Abstract
Autistic perceptual differences can be explained in terms of dysfunction of the magnocellular visual pathway [1]. Superior search ability across multiple saccades in autistic individuals suggests that saccadic suppression may be altered in high autistic tendency. In normal controls, suppression of vision during saccades affects predominantly the magnocellular system [2]. Thus we compared the relative contributions of the magnocellular and parvocellular systems during saccadic and fixation conditions in 10 young adults with high and 10 with low autistic tendency, selected from a normal population using Baron-Cohen’s autism spectrum quotient (AQ) test. Contrast thresholds for achromatic gratings of low or high spatial frequency (0.2 cpd, 2.0 cpd) presented either during the saccade or after a 100 ms delay were measured. Saccadic suppression was observed in for high but not low spatial frequency gratings in the High AQ group. However, suppression was observed for both spatial frequencies for the low AQ group. Nonlinear Visual Evoked Potentials (VEPs) were recorded using a horizontal rectangular (40° × 8°) stimulus pseudo-randomly flashing with temporal contrast of either 24% or 96% during eye fixations or during horizontal 20° saccades at a rate of 2 Hz. A reduction in the magnocellular derived positivity of the second order kernel response was observed at ∼100 ms under saccadic conditions, suggesting that impairment in magnocellular transient attention may be the underlying basis of saccadic suppression. An interaction between AQ, magnocellular physiology and saccade condition may help explain perceptual differences in autism.
[1] Sutherland, A, Crewther DP (2010). Magnocellular visual evoked potential delay with high autism spectrum quotient yields a neural mechanism for altered perception, Brain Res, 133, 2089-2097.
[2] Burr DC, Morrone MC, Ross J (1994). Selective suppression of the magnocellular visual pathway during saccadic eye movements. Nature, 371, 511-513.