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Keith Conners, whose work with hyperactive children established the first standards for diagnosing and treating what is now known as attention deficit hyperactivity disorder, or A.D.H.D. — and who late in life expressed misgivings about how loosely applied that label had become — died on July 5 in Durham, N.C. He was 84.

His wife, Carolyn, said the cause was heart failure.

The field of child psychiatry was itself still young when Dr. Conners joined the faculty of the Johns Hopkins University School of Medicine in the early 1960s as a clinical psychologist. Children with emotional and behavioral problems often got a variety of diagnoses, depending on the clinic, and often ended up being given strong tranquilizers as treatment. Working with Dr. Leon Eisenberg, a prominent child psychiatrist, Dr. Conners focused on a group of youngsters who were chronically restless, hyperactive and sometimes aggressive.

Doctors had recognized this type — “hyperkinesis,” it was called, or “minimal brain dysfunction” — but Dr. Conners combined existing descriptions and, using statistical analysis, focused on the core symptoms.

The 39-item questionnaire he devised, called the Conners Rating Scale, quickly became the worldwide standard for assessing the severity of such problems and measuring improvement. It was later abbreviated to 10 items, giving child psychiatry a scientific foothold and anticipating by more than a decade the kind of checklists that would come to define all psychiatric diagnosis.

He used his scale to study the effects of stimulant drugs on hyperactive children. Doctors had known since the 1930s that amphetamines could, paradoxically, calm such youngsters; a Rhode Island doctor, Charles Bradley, had published a well-known report detailing striking improvements in attention and academic performance among many children at a children’s inpatient home he ran near Providence. But it was a series of rigorous studies by Dr. Conners, in the 1960s and ’70s, that established stimulants — namely Dexedrine and Ritalin — as the standard treatments.

In recent years, rates of A.D.H.D. diagnosis have soared and drugs like Adderall and Concerta have become so widely prescribed that many patient advocates and doctors see an epidemic of overmedication. The drugs have also become a staple on college and high school campuses as de facto study aids for any striving student, diagnosis or not.

But when Dr. Conners began publishing his trials, the diagnosis was handed out far less commonly, and the treatments often made children worse.

“We take the drugs for granted today, and they’ve become controversial, but at the time these kids were being given much stronger medications — tranquilizers — that had all sorts of side effects,” James Swanson, a professor of pediatrics at the University of California, Irvine, said in an interview. “Keith was a leader in switching the field from drugs that knocked kids out to those that enhance behavior and performance.”

Through the 1990s, Dr. Conners was a force in A.D.H.D. research. He played a leading role in a long-term government-financed trial — it began recruiting patients in 1994, published its first main finding in 1999 and ran through 2014 — that compared drug treatment with behavioral therapy, a system of incremental rewards that teaches self-control and has also proved effective.

After a year, the study found that drug treatment was most effective, and sales of stimulant medications spiked. But two years into the study, the gains on medication had vanished — and, in what was considered a concession, Dr. Conners wrote in 2001 that combined behavior-drug treatment was probably the best approach.

“Keith was the godfather of medication treatment for A.D.H.D.,” said William E. Pelham, director of the Center for Children and Families at Florida International University. “That’s the best way to put it.”

Carmen Keith Conners was born on March 20, 1933, in Bingham, Utah, one of three children of Michael and Merle Conners. His father was a machinist, and his mother ran the household and worked at a department store.

The family moved frequently, as Michael Conners chased work, and eventually settled in Salt Lake City (Bingham was later razed to accommodate a copper mine). Keith entered high school there and soon proved himself an exceptional student. On a teacher’s recommendation, he applied for — and won — early entry to the University of Chicago. He left for college at 15 and never got a high school diploma.

After graduating from Chicago in 1953, he became a Rhodes scholar, earning a master’s degree from Oxford, Queens College, in 1955 in philosophy, psychology and physiology. In 1960, he completed a doctorate in clinical psychology at Harvard.

Dr. Conners’s long career took him from Johns Hopkins to Harvard Medical School to the University of Pittsburgh, George Washington University and, finally, the Duke University School of Medicine, where he founded the Duke A.D.H.D. Clinic.

