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No transfer of arousal from other’s eyes in Williams syndrome
Stockholm University, Faculty of Social Sciences, Department of Psychology, Personality, Social and Developmental Psychology. Karolinska Institutet, Stockholm, Sweden.ORCID iD: 0000-0001-8222-1699
Stockholm University, Faculty of Social Sciences, Department of Psychology, Personality, Social and Developmental Psychology. Karolinska Institutet, Stockholm, Sweden.
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2023 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 13, no 1, article id 18397Article in journal (Refereed) Published
Abstract [en]

Typically developing humans automatically synchronize their arousal levels, resulting in pupillary contagion, or spontaneous adaptation of pupil size to that of others. This phenomenon emerges in infancy and is believed to facilitate social interaction. Williams syndrome (WS) is a genetic condition characterized by a hyper-social personality and social interaction challenges. Pupillary contagion was examined in individuals with WS (n = 44), age-parallel-matched typically developing children and adults (n = 65), and infants (n = 79). Bayesian statistics were used. As a group, people with WS did not show pupillary contagion (Bayes factors supporting the null: 25–50) whereas control groups did. This suggests a very early emerging atypical developmental trajectory. In WS, higher pupillary contagion was associated with lower autistic symptoms of social communication. Diminished synchronization of arousal may explain why individuals with WS have social challenges, whereas synchronization of arousal is not a necessary correlate of high social motivation.

Place, publisher, year, edition, pages
2023. Vol. 13, no 1, article id 18397
Keywords [en]
Williams syndrome, WS, pupillary contagion, social interaction, hyper-social personality, synchronization of arousal, autistic symptoms
National Category
Psychology
Research subject
Psychology
Identifiers
URN: urn:nbn:se:su:diva-225004DOI: 10.1038/s41598-023-45521-5ISI: 001104520000054PubMedID: 37884631Scopus ID: 2-s2.0-85175065050OAI: oai:DiVA.org:su-225004DiVA, id: diva2:1824211
Note

Open access funding provided by Stockholm University. This work was funded by Sävstaholm Foundation, ST 2021-026, Strategic Research Area Neuroscience (StratNEURO), Crown Princess Lovisa Foundation., Linnea and Josef Carlsson Foundation, Sunnderdahls handikappfond, Promobilia foundation, Hjärnfonden, The Hållsten Research Foundation and the Rare Diseases Fund (Sällsyntafonden).

Available from: 2024-01-04 Created: 2024-01-04 Last updated: 2024-01-16Bibliographically approved

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Kleberg, Johan L.Hallman, AstridFawcett, Christine

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