Development and neural bases of face recognition in autism

Autism is a developmental disorder characterized by impairments in communication and social relationships, and a restricted range of activities. This disorder is associated with specific impairments in the processing of social and emotional information. The nature of these impairments in social processing suggests that autism involves dysfunction of brain regions responsible for early stage processing of social information. Here, we explore further the nature of early social processing impairments in autism, and discuss evidence that autism involves an early emerging impairment in face processing. We begin by discussing research on face recognition in autism. Next, we describe new data suggesting that this impairment is present early in children with autism. We then explore how a neural system for face recognition might emerge in normal development, and speculate on differences in the development of this system in autism. Studies of older children with autism have demonstrated impairments in face recognition. For example, Klin et al found that school aged children with autism performed worse on face recognition tests than developmentally disabled children without autism. Boucher and Lewis reported that children with autism performed worse on picture matching and recognition tasks than typically developing children. They found that children with autism were not impaired on similar tasks using pictures of buildings. Thus, face recognition impairments in autism do not appear to be the result of a general difficulty in visual discrimination. In a fMRI study of face processing, adults with autism failed to show activation of the fusiform face area, an area typically activated when viewing faces. In an event-related brain potentials (ERP) study of adolescents and adults with autism, McPartland, Dawson et al found that the ERP component associated with face processing (’N170’) differed between participants with autism and normal participants. This component is typically larger to faces than to nonfaces, and is especially prominent over the right hemisphere. In individuals with autism, N170 was larger for furniture than for faces, and was bilaterally distributed. The latency of the N170 component peaked was corre-