Dr. Conners, who lived in Durham, was married three times. In addition to his wife, he is survived by a twin sister, Carol Wagner; six children from his first two marriages, Anthony Conners, Rachel Carr, Sarah Homolka, Rebecca Conners, Michael Conners and Katie Conners; four grandchildren; and two great-grandchildren.

After a half-century of publishing treatment studies and maintaining a clinical practice, Dr. Conners came to see the ascendance of A.D.H.D. as a mixed blessing. The explosion of the diagnosis and the reckless prescribing of stimulant drugs were hardly on his account alone: In 1991, the United States Education Department made students with A.D.H.D. officially eligible for special education, which accelerated rates of diagnosis, and drugmakers have aggressively marketed their products to parents, doctors and adults who think they have attention deficits.

But in a 2013 interview with The New York Times, Dr. Conners, then a professor emeritus at Duke, expressed dismay that some 15 percent of high schoolers reported having been given an A.D.H.D. diagnosis.

“The numbers make it look like an epidemic. Well, it’s not. It’s preposterous,” he said. “This is a concoction to justify the giving out of the medication at unprecedented and unjustified levels.”

A version of this article appears in print

on July 14, 2017,

on Page B12 of the New York edition

with the headline:

Keith Conners, 84; Aided A.D.H.D. Diagnoses.

Keith Conners,
Psychologist Who Set Standard for Diagnosing A.D.H.D., Dies at 84,
NYT,
July 13, 2017,
https://www.nytimes.com/2017/07/13/
health/keith-conners-dead-psychologist-adhd-diagnosing.html

A Natural Fix for A.D.H.D.

OCT. 31, 2014

The New York Times

SundayReview | Opinion

By RICHARD A. FRIEDMAN

ATTENTION deficit hyperactivity disorder is now the most prevalent psychiatric illness of young people in America, affecting 11 percent of them at some point between the ages of 4 and 17. The rates of both diagnosis and treatment have increased so much in the past decade that you may wonder whether something that affects so many people can really be a disease.

And for a good reason. Recent neuroscience research shows that people with A.D.H.D. are actually hard-wired for novelty-seeking — a trait that had, until relatively recently, a distinct evolutionary advantage. Compared with the rest of us, they have sluggish and underfed brain reward circuits, so much of everyday life feels routine and understimulating.

To compensate, they are drawn to new and exciting experiences and get famously impatient and restless with the regimented structure that characterizes our modern world. In short, people with A.D.H.D. may not have a disease, so much as a set of behavioral traits that don’t match the expectations of our contemporary culture.

From the standpoint of teachers, parents and the world at large, the problem with people with A.D.H.D. looks like a lack of focus and attention and impulsive behavior. But if you have the “illness,” the real problem is that, to your brain, the world that you live in essentially feels not very interesting.

One of my patients, a young woman in her early 20s, is prototypical. “I’ve been on Adderall for years to help me focus,” she told me at our first meeting. Before taking Adderall, she found sitting in lectures unendurable and would lose her concentration within minutes. Like many people with A.D.H.D., she hankered for exciting and varied experiences and also resorted to alcohol to relieve boredom. But when something was new and stimulating, she had laserlike focus. I knew that she loved painting and asked her how long she could maintain her interest in her art. “No problem. I can paint for hours at a stretch.”

Rewards like sex, money, drugs and novel situations all cause the release of dopamine in the reward circuit of the brain, a region buried deep beneath the cortex. Aside from generating a sense of pleasure, this dopamine signal tells your brain something like, “Pay attention, this is an important experience that is worth remembering.”

The more novel and unpredictable the experience, the greater the activity in your reward center. But what is stimulating to one person may be dull — or even unbearably exciting — to another. There is great variability in the sensitivity of this reward circuit.

Clinicians have long known this to be the case, and everyday experience bears it out. Think of the adrenaline junkies who bungee jump without breaking a sweat and contrast them with the anxious spectators for whom the act evokes nothing but terror and dread.

