Incorporating Dis/ability Studies and Critical Race Theory to combat systematic exclusion of Black, Indigenous, and People of Color in clinical neuroscience.

This article reviews some of the ideological forces contributing to the systematic exclusion of Black, Indigenous, and People of Color (BIPOC) in clinical neuroscience. Limitations of functional near-infrared spectroscopy (fNIRS) and other methods systematically exclude individuals with coarse or curly hair and darker skin. Despite these well-known limitations, clinical neuroscience manuscripts frequently fail to report participant race or ethnicity or reasons for excluding participants. Grounding the discussion in Dis/ability Studies and Critical Race Theory (DisCrit), we review factors that exacerbate exclusion and contribute to the multiple marginalization of BIPOC, including (a) general methodological issues, (b) perceptions about race and disability, and (c) underreporting of methods. We also present solutions. Just as scientific practices changed in response to the replication crisis, we advocate for greater attention to the crisis of underrepresentation in clinical neuroscience and provide strategies that serve to make the field more inclusive.

The N170 event-related potential reflects delayed neural response to faces when visual attention is directed to the eyes in youths with ASD.

Atypical neural response to faces is thought to contribute to social deficits in autism spectrum disorder (ASD). Compared to typically developing (TD) controls, individuals with ASD exhibit delayed brain responses to upright faces at a face-sensitive event-related potential (ERP), the N170. Given observed differences in patterns of visual attention to faces, it is not known whether slowed neural processing may simply reflect atypical looking to faces. The present study manipulated visual attention to facial features to examine whether directed attention to the eyes normalizes N170 latency in ASD. ERPs were recorded in 30 children and adolescents with ASD as well as 26 TD children and adolescents. Results replicated prior findings of shorter N170 latency to the eye region of the face in TD individuals. In contrast, those with ASD did not demonstrate modulation of N170 latency by point of regard to the face. Group differences in latency were most pronounced when attention was directed to the eyes. Results suggest that well-replicated findings of N170 delays in ASD do not simply reflect atypical patterns of visual engagement with experimental stimuli. These findings add to a body of evidence indicating that N170 delays are a promising marker of atypical neural response to social information in ASD. LAY SUMMARY: This study looks at how children's and adolescents' brains respond when looking at different parts of a face. Typically developing children and adolescents processed eyes faster than other parts of the face, whereas this pattern was not seen in ASD. Children and adolescents with ASD processed eyes more slowly than typically developing children. These findings suggest that observed inefficiencies in face processing in ASD are not simply reflective of failure to attend to the eyes.