Neurocognitive and electrophysiological evidence of altered face processing in parents of children with autism: Implications for a model of abnormal development of social brain circuitry in autism

Abstract

Neuroimaging and behavioral studies have shown that children and adults with autism have impaired face recognition. Individuals with autism also exhibit atypical event-related brain potentials to faces, characterized by a failure to show a negative component (N170) latency advantage to face compared to nonface stimuli and a bilateral, rather than right lateralized, pattern of N170 distribution. In this report, performance by 143 parents of children with autism on standardized verbal, visual-spatial, and face recognition tasks was examined. It was found that parents of children with autism exhibited a significant decrement in face recognition ability relative to their verbal and visual spatial abilities. Event-related brain potentials to face and nonface stimuli were examined in 21 parents of children with autism and 21 control adults. Parents of children with autism showed an atypical event-related potential response to faces, which mirrored the pattern shown by children and adults with autism. These results raise the possibility that face processing might be a functional trait marker of genetic susceptibility to autism. Discussion focuses on hypotheses regarding the neurodevelopmental and genetic basis of altered face processing in autism. A general model of the normal emergence of social brain circuitry in the first year of life is proposed, followed by a discussion of how the trajectory of normal development of social brain circuitry, including cortical specialization for face processing, is altered in individuals with autism. The hypothesis that genetic-mediated dysfunction of the dopamine reward system, especially its functioning in social contexts, might account for altered face processing in individuals with autism and their relatives is discussed.

Social and attention factors during infancy and the later emergence of autism characteristics

“…By contrast, the latter two components are thought to be precursors to the N170 in adults, a face-sensitive component (de Haan, Johnson, & Halit, 2003) reported to be atypical in individuals with autism as well as their genetic relatives (Dawson et al, 2005). In our previous study with this pilot cohort, we found that infants at-risk as a group showed a slower P400 response to direct gaze relative to the control group (Elsabbagh, Volein, Csibra, et al, 2009).…”

“…Often debated is the relative contribution of potential infant precursors, i.e., infant capacities mediating the later-emerging characteristic symptoms of the condition. It has been suggested that a failure, or abnormality, in one or more of the underlying mechanisms that bias infants to orient towards and attend to socially relevant information from early in life, disrupts the typical emergence of the social brain network (Dawson et al, 2005;Johnson et al, 2005;Schultz, 2005). For example, atypical neural responses to face and/or eye contact may interfere with the emergence of critical developmental milestones relevant for social cognition, such as joint attention.…”

“…In adults the Broader Autism Phenotype refers to behavioural and brain characteristics associated with ASD found not only in affected individuals, but also in their relatives (Bolton et al, 1994;Dawson et al, 2005). As such, several characteristics of ASD might not be atypical, but their co-occurrence and severity within an individual determine whether they manifest as normative differences, as opposed to diagnosable symptoms.…”

Autism and the development of face processing

“…These anomalies include poor eye contact, and slow or absent mutual gaze in infants and children, but the underlying mechanisms are not well understood. In addition, recent evidence for anomalous gaze behavior in parents of some autistic children raises the possibility of complex interactions among genes and environmental factors affecting development of eye contact [51].…”

Using neuroscience as an outcome measure for behavioral interventions in Autism spectrum disorders (ASD): A review

“…Though the small sample size and lack of control group make it difficult to generalize these findings, results of Voos et al (2013) provide preliminary evidence that PRT can result in increased activation in regions previously identified as relevant to processing biological motion. Ventola et al (2014) measured activity in brain areas implicated in two distinct hypotheses about the neural underpinnings of social deficits in ASD: the social motivation hypothesis (Dawson et al, 2005), and the intense world hypothesis (Markram, Rinaldi, & Markram, 2007;Markram & Markram, 2010). The social motivation hypothesis posits that individuals with ASD may have diminished activation of the reward system to social information, and thus are less rewarded by social interactions compared to their typically developing peers.…”