Dr. Nora D. Volkow, a scientist who directs the National Institute on Drug Abuse, has studied the dopamine reward pathway in people with A.D.H.D. Using a PET scan, she and her colleagues compared the number of dopamine receptors in this brain region in a group of unmedicated adults with A.D.H.D. with a group of healthy controls. What she found was striking. The adults with A.D.H.D. had significantly fewer D2 and D3 receptors (two specific subtypes of dopamine receptors) in their reward circuits than did healthy controls. Furthermore, the lower the level of dopamine receptors was, the greater the subjects’ symptoms of inattention. Studies in children showed similar changes in dopamine function as well.
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These findings suggest that people with A.D.H.D are walking around with reward circuits that are less sensitive at baseline than those of the rest of us. Having a sluggish reward circuit makes normally interesting activities seem dull and would explain, in part, why people with A.D.H.D. find repetitive and routine tasks unrewarding and even painfully boring.

Psychostimulants like Adderall and Ritalin help by blocking the transport of dopamine back into neurons, thus increasing its level in the brain.

Another patient of mine, a 28-year-old man, was having a lot of trouble at his desk job in an advertising firm. Having to sit at a desk for long hours and focus his attention on one task was nearly impossible. He would multitask, listening to music and texting, while “working” to prevent activities from becoming routine.

Eventually he quit his job and threw himself into a start-up company, which has him on the road in constantly changing environments. He is much happier and — little surprise — has lost his symptoms of A.D.H.D.

My patient “treated” his A.D.H.D simply by changing the conditions of his work environment from one that was highly routine to one that was varied and unpredictable. All of a sudden, his greatest liabilities — his impatience, short attention span and restlessness — became assets. And this, I think, gets to the heart of what is happening in A.D.H.D.

Consider that humans evolved over millions of years as nomadic hunter-gatherers. It was not until we invented agriculture, about 10,000 years ago, that we settled down and started living more sedentary — and boring — lives. As hunters, we had to adapt to an ever-changing environment where the dangers were as unpredictable as our next meal. In such a context, having a rapidly shifting but intense attention span and a taste for novelty would have proved highly advantageous in locating and securing rewards — like a mate and a nice chunk of mastodon. In short, having the profile of what we now call A.D.H.D. would have made you a Paleolithic success story.

In fact, there is modern evidence to support this hypothesis. There is a tribe in Kenya called the Ariaal, who were traditionally nomadic animal herders. More recently, a subgroup split off and settled in one location, where they practice agriculture. Dan T. A. Eisenberg, an anthropologist at the University of Washington, examined the frequency of a genetic variant of the dopamine type-four receptor called DRD4 7R in the nomadic and settler groups of the Ariaal. This genetic variant makes the dopamine receptor less responsive than normal and is specifically linked with A.D.H.D. Dr. Eisenberg discovered that the nomadic men who had the DRD4 7R variant were better nourished than the nomadic men who lacked it. Strikingly, the reverse was true for the Ariaal who had settled: Those with this genetic variant were significantly more underweight than those without it.

So if you are nomadic, having a gene that promotes A.D.H.D.-like behavior is clearly advantageous (you are better nourished), but the same trait is a disadvantage if you live in a settled context. It’s not hard to see why. Nomadic Ariaal, with short attention spans and novelty-seeking tendencies, are probably going to have an easier time making the most of a dynamic environment, including getting more to eat. But this same brief attention span would not be very useful among the settled, who have to focus on activities that call for sustained focus, like going to school, growing crops and selling goods.
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You may wonder what accounts for the recent explosive increase in the rates of A.D.H.D. diagnosis and its treatment through medication. The lifetime prevalence in children has increased to 11 percent in 2011 from 7.8 percent in 2003 — a whopping 41 percent increase — according to the Centers for Disease Control and Prevention. And 6.1 percent of young people were taking some A.D.H.D. medication in 2011, a 28 percent increase since 2007. Most alarmingly, more than 10,000 toddlers at ages 2 and 3 were found to be taking these drugs, far outside any established pediatric guidelines.

Some of the rising prevalence of A.D.H.D. is doubtless driven by the pharmaceutical industry, whose profitable drugs are the mainstay of treatment. Others blame burdensome levels of homework, but the data show otherwise. Studies consistently show that the number of hours of homework for high school students has remained steady for the past 30 years.

