1. Cox CR, Eaton S, Ekas NV, Van Enkevort EA. {{Death concerns and psychological well-being in mothers of children with autism spectrum disorder}}. {Res Dev Disabil}. 2015; 45-46: 229-38.
PURPOSE: Utilizing a terror management theory perspective, the present research examined whether having a child with autism spectrum disorder (ASD) is associated with underlying cognitions and explicit worries about death, and their roles in psychological well-being. METHOD: 147 mothers of children with ASD (n=74) and typically developing children (n=73) completed a fear of death scale, as well as measures of death-thought accessibility, positive and negative affect, depression, and anxiety. RESULTS: Following previous research, mothers of children with ASD reported worse psychological health. Additionally, they evidenced greater death-thought accessibility compared to mothers of typically developing children, but did not differ in explicit worries about mortality. Greater death-thought accessibility, in turn, mediated the influence of ASD diagnosis on negative affect, depression, and anxiety. CONCLUSION: The current study offers an initial understanding of the association between mortality concerns and psychological health for mothers of children with ASD. Further, it underscores the importance of health care providers’ efforts to attend to, and educate parents about, their thoughts of mortality, even if the parent does not acknowledge such concerns. WHAT THIS PAPER ADDS: The present study examined the impact of both implicit and explicit worries about death in parents of children with Autism Spectrum Disorder (ASD). Specifically, we were able to demonstrate that increased death-thought accessibility among mothers of children with ASD was associated with worse psychological health. While it is possible for parents of children with ASD to report conscious worries about death, there were no observed differences on this measure. As far as we know, this work is the first to empirically examine the prevalence of mortality-related concerns in this population and the subsequent effects of death-thought accessibility on psychological health. This is an important avenue of research as parents of children with ASD may experience greater worries about leaving their children upon death with no one to care for them, or to leave their children in the care of individuals who may not understand their son or daughter’s unique needs. Additionally, the current findings highlight the importance of addressing mortality-related concerns, even when they may not be explicitly recognized, among parents of children with ASD. Given the effectiveness of parent education programs for children with ASD, a primary avenue for intervention may be education. Training care providers in ways to better discuss thoughts of death may help to alleviate stress and foster greater psychological well-being.
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2. Du L, Shan L, Wang B, Li H, Xu Z, Staal WG, Jia F. {{A Pilot Study on the Combination of Applied Behavior Analysis and Bumetanide Treatment for Children with Autism}}. {J Child Adolesc Psychopharmacol}. 2015.
OBJECTIVE: The purpose of this study was to investigate the therapeutic effects of combined bumetanide and applied behavior analysis (ABA) treatment in children with autism. METHODS: Sixty children diagnosed with autism according to the International Classification of Diseases, Tenth Revision (ICD-10) criteria (mean age of 4.5 years) were randomly divided into two groups: A single treatment group (n=28) and a combined treatment group (n=32). The combined treatment group received ABA training combined with oral bumetanide (0.5 mg twice a day). The single treatment group received ABA training only. Autism symptoms were evaluated with the Autism Behavior Checklist (ABC) and the Childhood Autism Rating Scale (CARS), whereas severity of disease (SI) and global improvement (GI) were measured with the Clinical Global Impressions (CGI). Assessment of ABC, CARS, and CGI was performed immediately before and 3 months after initiation of the treatment(s). RESULTS: Prior to intervention(s) no statistically significant differences in scores on the ABC, CARS, SI, or GI were found between the two groups. Total scores of the ABC, CARS, and SI were decreased in both groups after 3 months (p<0.05) compared with the scores prior to treatment. The total scores of the ABC and the CGI were significantly (p<0.05) lower in the combined treatment group than in the single treatment group. Although the total and item scores of the CARS in the combined treatment group were lower than in the single treatment group after a 3 month intervention, they did not reach statistical significance. No adverse effects of bumetanide were observed. CONCLUSIONS: Treatment with bumetanide combined with ABA training may result in a better outcome in children with autism than ABA training alone.
