Kate Plaisted-Grant


Kate Plaisted-Grant received a BSc in Psychology in 1991 from the Department of Psychology, University College London and became a post-graduate student at King’s College. She was awarded a PhD from the Department of Experimental Psychology, University of Cambridge in 1994 and was awarded the New Investigator Award by the American Psychological Society for the research conducted for her PhD. After a Research Fellowship at St. John’s College, she took up her lectureship at the Department of Experimental Psychology, University of Cambridge in 1998. 

Kate is a Fellow of St John's College, Cambridge, where she is Director of Studies in Experimental Psychology and Evolution and Behaviour. She is also Associate Editor of the Quarterly Journal of Experimental Psychology. She is currently funded by a Career Establishment Award from the MRC.

AVA Annual Meeting 2008: Magnocellular Processing in Autism

Children and adults with autism show marked difficulties in processing social information. Many studies have revealed deficits in making inferences about other people’s intentions and mental states, often characterised in the literature as deficits in social cognition. They attend less to faces and show abnormal face scanning, focussing on the mouth rather than the eye region, abnormalities that are referred to as deficits in social perception. In addition, general sensory and perceptual abnormalities have been observed in autism since the time the disorder was first described and abnormal sensory and perceptual interests provide important information for diagnosis. Despite the importance of this feature of autism, rather less research has focussed on the possible underlying mechanisms compared to the social perceptual and social cognitive features. However, a recent interest of the possibility of a dorsal stream processing deficit has raised a debate about the integrity of the magnocellular system in autism. In contrast to studies of dyslexia, very few studies assessing magnocellular functioning have yet been conducted in autism. Those that have suggest that functioning of the magnocellular system is equivalent to that of typical children. However, like studies in dyslexia, these previous studies conducted in autism did not employ the optimal stimulus. I will present two of our recent studies both of which suggest that magnocellular processing is impaired in autism. These findings highlight the need to consider the role of abnormal perceptual mechanisms in the aetiology of the disorder and to broaden current theories of autism beyond the constructs of deficits in social perception and social cognition. I will present some ideas about the impact of early magnocellular dysfunction on the achievement of early social developmental milestones, which might lead to the characteristic pattern of deficits in social perception and social cognition seen in autism.


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