1. Azad GF, Kim M, Marcus SC, Mandell DS, Sheridan SM. {{Parent-Teacher Communication about Children with Autism Spectrum Disorder: An Examination of Collaborative Problem-Solving}}. {Psychol Sch};2016 (Dec);53(10):1071-1084.
Effective parent-teacher communication involves problem-solving concerns about students. Few studies have examined problem solving interactions between parents and teachers of children with autism spectrum disorder (ASD), with a particular focus on identifying communication barriers and strategies for improving them. This study examined the problem-solving behaviors of parents and teachers of children with ASD. Participants included 18 teachers and 39 parents of children with ASD. Parent-teacher dyads were prompted to discuss and provide a solution for a problem that a student experienced at home and at school. Parents and teachers also reported on their problem-solving behaviors. Results showed that parents and teachers displayed limited use of the core elements of problem-solving. Teachers displayed more problem-solving behaviors than parents. Both groups reported engaging in more problem-solving behaviors than they were observed to display during their discussions. Our findings suggest that teacher and parent training programs should include collaborative approaches to problem-solving.
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2. Berggren S, Fletcher-Watson S, Milenkovic N, Marschik PB, Bolte S, Jonsson U. {{Emotion recognition training in autism spectrum disorder: A systematic review of challenges related to generalizability}}. {Dev Neurorehabil};2017 (Apr 10):1-14.
PURPOSE: To assess the generalizability of findings from randomized controlled trials (RCTs) evaluating emotion recognition (ER) training for children and adolescents with autism spectrum disorder (ASD). METHODS: We present a systematic review and narrative synthesis of the determinants of external validity in RCTs on ER training. Generalizability of the findings across situations, populations, settings, treatment delivery, and intervention formats was considered. RESULTS: We identified 13 eligible studies. Participants were predominantly boys with ASD in the normative IQ range (IQ > 70), with an age span from 4 to 18 years across studies. Interventions and outcome measures were highly variable. Several studies indicated that training may improve ER, but it is still largely unknown to what extent training effects are translated to daily social life. CONCLUSION: The generalizability of findings from currently available RCTs remains unclear. This underscores the importance of involving children with ASD and their caregivers in informed treatment decisions.
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3. Bjorklund G, Chirumbolo S, Geier DA, Kern JK, Geier MR. {{Histone deacetylase inhibitors, Thimerosal, and autism spectrum disorder}}. {Environ Res};2017 (Apr 11)
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4. Crosson J, Srivastava S, Bibat GM, Gupta S, Kantipuly A, Smith-Hicks C, Myers SM, Sanyal A, Yenokyan G, Brenner J, Naidu SR. {{Evaluation of QTc in Rett syndrome: Correlation with age, severity, and genotype}}. {Am J Med Genet A};2017 (Apr 10)
Rett syndrome (RTT) is caused by MECP2 mutations, resulting in various neurological symptoms. Prolonged corrected QT interval (QTc) is also reported and is a speculated cause of sudden death in RTT. The purpose of this study was to correlate QTc in RTT patients with age, clinical severity, and genotype. 100 RTT patients (98 females, 2 males) with MECP2 mutations underwent baseline neurological evaluation (KKI-RTT Severity Scale) and QTc measurement (standard 12 lead electrocardiogram) as part of our prospective natural history study. Mean QTc of the cohort was 422.6 msec, which did not exceed the normal values for age. 7/100 patients (7%) had QTc prolongation (>450 msec). There was a trend for increasing QTc with age and clinical severity (P = 0.09). No patients with R106C, R106W, R133C, R168*, R270*, R294*, R306C, R306H, and R306P mutations demonstrated QTc prolongation. There was a relatively high proportion of QTc prolongation in patients with R255* mutations (2/8, 25%) and large deletions (1/4, 25%). The overall presence of QTc prolongation did not correlate with mutation category (P = 0.52). Our findings demonstrate that in RTT, the prevalence of QTc prolongation is lower than previously reported. Hence, all RTT patients warrant baseline ECG; if QTc is prolonged, then cardiac followup is warranted. If initial QTc is normal, then annual ECGs, particularly in younger patients, may not be necessary. However, larger sample sizes are needed to solidify the association between QTc and age and clinical severity. The biological and clinical significance of mild QTc prolongation above the normative data remains undetermined.
