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Archive for the ‘ADHD stimulant treatment’ Category

Continued Increases in Adhd Diagnoses, Treatment With Meds Among US Children

In ADHD, ADHD child/adolescent, ADHD stimulant treatment, Child/Adolescent Psychology, Psychiatry, Psychopharmacology on Tuesday, 26 November 2013 at 07:09

Continued Increases in Adhd Diagnoses, Treatment With Meds Among US Children

Nov. 22, 2013 — A new study led by the CDC reports that half of U.S. children diagnosed with ADHD received that diagnosis by age 6.

The study published in the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP) found that an estimated two million more children in the United States (U.S.) have been diagnosed with attention-deficit/hyperactivity disorder (ADHD) between 2003-04 and 2011-12. One million more U.S. children were taking medication for ADHD between 2003-04 and 2011-12. According to the study conducted by the Centers for Disease Control and Prevention (CDC):

* 6.4 million children in the U.S. (11 percent of 4-17 year olds) were reported by their parents to have received an ADHD diagnosis from a healthcare provider, a 42 percent increase from 2003-04 to 2011-12.

* Over 3.5 million children in the U.S. (6 percent of 4-17 year olds) were reported by their parents to be taking medication for ADHD, a 28 percent increase from 2007-08 to 2011-12.

Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurobehavioral disorders of childhood. It often persists into adulthood. Children with ADHD may have trouble paying attention and/or controlling impulsive behaviors. Effective treatments for ADHD include medication, mental health treatment, or a combination of the two. When children diagnosed with ADHD receive proper treatment, they have the best chance of thriving at home, doing well at school, and making and keeping friends.

According to CDC scientists, children are commonly being diagnosed at a young age. Parents report that half of children diagnosed with ADHD were diagnosed by 6 years of age, but children with more severe ADHD tended to be diagnosed earlier, about half of them by the age of 4.

“This finding suggests that there are a large number of young children who could benefit from the early initiation of behavioral therapy, which is recommended as the first-line treatment for preschool children with ADHD,” said Susanna Visser, of the Centers for Disease Control and Prevention, lead author of the study.

The study increases our knowledge of ADHD treatment. Nearly 1 in 5 or 18 percent of children with ADHD did not receive mental health counseling or medication in 2011-2012. Of these children, one-third were reported to have moderate or severe ADHD.

“This finding raises concerns about whether these children and their families are receiving needed services,” said Dr. Michael Lu, Senior Administrator, Health Resources and Service Administration (HRSA).

The study also found that:

* Seven in 10 children (69 percent) with a current diagnosis of ADHD were taking medication to treat the disorder.

* Medication treatment is most common among children with more severe ADHD, according to parent reports.

* States vary widely in terms of the percentage of their child population diagnosed and treated with medication for ADHD. The percentage of children with a history of an ADHD diagnosis ranges from 15 percent in Arkansas and Kentucky to 4 percent in Nevada.

Nearly one in five high school boys and one in 11 high school girls in the U.S. were reported by their parents as having been diagnosed with ADHD by a healthcare provider. For this study, data from the 2011-2012 National Survey of Children’s Health (NSCH) were used to calculate estimates of the number of children in the U.S. ages 4-17 that, according to a parent, had received a diagnosis of ADHD by a healthcare provider and were currently taking medication for ADHD. The NSCH is conducted in collaboration between HRSA and CDC.

Retrieved from:  http://www.sciencedaily.com/releases/2013/11/131122112708.htm?goback=%2Egde_2450083_member_5810692543100264452#%21

ADHD Meds Don’t Raise Risk of Drug Abuse in Adulthood: Review

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment on Sunday, 23 June 2013 at 10:14

http://health.usnews.com/health-news/news/articles/2013/05/29/adhd-meds-dont-raise-risk-of-drug-abuse-in-adulthood-review

preschoolers and adhd…a six-year follow up.

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Neuropsychology, Psychiatry on Wednesday, 6 March 2013 at 16:04

http://www.jaacap.com/article/S0890-8567(12)00993-8/abstract

“ADHD in preschoolers is a relatively stable diagnosis over a 6-year period. The course is generally chronic, with high symptom severity and impairment, in very young children with moderate-to-severe ADHD, despite treatment with medication. Development of more effective ADHD intervention strategies is needed for this age group.”

adhd outcome data. a look at adhd 33 years later. two interesting pieces of research!

