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The 21st century has seen dramatic changes in our understanding of the visual physio-perceptual anomalies of autism and also in the structure and development of the primate visual system. This review covers the past 20 years of research into motion perceptual/dorsal stream anomalies in autism, as well as new understanding of the development of primate vision. The convergence of this literature allows a novel developmental hypothesis to explain the physiological and perceptual differences of the broad autistic spectrum. Central to these observations is the development of motion areas MT+, the seat of the dorsal cortical stream, central area of pre-attentional processing as well as being an anchor of binocular vision for 3D action. Such development normally occurs via a transfer of thalamic drive from the inferior pulvinar → MT to the anatomically stronger but later-developing LGN → V1 → MT connection. We propose that autistic variation arises from a slowing in the normal developmental attenuation of the pulvinar → MT pathway. We suggest that this is caused by a hyperactive amygdala → thalamic reticular nucleus circuit increasing activity in the PIm → MT via response gain modulation of the pulvinar and hence altering synaptic competition in area MT. We explore the probable timing of transfer in dominance of human MT from pulvinar to LGN/V1 driving circuitry and discuss the implications of the main hypothesis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Spiteri and Crewther.)

The magnocellular system has been implicated in the rapid processing of facial emotions, such as fear. Of the various anatomical possibilities, the retino-colliculo-pulvinar route to the amygdala is currently favored. However, it is not clear whether and when amygdala arousal activates the primary visual cortex (V1). Non-linear visual evoked potentials provide a well-accepted technique for examining temporal processing in the magnocellular and parvocellular pathways in the visual cortex. Here, we investigated the relationship between facial emotion processing and the separable magnocellular (K2.1) and parvocellular (K2.2) components of the second-order non-linear multifocal visual evoked potential responses recorded from the occipital scalp (O Z ). Stimuli comprised pseudorandom brightening/darkening of fearful, happy, neutral faces (or no face) with surround patches decorrelated from the central face-bearing patch. For the central patch, the spatial contrast of the faces was 30% while the modulation of the per-pixel brightening/darkening was uniformly 10% or 70%. From 14 neurotypical young adults, we found a significant interaction between emotion and contrast in the magnocellularly driven K2.1 peak amplitudes, with greater K2.1 amplitudes for fearful (vs. happy) faces at 70% temporal contrast condition. Taken together, our findings suggest that facial emotional information is present in early V1 processing as conveyed by the M pathway, and more activated for fearful as opposed to happy and neutral faces. An explanation is offered in terms of the contest between feedback and response gain modulation models., (Copyright © 2020 Mu and Crewther.)

As the visual system ages, flicker sensitivity decreases and the latencies of cortical visual evoked potentials (VEP) increase. However, the extent to which these effects reflect age-related changes in the magnocellular (M) and or parvocellular (P) pathways remain unclear. Here, we investigated the relation between flicker fusion frequencies and VEP non-linearities induced by rapid stimulation, as a function of age over 6 decades. The approach, using Wiener kernel analysis of multifocal flash (mf)VEP, allows the extraction of signatures of both M and P processing and hence establishing a neural basis of the known decline in flicker fusion threshold. We predicted that, in a sample of 86 participants, age would be associated with a latency increase in early mfVEP response components and that flicker fusion thresholds, for both low and high contrast stimuli, would relate to the temporal efficiency of the M-generated VEP component amplitudes. As expected, flicker fusion frequency reduced with age, while latencies of early second order peaks of the mfVEP increased with age, but M temporal efficiency (amplitude ratio of first to second order peaks) was not strongly age-related. The steepest increases in latency were associated with the M dominated K2.1 (second order first slice) N70 components recorded at low and high contrast (6.7 and 5.9 ms/decade, respectively). Interestingly, significant age-related latency shifts were not observed in the first order responses. Significant decreases in amplitude were found in multiple first and second order components up to 30 years of age, after which they remained relatively constant. Thus, aging and decline in visual function appears to be most closely related to the response latencies of non-linearities generated by the M pathway.

Low spatial frequency (LSF) visual information is extracted rapidly from fearful faces, suggesting magnocellular involvement. Autistic phenotypes demonstrate altered magnocellular processing, which we propose contributes to a decreased P100 evoked response to LSF fearful faces. Here, we investigated whether rapid processing of fearful facial expressions differs for groups of neurotypical adults with low and high scores on the Autistic Spectrum Quotient (AQ). We created hybrid face stimuli with low and high spatial frequency filtered, fearful, and neutral expressions. Fearful faces produced higher amplitude P100 responses than neutral faces in the low AQ group, particularly when the hybrid face contained a LSF fearful expression. By contrast, there was no effect of fearful expression on P100 amplitude in the high AQ group. Consistent with evidence linking magnocellular differences with autistic personality traits, our non-linear VEP results showed that the high AQ group had higher amplitude K2.1 responses than the low AQ group, which is indicative of less efficient magnocellular recovery. Our results suggest that magnocellular LSF processing of a human face may be the initial visual cue used to rapidly and automatically detect fear, but that this cue functions atypically in those with high autistic tendency.