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

自闭症视觉运动异常的神经机制:二十年最新进展及新的病因学

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Abstract

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.

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