Journal of the American Academy of Child and Adolescent Psychiatry · 2026
Specific, Replicable Behavioral and Neural Correlates of Sensory Over-Responsivity in Childhood.
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Luo Hexin, Kim Andrew W, Abbacchi Anna M, Constantino John N, Gurnett Christina A, Luby Joan L, Perino Michael T, Barch Deanna M, Sylvester Chad M, Camacho M Catalina, Schwarzlose Rebecca F
Аннотация
OBJECTIVE: Sensory over-responsivity (SOR), characterized by strong negative reactions to typically innocuous stimuli, is considered a symptom of autism spectrum disorder. However, SOR also affects 15% to 20% of children overall, including a majority of children with common psychiatric conditions. Despite its prevalence, the clinical specificity and neurobiological bases of SOR remain poorly understood. Our study aims to determine the specific clinical significance of SOR across diverse child samples, and to establish whether SOR is associated with replicable patterns of functional connectivity (FC).
METHOD: We analyzed data from 15,728 children and adolescents (6-17.9 years of age) across 5 datasets: 3 community samples, including the Adolescent Brain Cognitive Development℠ (ABCD) study and the Healthy Brain Network (HBN) study, and 2 autism-enriched samples. Bivariate and multivariate models examined associations between SOR and symptoms of anxiety, attention-deficit/hyperactivity disorder, depression, conduct disorder, and oppositional defiant disorder, as well as autistic traits. Analysis of resting-state functional magnetic resonance imaging (fMRI) data from the ABCD Study (n = 4,195) identified candidate brain-wide and circuit-specific FC correlates of mild SOR, and tested replication of effects in an independent ABCD subsample (n = 4,190). Additional analyses tested extension to children with severe SOR in ABCD and replication in smaller samples (HBN, n = 356; ABCD subset, n = 356).
RESULTS: Multivariate analyses revealed that SOR is associated with a remarkably consistent profile across samples: greater levels of both autistic traits and anxiety symptoms and, in community samples, lower levels of conduct disorder symptoms. Across samples, SOR is not reliably associated with symptoms of any other analyzed psychiatric conditions. Mild SOR is associated with brain-wide FC patterns and, specifically, reduced FC between cingulo-parietal network and bilateral caudate nucleus; these patterns show robust replication across independent ABCD subsamples and extension to severe SOR in ABCD but are not significant in smaller samples, indicating that large sample size is needed to reliably detect brain effects.
CONCLUSION: Results suggest that SOR may constitute a latent trait associated with both specific clinical risk and protection, and with replicable cortico-subcortical neural correlates. These findings advance our understanding of the neurobiology and clinical relevance of SOR. They may also inform clinical practice and future research aimed at understanding and supporting individuals with sensory challenges.
DIVERSITY & INCLUSION STATEMENT: We worked to ensure sex balance in the recruitment of human participants. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. We worked to ensure that the study questionnaires were prepared in an inclusive way.
METHOD: We analyzed data from 15,728 children and adolescents (6-17.9 years of age) across 5 datasets: 3 community samples, including the Adolescent Brain Cognitive Development℠ (ABCD) study and the Healthy Brain Network (HBN) study, and 2 autism-enriched samples. Bivariate and multivariate models examined associations between SOR and symptoms of anxiety, attention-deficit/hyperactivity disorder, depression, conduct disorder, and oppositional defiant disorder, as well as autistic traits. Analysis of resting-state functional magnetic resonance imaging (fMRI) data from the ABCD Study (n = 4,195) identified candidate brain-wide and circuit-specific FC correlates of mild SOR, and tested replication of effects in an independent ABCD subsample (n = 4,190). Additional analyses tested extension to children with severe SOR in ABCD and replication in smaller samples (HBN, n = 356; ABCD subset, n = 356).
RESULTS: Multivariate analyses revealed that SOR is associated with a remarkably consistent profile across samples: greater levels of both autistic traits and anxiety symptoms and, in community samples, lower levels of conduct disorder symptoms. Across samples, SOR is not reliably associated with symptoms of any other analyzed psychiatric conditions. Mild SOR is associated with brain-wide FC patterns and, specifically, reduced FC between cingulo-parietal network and bilateral caudate nucleus; these patterns show robust replication across independent ABCD subsamples and extension to severe SOR in ABCD but are not significant in smaller samples, indicating that large sample size is needed to reliably detect brain effects.
CONCLUSION: Results suggest that SOR may constitute a latent trait associated with both specific clinical risk and protection, and with replicable cortico-subcortical neural correlates. These findings advance our understanding of the neurobiology and clinical relevance of SOR. They may also inform clinical practice and future research aimed at understanding and supporting individuals with sensory challenges.
DIVERSITY & INCLUSION STATEMENT: We worked to ensure sex balance in the recruitment of human participants. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. We worked to ensure that the study questionnaires were prepared in an inclusive way.