Magnocellular visual evoked potential delay with high autism spectrum quotient yields a neural mechanism for altered perception.
Everyone has autistic characteristics to a greater or lesser degree, encapsulated in the Autism Spectrum Quotient, a scale that measures the degree to which an adult of normal intelligence displays traits associated with autism spectrum disorders. Recent psychophysical analyses of autism spectrum disorders point to superior local processing, and impaired or ignored global and contextual processing. The aim of this study was to test whether low- and high-scoring individuals on the Autism Spectrum Quotient differ on a measure of local and global processing, motion processing and visual pathway integrity. Fifteen low-scoring individuals and 14 high-scoring individuals derived from a normal population participated in the study. The results indicate that the initial cortical response to the magnocellular afferents is weaker at low contrast in the high autistic tendency group and that a second-order response, reflecting magnocellular activity, demonstrated a delay for high versus low scorers when the parvocellular pathway was also active in response to a high contrast stimulus. High-scoring individuals also demonstrated difficulty in identifying the global components of locally salient hierarchical Navon figures. Furthermore, cross-validated discriminant analysis, using four physiologically and three psychophysically derived parameters, correctly classified 83% of individuals who scored either high or low on the Autism Spectrum Quotient. These findings in the group scoring high on the Autism Spectrum Quotient indicate that a delay in primary visual/prestriate cortical processing of magnocellular input diminishes the advantage of its early arrival to primary visual cortex. This appears to be associated with impaired global visual perception, predicting with high accuracy behavioural tendencies associated with autism spectrum disorders. It has been proposed that perceptual impairment in autism may be attributed to a dysfunction of horizontal connections within early visual areas, presumably parvocellular in nature. However, the timing of such form processing aberrations is much later than the timing of abnormal magnocellular visual processing measured directly here. Thus it is proposed that a magnocellular processing delay decreases the ability of autistic individuals to benefit perceptually from feedback normally associated with the magnocellular advantage.
Brain Sciences Institute, Swinburne University of Technology, Melbourne 3122, Australia.
Alexandra
A
Sutherland
David P
DP
Crewther
D000328:Adult; D001321:Autistic Disorder / Q000175:diagnosis / Q000503:physiopathology; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000175:diagnosis* / Q000503:physiopathology*; D005074:Evoked Potentials, Visual / Q000502:physiology*; D006801:Humans; D009039:Motion Perception / Q000502:physiology*; D010775:Photic Stimulation / Q000379:methods; D011597:Psychomotor Performance / Q000502:physiology; D011930:Reaction Time / Q000502:physiology*; D014793:Visual Cortex / Q000502:physiology*; D014796:Visual Perception / Q000502:physiology