1. Refrigerator mothers and beyond….. The aetiology of autism Cognition and neuroscience

2. Main behavioural featuresMain cognitive (psychological) constructs Social cognition and social perceptionAtypical social interaction and social communication Gaze and eye contact, emotion perception, face processing, affective empathy and sympathy, pretend play, theory of mind, social motivation Executive functionRepetitive and stereotyped behaviour; atypical social interaction and social communication Cognitive flexibility, planning, attention shifting, working memory Bottom-up and top-down (local vs global) information processing Excellent attention to detail, restricted interests, repetitive behaviour, atypical social interaction and social communication Superior low-level sensory-perceptual processing, central coherence, systemising

3. In the mid-20th century, autism was thought to originate from the emotional coldness of the child’s mother (Refrigerator mothers) even though this hypothesis had no empirical support. By contrast, concurrent neurobiological hypotheses and Kanner’s proposal of an “innate inability to form the usual, biologically provided affective contact with people” have received scientific support. Cognition and neurobiology are related, and their development is characterised by a complex interplay between innate and environmental factors

4. Mentalising Since impaired theory of mind was specifically reported in children with autism in 1985, difficulties with mentalising—ie, understanding of mental states in both self and others—are believed to be core to social- communication deficits. Studies have confirmed that development is atypical not only for the behavioural expressions of mentalising, but also for their developmental precursors in social interaction (eg, joint attention and pretend play) and social perception (eg, eye contact, emotion perception, action–perception mirroring, social orienting, biological motion processing, and face processing).

5. Although many (high-functioning) individuals with autism achieve some degree of explicit or controlled mentalising, the implicit, automatic, and intuitive components are still impaired, even in adulthood. Early-onset mentalising difficulties seem to be specific to autism, but late-onset deficits are reported in disorders such as schizophrenia. Mentalising is closely entwined with executive control and language. Also, deficits in the social domain are not only about difficulties in the processing of information about other people, but also about processing of self-referential information, the relationship that self has in a social context.

6. Differences in social tasks People with autism often have trouble in social situations They may learn clever ways to compensate for this Neurotypicals look at the eyes Autistic people look at the mouth

7. Executive dysfunction Executive functioning is the ability to control action (creating plans, shifting attention) and is linked to the prefrontal lobe cortex. Autistic people may have executive dysfunction due to the fact that developmentally the frontal lobes have matured in a atypical way. This explains repetitive behaviour (inability to plan or shift attention) and narrow interests and obsessions Executive dysfunction hypothesis: autism results mainly from deficits in working memory, planning, inhibition, and other executive functions. Executive processes such as voluntary eye movements slowly improve in time but do not reach typical adult levels. Predicts stereotyped behaviour and narrow interests.

8. Weak central coherence Autistic people have problems integrating information to make a coherent, global picture. They focus on the small, local details in a scene. It explains their attention to detail and their memory for detail. Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people. This theory maps well from the under connectivity theory of autism

9. Frith (1989) suggested that a weak drive for coherence may be relevant to understanding aspects of autism. The theory is based on an understanding of how information processing typically occurs in most people. In their interactions with the environment, or in recalling information most individuals will recall an overall impression or the gist of something e.g. a story or a conversation. Individuals on the autism spectrum tend to be more, sometimes overly focused on details; this can often be at the expense of understanding the actual meaning or appreciating the nature of a situation or context. The basis of this theory is that this detailed processing is suggestive of weak central coherence (Roth, 2010).

10. Processing information Individuals with autism often have a preference for, and superiority in, processing of local rather than global sensory-perceptual features. Individuals without autism often show the opposite profile. This difference could explain the excellent attention to detail, enhanced sensory-perceptual processing and discrimination, and idiosyncratic sensory responsivity (ie, hyper-reactivity or hyporeactivity to sensory input or unusual interest in sensory features of the environment) in autism. It could also contribute to the exceptional abilities disproportionately recorded in individuals with autism. Additionally, top-down information processing in individuals with autism is often characterised by reduced recognition of the global context, and a strong preference to derive rule-based systems.

11. Mirror Neuron System The mirror neuron system is a set of brain regions which respond when you: perform an action see someone else acting imitate an action understand an action

12. Mirror Neuron Theory Some researchers suggest that the mirror system is essential for social interaction. Mirror systems let us imitate they may contribute to language and empathy and other social skills Parietal areas of the brain: social learning and social interaction in autism. This network of brain areas is often referred to as the ‘mirror neuron network’ and some have suggested a lack of sensitivity of this network in those with autism Atypical function of the mirror neuron network may have important implications in understanding various features of autism, including difficulties with empathy, difficulties in the development of language through imitation, and perhaps the prevalence of hyper and hypo sensory sensitivities.

