“Since the 1940s, psychiatrists have applied various labels to children who are hyperactive and inordinately inattentive and impulsive. Such youngster have been considered to have “minimal brain dysfunction,” “brain-injured child syndrome,” hyperkinetic reaction of childhood,” hyperactive child syndrome,” and most recently, “attention deficit disorder.” The frequent name change reflects how researchers have been about the underlying causes of, and even the precise diagnostic criteria for, the disorder.”
Russell A. Barkley, Ph.D., is an internationally recognized authority on attention deficit hyperactivity disorder (ADHD or ADD) in children and adults. Barkley has specialized in ADHD for more than 35 years and is currently Clinical Professor of Psychiatry at the Medical University of South Carolina.
Interesting history of ADHD
Hippocrates (493 BCE) describes a condition that seems to be compatible with what we know now as ADHD. Hippocrates describes patients who had “quickened responses to sensory experience, but also less tenaciousness because the soul moves on quickly to the next impression.” Hippocrates attributed this condition to an “overbalance of fire over water.”
John Locke, 17th century philosopher, describes a perplexing group of young students who, “try as they might, they cannot keep their minds from straying.”
Sir Alexander Crichton (1798) describes what seems to be a mental state much like the inattentive subtype of ADHD when he describes a “mental restlessness.” He observes that, “In this disease of attention, if it can with propriety be called so, every impression seems to agitate the person, and gives him or her an unnatural state of mental restlessness.” He continues to opine “the incapacity of attending with a necessary degree of constancy to ay one object, almost always arises from an unnatural or morbid sensitivity of the nerves, by which means this faculty is incessantly withdrawn from one impression to another. It may be born with a person, or it may be the effect of accidental disease.” Crichton noted that, “they have a particular name for this state of their nerves, which is expressive enough of their feelings. They say they have the fidgets.”
Heinrich Hoffmann (1845) became interested in writing for children when he couldn’t find suitable materials to read to his 3-year-old son. The result was a book of poems, complete with illustrations, about children and their undesirable behaviors. One, The Story of Fidgety Philip, was a description of a little boy who could be interpreted as having ADHD.
President Abraham Lincoln third son Tad fits the picture. He was described as hyperactive, impulsive (bursting into Oval Office while chasing his brother), and inattentive. He had learning problems and many tutors quit, saying he was not teachable.
Mrs. Lincoln struggled with impulsivity and on a number of occasions she overspent the White House budget causing political embarrassment and ridicule for the president. One time when President Lincoln was reviewing troops, a young captain’s wife caught his eye. Mrs. Lincoln noticed and she started screaming at her husband in front of the troops.
George Still, (1902) a British pediatrician, could be credited for starting the medical record on ADHD. Still describes a group of children who were hyperactive, impulsive, and inattentive. He published an account of 20 children in his practice who were "passionate," defiant, spiteful, and lacking "inhibitory volition." Still made the then radical suggestion that bad parenting was not to blame; instead, he suspected a subtle brain injury. He didn’t understand ADHD as a medical term and labeled these children as “morally defective.”
In 1918-1919, Still’s theory gained greater credence in the years following the 1917-18 the world-wide influenza pandemic left many survivors with viral encephalitis when doctors observed that the infection left some children with impaired attention, memory and control over their impulses. This caused researchers and doctors to believe that the condition was the result of injury rather than heredity.
In the 1930s, children now labeled as having ADHD were now labeled “minimal brain damage.”
Charles Bradley, (1937), a Rhode Island pediatrician, gave stimulants (amphetamines) to boys in a hospital ward whose behavior was out of control (subjected to beatings) and noticed it stimulated focus. This discovery disturbed many people. Since Charles Bradley's initial 1937 report of effective treatment with stimulants of children at the Emma Pendleton Bradley Hospital in East Providence, ADHD has received more scientific scrutiny than any other childhood psychiatric disorder
In the 1966, the labeled changes from “minimal brain damage” to “minimal brain dysfunction”
In 1968, the DSM-II began to call what is now called ADHD as “hyperkinetic reaction of childhood”
Terms describing ADHD have been part of the psychiatric terminology since the inception of the Diagnostic and Statistical Manual of Mental Disorders (DSM, the diagnostic bible listing clinical criteria for various psychiatric disorders) since 1952 published by the American Psychiatric Association.
Leopold Bellak, Hans Hussey, and Paul Wender in the 1970s observed that ADHD didn’t necessarily disappear at puberty, some people continued to have this condition into adulthood. Now estimate that 60% of children who have ADHD as children have it as adults. They also discovered that females have ADHD but where less disrupted than males, were more inattentive and prone to daydreaming, did not call attention to themselves due to behavioral issues, and therefore weren’t diagnosed as often.
By the mid-1970s, Ritalin had become the most prescribed drug for what was eventually termed, in 1987, attention deficit hyperactivity disorder.
In 1980, the name Attention Deficit Disorder (ADD) with or without hyperactivity was first introduced in the DSM-III
In 1987, the terminology ADD technically expired with the revision to ADHD in the DSM-III-R
Alan Zametkin (1990) and his colleagues at the National Institute of Mental Health proved the biological existence of ADHD. Zametkin reached a milestone with the publication in the New England Journal of Medicine (November 15, 1990) a study that linked hyperactivity in adults with metabolism of glucose in the premotor cortex and the superior prefrontal cortex - areas of the brain involved in the control of attention, planning, and motor activity.
In 1994, the DSM-IV introduced ADHD with sub-types
Xavier Castellanos (2002) et al. shows that the brains of children with attention-deficit/hyperactivity disorder (ADHD) average smaller than children without ADHD. Their study provides compelling evidence that ADHD is a real, biologically based phenomenon not imagined by neither parents nor teachers nor caused by medical treatment for the condition.
Summary of the research of brain size differences in children with ADHD
The brain of children and adolescents in whom ADHD is diagnosed are on the average 3 percent to 4 percent smaller in volume than those children without the condition. More specifically, the dorsolateral frontal lobes are 5 percent smaller, the basal ganglia 7 percent smaller, and the cerebellum 11-to 15-percent smaller. However, people with smaller brains are not necessarily less intelligent.
The largest size differences found is in the cerebellum, a brain structure just above the brainstem, which is involved in muscle tone, balance, the synchronization of muscle activity, and perhaps other functions. The caudate nucleus, an area deep in the brain that is believed to serve as a relay station for information important in regulating attention and activity level, is also significantly smaller in younger children with ADHD. But by the time the children are 15, the caudate did not differ in size.
The greater the severity of a child’s symptoms, the greater the discrepancy in the size of the various brain areas, as measured on brain scans. The smaller the brain, the greater the symptoms.
Children’s brains with ADHD lag about two to three important years behind in their social-emotional development.
Reading and attention disorders both seem to stem from the same primitive part of the brain that governs thinking and muscle control. Researchers at Yale University discovered that children with ADHD had low activity in their basal ganglia. The basal ganglion is an inhibitory organ that can also activate areas of the brain.
The neurotransmitter dopamine regulates the basal ganglion. Ritalin apparently increases the inhibitory effect, dropping people with ADHD to a calmer and more attentive state. The drug blocks the dopamine transported, a system that clears away dopamine, allowing the dopamine to accumulate.