1. Chee DY, Lee HC, Patomella AH, Falkmer T. {{Driving Behaviour Profile of Drivers with Autism Spectrum Disorder (ASD)}}. {J Autism Dev Disord}. 2017.
The symptomatology of autism spectrum disorder (ASD) can make driving risky, but little is known about the on-road driving behaviour of individuals with ASD. This study assessed and compared the on-road driving performance of drivers with and without ASD, and explored how the symptomatology of ASD hinders or facilitates on-road driving performance. Sixteen drivers with ASD and 21 typically-developed drivers participated in the study. Drivers with ASD underperformed in vehicle manoeuvring, especially at left-turns, right-turns and pedestrian crossings. However, drivers with ASD outperformed the TD group in aspects related to rule-following such as using the indicator at roundabouts and checking for cross-traffic when approaching intersections. Drivers with ASD in the current study presented with a range of capabilities and weaknesses during driving.
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2. Cheng STT, Lam GYH, To CKS. {{Pitch Perception in Tone Language-Speaking Adults With and Without Autism Spectrum Disorders}}. {Iperception}. 2017; 8(3): 2041669517711200.
Enhanced low-level pitch perception has been universally reported in autism spectrum disorders (ASD). This study examined whether tone language speakers with ASD exhibit this advantage. The pitch perception skill of 20 Cantonese-speaking adults with ASD was compared with that of 20 neurotypical individuals. Participants discriminated pairs of real syllable, pseudo-syllable (syllables that do not conform the phonotactic rules or are accidental gaps), and non-speech (syllables with attenuated high-frequency segmental content) stimuli contrasting pitch levels. The results revealed significantly higher discrimination ability in both groups for the non-speech stimuli than for the pseudo-syllables with one semitone difference. No significant group differences were noted. Different from previous findings, post hoc analysis found that enhanced pitch perception was observed in a subgroup of participants with ASD showing no history of delayed speech onset. The tone language experience may have modulated the pitch processing mechanism in the speakers in both ASD and non-ASD groups.
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3. Constantino JN, Marrus N. {{The Early Origins of Autism}}. {Child Adolesc Psychiatr Clin N Am}. 2017; 26(3): 555-70.
Autism spectrum disorders (ASDs) are neurodevelopmental disorders whose core features of impaired social communication and atypical repetitive behaviors and/or restrictions in range of interests emerge in toddlerhood and carry significant implications at successive stages of development. The ability to reliably identify most cases of the condition far earlier than the average age of diagnosis presents a novel opportunity for early intervention, but the availability of such an intervention is disparate across US communities, and its impact is imperfectly understood. New research may transform the clinical approach to these conditions in early childhood.
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4. Dykens EM, Roof E, Hunt-Hawkins H, Dankner N, Lee EB, Shivers CM, Daniell C, Kim SJ. {{Diagnoses and characteristics of autism spectrum disorders in children with Prader-Willi syndrome}}. {J Neurodev Disord}. 2017; 9: 18.
BACKGROUND: A small percentage of people with autism spectrum disorders (ASD) have alterations in chromosome 15q11.2-q3, the critical region for Prader-Willi syndrome (PWS). Data are limited, however, on the rates and characteristics of ASD in PWS. Previous estimates of ASD in PWS (25 to 41%) are questionable as they are based solely on autism screeners given to parents. Inaccurate diagnoses of ASD in PWS can mislead intervention and future research. METHODS: One hundred forty-six children and youth with PWS aged 4 to 21 years (M = 11) were assessed with the Autism Diagnostic Observation Schedule-2 (ADOS-2). An expert clinical team-made best-estimate ASD diagnoses based on ADOS-2 videotapes, calibrated severity scores, and children’s developmental histories and indices of current functioning. Children were also administered the Kaufman Brief Intelligence Test-2, and parents completed the Repetitive Behavior Scale-Revised and Vineland Adaptive Behavior Scales. Scores were compared across children with PWS + ASD versus PWS only. The performance of an ASD screener, the Social Communication Questionnaire (SCQ) and the ADOS-2 were evaluated in relation to best-estimate diagnoses. RESULTS: Best-estimate diagnoses of ASD were made in 18 children, or 12.3% of the sample, and the majority of them had the maternal uniparental disomy (mUPD) PWS genetic subtype. Compared to the PWS-only group, children with PWS + ASD had lower verbal and composite IQ’s and adaptive daily living and socialization skills, as well as elevated stereotypies and restricted interests. Regardless of ASD status, compulsivity and insistence on sameness in routines or events were seen in 76-100% of children and were robustly correlated with lower adaptive functioning. The SCQ yielded a 29-49% chance that screen-positive cases will indeed have ASD. The ADOS-2 had higher sensitivity, specificity and predictive values. Communication problems were seen in children who were ADOS-2 positive but deemed not to have ASD by the clinical team. CONCLUSIONS: Autism screeners should not be the sole index of probable ASD in PWS; children need to be directly observed and evaluated. Compulsivity and insistence on sameness are salient in PWS and likely impede adaptive functioning. Most children with PWS only evidenced sub-threshold problems in social interactions that could signal risks for other psychopathologies.
