Abstract
Attention-Deficit/Hyperactivity Disorder is not a single pathophysiological entity and appears to have a complex etiology. There are multiple genetic and environmental risk factors with small individual effect that act in concert to create a spectrum of neurobiological liability. Structural imaging studies show that brains of children with Attention-Deficit/Hyperactivity Disorder are significantly smaller than unaffected controls. The prefrontal cortex, basal ganglia and cerebellum are differentially affected and evidence indicating reduced connectivity in white matter tracts in key brain areas is emerging. Genetic, pharmacological, imaging, and animal models highlight the important role of dopamine dysregulation in the neurobiology of Attention-Deficit/Hyperactivity Disorder. To date, stimulants are the most effective psychopharmacological treatments available for Attention-Deficit/Hyperactivity Disorder. Currently only immediate release methylphenidate and atomoxetine are approved for the treatment of ADHD in Italy. Drug treatment should always be part of a comprehensive plan that includes psychosocial, behavioural and educational advice and interventions.
Highlights
Attention-Deficit/Hyperactivity Disorder (ADHD) is a common, long-lasting, treatable childhood psychiatric disorder, characterised by a pattern of developmentally inappropriate inattention, motor restlessness, and impulsivity that affects approximately 3-7% of school-aged children [1].ADHD was first recognised 100 years ago as a childhood disorder found mainly in boys, and was initially described as “hyperactivity” or “hyperkinetic disorder of childhood”
In the 1960’s and 70’s much of the focus on what is called ADHD was on hyperactivity
Recent studies have focused on the joint effects of gene variants and prenatal substance exposures on subtypes of ADHD children, demonstrating that smoking during pregnancy is associated with the combined ADHD type in genetically susceptible children [36]
Summary
Attention-Deficit/Hyperactivity Disorder (ADHD) is a common, long-lasting, treatable childhood psychiatric disorder, characterised by a pattern of developmentally inappropriate inattention, motor restlessness, and impulsivity that affects approximately 3-7% of school-aged children [1]. Recent studies have focused on the joint effects of gene variants (of DRD4 and DAT1) and prenatal substance exposures on subtypes of ADHD children, demonstrating that smoking during pregnancy is associated with the combined ADHD type in genetically susceptible children [36]. Positron emission tomography (PET) studies have shown that methylphenidate hydrochloride (MPH) blocks dopamine active transporters (DAT) and that extracellular dopamine (DA) increases in proportion to the level of blockade and to the rate of DA release This process is associated with an enhanced perception of the external stimulus as salient in subjects with ADHD [50]. Because the current evidence is based on research that has not been designed to investigate the cardiovascular effects of these drugs, it is difficult to draw firm conclusions [67] Both MPH and ATX significantly increase activation in key cortical and subcortical regions subserving attention and executive functions. Somnolence, fatigue, upper abdominal pain, sedation both common and unusual potentially severe adverse effects
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