13. Reduced Functional Connectivity Minshew model of autism: complex information processing disorder, connectivity/disconnectivity/under connectivity disorder, a disorder of cortical development, a neuronal organization disorder, intact or enhanced simple information processing, but poor complex/higher order processing. fMRI and EEG studies suggest that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex. Underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.

14. So… The Autistic Brain is "Differently Wired" What all of the brain findings have in common is that they point to autism as a disorder of the cortex. The cortex is the proverbial "grey matter": the part of the brain which is largely responsible for higher brain functions, including sensation, voluntary muscle movement, thought, reasoning, and memory. In many autistic people, the brain develops too quickly beginning at about 12 months. By age ten, their brains are at a normal size, but "wired" atypically. With autism there's accelerated growth at the wrong time, and that creates havoc. The consequences, in terms of disturbing early development, include problems within the cortex and from the cortex to other regions of the cortex in ways that compromise language and reasoning abilities.

15. The Down and upside of Unique Wiring Autism really impacts on behavioural function in the brain very broadly. It effects sensory, motor, memory, and postural control. The symptoms are most prominent in social interaction and problem solving because they require highest degree of interaction. While social and communication skills may be compromised by unique wiring in the brain, other abilities are actually enhanced. Autistic people have a really stellar ability to use the visual parts of the right side of the brain to compensate for problems with language processing. This may be the basis for detail-orientated processing -- and may be a decided advantage!

16. BMC Medicine 27.02.13 BMC Medicine 27.02.13 A look at how the brain processes information finds a distinct pattern in children with autism spectrum disorders. Using EEGs to track the brain's electrical cross-talk, researchers from Boston Children's Hospital have found a structural difference in brain connections. Compared with neurotypical children, those with autism have multiple redundant connections between neighbouring brain areas at the expense of long distance links. They examined brain networks as a whole in terms of their capacity to transfer and process information,“ There were more short- range connections within different brain region, but fewer connections linking far-flung areas. A brain network that favours short-range over long-range connections seems to be consistent with autism's classic cognitive profile—a child who excels at specific, focused tasks like memorising streets, but who cannot integrate information across different brain area into higher-order concepts.

17. BMC Medicine 27.02.13 For example, a child with autism may not understand why a face looks really angry, because his visual brain centres and emotional brain centres have less cross-talk. The brain cannot integrate these areas. It's doing a lot with the information locally, but it's not sending it out to the rest of the brain. It's a simpler, less specialized network that's more rigid, less able to respond to stimulation from the environment. Those who also had autism had the pattern of increased short-range versus long-range connections.

18. Role of immune system Interaction between the immune and the nervous systems is substantial throughout life. Frequency of immunological anomalies is increased in individuals with autism and their families. In autism, altered immune processes affect a wide array of neurodevelopmental processes (eg, neurogenesis, proliferation, apoptosis, synaptogenesis, and synaptic pruning), with persistent active neuro inflammation, increased concentrations of pro-inflammatory cytokines in serum and cerebrospinal fluid, and altered cellular immune functions. Neuro immune mechanisms could have key roles also.

19. References Bauman, M., & Kemper, T. L. (1985). Histoanatomic observations of the brain in early infantile autism. Neurology, 35, 866-874. Bauman, M., & Kemper, T. L. (1988). Limbic and cerebellar abnormalities: Consistent findings in infantile autism. Journal of Neuropathology and Experimental Neurology, 47, 369. Bennetto, L., Pennington, B. F., & Rogers, S. J. (1996). Intact and impaired memory functions in autism. Child Development, 67, 1816-1835. Boucher, J. (1977). Alternation and sequencing behavior and the response to novelty in autistic children. Journal of Child Psychology & Psychiatry, 18, 67-72. Boucher, J. (1988). Word fluency in high-functioning autistic children. Journal of Autism and Developmental Disorders, 18, 637-645. Courchesne, E., Yeung-Courchesne, R., Press, G. A., Hesselink, J. R., & Jernigan, T. L. (1988). Hypoplasia of cerebellar vermal lobule-Vi and lobule-Vii in autism. New England Journal of Medicine, 318, 1349-1354. Dawson, G., Klinger, L. G., Panagiotides, H., & Lewy, A. (1993). Electrophysiological evidence for frontal lobe involvement in the social impairments of individuals with autism. Paper presented at biennial meeting for SRCD, New Orleans, LA, 25-28 March. Frith, U. (1972) Cognitive mechanisms in autism: experiments with color and tone sequence production. Journal of Autism and Child Schizophrenia, 2, 160-173. Gaffney, G. R., Kuperman, S., Tsai, L. Y., & Minchin, S. (1989). Forebrain structure in autism. Journal of the American Academy of Child and Adolescent Psychiatry, 28, 534-537. George, M. S., Costa, D. C., Kouris, K., Ring, H. A., & Ell, P. J. (1992). Cerebral blood flow abnormalities in adults with infantile autism. Journal of Nervous & Mental Disease, 180, 413-417.