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5. Fluegge K. {{Revisiting the Link Between Precipitation and the Risk of Autism: The Role of Environmental Nitrous Oxide Exposure}}. {JAMA Pediatr};2017 (Apr 10)
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6. Glod M, Creswell C, Waite P, Jamieson R, McConachie H, Don South M, Rodgers J. {{Comparisons of the Factor Structure and Measurement Invariance of the Spence Children’s Anxiety Scale-Parent Version in Children with Autism Spectrum Disorder and Typically Developing Anxious Children}}. {J Autism Dev Disord};2017 (Apr 09)
The Spence Children’s Anxiety Scale-Parent version (SCAS-P) is often used to assess anxiety in children with autism spectrum disorder (ASD), however, little is known about the validity of the tool in this population. The aim of this study was to determine whether the SCAS-P has the same factorial validity in a sample of young people with ASD (n = 285), compared to a sample of typically developing young people with anxiety disorders (n = 224). Poor model fit with all of the six hypothesised models precluded invariance testing. Exploratory factor analysis indicated that different anxiety phenomenology characterises the two samples. The findings suggest that cross-group comparisons between ASD and anxious samples based on the SCAS-P scores may not always be appropriate.
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7. Green J, Pickles A, Pasco G, Bedford R, Wan MW, Elsabbagh M, Slonims V, Gliga T, Jones EJ, Cheung CH, Charman T, Johnson MH. {{Randomised trial of a parent-mediated intervention for infants at high risk for autism: longitudinal outcomes to age 3 years}}. {J Child Psychol Psychiatry};2017 (Apr 10)
BACKGROUND: There has been increasing interest in the potential for pre-emptive interventions in the prodrome of autism, but little investigation as to their effect. METHODS: A two-site, two-arm assessor-blinded randomised controlled trial (RCT) of a 12-session parent-mediated social communication intervention delivered between 9 and 14 months of age (Intervention in the British Autism Study of Infant Siblings-Video Interaction for Promoting Positive Parenting), against no intervention. Fifty-four infants (28 intervention, 26 nonintervention) at familial risk of autism but not otherwise selected for developmental atypicality were assessed at 9-month baseline, 15-month treatment endpoint, and 27- and 39-month follow-up. PRIMARY OUTCOME: severity of autism prodromal symptoms, blind-rated on Autism Observation Schedule for Infants or Autism Diagnostic Observation Schedule 2nd Edition across the four assessment points. SECONDARY OUTCOMES: blind-rated parent-child interaction and child language; nonblind parent-rated communication and socialisation. Prespecified intention-to-treat analysis combined estimates from repeated measures within correlated regressions to estimate the overall effect of the infancy intervention over time. RESULTS: Effect estimates in favour of intervention on autism prodromal symptoms, maximal at 27 months, had confidence intervals (CIs) at each separate time point including the null, but showed a significant overall effect over the course of the intervention and follow-up period (effect size [ES] = 0.32; 95% CI 0.04, 0.60; p = .026). Effects on proximal intervention targets of parent nondirectiveness/synchrony (ES = 0.33; CI 0.04, 0.63; p = .013) and child attentiveness/communication initiation (ES = 0.36; 95% CI 0.04, 0.68; p = .015) showed similar results. There was no effect on categorical diagnostic outcome or formal language measures. CONCLUSIONS: Follow-up to 3 years of the first RCT of a very early social communication intervention for infants at familial risk of developing autism has shown a treatment effect, extending 24 months after intervention end, to reduce the overall severity of autism prodromal symptoms and enhance parent-child dyadic social communication over this period. We highlight the value of extended follow-up and repeat assessment for early intervention trials.
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8. Gunes S. {{Modified-Release Methylphenidate-Related Trichotillomania in a Boy with Autism Spectrum Disorder}}. {J Child Adolesc Psychopharmacol};2017 (Apr 10)
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9. Gupta AR, Westphal A, Yang DY, Sullivan CA, Eilbott J, Zaidi S, Voos A, Vander Wyk BC, Ventola P, Waqar Z, Fernandez TV, Ercan-Sencicek AG, Walker MF, Choi M, Schneider A, Hedderly T, Baird G, Friedman H, Cordeaux C, Ristow A, Shic F, Volkmar FR, Pelphrey KA. {{Neurogenetic analysis of childhood disintegrative disorder}}. {Mol Autism};2017;8:19.
