Adults with autism show a diminished brain response to hearing their own name

Whether you are at a party or in line at the supermarket, when you hear someone calling your name this usually elicits a strong orienting response. Hearing your own name typically signals that another person intends to attract your attention, and orienting to the own name is considered an important aspect of successful social interaction. Problems with social interaction and communication belong to the core symptoms of autism spectrum disorder (ASD). Studies with infants at risk for ASD have indicated that a diminished orienting response to the own name is one of the strongest predictors for developing ASD. Surprisingly however, this had not yet been studied in individuals with an ASD diagnosis.

In a new study from Ghent University, Belgium, the brain response to hearing one's own name versus other names was compared between a group of adults with ASD, and a control group of adults without an ASD diagnosis. Participants in the study were listening to their own name, and names of close and unfamiliar others, but did not need to respond to these names. Meanwhile, their brain activity was being recorded.

Results showed that, as expected, the brain response to one's own name was much stronger than for other names in neurotypical adults. Strikingly, this preferential effect for the own name was completely absent in adults with ASD. Furthermore, this group difference was related to diminished activity in the right temporoparietal junction (rTPJ). Previous research has related the rTPJ to the processes of self-other distinction and mentalizing (representing another person's mental states). During these processes, abnormal patterns of activity have been found in individuals with ASD.

This study is the first to show that brains of adults with ASD respond differently when hearing their own name, suggestive of a core deficit in self-other distinction associated with dysfunction of the rTPJ. This novel finding is important for our understanding of this complex condition and its development, and warrants further research on the possibility to use the atypical neural response to the own name as a potential biological marker of ASD.