Attention-deficit/hyperactivity disorder (ADHD) is among the most commonly diagnosed mental health disorders in childhood worldwide, with an estimated prevalence of 7.2%.1 At least two-thirds of those diagnosed with ADHD as children will continue to experience symptoms into adulthood.2 In childhood and adolescence, boys are more than twice as likely as girls to be diagnosed with ADHD. This suggests there is both under-recognition and undertreatment of ADHD in girls.3 Untreated ADHD can cause significant consequences, such as impairments in school and work performance as well as relationship difficulties, with subsequent mental health sequelae.3

Adults with ADHD experience negative outcomes as well. Untreated ADHD in adults is associated with increased rates of unemployment and poor performance in educational and work settings. Other significant personal and social costs include a higher rate of traffic accidents, accidental injuries of all types, and criminal convictions and incarcerations (42% among ADHD patients compared with 14% among controls).4 Barbaresi et al found that adults with ADHD experience a mortality rate that is almost 2 times higher than the rate in those without ADHD, with an increased probability of dying by suicide and car accidents.5 Furthermore, adults with ADHD are more likely than those without ADHD to have substance use disorder (SUD), comorbid depression, and anxiety disorders.5

With the increasing prevalence of ADHD, patients or family members often approach primary care providers (PCPs) for evaluation and treatment of ADHD. In 2015, the Centers for Disease Control and Prevention found that nearly half of all children with ADHD were first diagnosed by a PCP,6 making early identification and treatment crucial. PCPs build long-term trusting relationships with families and are uniquely positioned to manage conditions such as ADHD using the principles of chronic care and medical home models.

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Diagnostic Criteria

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) identifies the essential diagnostic feature of ADHD as a “persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with function or development.”7 Patients must meet 6 of 9 criteria for inattention and/or at least 6 of 9 criteria for hyperactivity/impulsivity. In addition, symptoms of the disorder must occur in more than 1 setting.7 Outside informants, such as parents, teachers, daycare providers, coaches, and religious leaders, are key to diagnostic accuracy and evaluation of social or occupational functioning across settings.


Patients with ADHD commonly have comorbid conditions with symptoms that obscure ADHD symptoms and complicate diagnosis and treatment. In a national parent survey, Danielson et al found that nearly two-thirds of children with a current ADHD diagnosis had at least one co-occurring condition. Behavioral or conduct problems were most common (51.5%), followed by anxiety (32.7%), depression (16.8%), autism spectrum disorder (13.7%), and Tourette syndrome (1.2%). In adolescents, SUD also was reported (1.2%).8

Adults with ADHD also experience comorbidities. The National Comorbidity Survey reported that adults with ADHD are 2.7 times more likely to develop major depressive disorder, 7.5 times more likely to develop dysthymia, and more than 5 times more likely to develop a mood disorder. In addition, substance use or dependence was twice as likely to occur in adults with ADHD.9


The brain regions and functions involved in ADHD are varied and fairly complex; a thorough explanation of the mechanisms is beyond the scope of this paper. Briefly, functional magnetic resonance imaging studies show that ADHD is correlated with dysfunction of frontal brain regions involving cognitive functions and sensorimotor processes. These are consistent with the classical model of ADHD as a disorder of deficient frontostriatal activation and inefficient information processing in the dorsolateral prefrontal cortex. In addition, dysfunction in inter-relationships and inter-regulation among neural networks is the foundation for inconsistent symptom presentation of individuals with ADHD.10

The key neurotransmitters involved in the pathogenesis of ADHD are dopamine and norepinephrine.11 Dopamine is involved in attention, pleasure/reward, and motivation, whereas norepinephrine influences alertness. These neurotransmitters have important functional linkages to the anterior cingulate cortex, prefrontal cortex, and posterior parietal cortex. Dopamine enhances signal conduction and improves focus, on-task behavior, and on-task cognition. Norepinephrine acts on alpha2 receptors, which are found in the prefrontal cortex, by enhancing network connections. This allows the frontal cortex to increase inhibitions and enhance executive functioning. In ADHD, these neurotransmitters are either over- or underfunctioning, leading to decreased connectivity in the prefrontal cortex. These neurotransmitters are key to the psychopharmacological interventions that have been successful in treating ADHD.11

Family studies support a genetic heritability of 71% to 90%. A multitude of genetic variants affect dopamine and norepinephrine synthesis and metabolism in specific brain regions; these variants are influenced by environmental factors (ie, maternal smoking), which results in increased susceptibility to ADHD.12