Brief report: inhibition of return in young people with autism and Asperger's disorder.

The aim of this study was to investigate whether the superior search abilities observed in autism/Asperger's disorder may in part be a consequence of a more pronounced inhibition of return (IOR). Contrary to our prediction, IOR in individuals with autism was comparable to the matched comparison group. However, the autism group committed more false alarm responses than the matched comparison group; this may reflect a possible inhibitory deficit, or suggest that individuals with autism rely more on probabilities to determine their behavioural responses. There was a borderline-significant trend (p=0.052) to indicate that IOR may be more pronounced in individuals with Asperger's disorder. In contrast to the autism group, the Asperger's disorder group had a pattern of false alarm responses similar to that of the comparison group. The findings further inform Minshew's complex information processing theory which seeks to establish which areas of neuropsychological functioning are preserved and deficit in autism.

Array CGH identifies reciprocal 16p13.1 duplications and deletions that predispose to autism and/or mental retardation.

Autism and mental retardation (MR) are often associated, suggesting that these conditions are etiologically related. Recently, array-based comparative genomic hybridization (array CGH) has identified submicroscopic deletions and duplications as a common cause of MR, prompting us to search for such genomic imbalances in autism. Here we describe a 1.5-Mb duplication on chromosome 16p13.1 that was found by high-resolution array CGH in four severe autistic male patients from three unrelated families. The same duplication was identified in several variably affected and unaffected relatives. A deletion of the same interval was detected in three unrelated patients with MR and other clinical abnormalities. In one patient we revealed a further rearrangement of the 16p13 imbalance that was not present in his unaffected mother. Duplications and deletions of this 1.5-Mb interval have not been described as copy number variants in the Database of Genomic Variants and have not been identified in >600 individuals from other cohorts examined by high-resolution array CGH in our laboratory. Thus we conclude that these aberrations represent recurrent genomic imbalances which predispose to autism and/or MR.

Psychopathology in children and adolescents with autism compared to young people with intellectual disability.

Autism is a neurodevelopmental disorder with a specific pattern of behavioural, communication and social problems. Additional mental health problems are often poorly understood and undetected. This study investigates the level and pattern of emotional and behavioural problems in young people with autism compared with children with intellectual disability (ID). Subjects were 381 young people with autism and a representative group of 581 Australian young people with ID aged 4-18 years. Parents/carers provided details of the emotional and behavioural problems of their child using the Developmental Behaviour Checklist (DBC-P). Young people with autism were found to suffer from significantly higher levels of psychopathology than young people with ID. The implications of this finding are discussed.

An examination of movement kinematics in young people with high-functioning autism and Asperger's disorder: further evidence for a motor planning deficit.

This paper examines upper-body movement kinematics in individuals with high-functioning autism (HFA) and Asperger's disorder (AD). In general, the results indicate that HFA is more consistently associated with impaired motoric preparation/initiation than AD. The data further suggest that this quantitative difference in motor impairment is not necessarily underpinned by greater executive dysfunction vulnerability in autism relative to AD. Quantitative motoric dissociation between autism and AD may have down-stream effects on later stages of movement resulting in qualitative differences between these disorder groups, e.g. "motor clumsiness" in AD versus "abnormal posturing" in autism. It will be important for future research to map the developmental trajectory of motor abnormalities in these disorder groups.

Pseudo-random number generation in children with high-functioning autism and Asperger's disorder: further evidence for a dissociation in executive functioning?

The repetitive, stereotyped and obsessive behaviours, which are core diagnostic features of autism, are thought to be underpinned by executive dysfunction. This study examined executive impairment in individuals with autism and Asperger's disorder using a verbal equivalent of an established pseudo-random number generating task. Different patterns of disinhibition emerged in the autism (n = 12) and Asperger's disorder (n = 12) groups. Consistent with previous research, the autism group repeated single numbers (e.g. 2, 2, 2) more frequently than the control group. In contrast to past research suggesting intact executive abilities, this study found that the Asperger's disorder group generated more repetitive number patterns (e.g. 45, 45) than the controls. Executive functioning in children with Asperger's disorder may be particularly vulnerable to a lack of visual cueing and concrete rules. Qualitative differences in executive dysfunction between these groups may implicate differential disruption within the fronto-striatal circuitry.

A neurobehavioral examination of individuals with high-functioning autism and Asperger's disorder using a fronto-striatal model of dysfunction.

The repetitive, stereotyped, and obsessive behaviors that characterize autism may in part be attributable to disruption of the region of the fronto-striatal system, which mediates executive abilities. Neuropsychological testing has shown that children with autism exhibit set-shifting deficiencies on tests such as the Wisconsin Card Sorting task but show normal inhibitory ability on variants of the Stroop color-word test. According to Minshew and Goldstein's multiple primary deficit theory, the complexity of the executive functioning task is important in determining the performance of individuals with autism. This study employed a visual-spatial task (with a Stroop-type component) to examine the integrity of executive functioning, in particular inhibition, in autism (n = 12) and Asperger's disorder (n = 12) under increasing levels of cognitive complexity. Whereas the Asperger's disorder group performed similarly to age- and IQ-matched control participants, even at the higher levels of cognitive complexity, the high-functioning autism group displayed inhibitory deficits specifically associated with increasing cognitive load.

Screening young people for autism with the developmental behavior checklist.

OBJECTIVE: To determine whether a subset of items from the Developmental Behavior Checklist (DBC) could be selected to construct a reliable autism screening tool. METHOD: A 29-item scale-the Developmental Behavior Checklist-Autism Screening Algorithm (DBC-ASA)-was developed by using items from the DBC and evaluated in a sample comprising 180 children who met criteria for autism and 180 controls matched for age, sex, and IQ range. RESULTS: This study found that the DBC-ASA has good validity in discriminating young people (4-18 years) with autism and IQ ranging from normal to severe intellectual disability from others using a cutoff score of 17. CONCLUSION: The DBC-ASA is an effective autism screening questionnaire for at-risk young people, including those with intellectual disability.