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3. Ellul P, Rotge JY, Choucha W. {{Resistant Catatonia in a High-Functioning Autism Spectrum Disorder Patient Successfully Treated with Amantadine}}. {J Child Adolesc Psychopharmacol}. 2015.
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4. Guastella AJ, Hickie IB. {{Oxytocin Treatment, Circuitry and Autism: A Critical Review of the Literature Placing Oxytocin into the Autism Context}}. {Biol Psychiatry}. 2015.
Observed impairment in reciprocal social interaction is a diagnostic hallmark of autism spectrum disorders. There is no effective medical treatment for these problems. Psychological treatments remain costly, time intensive, and developmentally sensitive for efficacy. In this review, we explore the potential of oxytocin-based therapies for social impairments in autism. Evidence shows that acute oxytocin administration improves numerous markers critical to the social circuitry underlying social deficits in autism. Oxytocin may optimize these circuits and enhance reward, motivation, and learning to improve therapeutic outcomes. Despite this, the current evidence of therapeutic benefit from extended oxytocin treatment remains very limited. We highlight complexity in crossing from the laboratory to the autism clinical setting in evaluation of this therapeutic. We discuss a clinical trial approach that provides optimal opportunity for therapeutic response by using personalized methods that better target specific circuitry to define who will obtain benefit, at what stage of development, and the optimal delivery approach for circuitry manipulation. For the autism field, the therapeutic challenges will be resolved by a range of treatment strategies, including greater focus on specific interventions, such as oxytocin, that have a strong basis in the fundamental neurobiology of social behavior. More sophisticated and targeted clinical trials utilizing such approaches are now required, placing oxytocin into the autism context.
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5. Kestemont J, Vandekerckhove M, Bulnes LC, Matthys F, Van Overwalle F. {{Causal attribution in individuals with subclinical and clinical autism spectrum disorder: An fMRI study}}. {Soc Neurosci}. 2015: 1-13.
This neuroimaging study compares brain activation during causal attribution to three different attribution loci (i.e., self, another person, and situation) across a typical population without (N = 20) or with subclinical autism spectrum symptoms (N = 18) and a clinical population with autism spectrum disorder (ASD; N = 11). While they underwent fMRI, all participants read short sentences describing positive and negative behaviors and thoughts of another person directed toward the participant (i.e., « you »). Participants were then asked to attribute these behaviors to themselves, the other person, or the situation. Behavioral measures revealed self-serving attributions (i.e., attributing positive events to the self, while attributing negative events externally from the self) in all three participant groups. Neural measures revealed a great deal of shared activation across the three attribution loci and across the three participant groups in the temporo-parietal junction, the posterior superior sulcus, and the precuneus. Comparison between groups revealed more widespread activation in both subclinical and clinical ASD participants, which may be indicative of the extraneural resources these participants invest to compensate their impairments.
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6. Kikuchi M, Yoshimura Y, Mutou K, Minabe Y. {{Magnetoencephalography in the study of children with autism spectrum disorder}}. {Psychiatry Clin Neurosci}. 2015.
AIMS: Magnetoencephalography (MEG) is a noninvasive neuroimaging technique that provides a measure of cortical neural activity on a millisecond time scale with high spatial resolution. MEG has been clinically applied to various neurological diseases, including epilepsy and cognitive dysfunction. In the past decade, MEG has also emerged as an important investigatory tool in neurodevelopmental studies. It is therefore an opportune time to review how MEG is able to contribute to the study of atypical brain development. METHOD: We limit this review to autism spectrum disorder (ASD). The relevant literature for children was accessed using PubMed on January 5, 2015. Case reports, case series, and papers on epilepsy were excluded. RESULTS: Owing to their accurate separation of brain activity in the right and left hemispheres and the higher accuracy of source localization, MEG studies have added new information related to auditory evoked brain responses to findings from previous EEG studies of children with ASD. In addition, evidence of atypical brain connectivity in children with ASD has accumulated over the past decade. CONCLUSIONS: MEG is well suited for the study of neural activity with high time resolution even in young children. Although further studies are still necessary, the detailed findings provided by neuroimaging methods may aid clinical diagnosis and even contribute to the refinement of diagnostic categories for neurodevelopmental disorders in the future.
