Abstract
Functional and neurobiological models of face perception posit separate pathways for identity and expression processing. Consistent with these models, in acquired prosopagnosia where a localized brain lesion leads to severe face recognition impairments, expression perception is often spared. On the other hand, in autism spectrum disorder (ASD) both identity and expression perception is affected. This presents an apparent contradiction: it seems unlikely for pathophysiological changes in ASD to simultaneously impact both identity and expression pathways. A resolution is offered by the social motivation hypothesis, which argues that a lack of interest in social interaction limits exposure to faces. Indeed, a front-end constraint on visual input would stunt the development of a range of processes, including identification and expression recognition. This leads to the prediction that performance in identity and expression tasks should be related in ASD but independent in typical observers. In a recent study (Oruc, Shafai & Iarocci, 2018) we tested adults with and without ASD (Ns=34) in psychophysical tasks of identity and expression perception and assessed their social motivation. Participants with ASD showed significantly diminished identity and expression perception, and social motivation compared to the control group. Importantly, identification and expression performance was significantly correlated in the ASD group but not in the control group. Social motivation was correlated with face ability only in the low-social-motivation group. These results provide support for the social motivation hypothesis and suggest that face deficits in ASD likely stem from a bottleneck in the quality and quantity of visual exposure to faces.