20. Guerts, H. M., Verté, S., Oosterlaan, J., Roeyers, H., & Sergeant, J. A. (2004). How specific are executive functioning deficits in attention deficit hyperactivity disorder and autism? Journal of Child Psychology and Psychiatry, 45, 836-854. Hetzler, B. E., & Griffiin, J. L. (1981). Infantile autism and the temporal lobe of the brain. Journal of Autism and Developmental Disorders, 11, 317-330. Hill, E. L. (2004). Executive dysfunction in autism. Trends in Cognitive Sciences, 8, 26-32. Hill, E. L. (2004). Evaluating the theory of executive dysfunction in autism. Developmental Review, 24, 189-233. Horwitz, B., Rumsey, J. M., Grady, C. L., & Rapoport, S. I. (1988). The cerebral metabolic landscape in autism: Intercorrelations of regional glucose utilization. Archives of Neurology, 45, 749-755. Hughes, C. (1998). Finding your marbles: Does preschoolers’ strategic behavior predict later understanding of mind? Developmental Psychology, 34, 1326-1339. Hughes, C., & Russell, J. (1993). Autistic children’s difficulty with mental disengagement from an object: Its implications for theories of autism. Developmental Psychology, 29, 498-510. Hughes, C. et al. (1997). Executive function in parents of children with autism. Psychological Medicine, 27, 209-220. Jarrold, C., Boucher, J., & Smith, P. K. (1996). Generativity deficits in pretend play in autism. British Journal of Developmental Psychology, 14, 275-300. Koegel, R. L., & Schreibman, L. (1977). Teaching autistic children to respond to simultaneous multiple cues. Journal of Experimental Child Psychology, 24, 299-311. Koshino, H., Carpenter, P. A., Minshew, N. J., Cherassky, V. L., Keller, T. A., & Just, M. A. (2005). Functional connectivity in an fMRI working memory task with high-functioning autism. Neuroimage, 24, 810-821. Lewis, V., & Boucher, J. (1991). Skill, content and generative strategies in autistic children’s drawings. British Journal of Developmental Psychology, 9, 393-416.

21. Lovaas, O. I., Koegel, R. L., & Schreibman, L. (1979). Stimulus overselectivity in autism: A review of research. Psychological Bulletin, 86, 1236-1254. Luna, B. et al. (2002). Neocortical system abnormalities in autism. An fMRI study of spatial working memory. Neurology, 59, 834-840. Minshew, N. J., Goldstein, G., Muenz, L. R., & Payton, L. R. (1992). Neuropsychological functioning in nonmentally retarded autistic individuals. Journal of Clinical and Experimental Neuropsychology, 14, 749-761. Ohnishi, T. et al. (2000). Abnormal regional cerebral blood flow in childhood autism. Brain, 123, 1838-1844. Ozonoff, S. (1997). Components of executive function in autism and other disorders. In J. Russell (ed.). Autism as an Executive Disorder. Oxford: OUP. Ozonoff, S., Pennington, B. F., & Rogers, S. J. (1991). Executive function deficits in high-functioning autistic individuals: Relationship to theory of mind. Journal of Child Psychology and Psychiatry, 32, 1081-1105. Pennington, B. F., & Ozonoff, S. (1996). Executive functions and developmental psychopathology. Journal of Child Psychology and Psychiatry, 37, 51-87. Perner, J. (1998). The meta-intentional nature of executive functions and theory of mind. In P. Carruthers & J. Boucher (eds.). Language and thought: Interdisciplinary themes. Cambridge: Cambridge University Press. Prior, M. R., & Hoffman, W. (1990). Brief report: Neuropsychological testing of autistic children through an exploration with frontal lobe tests. Journal of Autism and Developmental Disorders, 20, 581-590. Salmond, C. H. et al. (2003). Investigating individual differences in brain abnormalities in autism. Philosophical Transactions of the Royal Society of London, B, 358, 405-413. Zilbovicius, M., Garreau, B., Samson, Y., Remy, P., Barthelemy, C., Syrota, A., & Lelord, G. (1995). Delayed maturation of the frontal cortex in childhood autism. American Journal of Psychiatry, 152, 248-252.