Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder with a prevalence of around 8% in school-aged children. The majority of affected children experience impairing symptoms into adulthood, and are at increased risk for ongoing educational, occupational, and socioeconomic deficits. Comorbidity with other neurodevelopmental conditions occurs in most cases. Although the biological mechanisms underlying ADHD have yet to be explicated, multiple associated factors in genetic, environmental, and neurocognitive domains have been identified. ADHD is likely the result of heritable genetic variants differentially expressed during gene-environment interplay, beginning in utero. Elucidating common risk variants requires exceptionally large sample sizes, and genome-wide significant risk loci have only recently been detected. Deficits in executive function likely contribute to the ADHD phenotype, as does dysfunction of large-scale “resting-state” networks. Meta-analyses of task-based functional magnetic resonance imaging report ADHD-associated hypoactivation of regions involved in executive function and perceptual timing. Among treatment approaches, stimulants consistently display the greatest efficacy in acutely reducing core symptoms. Combining pharmacological and behavioral interventions provides additional benefit over either intervention alone.

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The Spectrum of Neuropsychiatric Outcomes in Attention-Deficit/Hyperactivity Disorder

  • F. Xavier Castellanos,
  • Argelinda Baroni,
  • Shereen E. Elmaghrabi

摘要

Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder with a prevalence of around 8% in school-aged children. The majority of affected children experience impairing symptoms into adulthood, and are at increased risk for ongoing educational, occupational, and socioeconomic deficits. Comorbidity with other neurodevelopmental conditions occurs in most cases. Although the biological mechanisms underlying ADHD have yet to be explicated, multiple associated factors in genetic, environmental, and neurocognitive domains have been identified. ADHD is likely the result of heritable genetic variants differentially expressed during gene-environment interplay, beginning in utero. Elucidating common risk variants requires exceptionally large sample sizes, and genome-wide significant risk loci have only recently been detected. Deficits in executive function likely contribute to the ADHD phenotype, as does dysfunction of large-scale “resting-state” networks. Meta-analyses of task-based functional magnetic resonance imaging report ADHD-associated hypoactivation of regions involved in executive function and perceptual timing. Among treatment approaches, stimulants consistently display the greatest efficacy in acutely reducing core symptoms. Combining pharmacological and behavioral interventions provides additional benefit over either intervention alone.