1. Christensen DL, Bilder DA, Zahorodny W, Pettygrove S, Durkin MS, Fitzgerald RT, Rice C, Kurzius-Spencer M, Baio J, Yeargin-Allsopp M. {{Prevalence and Characteristics of Autism Spectrum Disorder Among 4-Year-Old Children in the Autism and Developmental Disabilities Monitoring Network}}. {J Dev Behav Pediatr};2015 (Dec 9)
OBJECTIVE: Early identification of children with autism spectrum disorder (ASD) facilitates timely access to intervention services. Yet, few population-based data exist on ASD identification among preschool-aged children. The authors aimed to describe ASD prevalence and characteristics among 4-year-old children in 5 of 11 sites participating in the 2010 Autism and Developmental Disabilities Monitoring Network. METHOD: Children with ASD were identified through screening of health and education records for ASD indicators, data abstraction and compilation for each child, and clinician review of records. ASD prevalence estimates, ages at first evaluation and ASD diagnosis, cognitive test scores, and demographics were compared for 4-year-old children and 8-year-old children living in the same areas. RESULTS: Among 58,467 children in these 5 sites, 4-year-old ASD prevalence was 13.4 per 1000, which was 30% lower than 8-year-old ASD prevalence. Prevalence of ASD without cognitive impairment was 40% lower among 4-year-olds compared with 8-year-olds, but prevalence of ASD with cognitive impairment was 20% higher among 4-year-olds compared with 8-year-olds. Among 4-year-olds with ASD, female and non-Hispanic white children were more likely to receive their first comprehensive evaluation by age 36 months compared with male and non-Hispanic black children, respectively. Among children diagnosed with ASD by age 48 months, median age at first comprehensive evaluation was 27 months for 4-year-olds compared with 32 months for 8-year-olds. CONCLUSION: Population-based ASD surveillance among 4-year-old children provides valuable information about the early identification of children with ASD and suggests progression toward lowering the age of first ASD evaluation within participating Autism and Developmental Disabilities Monitoring communities.
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2. Denman I, Banajee M, Hurley A. {{Dichotic listening training in children with autism spectrum disorder: A single subject design}}. {Int J Audiol};2015 (Dec);54(12):991-996.
OBJECTIVE: Previous research has shown that dichotic listening training has improved auditory and language processing for individuals with large interaural asymmetries on dichotic listening tasks. This training can be a useful treatment for children with autism spectrum disorder (ASD). DESIGN: A single subject, multiple baseline across subjects study was utilized. STUDY SAMPLE: Three children with ASD, between the ages of 8-12, participated in the study. RESULTS: This training demonstrated improvement in language and auditory processing tasks following completion of up to twelve weeks of auditory training. CONCLUSION: This study supports the idea that deficit specific, dichotic auditory training can remediate auditory and language deficits for children with ASD. More research is needed, with a group design and controls, in order to generalize these results to the larger ASD population.
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3. Kitzerow J, Teufel K, Wilker C, Freitag CM. {{Using the brief observation of social communication change (BOSCC) to measure autism-specific development}}. {Autism Res};2015 (Dec 8)
To date no reliable and objective, change sensitive instrument for autistic symptoms is available. The brief observation of social communication change (BOSCC) was specifically developed to measure change of core autistic symptoms, for example, for use as outcome measure in early intervention trials. This study investigated quality criteria of a preliminary research version of the BOSCC in N = 21 children with autism spectrum disorder (ASD) who had participated for 1 year in the Frankfurt early intervention program (FFIP). BOSCC rating was done on play based ADOS video scenes. Inter-rater agreement on the BOSCC average total was very high. The BOSCC showed a significant decrease of autistic symptoms after 1 year with a medium effect size. Symptom specific improvements were captured by the social communication subscale and most single items. The BOSCC showed comparable change sensitivity to other autism specific instruments. Future studies should focus on the finalized BOSCC version, and replicate findings in a larger sample. Autism Res 2015. (c) 2015 International Society for Autism Research, Wiley Periodicals, Inc.
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4. Kogan JH, Gross AK, Featherstone RE, Shin R, Chen Q, Heusner CL, Adachi M, Lin A, Walton NM, Miyoshi S, Miyake S, Tajinda K, Ito H, Siegel SJ, Matsumoto M. {{Mouse Model of Chromosome 15q13.3 Microdeletion Syndrome Demonstrates Features Related to Autism Spectrum Disorder}}. {J Neurosci};2015 (Dec 9);35(49):16282-16294.
