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The goal of early autism screening is earlier treatment. We pilot-tested a 12-week, low-intensity treatment with seven symptomatic infants ages 7–15 months. Parents mastered the intervention and maintained skills after treatment ended. Four comparison groups were matched from a study of infant siblings. The treated group of infants was significantly more symptomatic than most of the comparison groups at 9 months of age but was significantly less symptomatic than the two most affected groups between 18 and 36 months. At 36 months, the treated group had much lower rates of both ASD and DQs under 70 than a similarly symptomatic group who did not enroll in the treatment study. It appears feasible to identify and enroll symptomatic infants in parent-implemented intervention before 12 months, and the pilot study outcomes are promising, but testing the treatment’s efficacy awaits a randomized trial.

Identification of genetic biomarkers associated with autism spectrum disorders (ASDs) could improve recurrence prediction for families with a child with ASD. Here, we describe clinical microarray findings for 253 longitudinally phenotyped ASD families from the Baby Siblings Research Consortium (BSRC), encompassing 288 infant siblings. By age 3, 103 siblings (35.8%) were diagnosed with ASD and 54 (18.8%) were developing atypically. Thirteen siblings have copy number variants (CNVs) involving ASD-relevant genes: 6 with ASD, 5 atypically developing, and 2 typically developing. Within these families, an ASD-related CNV in a sibling has a positive predictive value (PPV) for ASD or atypical development of 0.83; the Simons Simplex Collection of ASD families shows similar PPVs. Polygenic risk analyses suggest that common genetic variants may also contribute to ASD. CNV findings would have been pre-symptomatically predictive of ASD or atypical development in 11 (7%) of the 157 BSRC siblings who were eventually diagnosed clinically. Siblings of those with autism spectrum disorder (ASD) have increased likelihood of ASD or related subclinical traits. Here, studying 253 ASD families, D’Abate et al. test the predictive value of genomic copy number variation involving ASD-associated loci, with confirmation in a second cohort.

The executive function theory was utilized to examine the relationship between cognitive process and the restricted, repetitive symptoms of Autistic Disorder (AD). Seventeen adults with AD were compared to 17 nonautistic controls on a new executive function battery (Delis-Kaplin Executive Function Scales). Restricted, repetitive symptoms were measured by a variety of instruments (i.e., the Autism Diagnostic Observation Schedule, Autism Diagnostic Interview-Revised, Gilliam Autism Rating Scale, and the Aberrant Behavior Checklist). The study replicated the executive function profile that has been reported in adults with AD. In addition to the replication findings, the study found several executive processes (i.e., cognitive flexibility, working memory, and response inhibition) were highly related to the restrictive, repetitive symptoms of AD; whereas, other executive process (i.e., planning and fluency) were not found to be significantly correlated with restricted, repetitive symptoms. Similarly, we found an executive function model consisting of relative strengths and deficits was the best predictor of restricted, repetitive symptoms of autism. The implications for the executive function theory and how the theory predicts core symptoms of autism are discussed.

Although repetitive behaviors are a core diagnostic domain for autism spectrum disorders, research in this area has been neglected. This study had two major aims (1) to provide a detailed characterization of repetitive behaviors in individuals with Asperger Syndrome (AS), high-functioning autism (HFA), and typically developing controls (TD); and (2) to examine whether differences in repetitive behavior profiles could provide evidence for the external validity of AS separate from HFA. Specifically, it was hypothesized that circumscribed interests would be more prevalent and cause more impairment in the AS group than the HFA group, while the reverse would be true for other categories of repetitive behavior. The parent(s) of 61 children and adolescents (19 with AS, 21 with HFA, and 21 TD) completed two interviews focused specifically on lifetime and current repetitive behavior symptoms. No reliable differences in repetitive behavior between AS and HFA children were found. Results suggested that circumscribed interests differ in developmental course from the three other DSM-IV-TR categories of repetitive behavior. Internal consistency among the four DSM-IV-TR categories of repetitive behavior was high, alpha = 0.84, providing evidence for a unitary repetitive behaviors factor. The importance of expanding research in the repetitive behavior domain is highlighted as part of the necessary integration of behavioral and neurobiological approaches to understanding the etiology of autism.

It has been proposed that deficient executive functions may be primary cognitive deficits of autism. Executive deficits may also play a part in several other developmental and neurological disorders, raising the question as to how disorders differing in behavioral phenotype can share the same cognitive underpinnings. Suggests that specific types of executive impairment may be associated with specific neurodevelopmental disorders. Hypothesized that when the broad domain of executive function was parsed into specific components, different disorders would demonstrate different executive profiles. The Wisconsin Card Sorting Task, the Tower of Hanoi, and the Stroop Color-Word Test, were administered to children with autism, Tourette syndrome, and attention deficit hyperactivity disorder; discusses findings. (Quotes from original text)

This study compared executive functions in children with autism (N=40), Tourette syndrome (N=30), attention-deficit hyperactivity disorder (N=24), or controls (N=29). Groups differed in patterns of performance on the Wisconsin Card Sorting Task, a measure of flexibility, the Tower of Hanoi, a measure of planning capacity, and the Stroop, a test of inhibition. (DB)

Earlier investigations have found mixed evidence of working memory impairment in autism. The present study examined working memory in a high-functioning autistic sample, relative to both a clinical control group diagnosed with Tourette Syndrome and a typically developing control group. No group differences were found across three tasks and five dependent measures of working memory. Performance was significantly correlated with both age and IQ. It is concluded that working memory is not one of the executive functions that is seriously impaired in autism. We also suggest that the format of administration of working memory tasks may be important in determining whether or not performance falls in the impaired range.

Recent structural and functional imaging work, as well as neuropathology and neuropsychology studies, provide strong empirical support for the involvement of frontal cortex in autism. The Cambridge Neuropsychological Test Automated Battery (CANTAB) is a computer-administered set of neuropsychological tests developed to examine specific components of cognition. Previous studies document the role of frontal cortex in performance of two CANTAB subtests: the Stockings of Cambridge, a planning task, and the Intradimensional/Extradimensional Shift task, a measure of cognitive set shifting. To examine the integrity of frontal functions, these subtests were administered to 79 participants with autism and 70 typical controls recruited from seven universities who are part of the Collaborative Programs of Excellence in Autism network. The two groups were matched on age, sex, and fullscale IQ. Significant group differences were found in performance on both subtests, with the autism group showing deficits in planning efficiency and extradimensional shifting relative to controls. Deficits were found in both lower- and higher-IQ individuals with autism across the age range of 6 to 47 years. Impairment on the CANTAB executive function subtests did not predict autism severity or specific autism symptoms (as measured by the ADI-R and ADOS), but it was correlated with adaptive behavior. If these CANTAB subtests do indeed measure prefrontal function, as suggested by previous research with animals and lesion patients, this adds to the accumulating evidence of frontal involvement in autism and indicates that this brain region should remain an active area of investigation.

This project evaluated the effectiveness of the Treatment and Education of Autistic and related Communication handicapped CHildren (TEACCH) home program intervention model for young children with autism, which encourages parents to be active, ongoing co-therapists. The 11 children in the treatment group, compared to the control, improved significantly in four months on subtests of imitation, fine and gross motor, and nonverbal conceptual skills. (DB)