BACKGROUND: Childhood disintegrative disorder (CDD) is a rare form of autism spectrum disorder (ASD) of unknown etiology. It is characterized by late-onset regression leading to significant intellectual disability (ID) and severe autism. Although there are phenotypic differences between CDD and other forms of ASD, it is unclear if there are neurobiological differences. METHODS: We pursued a multidisciplinary study of CDD (n = 17) and three comparison groups: low-functioning ASD (n = 12), high-functioning ASD (n = 50), and typically developing (n = 26) individuals. We performed whole-exome sequencing (WES), copy number variant (CNV), and gene expression analyses of CDD and, on subsets of each cohort, non-sedated functional magnetic resonance imaging (fMRI) while viewing socioemotional (faces) and non-socioemotional (houses) stimuli and eye tracking while viewing emotional faces. RESULTS: We observed potential differences between CDD and other forms of ASD. WES and CNV analyses identified one or more rare de novo, homozygous, and/or hemizygous (mother-to-son transmission on chrX) variants for most probands that were not shared by unaffected sibling controls. There were no clearly deleterious variants or highly recurrent candidate genes. Candidate genes that were found to be most conserved at variant position and most intolerant of variation, such as TRRAP, ZNF236, and KIAA2018, play a role or may be involved in transcription. Using the human BrainSpan transcriptome dataset, CDD candidate genes were found to be more highly expressed in non-neocortical regions than neocortical regions. This expression profile was similar to that of an independent cohort of ASD probands with regression. The non-neocortical regions overlapped with those identified by fMRI as abnormally hyperactive in response to viewing faces, such as the thalamus, cerebellum, caudate, and hippocampus. Eye-tracking analysis showed that, among individuals with ASD, subjects with CDD focused on eyes the most when shown pictures of faces. CONCLUSIONS: Given that cohort sizes were limited by the rarity of CDD, and the challenges of conducting non-sedated fMRI and eye tracking in subjects with ASD and significant ID, this is an exploratory study designed to investigate the neurobiological features of CDD. In addition to reporting the first multimodal analysis of CDD, a combination of fMRI and eye-tracking analyses are being presented for the first time for low-functioning individuals with ASD. Our results suggest differences between CDD and other forms of ASD on the neurobiological as well as clinical level.
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10. Irimia A, Torgerson CM, Jacokes ZJ, Van Horn JD. {{The connectomes of males and females with autism spectrum disorder have significantly different white matter connectivity densities}}. {Sci Rep};2017 (Apr 11);7:46401.
Autism spectrum disorder (ASD) encompasses a set of neurodevelopmental conditions whose striking sex-related disparity (with an estimated male-to-female ratio of 4:1) remains unknown. Here we use magnetic resonance imaging (MRI) and diffusion weighted imaging (DWI) to identify the brain structure correlates of the sex-by-ASD diagnosis interaction in a carefully selected cohort of 110 ASD patients (55 females) and 83 typically-developing (TD) subjects (40 females). The interaction was found to be predicated primarily upon white matter connectivity density innervating, bilaterally, the lateral aspect of the temporal lobe, the temporo-parieto-occipital junction and the medial parietal lobe. By contrast, regional gray matter (GM) thickness and volume are not found to modulate this interaction significantly. When interpreted in the context of previous studies, our findings add considerable weight to three long-standing hypotheses according to which the sex disparity of ASD incidence is (A) due to WM connectivity rather than to GM differences, (B) modulated to a large extent by temporoparietal connectivity, and (C) accompanied by brain function differences driven by these effects. Our results contribute substantially to the task of unraveling the biological mechanisms giving rise to the sex disparity in ASD incidence, whose clinical implications are significant.