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5. Kamp-Becker I, Poustka L, Bachmann C, Ehrlich S, Hoffmann F, Kanske P, Kirsch P, Krach S, Paulus FM, Rietschel M, Roepke S, Roessner V, Schad-Hansjosten T, Singer T, Stroth S, Witt S, Wermter AK. {{Study protocol of the ASD-Net, the German research consortium for the study of Autism Spectrum Disorder across the lifespan: from a better etiological understanding, through valid diagnosis, to more effective health care}}. {BMC Psychiatry}. 2017; 17(1): 206.
BACKGROUND: Autism Spectrum Disorder (ASD) is a severe, lifelong neurodevelopmental disorder with early onset that places a heavy burden on affected individuals and their families. Due to the need for highly specialized health, educational and vocational services, ASD is a cost-intensive disorder, and strain on health care systems increases with increasing age of the affected individual. METHODS: The ASD-Net will study Germany’s largest cohort of patients with ASD over the lifespan. By combining methodological expertise from all levels of clinical research, the ASD-Net will follow a translational approach necessary to identify neurobiological pathways of different phenotypes and their appropriate identification and treatment. The work of the ASD-Net will be organized into three clusters concentrating on diagnostics, therapy and health economics. In the diagnostic cluster, data from a large, well-characterized sample (N = 2568) will be analyzed to improve the efficiency of diagnostic procedures. Pattern classification methods (machine learning) will be used to identify algorithms for screening purposes. In a second step, the developed algorithm will be tested in an independent sample. In the therapy cluster, we will unravel how an ASD-specific social skills training with concomitant oxytocin administration can modulate behavior through neurobiological pathways. For the first time, we will characterize long-term effects of a social skills training combined with oxytocin treatment on behavioral and neurobiological phenotypes. Also acute effects of oxytocin will be investigated to delineate general and specific effects of additional oxytocin treatment in order to develop biologically plausible models for symptoms and successful therapeutic interventions in ASD. Finally, in the health economics cluster, we will assess service utilization and ASD-related costs in order to identify potential needs and cost savings specifically tailored to Germany. The ASD-Net has been established as part of the German Research Network for Mental Disorders, funded by the BMBF (German Federal Ministry of Education and Research). DISCUSSION: The highly integrated structure of the ASD-Net guarantees sustained collaboration of clinicians and researchers to alleviate individual distress, harm, and social disability of patients with ASD and reduce costs to the German health care system. TRIAL REGISTRATION: Both clinical trials of the ASD-Net are registered in the German Clinical Trials Register: DRKS00008952 (registered on August 4, 2015) and DRKS00010053 (registered on April 8, 2016).
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6. Pavlova MA, Guerreschi M, Tagliavento L, Gitti F, Sokolov AN, Fallgatter AJ, Fazzi E. {{Social cognition in autism: Face tuning}}. {Sci Rep}. 2017; 7(1): 2734.
Faces convey valuable information for social cognition, effective interpersonal interaction, and non-verbal communication. Face perception is believed to be atypical in autism, but the origin of this deficit is controversial. Dominant featural face encoding is suggested to be responsible for face tuning scarcity. Here we used a recently developed Face-n-Food paradigm for studying face tuning in individuals with autistic spectrum disorders (ASD). The key benefit of these images is that single components do not explicitly trigger face processing. In a spontaneous recognition task, adolescents with autism and typically developing matched controls were presented with a set of Face-n-Food images in different degree resembling a face (slightly bordering on the Giuseppe Arcimboldo style). The set of images was shown in a predetermined order from the least to most resembling a face. Thresholds for recognition of the Face-n-Food images as a face in ASD individuals were substantially higher than in typically developing controls: they did not report seeing a face on the images, which controls easily recognized as a face, and gave overall fewer face responses. This outcome not only lends support to atypical face tuning, but provides novel insights into the origin of face encoding deficits in autism.
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7. Shmaya Y, Eilat-Adar S, Leitner Y, Reif S, Gabis LV. {{Meal time behavior difficulties but not nutritional deficiencies correlate with sensory processing in children with autism spectrum disorder}}. {Res Dev Disabil}. 2017; 66: 27-33.
BACKGROUND: Food aversion and nutritional difficulties are common in children with autism spectrum disorder. AIM: To compare meal time behavior of children with autism to their typically developing siblings and to typical controls and to examine if sensory profiles can predict meal time behavior or nutritional deficiencies in the autism group.
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8. Singh S, Yazdani U, Gadad B, Zaman S, Hynan LS, Roatch N, Schutte C, Marti CN, Hewitson L, German DC. {{Serum thyroid-stimulating hormone and interleukin-8 levels in boys with autism spectrum disorder}}. {J Neuroinflammation}. 2017; 14(1): 113.
