964 research outputs found

    Memory, learning and language in autism spectrum disorder

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    Background and aims: The ‘dual-systems’ model of language acquisition has been used by Ullman and colleagues to explain patterns of strength and weakness in the language of higher-functioning people with autism spectrum disorder (ASD). Specifically, intact declarative/explicit learning is argued to compensate for a deficit in non-declarative/implicit procedural learning, constituting an example of the so-called ‘see-saw’ effect. Ullman and Pullman (2015) extended their argument concerning a see-saw effect on language in ASD to cover other perceived anomalies of behaviour, including impaired acquisition of social skills. The aim of this paper is to present a critique of Ullman and colleagues’ claims, and to propose an alternative model of links between memory systems and language in ASD. Main contribution: We argue that a 4-systems model of learning, in which intact semantic and procedural memory are used to compensate for weaknesses in episodic memory and perceptual learning, can better explain patterns of language ability across the autistic spectrum. We also argue that attempts to generalise the ‘impaired implicit learning/spared declarative learning’ theory to other behaviours in ASD are unsustainable. Conclusions: Clinically significant language impairments in ASD are under-researched, despite their impact on everyday functioning and quality of life. The relative paucity of research findings in this area lays it open to speculative interpretation which may be misleading. Implications: More research is need into links between memory/learning systems and language impairments across the spectrum. Improved understanding should inform therapeutic intervention, and contribute to investigation of the causes of language impairment in ASD with potential implications for prevention

    Defining language impairments in a subgroup of children with autism spectrum disorder

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    Autism spectrum disorder (ASD) is diagnosed on the basis of core impairments in pragmatic language skills, which are found across all ages and subtypes. In contrast, there is significant heterogeneity in language phenotypes, ranging from nonverbal to superior linguistic abilities, as defined on standardized tests of vocabulary and grammatical knowledge. The majority of children are verbal but impaired in language, relative to age-matched peers. One hypothesis is that this subgroup has ASD and co-morbid specific language impairment (SLI). An experiment was conducted comparing children with ASD to children with SLI and typically developing controls on aspects of language processing that have been shown to be impaired in children with SLI: repetition of nonsense words. Patterns of performance among the children with ASD and language impairment were similar to those with SLI, and contrasted with the children with ASD and no language impairment and typical controls, providing further evidence for the hypothesis that a subgroup of children with ASD has co-morbid SLI. The findings are discussed in the context of brain imaging studies that have explored the neural bases of language impairment in ASD and SLI, and overlap in the genes associated with elevated risk for these disorders.M01 RR00533 - NCRR NIH HHS; R01 DC10290 - NIDCD NIH HHS; U19 DC03610 - NIDCD NIH HH

    A Comprehensive Profile of Decoding and Comprehension in Autism Spectrum Disorders

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    The present study examined intake data from 384 participants with autism spectrum disorders (ASD) and a comparison group of 100 participants with dyslexia on nine standardized measures of decoding and comprehension. Although diagnostic groups were based on parental reports and could not be verified independently, we were able to observe significant distinctions between subject groups. Overall findings confirm previous results of a disassociation between decoding and comprehension in ASD. Using a larger sample than previous studies and a greater variety of measures, a pattern of relatively intact decoding skills paired with low comprehension was found in autism, PDD-NOS, and Asperger’s. In contrast, the dyslexic group showed the opposite pattern of stronger comprehension and weaker decoding

    Defining the cognitive phenotype of autism

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    Although much progress has been made in determining the cognitive profile of strengths and weaknesses that characterise individuals with autism spectrum disorders (ASDs), there remain a number of outstanding questions. These include how universal strengths and deficits are; whether cognitive subgroups exist; and how cognition is associated with core autistic behaviours, as well as associated psychopathology. Several methodological factors have contributed to these limitations in our knowledge, including: small sample sizes, a focus on single domains of cognition, and an absence of comprehensive behavioural phenotypic information. To attempt to overcome some of these limitations, we assessed a wide range of cognitive domains in a large sample (N = 100) of 14- to 16-year-old adolescents with ASDs who had been rigorously behaviourally characterised. In this review, we will use examples of some initial findings in the domains of perceptual processing, emotion processing and memory, both to outline different approaches we have taken to data analysis and to highlight the considerable challenges to better defining the cognitive phenotype(s) of ASDs. Enhanced knowledge of the cognitive phenotype may contribute to our understanding of the complex links between genes, brain and behaviour, as well as inform approaches to remediation

    Large-scale associations between the leukocyte transcriptome and BOLD responses to speech differ in autism early language outcome subtypes.

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    Heterogeneity in early language development in autism spectrum disorder (ASD) is clinically important and may reflect neurobiologically distinct subtypes. Here, we identified a large-scale association between multiple coordinated blood leukocyte gene coexpression modules and the multivariate functional neuroimaging (fMRI) response to speech. Gene coexpression modules associated with the multivariate fMRI response to speech were different for all pairwise comparisons between typically developing toddlers and toddlers with ASD and poor versus good early language outcome. Associated coexpression modules were enriched in genes that are broadly expressed in the brain and many other tissues. These coexpression modules were also enriched in ASD-associated, prenatal, human-specific, and language-relevant genes. This work highlights distinctive neurobiology in ASD subtypes with different early language outcomes that is present well before such outcomes are known. Associations between neuroimaging measures and gene expression levels in blood leukocytes may offer a unique in vivo window into identifying brain-relevant molecular mechanisms in ASD
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