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11. Kim SH, Grammer J, Benrey N, Morrison F, Lord C. {{Stimulus processing and error monitoring in more-able kindergarteners with Autism Spectrum Disorder (ASD): A short review and a preliminary ERP study}}. {Eur J Neurosci};2017 (Apr 10)
Deficits in executive functions (EF) in individuals with autism spectrum disorder (ASD) have been identified. However, there is limited evidence about patterns of deficits in EF-related skills, especially at the neurobiological level, in young children with ASD and little is known about how these skills are related to other domains of functioning and symptom severity. In this study, we provide a focused review of EF-related Event-Related Potentials (ERP) studies in children with ASD, accompanied by preliminary data for neurophysiological correlates of EF on a child-friendly Go/No-go task. We focus our preliminary investigation on ERPs associated with stimulus processing (N2, P3) and error monitoring (error/correct-related negativity [ERN, CRN], error positivity [Pe]) in 5-year-old kindergarteners with ASD and typical controls matched on age, gender, and task accuracy. Children with ASD showed significantly greater amplitudes of ERN/CRN compared to matched controls, suggesting heightened response monitoring. The ASD group also showed less distinct inhibitory P3 compared to the TD group, potentially suggesting atypical stimulus processing. In children with ASD, higher autism symptom severity was correlated with larger P3. Better behavioral performance on an EF-related task was correlated with smaller CRN. Our study is the first investigation to demonstrate the presence of N2, P3, ERN/CRN and Pe in kindergartners with ASD. The potential links between ERP patterns and behavioral and clinical features in more-able children with ASD highlight the need for further exploration into the functional mechanisms of these atypical neural activities and for more focused behavioral interventions targeting cognitive control and response monitoring. This article is protected by copyright. All rights reserved.
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12. Lamonica JM, Kwon DY, Goffin D, Fenik P, Johnson BS, Cui Y, Guo H, Veasey S, Zhou Z. {{Elevating expression of MeCP2 T158M rescues DNA binding and Rett syndrome-like phenotypes}}. {J Clin Invest};2017 (Apr 10)
Mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome (RTT), a neurological disorder affecting cognitive development, respiration, and motor function. Genetic restoration of MeCP2 expression reverses RTT-like phenotypes in mice, highlighting the need to search for therapeutic approaches. Here, we have developed knockin mice recapitulating the most common RTT-associated missense mutation, MeCP2 T158M. We found that the T158M mutation impaired MECP2 binding to methylated DNA and destabilized MeCP2 protein in an age-dependent manner, leading to the development of RTT-like phenotypes in these mice. Genetic elevation of MeCP2 T158M expression ameliorated multiple RTT-like features, including motor dysfunction and breathing irregularities, in both male and female mice. These improvements were accompanied by increased binding of MeCP2 T158M to DNA. Further, we found that the ubiquitin/proteasome pathway was responsible for MeCP2 T158M degradation and that proteasome inhibition increased MeCP2 T158M levels. Together, these findings demonstrate that increasing MeCP2 T158M protein expression is sufficient to mitigate RTT-like phenotypes and support the targeting of MeCP2 T158M expression or stability as an alternative therapeutic approach.
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13. Lewis LF. {{« We will never be normal »: The Experience of Discovering a Partner Has Autism Spectrum Disorder}}. {J Marital Fam Ther};2017 (Apr 10)
Online forums and lay literature suggest that partners of individuals with Autism Spectrum Disorder (ASD) experience depression, distress, and trauma in their everyday lives, exacerbated during the time surrounding diagnosis. In this content analysis, 29 participants were provided with an online open-ended statement asking them to describe in writing their experiences of discovering that their partners had ASD during their relationships. Six themes emerged, including: facing unique challenges within relationships; insisting partners seek diagnosis; initial shock and relief; losing hope for normalcy; making accommodations within relationships; and wishing for professional support. Marriage and family therapists should help couples minimize blaming and promote self-awareness, appropriate relationship expectations, and mutual understanding. Future research should explore the overall experience of neuro-mixed relationships for both partners.
