Abnormal global processing along the magnocellular visual pathway in autism: a possible mechanism for weak visuospatial coherence?

Frith and Happé (1994) argue that individuals with autism exhibit ‘weak central coherence’: an inability to integrate elements of information into coherent wholes. Some authors have speculated that a higher-level impairment might be present in the magnocellular visual pathway in autism, and furthermore, that this might account for weak central coherence, at least at the visuospatial level. We assessed the integrity of the magnocellular pathway in children diagnosed with an autism spectrum disorder (ASD), and in typically developing children using two visual tasks, one assessing lower-level magnocellular functioning (Flicker Contrast Sensitivity; FCS), the other (Global Dot Motion; GDM) examining functioning at higher levels of the cortical stream fed by the magnocellular pathway. Central coherence was tested using the Children’s Embedded Figures Test (CEFT). Relative to the typically developing children, the children with ASD had shorter CEFT latencies and higher GDM thresholds but equivalent FCS thresholds. Additionally, CEFT latencies were inversely related to GDM thresholds in the ASD group. These outcomes suggest that the elevated global motion thresholds in autism are the result of higher-level impairments in the cortical regions receiving predominant input from the magnocellular pathway. Visuospatial impairments in autism may be in the form of abnormal cooperative mechanisms in extra-striate cortical areas, which might contribute to differential performance when processing stimuli as Gestalts, including both dynamic (i.e., global motion perception) and static (i.e., disembedding performance) stimuli.