The Neurodevelopmental Architecture of ADHD: Executive Function, Emotional Dysregulation, and Circuit-Level Mechanisms

Abstract

Attention-Deficit/Hyperactivity Disorder (ADHD) is a complex neurodevelopmental condition characterized by pervasive deficits in executive control, motivational regulation, and emotional stability. Contemporary neuroscience conceptualizes ADHD as a disorder of distributed neural systems rather than localized dysfunction. This paper examines the neurodevelopmental architecture of ADHD through the integration of cognitive, affective, and circuit-level perspectives. Longitudinal imaging studies demonstrate delayed cortical maturation and disrupted connectivity within prefrontal and parietal regions, contributing to deficits in working memory, inhibition, and sustained attention. Emotional dysregulation is traced to impaired prefrontal–limbic communication, particularly between the amygdala and ventromedial prefrontal cortex, resulting in heightened reactivity and poor affective control. At the systems level, functional network analyses reveal instability across frontostriatal, frontoparietal, default mode, limbic, and cerebellar circuits. These networks exhibit abnormal coupling, reduced segregation, and inconsistent transitions between internal and external attentional states. Genetic and neurochemical studies implicate dopaminergic and noradrenergic dysregulation as primary modulators of these circuit abnormalities. Translational evidence indicates that stimulant and non-stimulant pharmacotherapy partially normalize network activation, while behavioral, cognitive, and neuromodulatory interventions strengthen regulatory circuitry through neuroplastic adaptation. Collectively, these findings support a dynamic systems model in which ADHD emerges from disrupted developmental synchronization across executive and emotional networks. Understanding this architecture offers a foundation for precision interventions targeting the neural mechanisms underlying self-regulation across the lifespan.