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14. Perets N, Segal-Gavish H, Gothelf Y, Barzilay R, Barhum Y, Abramov N, Hertz S, Morozov D, London M, Offen D. {{Long Term Beneficial Effect of Neurotrophic Factors-Secreting Mesenchymal Stem Cells Transplantation in the BTBR Mouse Model of Autism}}. {Behav Brain Res};2017 (Apr 06)
Autism spectrum disorders (ASD) are neurodevelopmental disabilities characterized by severe impairment in social communication skills and restricted, repetitive behaviors. We have previously shown that a single transplantation of mesenchymal stem cells (MSC) into the cerebral lateral ventricles of BTBR autistic-like mice resulted in an improvement across all diagnostic criteria of ASD. We suggested that brain-derived neurotrophic factor (BDNF), a protein which supports the survival and regeneration of neurons secreted by MSC, largely contributed to the beneficial behavioral effect. In this study, we investigated the behavioral effects of transplanted MSC induced to secrete higher amounts of neurotrophic factors (NurOwn(R)), on various ASD-related behavioral domains using the BTBR mouse model of ASD. We demonstrate that NurOwn(R) transplantation had significant advantages over MSC transplantation in terms of improving communication skills, one and six months following treatment, as compared to sham-treated BTBR mice. Furthermore, NurOwn(R) transplantation resulted in reduced stereotypic behavior for as long as six months post treatment, compared to the one month improvement observed in the MSC treated mice. Notably, NurOwn(R) treatment resulted in improved cognitive flexibility, an improvement that was not observed by MSC treatment. Both MSC and NurOwn(R) transplantation induced an improvement in social behavior that lasted for six months. In conclusion, the present study demonstrates that a single transplantation of MSC or NurOwn(R) have long-lasting benefits, while NurOwn(R) may be superior to MSC treatment.
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15. Platt RJ, Zhou Y, Slaymaker IM, Shetty AS, Weisbach NR, Kim JA, Sharma J, Desai M, Sood S, Kempton HR, Crabtree GR, Feng G, Zhang F. {{Chd8 Mutation Leads to Autistic-like Behaviors and Impaired Striatal Circuits}}. {Cell Rep};2017 (Apr 11);19(2):335-350.
Autism spectrum disorder (ASD) is a heterogeneous disease, but genetically defined models can provide an entry point to studying the molecular underpinnings of this disorder. We generated germline mutant mice with loss-of-function mutations in Chd8, a de novo mutation strongly associated with ASD, and demonstrate that these mice display hallmark ASD behaviors, macrocephaly, and craniofacial abnormalities similar to patient phenotypes. Chd8+/- mice display a broad, brain-region-specific dysregulation of major regulatory and cellular processes, most notably histone and chromatin modification, mRNA and protein processing, Wnt signaling, and cell-cycle regulation. We also find altered synaptic physiology in medium spiny neurons of the nucleus accumbens. Perturbation of Chd8 in adult mice recapitulates improved acquired motor learning behavior found in Chd8+/- animals, suggesting a role for CHD8 in adult striatal circuits. These results support a mechanism linking chromatin modification to striatal dysfunction and the molecular pathology of ASD.
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16. Roberts AL, Lyall K, Weisskopf MG. {{Maternal Exposure to Childhood Abuse is Associated with Mate Selection: Implications for Autism in Offspring}}. {J Autism Dev Disord};2017 (Apr 09)
Maternal experience of childhood abuse has been associated with offspring autism. To explore whether familial tendency towards autistic traits-presumably related to genetic predisposition-accounts for this association, we examined whether women who experienced childhood abuse were more likely to select mates with high levels of autistic traits, and whether parental autistic traits accounted for the association of maternal abuse and offspring autism in 209 autism cases and 833 controls. Maternal childhood abuse was strongly associated with high paternal autistic traits (severe abuse, OR = 3.98, 95% CI = 1.26, 8.31). Maternal and paternal autistic traits accounted for 21% of the association between maternal abuse and offspring autism. These results provide evidence that childhood abuse affects mate selection, with implications for offspring health.
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17. Sarvana Babu MS, Aggarwal N, Asha A, Ashok DS, Koshy T. {{Importance of 3D real time perioperative tee in ASD device embolisation}}. {Ann Card Anaesth};2017 (Apr-Jun);20(2):278.
