Driven to Distraction (Revised)
Page 33
7. It is difficult to decide whom to tell about ADD, and difficult to decide how to tell about it.
It should be possible to talk about having ADD without encountering suspicions or disbelief. However, this is rarely the case. People who know nothing about what ADD is—and that includes most people—can easily misunderstand a description of ADD. They may think it is an excuse for being lazy, or that it means the person is mentally ill, or that it is just a fancy word for stupid. In telling other people about ADD, one should anticipate these misunderstandings and not be thrown off by them. Have information ready with which to correct the misconceptions. Try not to get defensive, but rather be sympathetic with the other person’s point of view. They have never heard of ADD and at first it sounds pretty fishy. “You mean, there’s a neurological condition to explain why you’re late, forgetful, impulsive, and disorganized? Give me a break,” they may say. Be patient. Over time you will be able to explain it to them, and you may find they start thinking of other people who have it, maybe even themselves.
Bringing it up in the workplace can be particularly tricky. There is a law now to protect against discrimination on the basis of disabilities, and this includes ADD. The Americans with Disabilities Act of 1990 (ADA) makes it unlawful to discriminate in employment against a qualified individual with a disability. ADD is considered a disability that is guaranteed protection under this law. (For further information about this very significant law, write to the Equal Employment Opportunity Commission, 1801 L Street, NW, Washington, D.C. 20507, or telephone 202-663-4900.)
However, one may still fear the kind of discrimination that is hard to pin down, the kind of discrimination that invisibly can undermine one’s career without being explicit enough to file a grievance over.
The best way of dealing with this situation is to find your way slowly. Make inroads, form alliances, and when you feel you have some basis of trust, bring up the subject of ADD in the abstract. Do some advance educating before you volunteer the fact that you have it yourself. It is well worth doing this, because if your boss can understand what ADD is, it can make your work life much more satisfying and productive. It is simple to devise an ADD program for the workplace as long as the workplace is receptive to it—and remember, an employer is bound, under law, to be receptive to what are called “reasonable accommodations” in the workplace. The same kinds of strategies that work in the classroom—structure, lists, reminders, breaking large tasks down into small, elimination of time limits, reduction of distracting stimuli, encouragement, and support—help a great deal in the workplace as long as the environment is receptive. And not only does the law mandate that the employer be receptive, it is also in the employer’s best interest: people with ADD are hard, energetic workers. Tapping into their true potential is like harnessing rushing rapids to a hydroelectric turbine.
8. It is impossible to find a knowledgeable clinician in your area to diagnose and/or treat ADD, or you can’t find information on ADD.
There are several good places to go for information on where to get treatment. First, there is your state medical society, as well as your state neurological, pediatric, and psychiatric societies. Second, any medical school in your area can help you find a specialist in ADD. Just ask for the department of neurology or the department of pediatrics or the department of psychiatry or child psychiatry. Third, there are several organizations and newsletters devoted to ADD. These are excellent sources of information as well as support groups. We offer a partial listing here and a fuller listing at the end of this book.
Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD), a national organization, is a robust and active group offering information and support to all people involved with ADD. CHADD and its indefatigable staff have been at the forefront of advocating both politically and socially for all those with ADD. Although originally founded to help children with ADD, CHADD has now expanded to include adult ADD as well. The address of its headquarters is 499 NW 70th Avenue, Suite 308, Plantation, FL 33317. Telephone: (305) 587-3700.
The Attention Deficit Information Network (AD-IN) is another excellent national organization devoted to helping people with ADD. Its address is 475 Hillside Avenue, Needham, MA 02194. Telephone: (617) 455-9895.
ADDendum is a newsletter for adults with ADD. For more information, write to its editor, Paul Jaffe, Box 296, Scarborough, NY 10510.
The ADDult Support Network is an innovative organization that publishes a newsletter for adults called the ADDult News. Address: 2620 Ivy Place, Toledo, OH 43613.
Challenge, Inc., publishes an excellent newsletter on ADD. Address: Box 488, West Newbury, MA 01985. Telephone: (508) 462-0495.
The Orton Dyslexia Society is a national organization devoted to the treatment of dyslexia in children and adults. The society and its highly distinguished directors and advisors are active in promoting the understanding of ADD, particularly as it interfaces with dyslexia. Address: Chester Building, Suite 382, 8600 LaSalle Road, Baltimore, MD 21204-6020. Telephone: (301) 296-6232.
The Appendix to this book contains more listings.
9. Attempts at structuring keep falling apart.
Once the individual understands the importance of structure and goes to the trouble of setting up a solid system of organization for himself, he often finds that the system keeps collapsing, or that his attempts to abide by the system repeatedly fail. This is where a coach can be invaluable. Rather than letting the system collapse, the coach can help the individual revise the system, or can offer encouragement to stay with the system. It is not surprising, after all, for it to take a while for the new system to start to work; it is replacing a lifetime of no system. However, the person with ADD can get discouraged very quickly, not wanting to experience another failure, and so back away. At these moments the coach can intervene, offering reassurance, support, and hope.
10. There are lingering feelings of shame and embarrassment about having ADD.
This is a very common reaction, particularly if the syndrome is not explained properly. We tend to stigmatize any condition that affects the brain. However, with support and education the individual should come to realize that ADD has as many advantages as disadvantages, that there are many highly successful people in the world who have ADD, that the company of Mozart, Edison, Einstein, and Dustin Hoffman isn’t bad, and that the most dangerous stigma comes from within. People with ADD should stand up and be proud. While their lives may be full of struggle, their contributions to the joy and humor, as well as the productivity, of this world are great.
9
A Local Habitation and a Name
THE BIOLOGY OF ADD
Attention deficit disorder lives in the biology of the brain and the central nervous system. Although environmental factors do influence the course of ADD over a lifetime, most practitioners in the field now agree that the characteristic problems of people with ADD stem from neurobiological malfunctioning. It is our understanding of the biological component of the syndrome that has revolutionized our thinking about ADD in the past decade and shaped our ability to treat it as effectively as we can today.
We still have much to learn. The exact mechanism underlying ADD remains unknown. There is no single lesion of the brain, no single neurotransmitter system, no single gene we have identified that triggers ADD. The precise workings of the brain that underlie ADD have so far escaped us, in part due to the extraordinary complexity of the attentional system.
The attentional system involves nearly all structures of the brain in one way or another. It governs our consciousness, our waking experience, our actions and reactions. It is the means through which we interact with our environment, whether that environment is composed of math problems, other people, or the mountains on which we ski.
Still, we have been able to take some steps toward defining, in terms of the anatomy and chemistry of the brain, the underpinnings of ADD. With every step forward we become more sure what the disorder is not: it is not willful
misbehaving, it is not a moral failing, it is not a lack of trying nor an inability to take an interest in the world. Neurobiological data now show that the syndrome is rooted in the central nervous system.
How psychologists and medical researchers, building on one another’s insights over the past century, have come this far in defining the nature and causes of ADD is a fascinating story of deduction and persistence.
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
“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;
He wriggles,
And giggles,
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 …
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?
The story might start with the earlier-mentioned 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 conduct.
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 discoveries 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 the syndrome.
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 information.
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 ADD.