1. Ameis SH, Kassee C, Corbett-Dick P, Cole L, Dadhwal S, Lai MC, Veenstra-VanderWeele J, Correll CU. {{Systematic review and guide to management of core and psychiatric symptoms in youth with autism}}. {Acta Psychiatr Scand}. 2018.
OBJECTIVE: Evidence-based guidance of clinical decision-making for the management of Autism Spectrum Disorder (ASD) is lacking, particularly for co-occurring psychiatric symptoms. This review evaluates treatment evidence for six common symptom targets in children/adolescents with ASD and provides a resource to facilitate application of the evidence to clinical practice. METHOD: A systematic search identified randomized controlled trials (RCTs) and high-quality systematic reviews published between 2007 and 2016, focused on: social interaction/communication impairment, stereotypic/repetitive behaviours, irritability/agitation, attention-deficit/hyperactivity disorder symptoms, mood or anxiety symptoms, and sleep difficulties. We then completed qualitative evaluation of high-quality systematic reviews/meta-analyses and quantitative evaluation of recently published RCTs not covered by prior comprehensive systematic reviews. RESULTS: Recently published RCTs focused on social interaction and communication impairment (trials = 32) using psychosocial interventions. Interventions for irritability/agitation (trials = 16) were mainly pharmacological. Few RCTs focused on other symptom targets (trials = 2-5/target). Integration of these results with our qualitative review indicated that few established treatment modalities exist, and available evidence is limited by small studies with high risk of bias. CONCLUSION: Given the current evidence-base, treatment targets must be clearly defined, and a systematic approach to intervention trials in children/adolescents with ASD must be undertaken with careful consideration of the limitations of safety/efficacy data.
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2. Arnold Anteraper S, Guell X, D’Mello A, Joshi N, Whitfield-Gabrieli S, Joshi G. {{Disrupted Cerebro-cerebellar Intrinsic Functional Connectivity in Young Adults with High-functioning Autism Spectrum Disorder: A Data-driven, Whole-brain, High Temporal Resolution fMRI Study}}. {Brain Connect}. 2018.
OBJECTIVES: To examine the resting-state functional-connectivity (RsFc) in young adults with high-functioning autism spectrum disorder (HF-ASD) using state-of-the-art fMRI data acquisition and analysis techniques. METHODS: Simultaneous multi-slice, high temporal resolution fMRI acquisition; unbiased whole-brain connectome-wide multivariate pattern analysis (MVPA) techniques for assessing RsFc; and post-hoc whole-brain seed-to-voxel analyses using MVPA results as seeds. RESULTS: MVPA revealed two clusters of abnormal connectivity in the cerebellum. Whole-brain seed-based functional connectivity analyses informed by MVPA-derived clusters showed significant under connectivity between the cerebellum and social, emotional, and language brain regions in the HF-ASD group compared to healthy controls. The results we report are coherent with existing structural, functional, and RsFc literature in autism, extend previous literature reporting cerebellar abnormalities in the neuropathology of autism, and highlight the cerebellum as a potential target for therapeutic, diagnostic, predictive, and prognostic developments in ASD. CONCLUSIONS: The description of functional connectivity abnormalities using whole-brain, data-driven analyses as reported in the present study may crucially advance the development of ASD biomarkers, targets for therapeutic interventions, and neural predictors for measuring treatment response.
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3. Clements CC, Zoltowski AR, Yankowitz LD, Yerys BE, Schultz RT, Herrington JD. {{Evaluation of the Social Motivation Hypothesis of Autism: A Systematic Review and Meta-analysis}}. {JAMA Psychiatry}. 2018.
