Prevalence rates of ADHD in the childhood population vary, with expert opinion most often citing an incidence of approximately 3%–7% (American Psychiatric Association, 2000). The majority of children with the disorder continue to exhibit some symptoms in adulthood. Prevalence rates in adults are estimated to be about 4.4% (Kessler et al., 2006). The disorder is more common in males, with 6:1 frequency among clinic-referred samples and a 3.4:1 frequency among nonclinic-referred samples for males to females (Barkley, 2006).

There is considerable evidence to suggest a genetic basis for ADHD. The disorder is highly heritable, with a risk of 57% of occurrence from parents with ADHD to their children. Most of the genetic research has focused on candidate genes involved in dopaminergic transmission, although noradrenergic and serotonin systems are also studied. The most reliable findings in ADHD are associated with the DRD4 repeat polymorphism (Barkley, 2006). Other associations for candidate genes have included DAT1, DBH, DRD5, SNAP-25, 5HTT, and HTR1B. ADHD also has been associated with markers at several chromosomes including, but not limited to, regions 5p, 6q, 9q, 11q, 16q, and 17p. Additional factors thought to contribute to ADHD include low birth weight, environmental toxins such as prenatal exposure to maternal smoking and alcohol consumption, and postnatal exposure to lead.

Neuroimaging research into brain structure and function in ADHD repeatedly finds significant differences between ADHD and controls in frontal, anterior cingulate, basal ganglia, and cerebellar anatomy and function. Reviews of the literature from structural MRI methods (e.g., Krain & Castellanos, 2006) reveal perhaps the most consistent findings in regard to ADHD imaging studies. Comparisons in global brain volume between children with ADHD and healthy comparison children have repeatedly found evidence of significantly reduced total brain volume, frontal cortical volume, and reductions in frontal regions in ADHD using gray-white matter segmentation techniques. Measures of cortical thickness via a recent longitudinal study (Shaw et al., 2007) revealed a delay of approximately three years in an ADHD group compared to controls in attaining peak thickness throughout the cerebrum, with delays ranging from two to five years in the prefrontal regions. Interestingly, the ADHD group had slightly earlier peak thickness (about four months) in the primary motor cortex compared to the control group.

Studies that use a variety of functioning imaging techniques suggest decreased brain activation in the frontal cortex in ADHD, although a number of studies have also shown relative increased brain activation in ADHD (see Fassbender & Schweitzer, 2006). Accumulating evidence also suggests that the anterior cingulate cortex is implicated in ADHD and is often hypoactive in both child and adult participants. The basal ganglia are another structure of inherent interest in ADHD, given the functional attributes of this structure and the fact that it is a clear target of the most common treatment for ADHD, which is stimulant medication. Methylphenidate appears to increase dopamine levels in the basal ganglia via blocking its reuptake. Alterations are consistently found in the basal ganglia during functional brain-imaging studies, with the evidence mixed about whether the alterations in basal ganglia activation are increased or decreased (see Fassbender & Schweitzer, 2006). Stimulants appear to increase basal ganglia activation in children with ADHD.

Another subcortical structure, the cerebellum, also appears to be altered in structure and function in ADHD. The cerebellar vermis and hemispheres are smaller in children with ADHD than in comparison groups of healthy controls. Methylphenidate appears to increase cerebellar vermis activity, but only in a nontask-related fashion. Rates of hyperactivity and response to methylphenidate treatment also appear to be linked to the degree of activity in the cerebellar vermis (Fassbender & Schweitzer, 2006). Associations between the cerebellum, the basal ganglia, and the PFC suggest that abnormalities found in these regions may reflect a circuit-wide dysfunction in prefrontal-basal ganglia-cerebellar loops in ADHD. Ultimately, methods combining behavioral, imaging, and genetic techniques should help identify ADHD subgroups and potentially develop more targeted treatment efforts for the subgroups.

Practice parameters for ADHD have been identified by several organizations including the American Academy of Pediatrics (AAP) and the American Academy of Child and Adolescent Psychiatry. These organizations include recommendations for the evaluation of ADHD and, via AAP, access to rating scales for evaluating ADHD and monitoring treatment response. A comprehensive evaluation of ADHD in adults or children should assess the presence or absence of symptomatology, differential diagnosis from other disorders that mimic ADHD, and the possibility of comorbid psychiatric disorders. At a minimum, the evaluation should include a clinical interview, a medical evaluation conducted within the past year, standardized behavior-rating scales from parents and teachers, and a direct observation of the patient. Evaluations for both children and adults also should include a family history as well as documentation regarding developmental, social, and academic functioning.

An evaluation for adults also ought to include information regarding childhood via academic records and retrospective-childhood ratings by the adult patient and a parent or another individual who knew the patient as a child. An assessment of intellectual, academic, neuropsychological, and attentional functioning is desirable for purposes of differential diagnosis, as well as for pointing out individual strengths and weaknesses. Psychoeducational testing can also be useful when a low level of intellectual functioning or a learning disability mimics or coexists with ADHD. Preferably, the evaluation should be individualized to address areas of concern for each patient.

Although the evidence for the efficacy of pharmacological treatments for ADHD has strong empirical support (Jensen, 2002; MTA Cooperative Group, 1999; MTA Cooperative Group, 2004), there is also a role for behavioral interventions in the treatment of the disorder. Behavioral interventions are necessary for the 20%–30% of patients who do not respond to stimulants and for those who experience significant side effects from pharmacological agents. Perhaps most importantly, these interventions can also address comorbidity such as anxiety, academic performance, parent-child conflict, and stress in the parent (MTA Cooperative Group, 1999). Behavioral interventions for children include social skills training, school interventions, and parent training in contingency management. There is recent support for the use of behavioral and cognitive-behavioral treatments for adults with ADHD (e.g., Solanto et al., 2008) as well. The adult interventions teach compensatory strategies, organizational skills, planning, and the development of new habits to help resist distracters. Adults and adolescents may also benefit from “coaching” to monitor progress toward academic, career, and social goals.

The use of pharmacological interventions is warranted if the symptoms are interfering significantly with functioning. Most medications for ADHD appear to affect the dopaminergic and/or noradrenergic system. The majority of individuals (children and adults) are responsive to psychostimulant medications (e.g., methylphenidate and dextroamphetamine), and these compounds are considered safe and effective treatments for ADHD. Stimulants, typically considered the first line of defense, can produce improvements in impulse control, attention, on-task behavior, and social behavior. A number of fairly new delivery systems (including a pill and a transdermal “patch”) for psychostimulant medications are commercially available, including several with long-acting or extended-release options, such as Concerta, Metadate, Ritalin SR, and Ritalin LA. A recently released drug, Vyvanse (lisdexamfetamine dimesylate and mixed amphetamine salts), is an extended-release formulation of d-amphetamine that becomes therapeutically active following oral ingestion. Thus, Vynase should be less likely to be abused than other stimulants. Atomoxetine, a nonstimulant compound that is a highly selective inhibitor of the presynaptic norad-renergic transporter, has FDA approval for treatment of ADHD in adults and children. Other pharmacological options include bupropion and tricyclic antidepressants, but these drugs are prescribed less frequently than the stimulants. The most common side effects for stimulants and atomoxetine include decreased appetite, mild stomachaches or headaches, insomnia, increased anxiety, and/or irritability. All medications need to be monitored on a frequent and regular basis, given that children’s needs may change as they mature.

Psychostimulant Treatment for Children.