I think another social factor that, in part, may be driving the “epidemic” of A.D.H.D. has gone unnoticed: the increasingly stark contrast between the regimented and demanding school environment and the highly stimulating digital world, where young people spend their time outside school. Digital life, with its vivid gaming and exciting social media, is a world of immediate gratification where practically any desire or fantasy can be realized in the blink of an eye. By comparison, school would seem even duller to a novelty-seeking kid living in the early 21st century than in previous decades, and the comparatively boring school environment might accentuate students’ inattentive behavior, making their teachers more likely to see it and driving up the number of diagnoses.

Not all the news is so bad. Curiously, the prevalence of adult A.D.H.D. is only 3 to 5 percent, a fraction of what it is in young people. This suggests that a substantial number of people simply “grow out” of it. How does that happen?

Perhaps one explanation is that adults have far more freedom to choose the environment in which they live and the kind of work they do so that it better matches their cognitive style and reward preferences. If you were a restless kid who couldn’t sit still in school, you might choose to be an entrepreneur or carpenter, but you would be unlikely to become an accountant. But what is happening at the level of the brain that may explain this spontaneous “recovery”?

To try to answer that question, Aaron T. Mattfeld, a neuroscientist at the Massachusetts Institute of Technology, now at Florida International University in Miami, compared the brain function with resting-state M.R.I.s of three groups of adults: those whose childhood A.D.H.D persisted into adulthood; those whose had remitted; and a control group who never had a diagnosis of it. Normally, when someone is unfocused and at rest, there is synchrony of activity in brain regions known as the default mode network, which is typically more active during rest than during performance of a task. (In contrast, these brain regions in people with A.D.H.D. appear functionally disconnected from each other.) Dr. Mattfeld found that adults who had had A.D.H.D as children but no longer had it as adults had a restoration of the normal synchrony pattern, so their brains looked just like those of people who had never had it.

WE don’t yet know whether these brain changes preceded or followed the behavioral improvement, so the exact mechanism of adult recovery is unclear.

But in another measure of brain synchrony, the adults who had recovered looked more like adults with A.D.H.D.

In people without it, when the default mode network is active, another network, called the task-positive network, is inhibited. When the brain is focusing, the task-positive network takes over and quiets the default mode network. This reciprocal relationship is necessary in order to focus.

Both groups of adult A.D.H.D. patients, including those who had recovered, displayed simultaneous activation of both networks, as if the two regions were out of step, working at cross-purposes. Thus, adults who lost most of their symptoms did not have entirely normal brain activity.

What are the implications of this new research for how we think about and treat kids with A.D.H.D.? Of course, I am not suggesting that we take our kids out of school and head for the savanna. Nor am I saying we that should not use stimulant medications like Adderall and Ritalin, which are safe and effective and very helpful to many kids with A.D.H.D.

But perhaps we can leverage the experience of adults who grew out of their symptoms to help these kids. First, we should do everything we can to help young people with A.D.H.D. select situations — whether schools now or professions later on — that are a better fit for their novelty-seeking behavior, just the way adults seem to self-select jobs in which they are more likely to succeed.

In school, these curious, experience-seeking kids would most likely do better in small classes that emphasize hands-on-learning, self-paced computer assignments and tasks that build specific skills.

This will not eliminate the need for many kids with A.D.H.D. to take psychostimulants. But let’s not rush to medicalize their curiosity, energy and novelty-seeking; in the right environment, these traits are not a disability, and can be a real asset.

Richard A. Friedman is a professor of clinical psychiatry and the director of the psychopharmacology clinic at the Weill Cornell Medical College.

A version of this op-ed appears in print on November 2, 2014, on page SR1 of the New York edition with the headline: A Natural Fix for A.D.H.D..

A Natural Fix for A.D.H.D.,
NYT,
31.10.2014,
http://www.nytimes.com/2014/11/02/
opinion/sunday/a-natural-fix-for-adhd.html

Use of Antipsychotics in Children

Is Criticized

November 19, 2008

The New York Times

By GARDINER HARRIS

WASHINGTON — Powerful antipsychotic medicines are being used far too cavalierly in children, and federal drug regulators must do more to warn doctors of their substantial risks, a panel of federal drug experts said Tuesday.