Importance: The social motivation hypothesis posits that individuals with autism spectrum disorder (ASD) find social stimuli less rewarding than do people with neurotypical activity. However, functional magnetic resonance imaging (fMRI) studies of reward processing have yielded mixed results. Objectives: To examine whether individuals with ASD process rewarding stimuli differently than typically developing individuals (controls), whether differences are limited to social rewards, and whether contradictory findings in the literature might be due to sample characteristics. Data Sources: Articles were identified in PubMed, Embase, and PsycINFO from database inception until June 1, 2017. Functional MRI data from these articles were provided by most authors. Study Selection: Publications were included that provided brain activation contrasts between a sample with ASD and controls on a reward task, determined by multiple reviewer consensus. Data Extraction and Synthesis: When fMRI data were not provided by authors, multiple reviewers extracted peak coordinates and effect sizes from articles to recreate statistical maps using seed-based d mapping software. Random-effects meta-analyses of responses to social, nonsocial, and restricted interest stimuli, as well as all of these domains together, were performed. Secondary analyses included meta-analyses of wanting and liking, meta-regression with age, and correlations with ASD severity. All procedures were conducted in accordance with Meta-analysis of Observational Studies in Epidemiology guidelines. Main Outcomes and Measures: Brain activation differences between groups with ASD and typically developing controls while processing rewards. All analyses except the domain-general meta-analysis were planned before data collection. Results: The meta-analysis included 13 studies (30 total fMRI contrasts) from 259 individuals with ASD and 246 controls. Autism spectrum disorder was associated with aberrant processing of both social and nonsocial rewards in striatal regions and increased activation in response to restricted interests (social reward, caudate cluster: d = -0.25 [95% CI, -0.41 to -0.08]; nonsocial reward, caudate and anterior cingulate cluster: d = -0.22 [95% CI, -0.42 to -0.02]; restricted interests, caudate and nucleus accumbens cluster: d = 0.42 [95% CI, 0.07 to 0.78]). Conclusions and Relevance: Individuals with ASD show atypical processing of social and nonsocial rewards. Findings support a broader interpretation of the social motivation hypothesis of ASD whereby general atypical reward processing encompasses social reward, nonsocial reward, and perhaps restricted interests. This meta-analysis also suggests that prior mixed results could be driven by sample age differences, warranting further study of the developmental trajectory for reward processing in ASD.
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4. Dichter GS. {{Motivational Impairments in Autism May Be Broader Than Previously Thought}}. {JAMA Psychiatry}. 2018.
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5. Kuehn B. {{Uptick in Autism}}. {Jama}. 2018; 319(22): 2264.
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6. Kuno M, Hirano Y, Nakagawa A, Asano K, Oshima F, Nagaoka S, Matsumoto K, Masuda Y, Iyo M, Shimizu E. {{White Matter Features Associated With Autistic Traits in Obsessive-Compulsive Disorder}}. {Frontiers in psychiatry}. 2018; 9: 216.
Obsessive-compulsive disorder (OCD) is among the most debilitating psychiatric disorders. Comorbid autism spectrum disorder (ASD) or autistic traits may impair treatment response in OCD. To identify possible neurostructural deficits underlying autistic traits, we performed white matter tractography on diffusion tensor images (DTI) and assessed autistic trait severity using the Autism-Spectrum Quotient (AQ) in 33 OCD patients. Correlations between AQ and the DTI parameters, fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) were examined in major white matter tracts that were suggested to be altered in previous OCD studies. We found a negative correlation between AQ and FA and positive correlations between AQ and MD, AD and RD in the left uncinate fasciculus using age, Beck Depression Inventory, Yale-Brown Obsessive-Compulsive Scale, intelligence quotient and medication as covariates. However, we could not detect the significant results between AQ and all DTI parameters when adding gender as a covariate. In addition, in the ASD comorbid group, FA in the left uncinate fasciculus was significantly lower than in the non-ASD comorbid group and MD and RD were significantly higher than in the non-ASD group. These results did not survive correction for multiple comparisons. In ASD, the socio-emotional dysfunction is suggested to be related to the alteration of white matter microstructure in uncinate fasciculus. Our results suggest that variations in white matter features of the left uncinate fasciculus might be partly explained by autistic traits encountered in OCD patients.
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7. Lv Q, Du A, Wei W, Li Y, Liu G, Wang XP. {{Deep Brain Stimulation: A Potential Treatment for Dementia in Alzheimer’s Disease (AD) and Parkinson’s Disease Dementia (PDD)}}. {Front Neurosci}. 2018; 12: 360.
