Neural Mechanisms of Visual Motion Anomalies in Autism: A Two-Decade Update and Novel Aetiology

Spiteri, Samuel; Crewther, David P. · 2021 · OpenAlex-citations

DOI: 10.3389/fnins.2021.756841

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Summary

This review synthesizes two decades of research on visual motion anomalies in autism spectrum disorder (ASD), proposing a novel developmental hypothesis to explain dorsal stream vulnerabilities. The authors address the persistent gap in understanding the fundamental causes of ASD, noting that while sensory hypo- and hyper-reactivity affects over 90% of autistic individuals, effective treatments remain elusive. The paper integrates historical cognitive theories, such as weak central coherence and enhanced perceptual function, with recent advances in primate neuroanatomy and non-linear visual evoked potential (VEP) analysis to identify specific neural mechanisms underlying these perceptual differences. The authors analyze literature on primate visual development, particularly studies using marmosets, which reveal that the dorsal stream (motion processing) develops earlier than the ventral stream (object recognition). Crucially, they highlight a developmental shift in thalamic drive to area MT+ (motion area). In typical development, early robust connections from the inferior pulvinar to MT are pruned and replaced by stronger, later-developing connections from the lateral geniculate nucleus (LGN) via primary visual cortex (V1). The review also examines human data using Wiener kernel analysis of VEPs, which isolates magnocellular (M) and parvocellular (P) pathway responses. This method allows for the assessment of neural efficiency and temporal dynamics in both neurotypical and autistic populations. The central finding is a proposed aetiology where autistic variation arises from a failure to attenuate the early pulvinar-to-MT pathway. The authors hypothesize that a hyperactive amygdala-to-thalamic reticular nucleus circuit increases activity in the inferior pulvinar via response gain modulation. This heightened activity alters synaptic competition in area MT, preventing the normal takeover by the LGN-V1-MT circuit. Evidence supporting this includes non-linear VEP studies showing that individuals with high autistic traits exhibit significantly higher amplitude second-order kernel responses (K2.1), indicative of impaired neural efficiency in the M-pathway. These abnormalities are localized to early cortical stages, likely in MT+ or V1, rather than higher-order areas like the posterior superior temporal sulcus. The significance of this work lies in redefining the site of initial dysfunction in autism from higher-order social processing areas to early visual cortical mechanisms. By linking amygdala-driven emotional attention circuits to visual pathway development, the authors provide a physiological basis for the dorsal stream vulnerability observed in ASD. This model suggests that sensory anomalies are not merely secondary symptoms but are rooted in specific developmental disruptions of thalamocortical connectivity, offering new targets for understanding the neurobiology of autism.

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• peripheral attention