with autism spectrum disorder (ASD) is based on post-diagnostic, retrospective, self-select studies. Oftentimes, there is no direct comparison between trajectories of children with ASD and children without ASD. Methods: To circumvent both of these problems, the present secondary data analysis utilised a large-scale longitudinal general population survey of children born in the year 2000 (i.e. the Millennium Cohort Study; MCS; n = 18 522). Bi-annual MCS data were available from five data sweeps (children aged 9 months to 11 years of age). Results: Pre-diagnostic data showed early health problems differentiated children later diagnosed with autism from non-diagnosed peers. Prevalence was much higher than previously estimated (3.5% for 11-year olds). Post-diagnosis, trajectories deteriorated significantly for the children with ASD and their families in relation to education, health and economic wellbeing. Conclusion: These findings raise many issues for service delivery and the rights of persons with disabilities and their families.
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7. Downs R, Perna J, Vitelli A, Cook D, Dhurjati P. {{Model-based hypothesis of gut microbe populations and gut/brain barrier permeabilities in the development of regressive autism}}. {Med Hypotheses};2014 (Sep 18)
Regressive autism is a devastating disorder affecting children between the ages of 15-30months. The disorder is characterized by the loss of social interaction and communication ability following otherwise healthy development. In spite of rising autism prevalence, current detection methods and treatment options for this disease are lacking. Therefore, this study introduces a systems-level model, which suggests that gut microbes and intestinal inflammation influence the onset of regressive autism through increasing gut permeability. This computational model provides a framework for quantitative understanding of how imbalances in populations of gut microbes alters the whole-body and brain distributions of neurotoxins produced by GI tract bacteria. Our results indicate that increased levels of the bacteria Bacteroides vulgatus lead to increased brain levels of propionic acid, a neurotoxin which has been known to cause symptoms characteristic of autism when injected into the brain of rats. Our results further indicate that immune response to virulence factors produced by bacteria in the gut leads to increased systemic levels of inflammatory cytokines, such as IL-1beta, which significantly alter the permeability of the gut epithelial layer and the blood-brain barrier. Due to the large size of cytokines, however, we predict the time required for concentrations in the brain to stabilize to be on the order of years. This suggests that treatments preventing autism development could be administered after identifying microbial biomarkers of disease but before debilitating brain inflammation leads to regressive autism progression. Future research extending this work could provide new treatment options and diagnostic techniques to help combat regressive autism.
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8. Foody C, James JE, Leader G. {{Parenting Stress, Salivary Biomarkers, and Ambulatory Blood Pressure: A Comparison Between Mothers and Fathers of Children with Autism Spectrum Disorders}}. {J Autism Dev Disord};2014 (Oct 7)
Parents of children with autism spectrum disorders (ASD) may experience higher levels of stress and health problems than parents of children with typical development. However, most research has focused on mothers, with emphasis on parent-reported stress and wellbeing. This study compared parenting responsibility, distress, anxiety, depression, cortisol, alpha-amylase, and cardiovascular activity between 19 mother-father dyads of children with ASD. Mothers reported higher parenting responsibility, distress, anxiety, and depression than fathers, while fathers had higher blood pressure and heart rate variability. Mothers and fathers had lower than average morning cortisol levels, suggesting stress effects on the hypothalamic-pituitary-adrenal-axis. Parents of children with ASD may benefit from routine health screening (particularly adrenal and cardiovascular function) and referral for stress reduction interventions or supports.
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9. Frazier TW, Embacher R, Tilot AK, Koenig K, Mester J, Eng C. {{Molecular and phenotypic abnormalities in individuals with germline heterozygous PTEN mutations and autism}}. {Mol Psychiatry};2014 (Oct 7)
PTEN is a tumor suppressor associated with an inherited cancer syndrome and an important regulator of ongoing neural connectivity and plasticity. The present study examined molecular and phenotypic characteristics of individuals with germline heterozygous PTEN mutations and autism spectrum disorder (ASD) (PTEN-ASD), with the aim of identifying pathophysiologic markers that specifically associate with PTEN-ASD and that may serve as targets for future treatment trials. PTEN-ASD patients (n=17) were compared with idiopathic (non-PTEN) ASD patients with (macro-ASD, n=16) and without macrocephaly (normo-ASD, n=38) and healthy controls (n=14). Group differences were evaluated for PTEN pathway protein expression levels, global and regional structural brain volumes and cortical thickness measures, neurocognition and adaptive behavior. RNA expression patterns and brain characteristics of a murine model of Pten mislocalization were used to further evaluate abnormalities observed in human PTEN-ASD patients. PTEN-ASD had a high proportion of missense mutations and showed reduced PTEN protein levels. Compared with the other groups, prominent white-matter and cognitive abnormalities were specifically associated with PTEN-ASD patients, with strong reductions in processing speed and working memory. White-matter abnormalities mediated the relationship between PTEN protein reductions and reduced cognitive ability. The Ptenm3m4 murine model had differential expression of genes related to myelination and increased corpus callosum. Processing speed and working memory deficits and white-matter abnormalities may serve as useful features that signal clinicians that PTEN is etiologic and prompting referral to genetic professionals for gene testing, genetic counseling and cancer risk management; and could reveal treatment targets in trials of treatments for PTEN-ASD.Molecular Psychiatry advance online publication, 7 October 2014; doi:10.1038/mp.2014.125.
