By conceiving of autism and psychosis as diametrically opposite phenotypes of underactive and overactive mentalizing, respectively, Crespi & Badcock (C&B) commit themselves to a continuum view of intercorrelated mentalizing functions. This view fails to acknowledge dissociations between mentalizing functions and that psychotic people show a mixture of both hypo- and hyper-mentalizing.

Williams syndrome is a rare genetic disorder in which, it is claimed, language abilities are relatively strong despite mild to moderate mental retardation. Such claims have, in turn, been interpreted as evidence either for modular preservation of language or for atypical constraints on cognitive development. However, this review demonstrates that there is, in fact, little evidence that syntax, morphology, phonology, or pragmatics are any better than predicted by nonverbal ability, although performance on receptive vocabulary tests is relatively good. Similarly, claims of an imbalance between good phonology and impaired or atypical lexical semantics are without strong support. There is, nevertheless, consistent evidence for specific deficits in spatial language that mirror difficulties in nonverbal spatial cognition, as well as some tentative evidence that early language acquisition proceeds atypically. Implications for modular and neuroconstructivist accounts of language development are discussed.The preparation of this paper was supported by the Williams Syndrome Foundation (United Kingdom) and the Medical Research Council. I thank Courtenay Norbury and Kate Nation for comments on the manuscript and Chris Jarrold, Jill Boucher, and Teresa McCormack for many useful discussions.

Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication.