A History of Explanations

The following is adapted from Hallowell’s Driven to Distraction - specifically, Chapter 9 titled Local Habitation and a Name - The Biology of ADD, where he analyzes the history of various conceptualizations of the brain physiology of ADD/ADHD.

It might be said that ADD/ADHD was first described in 1902 by George Still. He found a group of 15 boys and 5 girls that were defiant, excessively emotional, passionate, lawless, spiteful, and with little inhibitory volition. Because these children were from adequate, non-dysfunctional families, Still postulated that there was a biological underpinning to ADD/ADHD, and it was not merely a psychological phenomenon.

The stimulant Benzedrine was first used in 1937 - by Charles Bradley - to treat ADD/ADHD children. Soon after, this condition was labeled Minimum Brain Dysfunction (MBD), and was treated with the stimulants Ritalin and Cylert.

In 1957, the condition was labeled Hyperkinetic Syndrome by Maurice Laufer, who claimed it was the result of overactivity of the thalamus. By the early 1970s, the more subtle symptoms of impulsivity and distractibility were added to hyperactivity in defining what was then called ADD/ADHD. It was proposed that hyperactivity was caused by a problem with the neurotransmitters called catecholamines.

Alan Zametkin carefully measured the brain glucose consumption of a group of 25 subjects identified as having ADD/ADHD - hyperactive as children and diagnosed according to Wender’s Utah Criteria. By using a PET scan, he found that the group had an average 8% decrease in glucose consumption compared to the control group.

In 1986, Chelune formulated the Frontal Lobe Hypothesis which states the hyperactivity and impulsivity are forms of disinhibition - the brain loses its ability to put on the brakes due to disturbed inhibition of the cortex. Also, Lou’s study showed a decrease in glucose consumption by the right hemisphere of the brain. The right hemisphere controls decision making capacities, visual-spatial abilities, and multi-tasking information processing. Right hemisphere disabilities sound like the AH qualities of losing their keys, always getting lost, never paying attention to the big picture, and never quite understanding other people.

Patricia Goldman-Rakic postulates that ADD/ADHD is a problem of working memory - an inability to profit from their experiences, focus on consequences, and navigate tasks and social situations. Accordingly, life seems discontinuous; no sense of history and each experience is met cold. The ADDer can’t stop the relentless flow of events. All runs together unbraked, uninhibited - the verbal rush, the inability to stop the words, and the verbal paralysis or stuttering resulting from an inability to stop the thoughts long enough to find the words. Social intrusiveness is an inability to stop at another's boundaries. Failure to form intimate relationships due to inability to pause long enough to listen to the other. Impulsivity, lack of planning, and outbursts are the inability to restrain the flow of action and feeling.

It has been estimated that if both parents have ADD/ADHD, then the likelihood of the children having it as well is between 30% and 70%. To determine the genetic nature of ADD/ADHD, 127 sets of identical and 111 sets of fraternal twins were studied. It was found that if one of the identical twins had ADD/ADHD, then 51% of the counterpart had it as well, compared to only 33% in the case of fraternal twins. This established ADD/ADHD as a condition with genetic origins, since identical twins studies of most genetic disorders have shown an approximate 50% concordance rate.

In 1991, David and Brenda Comings concluded their study of the relationship between the D2 Dopamine Receptor Gene and neuropsychiatric disorders. In a sample of over 300, they found the gene more frequently in those assessed as having Tourette’s Syndrome, ADD, Autism, or Alcoholism.