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10. James SJ, Shpyleva S, Melnyk S, Pavliv O, Pogribny IP. {{Elevated 5-hydroxymethylcytosine in the Engrailed-2 (EN-2) promoter is associated with increased gene expression and decreased MeCP2 binding in autism cerebellum}}. {Transl Psychiatry};2014;4:e460.
Epigenetic mechanisms regulate programmed gene expression during prenatal neurogenesis and serve as a mediator between genetics and environment in postnatal life. The recent discovery of 5-hydroxymethylcytosine (5-hmC), with highest concentration in the brain, has added a new dimension to epigenetic regulation of neurogenesis and the development of complex behavior disorders. Here, we take a candidate gene approach to define the role 5-hmC in Engrailed-2 (EN-2) gene expression in the autism cerebellum. The EN-2 homeobox transcription factor, previously implicated in autism, is essential for normal cerebellar patterning and development. We previously reported EN-2 overexpression associated with promoter DNA hypermethylation in the autism cerebellum but because traditional DNA methylation methodology cannot distinguish 5-methylcytosine (5-mC) from 5-hmC, we now extend our investigation by quantifying global and gene-specific 5-mC and 5-hmC. Globally, 5-hmC was significantly increased in the autism cerebellum and accompanied by increases in the expression of de novo methyltransferases DNMT3A and DNMT3B, ten-eleven translocase genes TET1 and TET3, and in 8-oxo-deoxyguanosine (8-oxo-dG) content, a marker of oxidative DNA damage. Within the EN-2 promoter, there was a significant positive correlation between 5-hmC content and EN-2 gene expression. Based on reports of reduced MeCP2 affinity for 5-hmC, MeCP2 binding studies in the EN-2 promoter revealed a significant decrease in repressive MeCP2 binding that may contribute to the aberrant overexpression of EN-2. Because normal cerebellar development depends on perinatal EN-2 downregulation, the sustained postnatal overexpression suggests that a critical window of cerebellar development may have been missed in some individuals with autism with downstream developmental consequences. Epigenetic regulation of the programmed on-off switches in gene expression that occur at birth and during early brain development warrants further investigation.
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11. Kidd SA, Lachiewicz A, Barbouth D, Blitz RK, Delahunty C, McBrien D, Visootsak J, Berry-Kravis E. {{Fragile X Syndrome: A Review of Associated Medical Problems}}. {Pediatrics};2014 (Oct 6)
Fragile X syndrome (FXS) is the most common known genetic cause of inherited intellectual disability and the most common known single-gene cause of autism spectrum disorder. It has been reported that a spectrum of medical problems are commonly experienced by people with FXS, such as otitis media, seizures, and gastrointestinal problems. Previous studies examining the prevalence of medical problems related to FXS have been challenging to interpret because of their marked differences in population, setting, and sampling. Through this comprehensive review, we update the literature by reviewing studies that have reported on prominent medical problems associated with FXS. We then compare prevalence results from those studies with results from a large cross-sectional database consisting of data collected by fragile X clinics that specialize in the care of children with FXS and are part of the Fragile X Clinical and Research Consortium. It is vital for pediatricians and other clinicians to be familiar with the medical problems related to FXS so that affected patients may receive proper diagnosis and treatment; improved care may lead to better quality of life for these patients and their families.
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12. Kodak T, Clements A, Paden AR, LeBlanc B, Mintz J, Toussaint KA. {{Examination of the relation between an assessment of skills and performance on auditory-visual conditional discriminations for children with autism spectrum disorder}}. {J Appl Behav Anal};2014 (Oct 8)
The current investigation evaluated repertoires that may be related to performance on auditory-to-visual conditional discrimination training with 9 students who had been diagnosed with autism spectrum disorder. The skills included in the assessment were matching, imitation, scanning, an auditory discrimination, and a visual discrimination. The results of the skills assessment showed that 4 participants failed to demonstrate mastery of at least 1 of the skills. We compared the outcomes of the assessment to the results of auditory-visual conditional discrimination training and found that training outcomes were related to the assessment outcomes for 7 of the 9 participants. One participant who did not demonstrate mastery of all assessment skills subsequently learned several conditional discriminations when blocked training trials were conducted. Another participant who did not demonstrate mastery of the auditory discrimination skill subsequently acquired conditional discriminations in 1 of the training conditions. We discuss the implications of the assessment for practice and suggest additional areas of research on this topic.