Damage to memory circuits may lead to dementia symptoms in Alzheimer’s disease (AD) and Parkinson’s disease dementia (PDD). Recently, deep brain stimulation (DBS) has been shown to be a novel means of memory neuromodulation when critical nodes in the memory circuit are targeted, such as the nucleus basalis of Meynert (NBM) and fornix. Potential memory improvements have been observed after DBS in patients with AD and PDD. DBS for the treatment of AD and PDD may be feasible and safe, but it is still preliminary. In this review, we explore the potential role of DBS for the treatment of dementia symptoms in AD and PDD. Firstly, we discuss memory circuits linked to AD and PDD. Secondly, we summarize clinical trials and case reports on NBM or fornix stimulation in AD or PDD patients and discuss the outcomes and limitations of these studies. Finally, we discuss the challenges and future of DBS for the treatment of AD and PDD. We include the latest research results from Gratwicke et al. (2017) and compare them with the results of previous relevant studies, and this would be a worthy update of the literature on DBS for dementia. In addition, we hypothesize that the differences between AD and PDD may ultimately lead to different results following DBS treatment.
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8. Lv QQ, You C, Zou XB, Deng HZ. {{Acyl-carnitine, C5DC, and C26 as potential biomarkers for diagnosis of autism spectrum disorder in children}}. {Psychiatry Res}. 2018; 267: 277-80.
Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders that shown a close association with impaired lipid metabolism. The acyl-carnitine spectrum status in Chinese children with ASD has not been reported. In this study, we assessed the levels of blood acyl-carnitines in Chinese children with ASD and examined the relation between acyl-carnitine profiles and the intelligence levels. Blood levels of acyl-carnitines were determined by tandem mass spectrometry in 60 children with ASD and 30 typically developing children. Chinese Wechsler Young Children Scale of Intelligence (C-WYCSI) was used in ASD group. Blood levels of free carnitine, glutaricyl carnitine, octyl carnitine, twenty four carbonyl carnitine and carnosyl carnitine in the ASD group were significantly lower than those in the control group. Glutaryl carnitine and carnosyl carnitine might be potential biomarkers for diagnosis of ASD. The changes in the acyl-carnitine spectrum indicate potential mitochondrial dysfunction and abnormal fatty acid metabolism in preschool ASD children.
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9. Rai D, Culpin I, Heuvelman H, Magnusson CMK, Carpenter P, Jones HJ, Emond AM, Zammit S, Golding J, Pearson RM. {{Association of Autistic Traits With Depression From Childhood to Age 18 Years}}. {JAMA Psychiatry}. 2018.
Importance: Population-based studies following trajectories of depression in autism spectrum disorders (ASD) from childhood into early adulthood are rare. The role of genetic confounding and of potential environmental intermediaries, such as bullying, in any associations is unclear. Objectives: To compare trajectories of depressive symptoms from ages 10 to 18 years for children with or without ASD and autistic traits, to assess associations between ASD and autistic traits and an International Statistical Classification of Diseases, 10th Revision (ICD-10) depression diagnosis at age 18 years, and to explore the importance of genetic confounding and bullying. Design, Setting, and Participants: Longitudinal study of participants in the Avon Longitudinal Study of Parents and Children birth cohort in Bristol, United Kingdom, followed up through age 18 years. Data analysis was conducted from January to November 2017. Main Outcomes and Measures: Depressive symptoms were assessed using the Short Mood and Feelings Questionnaire (SMFQ) at 6 time points between ages 10 and 18 years. An ICD-10 depression diagnosis at age 18 years was established using the Clinical Interview Schedule-Revised. Exposures were ASD diagnosis and 4 dichotomized autistic traits (social communication, coherence, repetitive behavior, and sociability). An autism polygenic risk score was derived using the Psychiatric Genomics Consortium autism discovery genome-wide association study summary data. Bullying was assessed at ages 8, 10, and 13 years. Results: The maximum sample with complete data was 6091 for the trajectory analysis (48.8% male) and 3168 for analysis of depression diagnosis at age 18 years (44.4% male). Children with ASD and autistic traits had higher average SMFQ depressive symptom scores than the general population at age 10 years (eg, for social communication 5.55 [95% CI, 5.16-5.95] vs 3.73 [95% CI, 3.61-3.85], for ASD 7.31 [95% CI, 6.22-8.40] vs 3.94 [95% CI, 3.83-4.05], remaining elevated in an upward trajectory until age 18 years (eg, for social communication 7.65 [95% CI, 6.92-8.37] vs 6.50 [95% CI, 6.29-6.71], for ASD 7.66 [95% CI, 5.96-9.35] vs 6.62 [95% CI, 6.43-6.81]). Social communication impairments were associated with depression at age 18 years (adjusted relative risk, 1.68; 95% CI, 1.05-2.70), and bullying explained a substantial proportion of this risk. There was no evidence of confounding by the autism polygenic risk score. Analysis in larger samples using multiple imputation led to similar but more precise results. Conclusions and Relevance: Children with ASD and ASD traits have higher depressive symptom scores than the general population by age 10 years, which persist to age 18 years, particularly in the context of bullying. Social communication impairments are an important autistic trait in relation to depression. Bullying, as an environmental intermediary, could be a target for interventions.
