Attention deficit hyperactive disorder (ADHD) is a neurobiological disorder whose prevalence has been estimated by the American Psychiatric Association (APA) at between 3 - 7% of children and by Woodruff et.al. to occur in 7 - 12% of children. Angold et. al. carried out epidemiological studies of preschool children where they found that 2 - 6% met diagnostic criteria for ADHD. Of those diagnosed as children, 70-85% continue to meet criteria as adolescents and about 60% continue to meet criteria as adults older that 25 years of age. The diagnosis is usually made between the ages of 7 to 10 years of age but sometimes much earlier when the child is 3 or 4 years old.
Neuropsychological, neuroimaging, and genetic studies have demonstrated the biological foundation of ADHD. The affected brain regions correlate with deficits in executive functioning, delay aversion, working memory, planning, vigilance, and response inhibition. Imaging studies have demonstrated smaller brain volumes on average than same age children and with smaller cerebellar volumes (Castellanos et.al.). Family, twin, and genotyping studies also support the biological nature of the disorder. Faraone has estimated the heritability at 76% and Biederman has estimated that the parents of ADHD children are 2 - 8 times more likely to have the disorder as are the siblings of the affected child.
The diagnostic criteria for ADHD require the positive endorsement of 6 of 9 inattentive symptoms and/or the endorsement of 6 of 9 hyperactive/impulsive symptoms with an age of onset before 7 years of age. These symptoms must result in clinically significant impairment in social, academic, and/or occupational functioning. These children tend to have an increase in injuries and accidents, problems with peer relations, academic troubles, more conflicts with parents than most children of the same age. In addition, adolescents with ADHD have more auto accidents, more substance abuse, more occupational impairment, more teen pregnancy, and higher rate of sexually transmitted diseases (STDs). In ADHD adults there is a continuation of those issues with more authority conflicts, job instability, and divorces.
A comprehensive initial appraisal is necessary because of the frequency and number of co-morbidities. The MTA Cooperative Group characterized an ADHD population of children (n=579, aged 7-9.9 years) and demonstrated that 31% had ADHD alone, 40% met criteria for oppositional defiant disorder, 38% met criteria for anxiety/mood disorder, 14% for conduct disorder, and 11% for tic disorders. The MTA study also randomized participating children to intensive behavioral therapy, pharmacotherapy with methylphenidate, a combination of the two, and standard community care. Pharmacotherapy alone and in combined demonstrated significant improvement and were superior to behavioral therapy alone. However, the combined therapy was not superior to pharmacotherapy alone. Medication therefore seems to have the most impact on the treatment of ADHD symptoms.
The role of medication as a first-line treatment is strongly supported by the literature and clinical experience. Stimulants have historically been considered the first-line treatment with about a 90% response rate. The stimulants approved for treatment of ADHD have either an amphetamine molecular structure (Dexedrine, Adderall, Vyvanse) or an methylphenidate molecular structure (Ritalin, Concerta, Metadate, Focalin, Daytrana), both of which enhance the neurotransmission of dopamine and to a lesser extent norepinephrine. Adverse effects cluster around a profile which includes delayed sleep onset, decreased appetite, weight loss, stomach upset, headache, increased pulse and blood pressure. Emotional adverse events with crabbiness, crying irritability are more frequent with preschool children. The second-line treatment is atomoxetine (Strattera) which is a norepinephrine reuptake inhibitor and is effective in about 60% of cases. Common acute adverse effects include nausea, vomiting, irritability, headaches, and sedation. The third-line of treatment are the alpha2 adrenergic agonists clonidine (Catapres, Kapvay) and guanfacine (Tenex, Intuniv). The most common adverse events (largely dose dependent) include headache, somnolence, fatigue, sedation, and upper abdominal pain.
In conclusion, careful and complete assessment and informed prescribing can optimize the outcomes for these patients who are otherwise at increased risk as adults for substance abuse, job instability, divorce, and a variety of legal problems.