David Pagliaccio1, Katherine Durham2, Kate D Fitzgerald3, Rachel Marsh2. 1. Division of Child and Adolescent Psychiatry, New York State Psychiatric Institute, New York, New York; Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York. Electronic address: david.pagliaccio@nyspi.columbia.edu. 2. Division of Child and Adolescent Psychiatry, New York State Psychiatric Institute, New York, New York; Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York. 3. Department of Psychiatry, University of Michigan, Ann Arbor, Michigan.
Abstract
BACKGROUND: Childhood obsessive-compulsive symptoms (OCSs) are common and can be an early risk marker for obsessive-compulsive disorder. The Adolescent Brain and Cognitive Development (ABCD) Study provides a unique opportunity to characterize OCSs in a large normative sample of school-age children and to explore corticostriatal and task-control circuits implicated in pediatric obsessive-compulsive disorder. METHODS: The ABCD Study acquired data from 9- and 10-year-olds (N = 11,876). Linear mixed-effects models probed associations between OCSs (Child Behavior Checklist) and cognition (NIH Toolbox), brain structure (subcortical volume, cortical thickness), white matter (diffusion tensor imaging), and resting-state functional connectivity. RESULTS: OCS scores showed good psychometric properties and high prevalence, and they were related to familial/parental factors, including family conflict. Higher OCS scores related to better cognitive performance (β = .06, t9966.60 = 6.28, p < .001, ηp2= .01), particularly verbal, when controlling for attention-deficit/hyperactivity disorder, which related to worse performance. OCSs did not significantly relate to brain structure but did relate to lower superior corticostriatal tract fractional anisotropy (β = -.03, t = -3.07, p = .002, ηp2= .02). Higher OCS scores were related to altered functional connectivity, including weaker connectivity within the dorsal attention network (β = -.04, t7262.87 = -3.71, p < .001, ηp2= .002) and weaker dorsal attention-default mode anticorrelation (β = .04, t7251.95 = 3.94, p < .001, ηp2 = .002). Dorsal attention-default mode connectivity predicted OCS scores at 1 year (β = -.04, t2407.61 = -2.23, p = .03, ηp2 = .03). CONCLUSIONS: OCSs are common and may persist throughout childhood. Corticostriatal connectivity and attention network connectivity are likely mechanisms in the subclinical-to-clinical spectrum of OCSs. Understanding correlates and mechanisms of OCSs may elucidate their role in childhood psychiatric risk and suggest potential utility of neuroimaging, e.g., dorsal attention-default mode connectivity, for identifying children at increased risk for obsessive-compulsive disorder.
BACKGROUND: Childhood obsessive-compulsive symptoms (OCSs) are common and can be an early risk marker for obsessive-compulsive disorder. The Adolescent Brain and Cognitive Development (ABCD) Study provides a unique opportunity to characterize OCSs in a large normative sample of school-age children and to explore corticostriatal and task-control circuits implicated in pediatric obsessive-compulsive disorder. METHODS: The ABCD Study acquired data from 9- and 10-year-olds (N = 11,876). Linear mixed-effects models probed associations between OCSs (Child Behavior Checklist) and cognition (NIH Toolbox), brain structure (subcortical volume, cortical thickness), white matter (diffusion tensor imaging), and resting-state functional connectivity. RESULTS: OCS scores showed good psychometric properties and high prevalence, and they were related to familial/parental factors, including family conflict. Higher OCS scores related to better cognitive performance (β = .06, t9966.60 = 6.28, p < .001, ηp2= .01), particularly verbal, when controlling for attention-deficit/hyperactivity disorder, which related to worse performance. OCSs did not significantly relate to brain structure but did relate to lower superior corticostriatal tract fractional anisotropy (β = -.03, t = -3.07, p = .002, ηp2= .02). Higher OCS scores were related to altered functional connectivity, including weaker connectivity within the dorsal attention network (β = -.04, t7262.87 = -3.71, p < .001, ηp2= .002) and weaker dorsal attention-default mode anticorrelation (β = .04, t7251.95 = 3.94, p < .001, ηp2 = .002). Dorsal attention-default mode connectivity predicted OCS scores at 1 year (β = -.04, t2407.61 = -2.23, p = .03, ηp2 = .03). CONCLUSIONS: OCSs are common and may persist throughout childhood. Corticostriatal connectivity and attention network connectivity are likely mechanisms in the subclinical-to-clinical spectrum of OCSs. Understanding correlates and mechanisms of OCSs may elucidate their role in childhood psychiatric risk and suggest potential utility of neuroimaging, e.g., dorsal attention-default mode connectivity, for identifying children at increased risk for obsessive-compulsive disorder.
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