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10. Salunkhe G, Weissbrodt K, Feige B, Saville CWN, Berger A, Dundon NM, Bender S, Smyrnis N, Beauducel A, Biscaldi M, Klein C. {{Examining the Overlap Between ADHD and Autism Spectrum Disorder (ASD) Using Candidate Endophenotypes of ADHD}}. {Journal of attention disorders}. 2018: 1087054718778114.
OBJECTIVE: Recent discussions of aetiological overlap between ADHD and Autism Spectrum Disorder (ASD) require comparative studying of these disorders. METHOD: We examined performance of ASD patients with (ASD+) and without (ASD-) comorbid ADHD, ADHD patients, and controls for selected putative endophenotypes of ADHD: Intrasubject Variability (ISV) of reaction times, working memory (WM), inhibition, and temporal processing. RESULTS: We found that patients with ADHD or ASD+, but not ASD-, had elevated ISV across the entire task battery and temporal processing deficits, and that none of the groups were impaired in WM or inhibition. High levels of ISV and generally poor performance in ASD+ patients were only partially due to additive effects of the pure disorders. CONCLUSION: Overall, we conclude that, within our limited but heterogeneous task battery, ISV and temporal processing deficits are most sensitive to ADHD symptomatology and that controlling for ADHD comorbidity is mandatory when assessing ISV in autism.
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11. Souza X, Abreu M, Resende VLS, Castilho LS. {{What Increases the Risk of Dental Traumatism in Patients with Developmental Disabilities?}}. {Brazilian dental journal}. 2018; 29(2): 154-8.
This study investigated risk factors for tooth injuries in individuals from a dental clinical reference service for patients with special needs in Belo Horizonte, MG, Brazil. This is a retrospective cohort study that evaluated 493 dental charts of individuals with or without tooth injuries at their first dental appointment. The dependent variable was the time of occurrence of new dental traumatic injuries and was measured in months. Gender, age, International Code of Diseases, mother’s education, mouth breathing, hyperkinesis, pacifier use, thumb sucking, psychotropic drug use, tooth injuries at the first dental examination, involuntary movements, open bite, having one or more siblings and reports of seizures were the covariates. The Cox proportional hazards regression model was used to estimate the unadjusted and adjusted hazard ratios and their respective 95% confidence intervals. The average time that individuals remained free of dental traumatism was 170.78 months (95% CI, 157.89-183.66) with median of 216 months. The incidence of new events was 11.88%. The covariate associated with an increased risk of dental traumatism was a history of tooth injuries at the first dental appointment. The increase in dental trauma risk was 3.59 (95% CI, 1.94-6.65). A history of traumatic dental injury was the risk factor for the dental trauma found in this group of individuals with developmental disabilities.
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12. Tan DW, Maybery MT, Clarke MW, Di Lorenzo R, Evans MO, Mancinone M, Panos C, Whitehouse AJO. {{No relationship between autistic traits and salivary testosterone concentrations in men from the general population}}. {PLoS One}. 2018; 13(6): e0198779.
It is suggested that testosterone may play a part in the higher prevalence of Autism Spectrum Disorder (ASD) in males compared to females. Previous studies have reported elevated postnatal testosterone levels in children and women with ASD but not in men. We compared levels of salivary testosterone across 67 undergraduate males (Mage 19.5 yrs, SD 1.92) selected for low, mid-range and high levels of autistic traits assessed using the Autism-spectrum Quotient. Analyses revealed no significant differences in testosterone concentrations across the three groups. The current data add to the increasing evidence for the lack of relationship between autistic traits and postnatal levels of testosterone in men.
