This slide gives a brief overview of how attention deficit hyperactivity disorder (ADHD) has evolved over the years Symptoms first described as early as 1902 by Dr. Still in Lancet The core symptoms of ADHD have always been defined on the basis of behavioral characteristics At first the symptoms were viewed as identical to those that would follow an insult to the brain, such as a head injury or a CNS infection. When these behavioral characteristics were seen in children with no history of such an insult, the damage to the CNS was considered to be so minimal that the only manifestations were behavioral. Hence the term “minimal brain damage” In the early 1960s, the term “minimal brain dysfunction,” or MBD, was used to describe a cluster of symptoms that included specific learning disabilities, hyperkinesis, impulsivity, and short attention span. But MBD was a vague, overinclusive diagnostic label, and it lacked predictive validity In 1968, DSM-II described this constellation of symptoms—overactivity, restlessness, distractibility, short attention span—as a specific syndrome: “hyperkinetic reaction of childhood.” The emphasis in this diagnostic label was on the motoric symptoms, which, we now know, represents only 1 part of this disorder Our more recent classifications—those in DSM-III, DSM-III-R, and DSM-IV—have described the signs and symptoms of the disorder without implying a specific etiology, as we saw that the “minimal brain damage” diagnosis did. Our current criteria emphasize 3 main behavioral areas: inattention, impulsivity, and hyperactivity
ADHD is most likely caused by a complex interplay of factors Biologic factors that predispose an individual for ADHD include post-traumatic or infectious encephalopathy, lead poisoning, and fetal alcohol syndrome Environmental influences include abuse or neglect, family adversity, and situational stress Emerging literature provides support for the hypothesis that abnormalities in frontal networks or frontal-striatal dysfunction and catecholamine dysregulation are involved Family and twin studies reveal compelling data regarding the genetic origin of ADHD; and recent advances in neuroimaging techniques have promoted closer study of neuroanatomic correlates
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