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7. Nirenberg MJ, Bhatt JM, Roda RH. {{Fragile X Tremor Ataxia Syndrome With Rapidly Progressive Myopathy}}. {JAMA Neurol}. 2015; 72(8): 946-8.
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8. Ouellette-Kuntz H, Shooshtari S, Balogh R, Martens P. {{Understanding Information About Mortality Among People with Intellectual and Developmental Disabilities in Canada}}. {J Appl Res Intellect Disabil}. 2015; 28(5): 423-35.
BACKGROUND: This paper reviews what is currently known about mortality among Canadians with intellectual and developmental disabilities and describes opportunities for ongoing monitoring. METHODS: In-hospital mortality among adults with intellectual and developmental disabilities in Ontario was examined using hospital data. Mortality was compared between age-, sex- and residence area-matched groups of Manitobans with and without intellectual and developmental disabilities using linked administrative data. A retrospective cohort study of mortality among individuals with intellectual and developmental disabilities in a region of Ontario focused on measuring excess mortality and risk factors. FINDINGS: There is evidence of excess mortality in persons with intellectual and developmental disabilities in Canada. Some of the excess is attributable to comorbidities that are more common in this population. Women may have a greater risk of death than men. Excess mortality occurs at all ages but is more pronounced in early life. DISCUSSION: High-quality ongoing monitoring of mortality among individuals with intellectual and developmental disabilities is possible in Canada. Examination of sex differences should be a priority.
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9. Park EY, Kim J. {{Factor structure of the childhood autism rating scale as per DSM-5}}. {Pediatr Int}. 2015.
BACKGROUND/OBJECTIVE: The DSM-5 recently proposed new diagnostic criteria for ASD. Although, many new or updated tools have been developed since the DSM-IV was published in 1994, the CARS has been used consistently in ASD diagnosis and research due to its technical adequacy, cost-effectiveness, and practicality. Additionally, items in the CARS did not alter following the release of the revised DSM-IV because the CARS factor structure was found to be consistent with the revised criteria after a factor analysis. For that reason, this study aimed to identify the factor structure of the Childhood Autism Rating Scale (CARS) using confirmatory factor analysis. METHOD: Participants (N = 150) were children who had received an ASD diagnosis or who met the criteria for having broader autism or emotional/behavior disorders with comorbid disorders such as ADHD, bipolar disorder, intellectual or developmental disabilities. Previous studies used one-, two-, and four-factor models, all of which we examined to confirm the best-fit model using confirmatory factor analysis. RESULTS: Results revealed appropriate comparative fit indices and root mean square errors for all four models. The two-factor model, based on DSM-5 criteria, was the most valid and reliable. The inter-item consistency of the CARS was .926 and demonstrated adequate reliability. These results supported the validity and reliability of the two-factor model of the CARS. CONCLUSIONS: Although the CARS was developed prior to the introduction of the DSM-5, its psychometric properties, conceptual relevance, and flexible administration procedures support its continued role as a screening device in the diagnostic decision-making process. This article is protected by copyright. All rights reserved.
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10. Segal-Gavish H, Karvat G, Barak N, Barzilay R, Ganz J, Edry L, Aharony I, Offen D, Kimchi T. {{Mesenchymal Stem Cell Transplantation Promotes Neurogenesis and Ameliorates Autism Related Behaviors in BTBR Mice}}. {Autism Res}. 2015.
Autism spectrum disorders (ASD) are characterized by social communication deficits, cognitive rigidity, and repetitive stereotyped behaviors. Mesenchymal stem cells (MSC) have a paracrine regenerative effect, and were speculated to be a potential therapy for ASD. The BTBR inbred mouse strain is a commonly used model of ASD as it demonstrates robust behavioral deficits consistent with the diagnostic criteria for ASD. BTBR mice also exhibit decreased brain-derived neurotrophic factor (BDNF) signaling and reduced hippocampal neurogenesis. In the current study, we evaluated the behavioral and molecular effects of intracerebroventricular MSC transplantation in BTBR mice. Transplantation of MSC resulted in a reduction of stereotypical behaviors, a decrease in cognitive rigidity and an improvement in social behavior. Tissue analysis revealed elevated BDNF protein levels in the hippocampus accompanied by increased hippocampal neurogenesis in the MSC-transplanted mice compared with sham treated mice. This might indicate a possible mechanism underpinning the behavioral improvement. Our study suggests a novel therapeutic approach which may be translatable to ASD patients in the future. Autism Res 2015. (c) 2015 International Society for Autism Research, Wiley Periodicals, Inc.