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment on Thursday, 24 January 2013 at 10:25

ADHD Outcome Data in Adults Shows Value of Early Treatment

By: Joan Arehart-Treichel

When men diagnosed with ADHD in childhood were followed up several decades later, some were found to have very poor outcomes. Most, however, were leading productive lives. 

Having attention-deficit/hyperactivity disorder (ADHD) in childhood portends a number of negative outcomes later in life, a 33-year follow-up of childhood ADHD subjects has found.

The study, which was headed by Rachel Klein, Ph.D., a professor of child and adolescent psychiatry at the New York University Child Study Center, was reported online October 15 in the Archives of General Psychiatry.

The study included 271 white men who were 41 years old. Out of the subjects, 135 had had childhood ADHD without conduct disorder. The remaining 136 had not had childhood ADHD, but had parents whose occupations matched those of the ADHD subjects. They served as control subjects.

The researchers compared the two groups on several outcomes and found that the former were generally doing more poorly than the controls were. They had significantly worse educational, occupational, economic, and social outcomes, as well as more divorces and higher rates of antisocial personality disorder, substance use disorder, and nicotine dependence.

For example, 31 percent of the ADHD subjects did not complete high school, compared with 5 percent of control subjects. The ADHD subjects were earning, on average, $40,000 a year less than the control subjects. Although most individuals in both groups were living with a spouse (70 percent and 79 percent), significantly more ADHD subjects were currently divorced (10 percent versus 3 percent) or had ever been divorced (31 percent versus 12 percent). The ADHD subjects were about three times more likely to have a substance use disorder and nicotine dependence than controls.

Moreover, 16 percent of ADHD subjects had antisocial personality disorder, while no controls did.

That none of the controls had antisocial personality disorder a third-of-a-century later needs clarification, Klein said in an interview. Some of the controls did have conduct disorder during adolescence, and about 8 percent developed antisocial personality disorder, but the prevalence at the average age of 25 was low, around 3 percent, and of these none retained the diagnosis at the average age of 41. “I was surprised that none of the controls continued on the path of antisocial personality, especially since, in contrast, the ADHD children fared much worse in this regard. The finding points to the possibility that among boys without ADHD, the extended prognosis for conduct disorder is good.”

Also, since the 12-month prevalence rate for antisocial personality disorder in American adults is 1 percent according to the National Comorbidity Survey Replication, “it is not surprising that the disorder is not found in a single sample,” Klein said.

But what is striking in any case, she concluded, is that “antisocial personality disorder disappeared completely among the men who did not have a childhood history of ADHD.”

Finally, the worst outcome for those in the ADHD sample was for those who developed both antisocial personality disorder and a substance use disorder. Also, the 22 percent of ADHD subjects whose illness had persisted into adolescence or early adulthood were especially at risk of developing an antisocial personality disorder and a substance use disorder.

Yet some good news also emerged from the study. While 84 of the 135 ADHD subjects developed a conduct disorder during adolescence, only 22 went on to develop antisocial personality disorder.

An unexpected finding, Klein added, was “that the men who had ADHD in childhood did not have relatively more new psychopathology during adulthood.” For instance, they had no more mood or anxiety disorders at age 41 than controls did. Indeed, “ADHD was not a lifelong disorder in the majority of cases,” Klein emphasized. “Most children went on to live fruitful lives, most were employed, most were in rewarding relationships, and most were happy with their situation.”

“This is a long-term follow-up study of 6- to 12-year-old boys who were diagnosed with ADHD,” child psychiatrist David Fassler, M.D., a clinical professor of psychiatry at the University of Vermont and APA treasurer, told Psychiatric News. “Of significant concern, they noted an increased incidence of incarceration and death compared to a matched control group. The results remind us that ADHD in childhood is often associated with persistent adverse consequences later in life. The findings also underscore the importance of early recognition and ongoing access to appropriate and effective treatment for children, adolescents, and adults with ADHD.”

The study was funded by the National Institutes of Health. ■

An abstract of “Clinical and Functional Outcome of Childhood Attention-Deficit/Hyperactivity Disorder 33 Years later” is posted athttp://archpsyc.jamanetwork.com/article.aspx?articleid=1378851.

