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The relationship between adaptive functioning (ability) and autism symptomatology (disability) remains unclear, especially for higher functioning individuals with autism spectrum disorder (ASD). This study investigates ability and disability using the Vineland and Autism Diagnostic Observation Schedule (ADOS), respectively, in two clinical samples of children with ASD. Participants included 187 males with VIQ > 70. Vineland scores were substantially below VIQ, highlighting the magnitude of adaptive impairments despite cognitive potential. A weak relationship was found between ability and disability. Negative relationships were found between age and Vineland scores and no relationships were found between age and ADOS scores. Positive relationships were found between IQ and Vineland Communication. Results stress the need for longitudinal studies on ability and disability in ASD and emphasize the importance of adaptive skills intervention.

The relationship between adaptive functioning and autism symptomatology was examined in 1,089 verbal youths with ASD examining results on Vineland-II, IQ, and measures of ASD severity. Strong positive relationships were found between Vineland subscales and IQ. Vineland Composite was negatively associated with age. IQ accounted a significant amount of the variance in overall adaptive skills (55%) beyond age and ASD severity. Individuals with ASD demonstrated significant adaptive deficits and negligible associations were found between the level of autism symptomatology and adaptive behavior. The results indicate that IQ is a strong predictor of adaptive behavior, the gap between IQ and adaptive impairments decreases in lower functioning individuals with ASD, and older individuals have a greater gap between IQ and adaptive skills.

Individuals with autistic spectrum disorders (ASDs) often experience, describe and exhibit unusual patterns of sensation and attention. These anomalies have been hypothesized to result from overarousal and consequent overfocused attention. Parents of individuals with ASD rated items in three domains, 'sensory overreactivity', 'sensory underreactivity' and 'sensory seeking behaviors', of an expanded version of the Sensory Profile, a 103-item rating scale developed for the present study. Parents also rated symptom severity, overselective attention and exceptional memory, and completed the Vineland Adaptive Behavior Scales. Of 222 rated subjects, 144 had complete data. Cluster analysis showed the predicted overfocused pattern of sensation and attention, comprising overreactivity, perseverative behavior and interests, overfocused attention and exceptional memory in 43 percent of this sample. This pattern was striking in 10 percent. The neurological basis of overreactivity and overfocusing is discussed in relation to the overarousal hypothesis. Attention is drawn to its considerable prevalence in the ASD population.

We conducted a comprehensive review and meta-analysis of research regarding feeding problems and nutrient status among children with autism spectrum disorders (ASD). The systematic search yielded 17 prospective studies involving a comparison group. Using rigorous meta-analysis techniques, we calculated the standardized mean difference (SMD) with standard error and corresponding odds ratio (OR) with 95 % confidence intervals (CI). Results indicated children with ASD experienced significantly more feeding problems versus peers, with an overall SMD of 0.89 (0.08) and a corresponding OR of 5.11, 95 % CI 3.74-6.97. Nutrient analyses indicated significantly lower intake of calcium (SMD: -0.65 [0.29]; OR: 0.31, 95 % CI 0.11-0.85) and protein (SMD: -0.58 [0.25]; OR: 0.35, 95 % CI: 0.14-0.56) in ASD. Future research must address critical questions regarding the cause, long-term impact, and remediation of atypical feeding in this population.

Functional magnetic resonance imaging of brain responses to biological motion in children with autism spectrum disorder (ASD), unaffected siblings (US) of children with ASD, and typically developing (TD) children has revealed three types of neural signatures: (i) state activity, related to the state of having ASD that characterizes the nature of disruption in brain circuitry; (ii) trait activity, reflecting shared areas of dysfunction in US and children with ASD, thereby providing a promising neuroendophenotype to facilitate efforts to bridge genomic complexity and disorder heterogeneity; and (iii) compensatory activity, unique to US, suggesting a neural systemlevel mechanism by which US might compensate for an increased genetic risk for developing ASD. The distinct brain responses to biological motion exhibited by TD children and US are striking given the identical behavioral profile of these two groups. These findings offer far-reaching implications for our understanding of the neural systems underlying autism.endophenotype | functional magnetic resonance imaging

Context Clinical best estimate diagnoses of specific autism spectrum disorders (autistic disorder, pervasive developmental disorder-not otherwise specified, Asperger’s disorder) have been used as the diagnostic gold standard, even when information from standardized instruments is available. Objective To determine if the relationships between behavioral phenotypes and clinical diagnoses of different autism spectrum disorders vary across 12 university-based sites. Design Multi-site observational study collecting clinical phenotype data (diagnostic, developmental and demographic) for genetic research. Classification trees were employed to identify characteristics that predicted diagnosis across and within sites. Setting Participants were recruited through 12 university-based autism service providers into a genetic study of autism. Participants 2102 probands (1814 males) between 4 and 18 years of age (M age=8.93, SD=3.5 years) who met autism spectrum criteria on the Autism Diagnostic Interview–Revised and Autism Diagnostic Observation Schedule and had a clinical diagnosis of an autism spectrum disorder. Main Outcome Measures Best estimate clinical diagnoses predicted by standardized scores from diagnostic, cognitive, and behavioral measures. Results Though distributions of scores on standardized measures were similar across sites, significant site differences emerged in best estimate clinical diagnoses of specific autism spectrum disorders. Relationships between clinical diagnoses and standardized scores, particularly verbal IQ, language level and core diagnostic features, varied across sites in weighting of information and cut-offs. Conclusions Clinical distinctions among categorical diagnostic subtypes of autism spectrum disorders were not reliable even across sites with well-documented fidelity using standardized diagnostic instruments. Results support the move from existing sub-groupings of autism spectrum disorders to dimensional descriptions of core features of social affect and fixated, repetitive behaviors, together with characteristics such as language level and cognitive function.

OBJECTIVES: African American (AA) children affected by autism spectrum disorder (ASD) experience delays in diagnosis and obstacles to service access, as well as a disproportionate burden of intellectual disability (ID) as documented in surveillance data recently published by the US Centers for Disease Control and Prevention. Our objective in this study was to analyze data from the largest-available repository of diagnostic and phenotypic information on AA children with ASD, and to explore the wide variation in outcome within the cohort as a function of sociodemographic risk and specific obstacles to service access for the purpose of informing a national approach to resolution of these disparities. METHODS: Parents of 584 AA children with autism consecutively enrolled in the Autism Genetic Resource Exchange across 4 US data collection sites completed event history calendar interviews of the diagnostic odysseys for their children with ASD. These data were examined in relation to developmental outcomes of the children with autism and their unaffected siblings. RESULTS: The average age of ASD diagnosis was 64.9 months (649.6), on average 42.3 months (645.1) after parents' first concerns about their children's development. The relationship between timing of diagnosis and ASD severity was complex, and ID comorbidity was not predicted in a straightforward manner by familial factors associated with cognitive variation in the general population. CONCLUSIONS: These findings document significant opportunity to expedite diagnosis, the need to further understand causes of ID comorbidity, and the necessity to identify effective approaches to the resolution of disparities in severity-of-outcome for AA children with autism. WHAT'S KNOWN ON THIS SUBJECT: African American (AA) children with autism experience racial disparities in timing of diagnosis and access to quality interventions. AA children experience twice the rate of comorbid intellectual disability and higher rates of misdiagnosis of autism compared with non-Hispanic white children. WHAT THIS STUDY ADDS: These data reveal a 3-year time lag between parental recognition of developmental delay and autism diagnosis among AAs, and that excess intellectual disability burden cannot be explained by ascertainment bias or by traditional familial predictors of cognitive outcome.