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13. Mohn JL, Alexander J, Pirone A, Palka CD, Lee SY, Mebane L, Haydon PG, Jacob MH. {{New molecular insights into cognitive and autistic-like disabilities}}. {Mol Psychiatry};2014 (Oct);19(10):1053.
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14. Qin M, Huang T, Liu Z, Kader M, Burlin T, Xia Z, Zeidler Z, Hukema RK, Smith CB. {{Cerebral protein synthesis in a knockin mouse model of the fragile x premutation}}. {ASN Neuro};2014;6(5)
The (CGG)n-repeat in the 5′-untranslated region of the fragile X mental retardation gene (FMR1) gene is polymorphic and may become unstable on transmission to the next generation. In fragile X syndrome, CGG repeat lengths exceed 200, resulting in silencing of FMR1 and absence of its protein product, fragile X mental retardation protein (FMRP). CGG repeat lengths between 55 and 200 occur in fragile X premutation (FXPM) carriers and have a high risk of expansion to a full mutation on maternal transmission. FXPM carriers have an increased risk for developing progressive neurodegenerative syndromes and neuropsychological symptoms. FMR1 mRNA levels are elevated in FXPM, and it is thought that clinical symptoms might be caused by a toxic gain of function due to elevated FMR1 mRNA. Paradoxically, FMRP levels decrease moderately with increasing CGG repeat length in FXPM. Lowered FMRP levels may also contribute to the appearance of clinical problems. We previously reported increases in regional rates of cerebral protein synthesis (rCPS) in the absence of FMRP in an Fmr1 knockout mouse model and in a FXPM knockin (KI) mouse model with 120 to 140 CGG repeats in which FMRP levels are profoundly reduced (80%-90%). To explore whether the concentration of FMRP contributes to the rCPS changes, we measured rCPS in another FXPM KI model with a similar CGG repeat length and a 50% reduction in FMRP. In all 24 brain regions examined, rCPS were unaffected. These results suggest that even with 50% reductions in FMRP, normal protein synthesis rates are maintained.
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15. Raz R, Weisskopf MG, Davidovitch M, Pinto O, Levine H. {{Differences in Autism Spectrum Disorders Incidence by Sub-Populations in Israel 1992-2009: A Total Population Study}}. {J Autism Dev Disord};2014 (Oct 7)
We analyzed data from the Israeli National Insurance Institute (NII). Autism Spectrum Disorder (ASD) incidence was calculated for all children born in Israel 1992-2009, and by population groups. Overall, 9,109 ASD cases among 2,431,649 children were identified. ASD cumulative incidence by age 8 years increased 10-fold during 2000-2011, from 0.49 % to 0.49 %, while other child disabilities in NII increased only 1.65-fold. There was a consistent increase in ASD incidence with advancing birth cohorts born 1992-2004, stabilizing among those born 2005-2009. ASD rates among Israeli Arabs were substantially lower, and increased about 10 years later than the general population. The findings suggest a role for ASD awareness, accessing of the government benefit, or the way the concept of ASD is perceived.
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16. Retico A, Tosetti M, Muratori F, Calderoni S. {{Neuroimaging-based methods for autism identification: a possible translational application?}}. {Funct Neurol};2014 (Oct 7):1-9.
Classification methods based on machine learning (ML) techniques are becoming widespread analysis tools in neuroimaging studies. They have the potential to enhance the diagnostic power of brain data, by assigning a predictive index, either of pathology or of treatment response, to the single subject’s acquisition. ML techniques are currently finding numerous applications in psychiatric illness, in addition to the widely studied neurodegenerative diseases. In this review we give a comprehensive account of the use of classification techniques applied to structural magnetic resonance images in autism spectrum disorders (ASDs). Understanding of these highly heterogeneous neurodevelopmental diseases could greatly benefit from additional descriptors of pathology and predictive indices extracted directly from brain data. A perspective is also provided on the future developments necessary to translate ML methods from the field of ASD research into the clinic.