BACKGROUND: Autism spectrum disorder (ASD) affects approximately 1 in 68 children in the USA. An ASD blood biomarker may enable early diagnosis and/or identification of new therapeutic targets. Serum samples from ASD and typically developing (TD) boys (n = 30/group) were screened for differences in 110 proteins using a multiplex immunoassay. RESULTS: Eleven proteins were found that together could confirm ASD with modest accuracy using multiple training and test sets. Two of the 11 proteins identified here were further tested using a different detection platform and with a larger sample of ASD and TD boys. The two proteins, thyroid-stimulating hormone (TSH) and interleukin-8 (IL-8), have been previously identified as putative biomarkers for ASD. TSH levels were significantly lower in ASD boys, whereas IL-8 levels were significantly elevated. The diagnostic accuracy for ASD based upon TSH or IL-8 levels alone varied from 74 to 76%, but using both proteins together, the diagnostic accuracy increased to 82%. In addition, TSH levels were negatively correlated with the Autism Diagnostic Observation Schedule subdomain scores. CONCLUSIONS: These data suggest that a panel of proteins may be useful as a putative blood biomarker for ASD.
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9. Varghese M, Keshav N, Jacot-Descombes S, Warda T, Wicinski B, Dickstein DL, Harony-Nicolas H, De Rubeis S, Drapeau E, Buxbaum JD, Hof PR. {{Autism spectrum disorder: neuropathology and animal models}}. {Acta Neuropathol}. 2017.
Autism spectrum disorder (ASD) has a major impact on the development and social integration of affected individuals and is the most heritable of psychiatric disorders. An increase in the incidence of ASD cases has prompted a surge in research efforts on the underlying neuropathologic processes. We present an overview of current findings in neuropathology studies of ASD using two investigational approaches, postmortem human brains and ASD animal models, and discuss the overlap, limitations, and significance of each. Postmortem examination of ASD brains has revealed global changes including disorganized gray and white matter, increased number of neurons, decreased volume of neuronal soma, and increased neuropil, the last reflecting changes in densities of dendritic spines, cerebral vasculature and glia. Both cortical and non-cortical areas show region-specific abnormalities in neuronal morphology and cytoarchitectural organization, with consistent findings reported from the prefrontal cortex, fusiform gyrus, frontoinsular cortex, cingulate cortex, hippocampus, amygdala, cerebellum and brainstem. The paucity of postmortem human studies linking neuropathology to the underlying etiology has been partly addressed using animal models to explore the impact of genetic and non-genetic factors clinically relevant for the ASD phenotype. Genetically modified models include those based on well-studied monogenic ASD genes (NLGN3, NLGN4, NRXN1, CNTNAP2, SHANK3, MECP2, FMR1, TSC1/2), emerging risk genes (CHD8, SCN2A, SYNGAP1, ARID1B, GRIN2B, DSCAM, TBR1), and copy number variants (15q11-q13 deletion, 15q13.3 microdeletion, 15q11-13 duplication, 16p11.2 deletion and duplication, 22q11.2 deletion). Models of idiopathic ASD include inbred rodent strains that mimic ASD behaviors as well as models developed by environmental interventions such as prenatal exposure to sodium valproate, maternal autoantibodies, and maternal immune activation. In addition to replicating some of the neuropathologic features seen in postmortem studies, a common finding in several animal models of ASD is altered density of dendritic spines, with the direction of the change depending on the specific genetic modification, age and brain region. Overall, postmortem neuropathologic studies with larger sample sizes representative of the various ASD risk genes and diverse clinical phenotypes are warranted to clarify putative etiopathogenic pathways further and to promote the emergence of clinically relevant diagnostic and therapeutic tools. In addition, as genetic alterations may render certain individuals more vulnerable to developing the pathological changes at the synapse underlying the behavioral manifestations of ASD, neuropathologic investigation using genetically modified animal models will help to improve our understanding of the disease mechanisms and enhance the development of targeted treatments.
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10. Whitaker LR, Simpson A, Roberson D. {{Brief Report: Is Impaired Classification of Subtle Facial Expressions in Children with Autism Spectrum Disorders Related to Atypical Emotion Category Boundaries?}}. {J Autism Dev Disord}. 2017.
Impairments in recognizing subtle facial expressions, in individuals with autism spectrum disorder (ASD), may relate to difficulties in constructing prototypes of these expressions. Eighteen children with predominantly intellectual low-functioning ASD (LFA, IQ <80) and two control groups (mental and chronological age matched), were assessed for their ability to classify emotional faces, of high, medium and low intensities, as happy or angry. For anger, the LFA group made more errors for lower intensity expressions than the control groups, classifications did not differ for happiness. This is the first study to find that the LFA group made more across-valence errors than controls. These data are consistent with atypical facial expression processing in ASD being associated with differences in the structure of emotion categories. Lien vers le texte intégral (Open Access ou abonnement)
