Attention-Deficit/Hyperactivity Disorder (ADHD), once thought to occur only in children, is now recognized as continuing into adulthood in many people. It is now understood to be a chronic condition with symptoms experienced over a lifetime; it is estimated to affect as many as 4% of adults worldwide. In the U.S., approximately 20% of adults who meet the criteria for ADHD have ever been diagnosed and treated for it.
ADHD is characterized by difficulty initiating or completing tasks, sustaining attention, and controlling impulsive actions. Patients may have difficulties with organization and time management. As a result of these difficulties, ADHD can have serious negative impacts on the educational, social, and occupational lives of those who experience these symptoms.
Three types of ADHD are diagnosed:
- Combined inattentive and hyperactive-impulsive (this is the most common type, found in about 80% percent of patients).
- Predominantly inattentive (about 15%).
- Predominantly hyperactive-impulsive (about 5%)
The terminology can be confusing. Attention Deficit Disorder (ADD) is an older term for what is now called Attention-Deficit/Hyperactivity Disorder (ADHD). There is no longer any actual disorder “officially” called ADD, but some people still use ADD (or Adult ADD) to refer to the type of ADHD that is predominantly inattentive, and use ADHD (or Adult ADHD) for the type of ADHD that is predominantly hyperactive or impulsive. However, these all refer to the same disorder, and in regard to medications, the treatments are generally the same. Hyperactive symptoms often improve by adulthood, and it is for this reason that it was previously thought that patients outgrow ADHD. It is now clear, however, that inattentive symptoms usually do not resolve, though they are not always outwardly apparent if someone has structured their life in a way that avoids situations requiring extended periods of sustained focus.
Although the exact mechanism is unknown, a number of associated neurochemical abnormalities have been observed, and considerable evidence suggests that the disorder has a strong genetic component and a biological underpinning; the pathophysiology includes dysfunction in both norepinephrine and dopamine activity, particularly in the frontal cortex.