17. Robinson EB, Samocha KE, Kosmicki JA, McGrath L, Neale BM, Perlis RH, Daly MJ. {{Autism spectrum disorder severity reflects the average contribution of de novo and familial influences}}. {Proc Natl Acad Sci U S A};2014 (Oct 6)
Autism spectrum disorders (ASDs) are a highly heterogeneous group of conditions-phenotypically and genetically-although the link between phenotypic variation and differences in genetic architecture is unclear. This study aimed to determine whether differences in cognitive impairment and symptom severity reflect variation in the degree to which ASD cases reflect de novo or familial influences. Using data from more than 2,000 simplex cases of ASD, we examined the relationship between intelligence quotient (IQ), behavior and language assessments, and rate of de novo loss of function (LOF) mutations and family history of broadly defined psychiatric disease (depressive disorders, bipolar disorder, and schizophrenia; history of psychiatric hospitalization). Proband IQ was negatively associated with de novo LOF rate (P = 0.03) and positively associated with family history of psychiatric disease (P = 0.003). Female cases had a higher frequency of sporadic genetic events across the severity distribution (P = 0.01). High rates of LOF mutation and low frequencies of family history of psychiatric illness were seen in individuals who were unable to complete a traditional IQ test, a group with the greatest degree of language and behavioral impairment. These analyses provide strong evidence that familial risk for neuropsychiatric disease becomes more relevant to ASD etiology as cases become higher functioning. The findings of this study reinforce that there are many routes to the diagnostic category of autism and could lead to genetic studies with more specific insights into individual cases.
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18. Rodriguez NM, Thompson RH. {{Behavioral variability and autism spectrum disorders}}. {J Appl Behav Anal};2014 (Oct 8)
Restricted and repetitive behavior is a diagnostic characteristic of autism spectrum disorder (ASD). To the extent that the behavior of individuals with ASD can be conceptualized as problems of invariance, our understanding of environmental variables that influence restricted and repetitive behavior may be informed by the basic and applied literature on response variability. The purposes of this paper are (a) to describe how restricted and repetitive behavior can be conceptualized as problems of invariance, (b) to consider the implications of a lack of varied responding for individuals with ASD, (c) to review relevant basic and applied research on response variability, (d) to present methods to address invariant responding for individuals with ASD, and (e) to suggest areas for future research.
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19. Sinha P, Kjelgaard MM, Gandhi TK, Tsourides K, Cardinaux AL, Pantazis D, Diamond SP, Held RM. {{Autism as a disorder of prediction}}. {Proc Natl Acad Sci U S A};2014 (Oct 6)
A rich collection of empirical findings accumulated over the past three decades attests to the diversity of traits that constitute the autism phenotypes. It is unclear whether subsets of these traits share any underlying causality. This lack of a cohesive conceptualization of the disorder has complicated the search for broadly effective therapies, diagnostic markers, and neural/genetic correlates. In this paper, we describe how theoretical considerations and a review of empirical data lead to the hypothesis that some salient aspects of the autism phenotype may be manifestations of an underlying impairment in predictive abilities. With compromised prediction skills, an individual with autism inhabits a seemingly « magical » world wherein events occur unexpectedly and without cause. Immersion in such a capricious environment can prove overwhelming and compromise one’s ability to effectively interact with it. If validated, this hypothesis has the potential of providing unifying insights into multiple aspects of autism, with attendant benefits for improving diagnosis and therapy.
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20. Xin JF, Leonard DA. {{Using iPads to Teach Communication Skills of Students with Autism}}. {J Autism Dev Disord};2014 (Oct 8)
The purpose of this study was to examine the effects of using an iPad to assist students with autism in learning communication skills. Three, 10 years old learners diagnosed with autism who present little or no functional speech, participated in the study. A multiple baseline design with AB phases across academic and social settings was used. During the baseline, students were given access to an iPad with the SonoFlex speech-generating device application, while no communicative attempts were observed. During the intervention, the students were taught to use the iPad to communicate with their teacher and peers for 6 weeks. With a least-to-most prompting hierarchy, all students increased initiating requests, responding to questions and making social comments in both class and recess settings.
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21. Zwicker JD, Emery JC. {{Autism Research Funding Allocation: Can Economics Tell Us If We Have Got It Right?}}. {Autism Res};2014 (Oct 6)
There is a concern that the allocation of autism spectrum disorder (ASD) research funding may be misallocating resources, overemphasizing basic science at the expense of translational and clinical research. Anthony Bailey has proposed that an economic evaluation of autism research funding allocations could be beneficial for funding agencies by identifying under- or overfunded areas of research. In response to Bailey, we illustrate why economics cannot provide an objective, technical solution for identifying the « best » allocation of research resources. Economic evaluation has its greatest power as a late-stage research tool for interventions with identified objectives, outcomes, and data. This is not the case for evaluating whether research areas are over- or underfunded. Without an understanding of how research funding influences the likelihood and value of a discovery, or without a statement of the societal objectives for ASD research and level of risk aversion, economic analysis cannot provide a useful normative evaluation of ASD research. Autism Res 2014, : -. (c) 2014 International Society for Autism Research, Wiley Periodicals, Inc.
