Where the story began is impossible to say. Certainly, the symptoms of ADD have
been with us as long as history has been recorded. However, the modern story of
ADD, the story of bringing those symptoms out of the realm of morality and
punishment and into the realm of science and treatment, began somewhere around
the turn of the century.
In 1904 one of the world's most prestigious medical journals, the British
journal Lancet published a little doggerel verse that might be
the first published account of ADD in the medical literature.
The Story of Fidgety Philip
Fidgety Phil has had many incarnations in popular culture, including Dennis the
Menace and Calvin from "Calvin and Hobbes." Most everybody knows a little boy
who bangs into things, climbs to the top of trees, scales the furniture, beats
up on his siblings, talks back, and displays all the characteristics of being
out of control, maybe a little bit of a bad seed, despite the generosity and
best efforts of the parents. How can this be explained? And how is it that this
person has existed throughout the centuries?
"Let me see if Philip can
Be a little gentleman;
Let me see if he is able
To sit still for once at the table."
Thus Papa bade Phil behave;
And Mama looked very grave.
But Fidgety Phil,
He won't sit still;
And then, I declare,
Swings backwards and forwards,
And tilts up his chair,
Just like any rocking horse--
"Philip! I am getting cross!"
See the naughty, restless child
Growing still more rude and wild,
Till his chair falls over quite.
Philip screams with all his might,
Catches at the cloth, but then
That makes matters worse again.
Down upon the ground they fall,
Glasses, plates, knives, forks and all.
How Mama did fret and frown,
When she saw them tumbling down!
And Papa made such a face!
Philip is in sad disgrace . . .
The story might start with . . . George Frederic Still, M.D.,
who in 1902 described a group of twenty children who were defiant, excessively
emotional, passionate, lawless, spiteful, and had little inhibitory volition.
This group consisted of three boys for every girl, and their troubling
behaviors all had appeared before the age of eight. What was most striking to
Still was that this group of kids had been raised in benign environments, with
"good-enough" parenting. Indeed, those children who had been subject to poor
child-rearing were excluded from his analysis. He speculated, in light of the
adequate rearing these children received, there might be a biological basis to
the unbounded behavior, a genetically inherited proneness toward moral
corruption. He gained confidence in his theory when he discovered that some
members of these children's families had psychiatric difficulties such as
depression, alcoholism, and conduct problems.
While it was certainly possible that the pathology was psychological only, and
was passed down from generation to generation as a kind of family neurosis,
Still proposed that genetics and biology should be considered at least as much
as free will in assessing the cause of these children's problems. This was a
new way of thinking.
Although it would be decades before there was conclusive evidence bearing Still
out, his new way of thinking was pivotal. In the nineteenth century--and
before--"bad" or uncontrollable behavior in children was seen as a moral
failing. Either the parents or the children or both should be held responsible.
The usual "treatment" for these children was physical punishment. Pediatric
textbooks from that era are full of descriptions of how to beat a child and
exhortations on the necessity of doing so. As clinicians began to speculate
that neurology, rather than the devil, was governing behavior, a kinder, more
effective approach to child-rearing emerged.
The puzzling contradiction between upbringing and behavior in this population
of children captured the imagination of turn-of-the-century psychologists.
Still's observations supported the theory of William James, the father of
American psychology. James saw the deficits in what he called inhibitory
volition, moral control, and sustained attention as being causally related to
each other through an underlying neurological defect. Cautiously, he speculated
on the possibility of either a decreased threshold in the brain for inhibition
of response to various stimuli, or a syndrome of disconnection within the
cortex of the brain in which intellect was dissociated from "will," or social
The trail of Still and James was picked up in 1934, when Eugene Kahn and Louis
H. Cohen published a piece called "Organic Driveness" in the New England
Journal of Medicine. Kahn and Cohen asserted that there was a
biological cause for the hyperactive, impulse-ridden, morally immature behavior
of the people they were seeing who had been hit by the encephalitis epidemic of
1917-18. This epidemic left some victims chronically immobile (as those
described by Oliver Sacks in his book Awakenings) and others
chronically insomniac, with impaired attention, impaired regulation of
activity, and poor impulse control. In other words, the characteristics
plaguing this latter group were what we now take to be the diagnostic triad of
ADD symptoms: distractibility, impulsivity, and restlessness. Kahn and Cohen
were the first to provide an elegant description of the relationship between an
organic disease and the symptoms of ADD.
