Electrophysiological Studies of Reception of Facial Communication in Autism Spectrum Disorder and Schizophrenia

Abstract

& KEYWORDSAutism spectrum disorder (ASD) and schizophrenia spectrum disorders (SZ) are both characterized by difficulty with social cognition. Likewise, social brain activity is atypical in both disorders and indicates atypical reception of facial communicationa key area in the Research Domain Criteria framework for identifying common biological underpinnings of psychiatric disorders. To identify areas of overlap and dissociation between ASD and SZ, this paper reviews studies of electrophysiological (EEG) response to facial stimuli across ASD and SZ populations. We focus on findings regarding amplitude and latency of four brain responses implicated in social perception: P100, N170, N250, and P300. There were many inconsistent findings in both the ASD and SZ literatures; however, replication across studies was strongest for delayed N170 latency in ASD and attenuated N170 amplitude in SZ. EEG responses corresponded with clinical symptoms in multiple samples. These results highlight the challenges associated with replicating research findings in heterogeneous clinical populations, as well as the need for transdiagnostic research and for designing studies to examine relationships among continuous quantifications of behavior and neural activity across neurodevelopmental disorders. Autism spectrum disorder (ASD) and schizophrenia spectrum disorders (SZ) are highly prevalent neurodevelopmental disorders (ND) with considerable public health impact, costing the United States a combined $423 billion per year (Cloutier et al. 2016). Though these disorders are classified in two separate diagnostic taxonomies, social deficits are diagnostic hallmarks of both, and diagnostic confusion is common. Social dysfunction is a core symptom of both ASD and SZ, evident in decreased social motivation, reduced social reward, impaired mentalizing, and decreased likelihood of social engagement (Dawson et al. 2005; Dowd and Barch 2010; Schultz 2005). Moreover, parallel lines of research indicate commonalities in affected genetic pathways and neural processes, suggesting shared neuropathology (Cristino et al. 2014; Mitchell 2011). These findings are consistent with the hypothesis that common mechanisms contribute to social communication deficits across behaviorally defined categories of ND. Despite these commonalities, few studies have directly compared distinct diagnostic groups or conceptualized these diagnostic classes as heterogeneous manifestations of shared dysfunction in overlapping neural substrates. For this reason, little is known about whether atypical social perception across NDs reflects common or distinct neural underpinnings. In this review, we focus on literature related to face and emotion processing across ASD and SZ, highlighting what is known, where the disorders converge and diverge, and what work remains to be done to understand social processes related to reception of facial communication across disorders.