Overview and neurobiology of attention-deficit/hyperactivity disorder.

Although attention-deficit/hyperactivity disorder (ADHD) impairs millions of people worldwide, both the prevalence and existence of the disorder are being reevaluated at the phenotypic level. To safeguard against overdiagnosis, the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), demands that individuals with ADHD have pervasive impairment, that is, impairment in more than 1 setting. However, the appropriateness of the DSM-IV classification of ADHD is also undergoing reevaluation. Like the symptoms of a developmental disability, the symptoms of ADHD must be evaluated in the context of age-based norms; therefore, the current criteria for ADHD, which are not age referenced, may minimize the rate of persistence of ADHD into adulthood. In an effort to better understand the pathophysiology of ADHD, recent research has focused on identifying the etiology of ADHD. These studies have revealed that the disorder is highly heritable and may be associated with neurobiological deficits in the prefrontal cortex and related subcortical systems. Etiologic studies have also identified candidate genes and prenatal and perinatal risk factors for ADHD. As the causes and course of ADHD are better understood, a new generation of medications is being developed for the disorder. Although stimulants are often effective in reducing the symptoms of the disorder, as a class they have limitations such as a lack of 24-hour-a-day coverage, unwanted side effects, potential for abuse, and lessened effectiveness in the context of some comorbidities. Therefore, the treatment characteristics of newer, more selective treatments such as atomoxetine should continue to be explored in ADHD.