bioRxiv : the preprint server for biology · 2026
Sub-Additive Effects of Autism-ADHD Comorbidity on Resting-State Pupillary and Oculomotor Phenotypes.
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Di Xin, Biswal Bharat B
Аннотация
BACKGROUND: Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) share substantial clinical and physiological overlap. While naturalistic and sensory-driven paradigms increasingly capture evoked neurophysiological responses, the intrinsic baseline physiology of these conditions remains poorly defined. We characterized resting-state pupillary volatility and oculomotor stability across the ASD-ADHD spectrum using dimensional and categorical (DSM-5) frameworks.
METHODS: We analyzed resting-state eye-tracking data from a large pediatric cohort (N = 2,315) from the Healthy Brain Network, extracting Pupil Relative Volatility (Coefficient of Variation [CV]) and Bivariate Contour Ellipse Area (BCEA) to index pupillary and spatial gaze stability. Data were evaluated via continuous regressions against Social Responsiveness Scale (SRS) and SWAN inventories, then 2×2 factorial ANCOVAs based on clinical diagnoses, with sensitivity analyses for extreme values, hardware heterogeneity, and psychostimulant medication.
RESULTS: Dimensional models revealed no significant association between either metric and continuous ASD or ADHD trait severity, apart from a modest sub-additive SRS × SWAN interaction on pupillary CV; an apparent pooled BCEA-trait association proved attributable to hardware differences and was absent within hardware-consistent subgroups. Categorical models showed robust diagnostic differentiation for both metrics: isolated ASD was associated with elevated CV and impaired BCEA, with ADHD additionally impairing BCEA. Comorbid ASD+ADHD produced a sub-additive CV interaction robust across outlier-resistant, hardware-stratified, and medication-adjusted analyses; an analogous BCEA interaction was directionally consistent but not significant under standard estimation.
CONCLUSIONS: Categorical diagnostic status was consistently associated with baseline pupillary and oculomotor physiology across the ASD-ADHD spectrum in this cohort, with a shared sub-additive comorbidity effect most robustly expressed in pupillary volatility; continuous trait severity showed little independent association with either metric. These findings, obtained using a rigorously validated, hardware-heterogeneous multi-site sample, establish a foundation for future naturalistic and sensory-evoked investigations of the shared physiological architecture underlying ASD-ADHD comorbidity.
METHODS: We analyzed resting-state eye-tracking data from a large pediatric cohort (N = 2,315) from the Healthy Brain Network, extracting Pupil Relative Volatility (Coefficient of Variation [CV]) and Bivariate Contour Ellipse Area (BCEA) to index pupillary and spatial gaze stability. Data were evaluated via continuous regressions against Social Responsiveness Scale (SRS) and SWAN inventories, then 2×2 factorial ANCOVAs based on clinical diagnoses, with sensitivity analyses for extreme values, hardware heterogeneity, and psychostimulant medication.
RESULTS: Dimensional models revealed no significant association between either metric and continuous ASD or ADHD trait severity, apart from a modest sub-additive SRS × SWAN interaction on pupillary CV; an apparent pooled BCEA-trait association proved attributable to hardware differences and was absent within hardware-consistent subgroups. Categorical models showed robust diagnostic differentiation for both metrics: isolated ASD was associated with elevated CV and impaired BCEA, with ADHD additionally impairing BCEA. Comorbid ASD+ADHD produced a sub-additive CV interaction robust across outlier-resistant, hardware-stratified, and medication-adjusted analyses; an analogous BCEA interaction was directionally consistent but not significant under standard estimation.
CONCLUSIONS: Categorical diagnostic status was consistently associated with baseline pupillary and oculomotor physiology across the ASD-ADHD spectrum in this cohort, with a shared sub-additive comorbidity effect most robustly expressed in pupillary volatility; continuous trait severity showed little independent association with either metric. These findings, obtained using a rigorously validated, hardware-heterogeneous multi-site sample, establish a foundation for future naturalistic and sensory-evoked investigations of the shared physiological architecture underlying ASD-ADHD comorbidity.