Common multimodal neuroimaging mechanism of attention deficit hyperactivity disorder and sleep initiation difficulty in the developing brain

• We unveiled shared multimodal neuroimaging biomarkers of ADHD and sleep initiation difficulty in a large-scale study. • Unidirectional mediation model found that ADHD impacts sleep initiation difficulty via shared neuroimaging features. • Three ADHD developmental trajectories were identified, with the remitting group showing the most severe sleep initiation difficulty and distinct neurostructural alterations. • The longitudinal ADHD - sleep initiation difficulty relationship is trajectory-specific, demonstrating bidirectional effects. • Converging multimodal evidence reveals integrated structural and functional neural substrates of ADHD - sleep initiation difficulty. Attention deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder. Studies indicate that 20–55% of individuals with ADHD experience comorbid sleep disturbances, among which, sleep initiation difficulty (SID) is highly correlated with hyperactivity behaviors. However, the underlying neuroimaging mechanisms common to ADHD and sleep initiation difficulty remain poorly understood. This study used multimodal neuroimaging data and ADHD, SID phenotype data from the ABCD Study (n=11,868; 52.1% male) to identify neuroimaging markers common to both conditions using linear regression. Then, these common neuroimaging features were analyzed across different ADHD trajectory groups, which were determined by latent class growth analysis (LCGA). Random-intercepts cross-lagged panel model (RI-CLPM) were further used to examine their longitudinal relationships. Inter-network connectivity between the dorsal attention network and default mode network (DMN-DAN) from rest-fMRI, specific cortico-striatal-thalamic circuits involving the right orbitofrontal cortex volume from brain structural imaging and several major white matter tracts were significantly associated with both ADHD symptoms and SID. These neuroimaging markers collectively mediated the relationship between ADHD and SID. Furthermore, three distinct ADHD trajectories were identified and showed different association pattern with neuroimaging features and lagged effects between ADHD and SID. Through multimodal neuroimaging analyses of ADHD and SID, we identified common neural substrates, which mediated the effect of ADHD symptoms on SID, and exhibited distinct patterns across different ADHD trajectory subgroups. The results suggest that common neural architecture and its dynamic expression may underlie the neurobiological link between ADHD and SID.