The chromosome 15q13.3 microdeletion is a pathogenic copy number variation conferring epilepsy, intellectual disability, schizophrenia, and autism spectrum disorder (ASD). We generated mice carrying a deletion of 1.2 Mb homologous to the 15q13.3 microdeletion in human patients. Here, we report that mice with a heterozygous deletion on a C57BL/6 background (D/+ mice) demonstrated phenotypes including enlarged/heavier brains (macrocephaly) with enlarged lateral ventricles, decreased social interactions, increased repetitive grooming behavior, reduced ultrasonic vocalizations, decreased auditory-evoked gamma band EEG, and reduced event-related potentials. D/+ mice had normal body weight, activity levels, sensory gating, and cognitive abilities and no signs of epilepsy/seizures. Our results demonstrate that D/+ mice represent ASD-related phenotypes associated with 15q13.3 microdeletion syndrome. Further investigations using this chromosome-engineered mouse model may uncover the common mechanism(s) underlying ASD and other neurodevelopmental/psychiatric disorders representing the 15q13.3 microdeletion syndrome, including epilepsy, intellectual disability, and schizophrenia. SIGNIFICANCE STATEMENT: Recently discovered pathologic copy number variations (CNVs) from patients with neurodevelopmental/psychiatric disorders show very strong penetrance and thus are excellent candidates for mouse models of disease that can mirror the human genetic conditions with high fidelity. A 15q13.3 microdeletion in humans results in a range of neurodevelopmental/psychiatric disorders, including epilepsy, intellectual disability, schizophrenia, and autism spectrum disorder (ASD). The disorders conferred by a 15q13.3 microdeletion also have overlapping genetic architectures and comorbidity in other patient populations such as those with epilepsy and schizophrenia/psychosis, as well as schizophrenia and ASD. We generated mice carrying a deletion of 1.2 Mb homologous to the 15q13.3 microdeletion in human patients, which allowed us to investigate the potential causes of neurodevelopmental/psychiatric disorders associated with the CNV.
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5. Kosidou K, Dalman C, Widman L, Arver S, Lee BK, Magnusson C, Gardner RM. {{Maternal polycystic ovary syndrome and the risk of autism spectrum disorders in the offspring: a population-based nationwide study in Sweden}}. {Mol Psychiatry};2015 (Dec 8)
Although many studies indicate the interplay of genetic and environmental factors in the etiology of autism spectrum disorder (ASD), our limited understanding of the underlying mechanisms hampers the development of effective ways of detecting and preventing the disorder. Recent studies support the hypothesis that prenatal androgen exposure contributes to the development of ASD. This would suggest that maternal polycystic ovary syndrome (PCOS), a condition associated with excess androgens, would increase the risk of ASD in the offspring. We conducted a matched case-control study nested within the total population of Sweden (children aged 4-17 who were born in Sweden from 1984 to 2007). The sample consisted of 23 748 ASD cases and 208 796 controls, matched by birth month and year, sex and region of birth. PCOS and ASD were defined from ICD codes through linkage to health-care registers. Maternal PCOS increased the odds of ASD in the offspring by 59%, after adjustment for confounders (odds ratio (OR) 1.59, 95% confidence interval (CI) 1.34-1.88). The odds of offspring ASD were further increased among mothers with both PCOS and obesity, a condition common to PCOS that is related to more severe hyperandrogenemia (OR 2.13, 95% CI 1.46-3.10). Risk estimates did not differ between sexes. In conclusion, children of women with PCOS appear to have a higher risk of developing ASD. This finding awaits confirmation, and exploration of potentially underlying mechanisms, including the role of sex steroids in the etiology of ASD.Molecular Psychiatry advance online publication, 8 December 2015; doi:10.1038/mp.2015.183.
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6. Leekam S. {{Social cognitive impairment and autism: what are we trying to explain?}}. {Philos Trans R Soc Lond B Biol Sci};2016 (Jan 19);371(1686)
Early psychological theories of autism explained the clinical features of this condition in terms of perceptual and sensory processing impairments. The arrival of domain-specific social cognitive theories changed this focus, postulating a ‘primary’ and specific psychological impairment of social cognition. Across the years, evidence has been growing in support of social cognitive and social attention explanations in autism. However, there has also been evidence for general non-social cognitive impairments in representational understanding, attention allocation and sensory processing. Here, I review recent findings and consider the case for the specificity and primacy of the social cognitive impairment, proposing that we should focus more explicitly on clinically valid features for insights on the integration of ‘social’ and ‘non-social’ cognition.
