Abstract
Attention deficit hyperactivity disorder (ADHD), classified in ICD-10 as hyperkinetic disorder (HD), is one of the most common neurodevelopmental conditions, affecting approx. 5–7% of children and 2.5–4% of adults. Despite decades of research, its clinical presentation remains heterogeneous and debated, with diagnostic differences between ICD-10 and DSM-5. Core symptoms – inattention, hyperactivity, and impulsivity – significantly impair social, academic, and emotional functioning and frequently co-occur with oppositional defiant disorder, conduct disorder, anxiety, depression, and substance use disorders. Historically, the concept of ADHD evolved from early descriptions of “moral control defects” to contemporary evidence of neurobiological underpinnings. Neuroimaging studies demonstrate reduced volumes of frontal lobes, basal ganglia, cerebellum, and abnormalities within fronto-striatal and limbic networks. Neuropsychological models highlight impaired response inhibition, executive dysfunction, and difficulties with delayed reward processing.
Attention deficit hyperactivity disorder is highly heritable (70–80%), with numerous candidate genes implicated in dopaminergic, noradrenergic, serotonergic, and glutamatergic pathways. However, its etiology is multifactorial, involving complex gene–environment interactions. Environmental risk factors include prenatal exposure to nicotine and alcohol, toxic pollutants, maternal stress, and broader psychosocial influences. Given its strong links with emotional difficulties, behavioural disorders, and addiction risk in adolescence, ADHD represents a major public-health challenge. A comprehensive understanding of its neurobiology, developmental trajectory, and etiological complexity is essential for accurate diagnosis and effective individualized treatment.