Biological evidence suggests that autism begins at the synapse - but where does it go from there? How does this abnormal neural substrate interact with normal developmental programmes and gradients to magnify initial conditions into the emergent syndrome of autism, and how might this interaction be therapeutically interfered with? Clues can be gleaned not only from people with autism spectrum conditions but also their clinically unaffected family members - people who share genetic susceptibility but who have escaped the full syndrome. Functional imaging suggests that local perturbations of neural function, especially in prefrontal cortices, are in many instances shared by these "unaffected" relatives and may be permissive but not determinative of autism, whereas long-range functional disconnections between widely separated brain regions are more characteristic of autism per se. These observations lead to a model in which perturbations of local neural connectivity decrease local network entropy, propagating an abnormality from the level of single synapses to the level of local computational networks. Because development of long-range connections depends in part on correlated activities within the regions being connected, this decreased entropy can further propagate the perturbation from local to long-distance networks. The endpoint is a brain that operates more as a collection of autonomous subprocessors than as a top-down coordinated and controlled network. Every individual, autistic or not, evolves a cognitive style that makes most effective use of the brain that they have. In the case of this autistic, disconnected brain, that cognitive style is a low-construal mode of iconic-over-symbolic, detail-over-gestalt, egocentric-over-allocentric perception, cognition, and action, in which only one process at a time can maintain access to the central executive, conscious attention is usurped by whichever is the most salient exogenous stimulus or endogenous cognitive process, and the everyday simultaneities of seeing and hearing, looking and thinking, thinking and speaking, or self-representation and other-representation become nearly impossible. Key to therapeutic strategies is to work with this cognitive style rather than against it, by matching a student's preferred input modality and by making communicative and educational content spatially and temporally coincident with the most physically salient, attention-capturing stimulus in the environment.