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18. Shen MD, Kim SH, McKinstry RC, Gu H, Hazlett HC, Nordahl CW, Emerson RW, Shaw D, Elison JT, Swanson MR, Fonov VS, Gerig G, Dager SR, Botteron KN, Paterson S, Schultz RT, Evans AC, Estes AM, Zwaigenbaum L, Styner MA, Amaral DG, Piven J, Piven J, Hazlett HC, Chappell C, Dager S, Estes A, Shaw D, Botteron K, McKinstry R, Constantino J, Pruett J, Schultz R, Zwaigenbaum L, Elison J, Evans AC, Collins DL, Pike GB, Fonov V, Kostopoulos P, Das S, Gerig G, Styner M, Gu H. {{Increased Extra-axial Cerebrospinal Fluid in High-Risk Infants Who Later Develop Autism}}. {Biol Psychiatry};2017 (Mar 06)
BACKGROUND: We previously reported that infants who developed autism spectrum disorder (ASD) had increased cerebrospinal fluid (CSF) in the subarachnoid space (i.e., extra-axial CSF) from 6 to 24 months of age. We attempted to confirm and extend this finding in a larger independent sample. METHODS: A longitudinal magnetic resonance imaging study of infants at risk for ASD was carried out on 343 infants, who underwent neuroimaging at 6, 12, and 24 months. Of these infants, 221 were at high risk for ASD because of an older sibling with ASD, and 122 were at low risk with no family history of ASD. A total of 47 infants were diagnosed with ASD at 24 months and were compared with 174 high-risk and 122 low-risk infants without ASD. RESULTS: Infants who developed ASD had significantly greater extra-axial CSF volume at 6 months compared with both comparison groups without ASD (18% greater than high-risk infants without ASD; Cohen’s d = 0.54). Extra-axial CSF volume remained elevated through 24 months (d = 0.46). Infants with more severe autism symptoms had an even greater volume of extra-axial CSF from 6 to 24 months (24% greater at 6 months, d = 0.70; 15% greater at 24 months, d = 0.70). Extra-axial CSF volume at 6 months predicted which high-risk infants would be diagnosed with ASD at 24 months with an overall accuracy of 69% and corresponding 66% sensitivity and 68% specificity, which was fully cross-validated in a separate sample. CONCLUSIONS: This study confirms and extends previous findings that increased extra-axial CSF is detectable at 6 months in high-risk infants who develop ASD. Future studies will address whether this anomaly is a contributing factor to the etiology of ASD or an early risk marker for ASD.
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19. Stergiakouli E, Davey Smith G, Martin J, Skuse DH, Viechtbauer W, Ring SM, Ronald A, Evans DE, Fisher SE, Thapar A, St Pourcain B. {{Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development}}. {Mol Autism};2017;8:18.
BACKGROUND: Shared genetic influences between attention-deficit/hyperactivity disorder (ADHD) symptoms and autism spectrum disorder (ASD) symptoms have been reported. Cross-trait genetic relationships are, however, subject to dynamic changes during development. We investigated the continuity of genetic overlap between ASD and ADHD symptoms in a general population sample during childhood and adolescence. We also studied uni- and cross-dimensional trait-disorder links with respect to genetic ADHD and ASD risk. METHODS: Social-communication difficulties (N Lien vers le texte intégral (Open Access ou abonnement)
20. Stronach ST, Wetherby AM. {{Observed and Parent-Report Measures of Social Communication in Toddlers With and Without Autism Spectrum Disorder Across Race/Ethnicity}}. {Am J Speech Lang Pathol};2017 (Apr 09):1-14.
Purpose: This study investigated whether measures of early social communication vary among young children of diverse racial/ethnic status with and without autism spectrum disorder (ASD). Method: Participants were 364 toddlers between ages 18 and 36 months with a diagnosis of ASD confirmed (n = 195) or ruled out (n = 169), from 3 racial/ethnic categories: non-Hispanic White (n = 226), non-Hispanic Black (n = 74), and Hispanic (n = 64). Group differences in social communication were examined using an observational measure-the Communication and Symbolic Behavior Scales Behavior Sample (CSBS-BS; Wetherby & Prizant, 2002)-and a parent-report measure, the Early Screening for Autism and Communication Disorders (Wetherby, Woods, & Lord, 2007). Results: Controlling for maternal education, children with ASD scored significantly lower on the CSBS-BS than children without, indicating poorer social communication skills, and higher on the Early Screening for Autism and Communication Disorders, indicating more ASD features. Racial/ethnic groups did not differ on 6 CSBS-BS clusters, but Non-Hispanic White toddlers scored significantly higher than both other groups on the Understanding cluster. There were no significant Diagnosis x Race/Ethnicity interactions. Conclusion: These findings indicate good agreement between observed and parent-report measures in this sample. Results suggest that the CSBS-BS and Early Screening for Autism and Communication Disorders could be viable tools in the detection process for toddlers with ASD in these racial/ethnic groups.