Lateralization in individuals with high-functioning autism and Asperger's disorder: a frontostriatal model.

Neurobiological and behavioural studies of possible left hemisphere dysfunction in autism have generated conflicting results. Left hemisphere dysfunction may manifest in autism only in tasks that invoke executive functions. Moreover, left hemisphere dysfunction may underpin autism but not Asperger's disorder. We thus aimed to systematically investigate reports of anomalous lateralization in individuals with high-functioning autism and Asperger's disorder. Two of the tasks were sensitive to executive dysfunction: a serial choice reaction-time task and a Posner-type paradigm; the remaining tasks instead investigated aspects of perceptual lateralisation. Compared with age- and IQ-matched controls, the autism group displayed deficiencies in right hemispace (and by implication, left hemisphere) performance on both executive function tasks; however, this group demonstrated normal lateralization effects on the nonexecutive, visual-perceptual tasks. In contrast, the Asperger's disorder group showed similar laterality effects to their age- and IQ-matched controls on both executive and nonexecutive function tasks. The etiological relevance of this neurobehavioral dissociation between high-functioning autism and Asperger's disorder was discussed; in particular, it was suggested that the period where dominance shifts from right to left hemisphere is important in whatever process might dictate the emergence of either autism or Asperger's disorder.

Adult outcomes in autism: community inclusion and living skills.

Longitudinal research has demonstrated that social outcomes for adults with autism are restricted, particularly in terms of employment and living arrangements. However, understanding of individual and environmental factors that influence these outcomes is far from complete. This longitudinal study followed a community sample of children and adolescents with autism into adulthood. Social outcomes in relation to community inclusion and living skills were examined, including the predictive role of a range of individual factors and the environment (socio-economic disadvantage). Overall, the degree of community inclusion and living skills was restricted for the majority, and while childhood IQ was an important determinant of these outcomes, it was not the sole predictor. The implications of these findings in relation to interventions are discussed.

Differential olfactory identification in children with autism and Asperger's disorder: a comparative and longitudinal study.

Key theories of autism implicate orbitofrontal cortex (OFC) compromise, while olfactory identification (OI) deficits are associated with OFC dysfunction. This study aimed to complete a 5-year follow-up of children with high-functioning autism (HFA) who previously lacked the normal age-OI association; and compare unirhinal-OI in children with HFA, Asperger's disorder (ASP), and controls. While both HFA and controls had improved birhinal-OI at follow-up, reduced OI in some HFA participants suggested OFC deterioration and heterogeneous OFC development. Unirhinal-OI was impaired in HFA but not ASP relative to controls, suggesting orbitofrontal compromise in HFA but integrity in ASP. Differing IQ-OI relationships existed between HFA and ASP. Findings support the hypothesis of separate neurobiological underpinnings in ASP and HFA, specifically differential orbitofrontal functioning.

Gait function in newly diagnosed children with autism: Cerebellar and basal ganglia related motor disorder.

We investigated gait in newly diagnosed children with autism. From our previous study with 6- to 14-year-olds, we hypothesized that motor symptoms indicative of basal ganglia and cerebellar dysfunction would appear across the developmental trajectory of autism. Two groups were recruited: children with autism (eight males, three females; mean age 5 y 10 mo [SD 9 mo]; range 4 y 4 mo-6 y 9 mo) and a comparison group of typically developing children (eight males, three females; mean age 5 y 9 mo [SD 1 y 1 mo]; range 4 y 3 mo-7 y 2 mo). The GAITRite Walkway was used to gather data from average gait and intra-walk measurements. Experienced physiotherapists analyzed gait qualitatively. Groups were matched according to age, height, weight, and IQ; although not statistically significant, IQ was lower in the group with autism. Spatiotemporal gait data for children with autism were compatible with findings from patients with cerebellar ataxia: specifically, greater difficulty walking along a straight line, and the coexistence of variable stride length and duration. Children with autism were also less coordinated and rated as more variable and inconsistent (i.e. reduced smoothness) relative to the comparison group. Postural abnormalities in the head and trunk suggest additional involvement of the fronto-striatal basal ganglia region. Abnormal gait features are stable across key developmental periods and are, therefore, promising for use in clinical screening for autism.

A clinical and neurobehavioural review of high-functioning autism and Asperger's disorder.

OBJECTIVE: To compare, contrast and review clinical and neuropsychological studies of high-functioning autism and Asperger's disorder. METHOD: This paper reviews past and contemporary conceptualizations of autism and Asperger's disorder, together with epidemiological information, genetic and neurobehavioural findings. This paper focuses on neurobehavioural studies, in particular, executive functioning, lateralization, visual-perceptual and motor processing, which have provided an important source of information about the potential neurobiological dissociation that may exist between autism and Asperger's disorder. RESULTS: The clinical profiles of autism and Asperger's disorder contain a mixture of psychiatric and neurological symptoms: for example, movement abnormalities (i.e. stereotyped behaviours, hand flapping, toe walking, whole-body movements), atypical processing of parts and wholes, verbal and non-verbal deficits, ritualistic/compulsive behaviour, disturbances in reciprocal social interaction and associated depression and anxiety. The considerable clinical overlap between autism and Asperger's disorder has led many to question whether Asperger's disorder is merely a mild form of autism, or whether it should be considered as a separate clinical entity. CONCLUSION: In light of the growing body of epidemiological information, genetic, and neurobehavioural evidence that distinguishes autism from Asperger's disorder, it is premature to rule out the possibility that these disorders may be clinically, and possibly neurobiologically separate.