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11. Urbain CM, Pang EW, Taylor MJ. {{Atypical spatiotemporal signatures of working memory brain processes in autism}}. {Transl Psychiatry}. 2015; 5: e617.
Working memory (WM) impairments may contribute to the profound behavioural manifestations in children with autism spectrum disorder (ASD). However, previous behavioural results are discrepant as are the few functional magnetic resonance imaging (fMRI) results collected in adults and adolescents with ASD. Here we investigate the precise temporal dynamics of WM-related brain activity using magnetoencephalography (MEG) in 20 children with ASD and matched controls during an n-back WM task across different load levels (1-back vs 2-back). Although behavioural results were similar between ASD and typically developing (TD) children, the between-group comparison performed on functional brain activity showed atypical WM-related brain processes in children with ASD compared with TD children. These atypical responses were observed in the ASD group from 200 to 600 ms post stimulus in both the low- (1-back) and high- (2-back) memory load conditions. During the 1-back condition, children with ASD showed reduced WM-related activations in the right hippocampus and the cingulate gyrus compared with TD children who showed more activation in the left dorso-lateral prefrontal cortex and the insulae. In the 2-back condition, children with ASD showed less activity in the left insula and midcingulate gyrus and more activity in the left precuneus than TD children. In addition, reduced activity in the anterior cingulate cortex was correlated with symptom severity in children with ASD. Thus, this MEG study identified the precise timing and sources of atypical WM-related activity in frontal, temporal and parietal regions in children with ASD. The potential impacts of such atypicalities on social deficits of autism are discussed.
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12. Watson KK, Miller S, Hannah E, Kovac M, Damiano CR, Sabatino-DiCrisco A, Turner-Brown L, Sasson NJ, Platt ML, Dichter GS. {{Increased reward value of non-social stimuli in children and adolescents with autism}}. {Front Psychol}. 2015; 6: 1026.
An econometric choice task was used to estimate the implicit reward value of social and non-social stimuli related to restricted interests in children and adolescents with (n = 12) and without (n = 22) autism spectrum disorder (ASD). Mixed effects logistic regression analyses revealed that groups differed in valuation of images related to restricted interests: control children were indifferent to cash payouts to view these images, but children with ASD were willing to receive less cash payout to view these images. Groups did not differ in valuation of social images or non-social images not related to restricted interests. Results highlight that motivational accounts of ASD should also consider the reward value of non-social stimuli related to restricted interests in ASD (Dichter and Adolphs, 2012).
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13. Yi JJ, Berrios J, Newbern JM, Snider WD, Philpot BD, Hahn KM, Zylka MJ. {{An Autism-Linked Mutation Disables Phosphorylation Control of UBE3A}}. {Cell}. 2015.
Deletion of UBE3A causes the neurodevelopmental disorder Angelman syndrome (AS), while duplication or triplication of UBE3A is linked to autism. These genetic findings suggest that the ubiquitin ligase activity of UBE3A must be tightly maintained to promote normal brain development. Here, we found that protein kinase A (PKA) phosphorylates UBE3A in a region outside of the catalytic domain at residue T485 and inhibits UBE3A activity toward itself and other substrates. A de novo autism-linked missense mutation disrupts this phosphorylation site, causing enhanced UBE3A activity in vitro, enhanced substrate turnover in patient-derived cells, and excessive dendritic spine development in the brain. Our study identifies PKA as an upstream regulator of UBE3A activity and shows that an autism-linked mutation disrupts this phosphorylation control. Moreover, our findings implicate excessive UBE3A activity and the resulting synaptic dysfunction to autism pathogenesis.