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21. Vanmarcke S, Noens I, Steyaert J, Wagemans J. {{Spatial Frequency Priming of Scene Perception in Adolescents With and Without ASD}}. {J Autism Dev Disord};2017 (Apr 09)
While most typically developing (TD) participants have a coarse-to-fine processing style, people with autism spectrum disorder (ASD) seem to be less globally and more locally biased when processing visual information. The stimulus-specific spatial frequency content might be directly relevant to determine this temporal hierarchy of visual information processing in people with and without ASD. We implemented a semantic priming task in which (in)congruent coarse and/or fine spatial information preceded target categorization. Our results indicated that adolescents with ASD made more categorization errors than TD adolescents and needed more time to process the prime stimuli. Simultaneously, however, our findings argued for a processing advantage in ASD, when the prime stimulus contains detailed spatial information and presentation time permits explicit visual processing.
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22. Wegiel J, Flory M, Kaczmarski W, Brown WT, Chadman K, Wisniewski T, Nowicki K, Kuchna I, Ma SY, Wegiel J. {{Partial Agenesis and Hypoplasia of the Corpus Callosum in Idiopathic Autism}}. {J Neuropathol Exp Neurol};2017 (Mar 01);76(3):225-237.
To test the hypothesis that developmental anomalies of the corpus callosum (CC), contribute to the pathogenesis of autism, we characterized the type, topography, and severity of CC pathology corresponding to reduced CC areas that are detected by magnetic resonance imaging in the brains of 11 individuals with autism and 11 controls. In the brains of 3 autistic subjects, partial CC agenesis resulted in complete or partial lack of interhemispheric axonal connections in CC segments III-V. In these cases, a combination of focal agenesis and uniform axonal deficit caused reduction of CC areas by 37%, of axon numbers by 62%, and of the numerical density of axons by 39%. In the CC of 8 autistic subjects without agenesis, there was an 18% deficit of the midsagittal CC area, 48.4% deficit of axon numbers, and 37% reduction of the numerical density of axons. The significantly thinner CC, reduced CC area, and uniform axonal deficit in all autistic subjects were classified as CC hypoplasia. Thus, the byproduct of partial CC agenesis and hypoplasia is reduction of axonal connections between cortical areas known to be involved in behavioral alterations observed in people with autism.
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23. Zeestraten EA, Gudbrandsen MC, Daly E, de Schotten MT, Catani M, Dell’Acqua F, Lai MC, Ruigrok AN, Lombardo MV, Chakrabarti B, Baron-Cohen S, Ecker C, Murphy DG, Craig MC. {{Sex differences in frontal lobe connectivity in adults with autism spectrum conditions}}. {Transl Psychiatry};2017 (Apr 11);7(4):e1090.
Autism spectrum conditions (ASC) are more prevalent in males than females. The biological basis of this difference remains unclear. It has been postulated that one of the primary causes of ASC is a partial disconnection of the frontal lobe from higher-order association areas during development (that is, a frontal ‘disconnection syndrome’). Therefore, in the current study we investigated whether frontal connectivity differs between males and females with ASC. We recruited 98 adults with a confirmed high-functioning ASC diagnosis (61 males: aged 18-41 years; 37 females: aged 18-37 years) and 115 neurotypical controls (61 males: aged 18-45 years; 54 females: aged 18-52 years). Current ASC symptoms were evaluated using the Autism Diagnostic Observation Schedule (ADOS). Diffusion tensor imaging was performed and fractional anisotropy (FA) maps were created. Mean FA values were determined for five frontal fiber bundles and two non-frontal fiber tracts. Between-group differences in mean tract FA, as well as sex-by-diagnosis interactions were assessed. Additional analyses including ADOS scores informed us on the influence of current ASC symptom severity on frontal connectivity. We found that males with ASC had higher scores of current symptom severity than females, and had significantly lower mean FA values for all but one tract compared to controls. No differences were found between females with or without ASC. Significant sex-by-diagnosis effects were limited to the frontal tracts. Taking current ASC symptom severity scores into account did not alter the findings, although the observed power for these analyses varied. We suggest these findings of frontal connectivity abnormalities in males with ASC, but not in females with ASC, have the potential to inform us on some of the sex differences reported in the behavioral phenotype of ASC.
