Processing of expressions by individuals with autistic traits: Empathy deficit or sensory hyper-reactivity?
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ABSTRACT: Individuals with autistic traits display impaired social interaction and communication in everyday life, but the underlying cognitive neural mechanisms remain very unclear and still remain controversial. The mind-blindness hypothesis suggests that social difficulties in individuals with autistic traits are caused by empathy impairment in individuals; however, the intense world theory suggests that these social difficulties are caused by sensory hyper-reactivity and sensory overload, rather than empathy impairment. To further test these two theories, this study investigated event-related potentials (ERPs) to explore the cognitive neural processing of repetitive expressions in individuals with autistic traits. This study employed the Mandarin version of the autism-spectrum quotient (AQ) to assess autistic traits in 2,502 healthy adults. Two subset groups were used, e.g., the participants of a high-AQ group were randomly selected among the 10% of individuals with the highest AQ scores; similarly, the participants in the low-AQ group were randomly selected from the 10% of participants with the lowest AQ scores. In an experiment, three different facial expressions (positive, neutral, or negative) of the same person were presented successively and pseudo-randomly in each trial. Participants needed to define the expression of the face that was presented last. The results showed that compared with the low-AQ group, the high-AQ group exhibited higher P1 amplitudes induced by the second and third presented expressions, as well as higher P3 amplitudes induced by the third presented negative expressions. This indicates that individuals with autistic traits may experience overly strong perception, attention, and cognitive evaluation to repetitive expressions, particularly negative expressions. This result supports the intense world theory more strongly than the mind-blindness hypothesis.
SUBMITTER: Meng C
PROVIDER: S-EPMC8270190 | biostudies-literature |
REPOSITORIES: biostudies-literature
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