Magno- and Parvocellular Contrast Responses in Varying Degrees of Autistic Trait.

Abstract

Autistic tendency has been associated with altered visual perception, especially impaired visual motion sensitivity and global/local integration, as well as enhanced visual search and local shape recognition. However, the neurophysiological mechanisms underlying these abnormalities remain poorly defined. The current study recruited 29 young adults displaying low, middle or high autistic trait as measured by Baron-Cohen's Autism spectrum Quotient (AQ), and measured motion coherence thresholds psychophysically, with manipulation of dot lifetime and stimulus contrast, as well as nonlinear cortical visual evoked potentials (VEPs) over a range of temporal luminance contrast levels from 10% to 95%. Contrast response functions extracted from the major first order and second order Wiener kernel peaks of the VEPs showed consistent variation with AQ group, and Naka-Rushton fits enabled contrast gain and semi-saturation contrasts to be elicited for each peak. A short latency second order response (previously associated with magnocellular processing) with high contrast gain and a saturating contrast response function showed higher amplitude for the High AQ (compared with Mid and Low groups) indicating poorer neural recovery after rapid stimulation. A non-linearity evoked at longer interaction times (previously associated with parvocellular processing) with no evidence of contrast saturation and lower contrast gain showed no difference between autism quotient groups across the full range of stimulus contrasts. In addition, the short latency first order response and a small, early second order second slice response showed gain and semi-saturation parameters indicative of magnocellular origin, while the longer latency first order response probably reflects a mixture of inputs (including feedback from higher cortical areas). Significant motion coherence (AQ group) * (dot lifetime) interactions with higher coherence threshold for limited dot lifetime stimuli is consistent with atypical magnocellular functioning, however psychophysical performance for those with High AQ is not explained fully, suggesting that other factors may be involved.