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The 'broken-mirror' theory of autism argues that dysfunction of the 'mirror neuron system' is a root cause of social disability in autism. The present paper aims to scrutinize this theory and, when it breaks down, to provide an alternative. Current evidence suggests that children with autism are able to understand and emulate goal-directed actions, but may have specific impairments in automatic mimicry of actions without goals. These data are not compatible with the broken-mirror theory, but can be accounted for by a new model called EP-M. The EP-M model segments the mirror neuron system into an indirect, parietal route for goal emulation and planning (EP) and a direct occipital-frontal route for mimicry (M). This fractionation is consistent with neuroimaging and behavioural studies of the mirror neuron system in typical children and adults. I suggest that top-down modulation of the direct M route may be dysfunctional in individuals with autism, leading to abnormal behaviours on mimicry tasks as well as other social disabilities.

Evidence is reviewed suggesting that, in the general population, empathizing and systemizing show strong sex differences. The function of systemizing is to predict lawful events, including lawful change, or patterns in data. Also reviewed is the evidence that individuals on the autistic spectrum have degrees of empathizing difficulties alongside hypersystemizing. The hypersystemizing theory of autism spectrum conditions (ASC) proposes that people with ASC have an unusually strong drive to systemize. This can explain their preference for systems that change in highly lawful or predictable ways; why they become disabled when faced with systems characterized by less lawful change; and their 'need for sameness' or 'resistance to change'. If 'truth' is defined as lawful patterns in data then, according to the hypersystemizing theory, people with ASC are strongly driven to discover the 'truth'.

Uta Frith has made a major contribution to our understanding of developmental disorders, especially autism and dyslexia. She has studied the cognitive and neurobiological bases of both disorders and demonstrated distinctive impairments in social cognition and central coherence in autism, and in phonological processing in dyslexia. In this enterprise she has encouraged psychologists to work in a theoretical framework that distinguishes between observed behaviour and the underlying cognitive and neurobiological processes that mediate that behaviour.