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7. Mitra A, Snyder AZ, Constantino JN, Raichle ME. {{The Lag Structure of Intrinsic Activity is Focally Altered in High Functioning Adults with Autism}}. {Cereb Cortex};2015 (Dec 9)
The behaviors that define autism spectrum disorders (ASDs) have been hypothesized to result from disordered communication within brain networks. Several groups have investigated this question using resting-state functional magnetic resonance imaging (RS-fMRI). However, the published findings to date have been inconsistent across laboratories. Prior RS-fMRI studies of ASD have employed conventional analysis techniques based on the assumption that intrinsic brain activity is exactly synchronous over widely separated parts of the brain. By relaxing the assumption of synchronicity and focusing, instead, on lags between time series, we have recently demonstrated highly reproducible patterns of temporally lagged activity in normal human adults. We refer to this analysis technique as resting-state lag analysis (RS-LA). Here, we report RS-LA as well as conventional analyses of RS-fMRI in adults with ASD and demographically matched controls. RS-LA analyses demonstrated significant group differences in rs-fMRI lag structure in frontopolar cortex, occipital cortex, and putamen. Moreover, the degree of abnormality in individuals was highly correlated with behavioral measures relevant to the diagnosis of ASD. In this sample, no significant group differences were observed using conventional RS-fMRI analysis techniques. Our results suggest that altered propagation of intrinsic activity may contribute to abnormal brain function in ASD.
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8. Park MO. {{Comparison of motor and process skills among children with different developmental disabilities}}. {J Phys Ther Sci};2015 (Oct);27(10):3183-3184.
[Purpose] The purpose of the present study was to compare the motor and process skills of children with different developmental disabilities. [Subjects] Thirty-nine children with developmental disabilities participated in this study which was conducted at N hospital in South Korea. [Methods] The motor and process skills of the participants were compared among three different disabilities: pervasive developmental disorder, cerebral palsy, and intellectual disorder. The data were analyzed using descriptive statistics and one-way ANOVA. [Results] Significant differences in motor skills were found among the diagnoses. The cerebral palsy group showed poorer motor skills than the pervasive developmental disability and intellectual disability groups. [Conclusion] The findings have clinical implications for strategies of rehabilitation for children with developmental disabilities.
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9. Quintin EM, Jo B, Hall SS, Bruno JL, Chromik LC, Raman MM, Lightbody AA, Martin A, Reiss AL. {{The cognitive developmental profile associated with fragile X syndrome: A longitudinal investigation of cognitive strengths and weaknesses through childhood and adolescence}}. {Dev Psychopathol};2015 (Dec 9):1-13.
Few studies have investigated developmental strengths and weaknesses within the cognitive profile of children and adolescents with fragile X syndrome (FXS), a single-gene cause of inherited intellectual impairment. With a prospective longitudinal design and using normalized raw scores (Z scores) to circumvent floor effects, we measured cognitive functioning of 184 children and adolescents with FXS (ages 6 to 16) using the Wechsler Scale of Intelligence for Children on one to three occasions for each participant. Participants with FXS received lower raw scores relative to the Wechsler Scale of Intelligence for Children normative sample across the developmental period. Verbal comprehension, perceptual organization, and processing speed Z scores were marked by a widening gap from the normative sample, while freedom from distractibility Z scores showed a narrowing gap. Key findings include a relative strength for verbal skills in comparison with visuospatial-constructive skills arising in adolescence and a discrepancy between working memory (weakness) and processing speed (strength) in childhood that diminishes in adolescence. Results suggest that the cognitive profile associated with FXS develops dynamically from childhood to adolescence. Findings are discussed within the context of aberrant brain morphology in childhood and maturation in adolescence. We argue that assessing disorder-specific cognitive developmental profiles will benefit future disorder-specific treatment research.
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10. Robins DL. {{Prevalence Counts: Commentary on « Prevalence and Characteristics of Autism Spectrum Disorder Among 4-Year-Old Children in the Autism and Developmental Disabilities Monitoring Network »}}. {J Dev Behav Pediatr};2015 (Dec 9)
