Abstract

Saccadic suppression—the reduction of visual sensitivity during rapid eye movements—has previously been proposed to reflect a specific suppression of the magnocellular visual system, with the initial neural site of that suppression at or prior to afferent visual information reaching striate cortex. Dysfunction in the magnocellular visual pathway has also been associated with perceptual and physiological anomalies in individuals with autism spectrum disorder or high autistic tendency, leading us to question whether saccadic suppression is altered in the broader autism phenotype. Here we show that individuals with high autistic tendency show greater saccadic suppression of low versus high spatial frequency gratings while those with low autistic tendency do not. In addition, those with high but not low autism spectrum quotient (AQ) demonstrated pre-cortical (35–45 ms) evoked potential differences (saccade versus fixation) to a large, low contrast, pseudo-randomly flashing bar. Both AQ groups showed similar differential visual evoked potential effects in later epochs (80–160 ms) at high contrast. Thus, the magnocellular theory of saccadic suppression appears untenable as a general description for the typically developing population. Our results also suggest that the bias towards local perceptual style reported in autism may be due to selective suppression of low spatial frequency information accompanying every saccadic eye movement.

Highlights

  • Deficits in magnocellular/dorsal stream processing have been proposed as an explanation for perceptual abnormalities in autism [9,10,11,12,13,14]

  • Findings of impaired magnocellular function in high autistic tendency raise the question of what differences in saccadic suppression of magnocellular function we would expect to find between high autism spectrum quotient (AQ) and low AQ groups

  • We predicted that saccadic suppression of the M-pathway would be greater in those 3 with high AQ than in those with lower autistic tendency, given the literature outlined above, describing a weakness or deficit in magnocellular processing in those with high autistic tendency

Read more

Summary

Introduction

Deficits in magnocellular/dorsal stream processing have been proposed as an explanation for perceptual abnormalities in autism [9,10,11,12,13,14]. Apart from the known alteration in VEP waveforms in the secondorder response associated with magnocellular processing in those with high AQ, we would observe both short and long latency VEP differences under saccade compared with fixation conditions for those with high AQ scores compared with those with low AQ. Any such differences would be expected to reflect magnocellular contributions to afferent input for cortical processing, and to top-down facilitation [35] of recognition and perception

Objectives
Methods
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call