We use a new model of metarepresentational development to predict a cognitive deficit which could explain a crucial component of the social impairment in childhood autism. One of the manifestations of a basic metarepresentational capacity is a 'theory of mind'. We have reason to believe that autistic children lack such a 'theory'. If this were so, then they would be unable to impute beliefs to others and to predict their behaviour. This hypothesis was tested using Wimmer and Perner's puppet play paradigm. Normal children and those with Down's syndrome were used as controls for a group of autistic children. Even though the mental age of the autistic children was higher than that of the controls, they alone failed to impute beliefs to others. Thus the dysfunction we have postulated and demonstrated is independent of mental retardation and specific to autism. *We are grateful to John Morton for his helpful comments on earlier drafts of this paper. We would also like to thank staff and children of the various schools which participated in the study. The experiment was carried out by Simon Baron-Cohen as part of his Ph.D thesis (

"Weak central coherence" refers to the detail-focused processing style proposed to characterise autism spectrum disorders (ASD). The original suggestion of a core deficit in central processing resulting in failure to extract global form/meaning, has been challenged in three ways. First, it may represent an outcome of superiority in local processing. Second, it may be a processing bias, rather than deficit. Third, weak coherence may occur alongside, rather than explain, deficits in social cognition. A review of over 50 empirical studies of coherence suggests robust findings of local bias in ASD, with mixed findings regarding weak global processing. Local bias appears not to be a mere side-effect of executive dysfunction, and may be independent of theory of mind deficits. Possible computational and neural models are discussed.

The mentalizing (theory of mind) system of the brain is probably in operation from ca. 18 months of age, allowing implicit attribution of intentions and other mental states. Between the ages of 4 and 6 years explicit mentalizing becomes possible, and from this age children are able to explain the misleading reasons that have given rise to a false belief. Neuroimaging studies of mentalizing have so far only been carried out in adults. They reveal a system with three components consistently activated during both implicit and explicit mentalizing tasks: medial prefrontal cortex (MPFC), temporal poles and posterior superior temporal sulcus (STS). The functions of these components can be elucidated, to some extent, from their role in other tasks used in neuroimaging studies. Thus, the MPFC region is probably the basis of the decoupling mechanism that distinguishes mental state representations from physical state representations; the STS region is probably the basis of the detection of agency, and the temporal poles might be involved in access to social knowledge in the form of scripts. The activation of these components in concert appears to be critical to mentalizing.

A multiple case study was conducted in order to assess three leading theories of developmental dyslexia: (i) the phonological theory, (ii) the magnocellular (auditory and visual) theory and (iii) the cerebellar theory. Sixteen dyslexic and 16 control university students were administered a full battery of psychometric, phonological, auditory, visual and cerebellar tests. Individual data reveal that all 16 dyslexics suffer from a phonological deficit, 10 from an auditory deficit, four from a motor deficit and two from a visual magnocellular deficit. Results suggest that a phonological deficit can appear in the absence of any other sensory or motor disorder, and is sufficient to cause a literacy impairment, as demonstrated by five of the dyslexics. Auditory disorders, when present, aggravate the phonological deficit, hence the literacy impairment. However, auditory deficits cannot be characterized simply as rapid auditory processing problems, as would be predicted by the magnocellular theory. Nor are they restricted to speech. Contrary to the cerebellar theory, we find little support for the notion that motor impairments, when found, have a cerebellar origin or reflect an automaticity deficit. Overall, the present data support the phonological theory of dyslexia, while acknowledging the presence of additional sensory and motor disorders in certain individuals.