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Functional Anatomy of Impaired Selective Attention and Compensatory Processing in Autism
Matthew Belmonte and Deborah Yurgelun-Todd
Cognitive Brain Research 17(3):651-664 (October 2003).
Abstract:
In autism, physiological indices of selective attention have been shown to be abnormal even in situations where behaviour is intact. This divergence between behaviour and physiology suggests the action of some compensatory process of attention, one which may hold clues to the aetiology of autism's characteristic cognitive phenotype. Six subjects with autism spectrum disorders and six normal control subjects were studied with fMRI while performing a bilateral visual spatial attention task. In normal subjects, the task evoked activation in a network of cortical regions including superior parietal lobe (p<0.001), left middle temporal gyrus (p=0.002), left inferior (p<0.001) and middle (p<0.02) frontal gyri, and medial frontal gyrus (p<0.02). Autistic subjects, in contrast, showed activation in bilateral ventral occipital cortex (p<0.03) and striate cortex (p<0.05). Within the task condition, a region-of-interest comparison of attend-left versus attend-right conditions indicated that modulation of activation in the autistic brain as a function of the lateral focus of spatial attention was abnormally decreased in left ventral occipital cortex (p<0.03), abnormally increased in left intraparietal sulcus (p<0.01), and abnormally variable in superior parietal lobe (p<0.03). These results are discussed in terms of a model of autism in which a pervasive defect of neural and synaptic development produces over-connected neural systems prone to noise and crosstalk, resulting in hyper-arousal and reduced selectivity. These low-level attentional traits may be the developmental basis for higher-order cognitive styles such as weak central coherence.
Theme: 100.000 DISORDERS OF THE NERVOUS SYSTEM
Topic: 100.007 Developmental disorders
Key words: autism, visual attention, arousal, fMRI, parietal, intraparietal sulcus
This work was supported by a grant from the National Alliance for Autism Research. In addition, a portion of the data analysis and writing was conducted while the first author was supported by a grant from Cure Autism Now. We thank Margaret Bauman, David Beversdorf, and Deborah Fein for subject referrals, David Beversdorf for sharing ADI-R scores of four of the subjects, and most of all our subjects for giving so much of their time.