What brain mechanisms underlie autism and how do they give rise to autistic behavioral symptoms? This article describes a neural model, called the iSTART model, which proposes how cognitive, emotional, timing, and motor processes that involve brain regions like prefrontal and temporal cortex, amygdala, hippocampus, and cerebellum may interact together to create and perpetuate autistic symptoms. These model processes were originally developed to explain data concerning how the brain controls normal behaviors. The iSTART model shows how autistic behavioral symptoms may arise from prescribed breakdowns in these brain processes, notably a combination of underaroused emotional depression in the amygdala and related affective brain regions, learning of hyperspecific recognition categories in temporal and prefrontal cortices, and breakdowns of adaptively timed attentional and motor circuits in the hippocampal system and cerebellum. The model clarifies how malfunctions in a subset of these mechanisms can, though a system-wide vicious circle of environmentally mediated feedback, cause and maintain problems with them all. ii

FMRI investigation of working memory for faces in autism: Visual coding and underconnectivity with frontal areas

connectivity

ABSTRACT: This article highlights the overlapping and converging goals and challenges of autism research and affective computing. We propose that a collaboration between autism research and affective computing could lead to several mutually beneficial outcomes—from developing new tools to assist people with autism in understanding and operating in the socioemotional world around them, to developing new computational models and theories that will enable technology to be modified to provide an overall better socioemotional experience to all people who use it. This article describes work toward this convergence at the MIT Media Lab, and anticipates new research that might arise from the interaction between research into autism, technology, and human socioemotional intelligence.

Past autism research has often been dedicated to tracing the causes of the disorder to a localized neurological abnormality, a single functional network, or a single cognitive-behavioral domain. In this review, I argue that autism is a ‘‘distributed disorder’ ’ on various levels of study (genetic, neuroanatomical, neurofunctional, behavioral). ‘‘Localizing’’ models are therefore not promising. The large array of potential genetic risk factors suggests that multiple (or all) emerging functional brain networks are affected during early development. This is supported by widespread growth abnormalities throughout the brain. Interactions during development between affected functional networks and atypical experiential effects (associated with atypical behavior) in children with autism further complicate the neurological bases of the disorder, resulting in an ‘‘exponentially distributed’ ’ profile. Promising approaches to a better characterization of neural endophenotypes in autism are provided by techniques investigating white matter and connectivity, such as MR spectroscopy, diffusion-tensor imaging (DTI), and functional connectivity MRI. According to a recent hypothesis, the autistic brain is generally characterized by ‘‘underconnectivity.’ ’ However, not all findings are consistent with this view. The concepts and methodology of functional connectivity need to be refined and results need to be corroborated by anatomical studies (such as DTI tractography) before definitive conclusions can be drawn.

Abstract: Neuropsychological theories have traditionally attempted to provide a unifying account of the complex and diverse behavioral manifestations of autism in terms of their underlying psychological mechanisms and associated brain bases. This article reviews three competing neuropsychological theories of autism: the executive dysfunction hypothesis, the weak central coherence hypothesis, and the limbic system hypothesis. Each theory is evaluated critically with regard to the primary neuropsychological deficit hypothesized and the research findings that have been offered in support of it. In a concluding section, some of the metatheoretical assumptions informing attempts to identify a “core ” neuropsychological impairment in autism are outlined and questioned, and new approaches to a neuropsychological understanding of autism are suggested.

and the Three Guineas Trust, during the period of this work. Part of this review is reprinted from Baron-Cohen et al (in press, Journal of Neurology and Neurosurgery). 1 Autism is diagnosed when a child or adult has abnormalities in a ‘triad ’ of behavioural domains: social development, communication, and repetitive behaviour/obsessive interests (APA, 1994; ICD-10, 1994). Autism can occur at any point on the IQ continuum, and IQ is a strong predictor of outcome (Rutter, 1978). Autism is also invariably accompanied by language delay (no single words before 2 years old). Asperger Syndrome (AS) (Asperger, 1944) is a subgroup on the autistic spectrum. People with AS share many of the same features as are seen in autism, but with no history of language delay and where IQ is in the average range or above. The main cognitive theories of autism are summarised next: Cognitive theories a. The Mindblindness theory The mindblindness theory of autism (Baron-Cohen, 1995) proposed that in autism

Enhanced and diminished visuo-spatial information processing in autism depends on stimulus complexity

Acknowledgements: SBC, JH, and RG were supported by the MRC during the period of this work. SW was supported by the McDonnell-Pew Trust. JL was supported by the Isaac Newton Trust. We are also grateful for support from the Shirley Foundation. Parts

Since Autism was first outlined (Kanner, 1943), an agreed-upon definition of Autism has been reached and standardized diagnostic methods produced. To date, however, no clear etiology has been established, and proposed treatments vary widely. Research has uncovered enough about Autism’s underlying neuroand cognitive psychology to allow us to outline treatment implications to benefit those families seeking help now who are unwilling to wait for the elusive ultimate answer. The Autism Treatment Center of America ™ has been using The Son-Rise Program ® (SRP) with families since 1983 in order to fulfill this need. The SRP was developed by parents experimenting with ways to reach their severely autistic child (Kaufman, 1976). Science at this time offered no guidance on facilitating the social development of children with Autism. Since their son emerged from Autism after 3 _ years of intensive work, the Kaufmans have offered SRP to families internationally. To date, no rigorous longitudinal testing of the efficacy of SRP has been performed yet it can be seen that the key principles of this approach draw