At about the same time, Charles Bradley was developing another line of evidence
linking ADD-like symptoms to biological roots. In 1937, Bradley reported
success in using benzedrine, a stimulant, to treat behaviorally disordered
children. This was a serendipitous discovery that was quite counterintuitive;
why should a stimulant help hyperactive children become less stimulated? Like
many important discoverers in medicine, Bradley couldn't explain his discovery;
he could only report its veracity.
Soon this population of children would be labeled MBD--minimal brain
dysfunction--and treated with Ritalin and Cylert, two other stimulants that
were found to have a dramatic effect on the behavioral and social symptoms of
the syndrome. By 1957 there was an attempt to match the symptoms of what was by
then called the "hyperkinetic syndrome" with a specific anatomical structure in
the brain. Maurice Laufer, in Psychosomatic Medicine, placed the
location of dysfunction at the thalamus, a midbrain structure. Laufer saw
hyperkinesis as proof that the work of the thalamus which was to filter
stimuli, had gone awry. Although his hypothesis was never proved, it did
promote the conception of the disorder as one defined by an overactivity of a
part of the brain.
Throughout the sixties, clinical skill with the hyperkinetic population
improved, and the clinician's powers of observation grew more attuned to the
nuances of the children's behavior. It became more apparent to the clinician's
eye that the syndrome somehow was due to genetically based malfunctioning of
biological systems rather than to bad parenting or bad behavior. The definition
of the syndrome has evolved through family studies and statistical analysis of
epidemiological data that absolve parents and children of blame (although the
pernicious and unfair tendency to blame parents and children persists to this
day among the ill informed).
By the early seventies the definition of the syndrome included not just the
behaviorally evident hyperactivity, but also the more subtle symptoms of
distractibility and impulsivity. By then, we knew that ADD clustered in
families and was not caused by bad parenting. We knew that the symptoms were
often improved by the use of stimulant medication. We thought we knew, but
couldn't prove, that ADD had a biological basis, and that it was genetically
transmitted. However, this more accurate and encompassing view was not
accompanied by any major new discoveries related to the biological causes of
Due to the lack of further biological evidence, some people argued that ADD was
a mythical disorder, an excuse contrived to exonerate reprobate children and
their parents. As is usually the case in psychiatry, the intensity of the
debate was inversely proportional to the availability of factual
As in a good mystery, the journey from suspicion to proof, from speculation to
empirical evidence, from Kahn and Cohen to Paul Wender and Alan Zametkin and
Rachel Gittleman-Klein and the other current researchers, has been riddled with
false leads, multiple possibilities, contradictory findings, and many gut
reactions of all kinds.
One of the first attempts to unite the effects of the stimulants with what we
know about the brain was made by C. Kornetsky, who in 1970 proposed the
Catecholamine Hypothesis of Hyperactivity. Catecholamines are a class of
compounds that includes the neurotransmitters norepinephrine and dopamine.
Since the stimulants affect the norepinephrine and dopamine neurotransmitter
systems by increasing the amount of these neurotransmitters, Kornetsky
concluded that ADD possibly was caused by an underproduction or
underutilization of these neurotransmitters. Although this hypothesis is still
tenable, biochemical studies and clinical tests of neurotransmitter metabolites
in urine over the past two decades have not been able to document the specific
role of the catecholamines in ADD.
No single neurotransmitter system may be the sole regulator of ADD. Neurons can
convert dopamine into norepinephrine. Many of the drugs that act on the
catecholamines act on serotonin. Some of the drugs that act on serotonin can
act on norepinephrine and dopamine. And we can't rule out the role of other
neurotransmitters like GABA (gamma amino butyric acid), which have showed up in
some biochemical studies. The most likely possibility is that the effect of
dopamine and norepinephrine and serotonin is key and drugs that alter these
neurotransmitters will have the most telling effect on the symptomatology of
So can we say that ADD is a chemical imbalance? Like most questions in
psychiatry, the answer is yes and then again no. No, we have not found a good
way to measure the specific imbalances in the neurotransmitter systems that may
be responsible for the ADD. But yes, there is enough evidence that
neurochemical systems are altered in people with ADD to state that the problem
derives from the chemistry of the brain. Most likely, it is a dysregulation
along the catecholamine-serotonin axis, a dance where one misstep by one
partner creates a misstep by the other, which creates another misstep by the
first. Before they know it, these dance partners are out of step not just with
each other but with the music--and who is to say how it happened?
home · watch the program · four families · adhd drugs · adhd · backlash
readings · adhd in schools · interviews · discussion · the producers · viewers' guide
synopsis · tapes & transcripts · press reaction · credits
frontline · wgbh · pbs online
pill photograph copyright ©2001 photodisc all rights reserved
web site copyright 1995-2014
WGBH educational foundation