More than 389,000 children and teenagers were treated last year with Risperdal, one of five popular medicines known as atypical antipsychotics. Of those patients, 240,000 were 12 or younger, according to data presented to the committee. In many cases, the drug was prescribed to treat attention deficit disorders.

But Risperdal is not approved for attention deficit problems, and its risks — which include substantial weight gain, metabolic disorders and muscular tics that can be permanent — are too profound to justify its use in treating such disorders, panel members said.

“This committee is frustrated,” said Dr. Leon Dure, a pediatric neurologist from the University of Alabama School of Medicine who was on the panel. “And we need to find a way to accommodate this concern of ours.”

The meeting on Tuesday was scheduled to be a routine review of the pediatric safety of Risperdal and Zyprexa, popular antipsychotic medicines made, respectively, by Johnson & Johnson and Eli Lilly & Company. Food and Drug Administration officials proposed that the committee endorse the agency’s routine monitoring of the safety of the medicines in children and support its previous efforts to highlight the drugs’ risks.

But committee members unanimously rejected the agency’s proposals, saying that far more needed to be done to discourage the medicines’ growing use in children, particularly to treat conditions for which the medicines have not been approved.

“The data show there is a substantial amount of prescribing for attention deficit disorder, and I wonder if we have given enough weight to the adverse-event profile of the drug in light of this,” Dr. Daniel Notterman, a senior health policy analyst at Princeton University and a panel member, said when speaking about Risperdal.

Drug agency officials responded that they had already placed strongly worded warnings on the drugs’ labels.

“I’m a little puzzled about the statement that the label is inadequate,” said Dr. Thomas Laughren, director of the agency’s division of psychiatry products. “I’m anxious to hear what more we can do in the labeling.”

Kara Russell, a spokeswoman for Johnson & Johnson, said, “Adverse drug reactions associated with Risperdal use in approved indications are accurately reflected in the label.”

But panelists said the current warnings were not enough.

While panel members spoke at length about Risperdal, they said their concerns applied to the other medicines in its class, including Zyprexa, Seroquel, Abilify and Geodon.

The committee’s concerns are part of a growing chorus of complaints about the increasing use of antipsychotic medicines in children and teenagers. Prescription rates for the drugs have increased more than fivefold for children in the past decade and a half, and doctors now use the drugs to settle outbursts and aggression in children with a wide variety of diagnoses, even though children are especially susceptible to their side effects.

A consortium of state Medicaid directors is evaluating the use of the drugs in children on state Medicaid rolls to ensure that they are being properly prescribed.

The growing use of the medicines has been driven partly by the sudden popularity of the diagnosis of pediatric bipolar disorder.

The leading advocate for the bipolar diagnosis is Dr. Joseph Biederman, a child psychiatrist at Harvard University whose work is under a cloud after a Congressional investigation revealed that he had failed to report to his university at least $1.4 million in outside income from the makers of antipsychotic medicines.

In the past year, Risperdal prescriptions to patients 17 and younger increased 10 percent, while prescriptions among adults declined 5 percent. Most of the pediatric prescriptions were written by psychiatrists.

From 1993 through the first three months of 2008, 1,207 children given Risperdal suffered serious problems, including 31 who died. Among the deaths was a 9-year-old with attention deficit problems who suffered a fatal stroke 12 days after starting therapy with Risperdal.

At least 11 of the deaths were children whose treatment with Risperdal was unapproved by the F.D.A. Once the agency approves a medicine for a particular condition, doctors are free to prescribe it for other problems.

Panel members said they had for years been concerned about the effects of Risperdal and similar medicines, but F.D.A. officials said no studies had been done to test the drugs’ long-term safety.

Dr. Dure said he was concerned that doctors often failed to recognize the movement disorders, including tardive dyskinesia and dystonia, that can result from using these medicines.

“I have a bias that extra-pyramidal side effects are being under-recognized with these agents,” Dr. Dure said.

Dr. Laughren of the F.D.A. said the agency could do little to fix the problem. Instead, he said, medical specialty societies must do a better job educating doctors about the drugs’ side effects.

Use of Antipsychotics in Children Is Criticized,
NYT,
19.11.2008,
https://www.nytimes.com/2008/11/19/
health/policy/19fda.html

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