Psychiatric News   |   December 07, 2012

Volume 47 Number 23 page 26-26

10.1176/appi.pn.2012.12a2

American Psychiatric Association

Retrieved from: http://psychnews.psychiatryonline.org/newsArticle.aspx?articleid=1484670

Clinical and Functional Outcome of Childhood Attention-Deficit/Hyperactivity Disorder 33 Years Later

Rachel G. Klein, PhD; Salvatore Mannuzza, PhD; María A. Ramos Olazagasti, PhD; Erica Roizen, MS; Jesse A. Hutchison, BA; Erin C. Lashua, MA; F. Xavier Castellanos, MD

Arch Gen Psychiatry. 2012;69(12):1295-1303. doi:10.1001/archgenpsychiatry.2012.271.

Context  Prospective studies of childhood attention-deficit/hyperactivity disorder (ADHD) have not extended beyond early adulthood.

Objective  To examine whether children diagnosed as having ADHD at a mean age of 8 years (probands) have worse educational, occupational, economic, social, and marital outcomes and higher rates of ongoing ADHD, antisocial personality disorder (ASPD), substance use disorders (SUDs), adult-onset psychiatric disorders, psychiatric hospitalizations, and incarcerations than non-ADHD comparison participants at a mean age of 41 years.

Design  Prospective, 33-year follow-up study, with masked clinical assessments.

Setting  Research clinic.

Participants  A total of 135 white men with ADHD in childhood, free of conduct disorder, and 136 men without childhood ADHD (65.2% and 76.4% of original cohort, respectively).

Main Outcome Measures  Occupational, economic, and educational attainment; marital history; occupational and social functioning; ongoing and lifetime psychiatric disorders; psychiatric hospitalizations; and incarcerations.

Results  Probands had significantly worse educational, occupational, economic, and social outcomes; more divorces; and higher rates of ongoing ADHD (22.2% vs 5.1%,P < .001), ASPD (16.3% vs 0%, P < .001), and SUDs (14.1% vs 5.1%, P = .01) but not more mood or anxiety disorders (P = .36 and .33) than did comparison participants. Ongoing ADHD was weakly related to ongoing SUDs (ϕ = 0.19, P = .04), as well as ASPD with SUDs (ϕ = 0.20, P = .04). During their lifetime, probands had significantly more ASPD and SUDs but not mood or anxiety disorders and more psychiatric hospitalizations and incarcerations than comparison participants. Relative to comparisons, psychiatric disorders with onsets at 21 years or older were not significantly elevated in probands. Probands without ongoing psychiatric disorders had worse social, but not occupational, functioning.

Conclusions  The multiple disadvantages predicted by childhood ADHD well into adulthood began in adolescence, without increased onsets of new disorders after 20 years of age. Findings highlight the importance of extended monitoring and treatment of children with ADHD.

Retrieved from: http://archpsyc.jamanetwork.com/article.aspx?articleid=1378851#qundefined

ABCs and ADHD…

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Psychiatry, School Psychology on Wednesday, 9 January 2013 at 07:04

The ABCs of ADHD

Learn about the specific characteristics of a child with ADHD and how it impacts their lives.

By Melvyn Hyman

Who today has not heard the term “attention deficit hyperactivity disorder,” or ADHD? No other term in the diagnostic lexicon has more information and misinformation attached to it than ADHD. Everyone you ask — parents, doctors, teachers, psychologists, nurses, neighbors or relatives — will have an opinion on this disorder, and likely their opinions will all differ. Some will toss it off and say, “Boys will be boys.” Some will insist that a child be medicated right away. Others will be adamant that children should never be medicated. Others will claim that eliminating sugar from the diet will eliminate the problem. Still others will question whether there is anything to the diagnosis at all.

Since first identified as a diagnosis, ADHD has been given a great deal of attention by neurologists and psychologists. ADHD is now widely recognized as a legitimate mental health problem. Although its exact definition continues to be debated, ADHD is thought to be a neurological impairment, probably originating in the frontal lobes of the brain, affecting a child’s ability to control his or her impulses. Lacking the ability to control their impulses, these children do and say whatever occurs to them from minute to minute. They are quite literally out of control.

There has been a great deal of research to understand just what causes children have ADHD. Among the identified causes are: heredity (a parent or other close relative with ADHD, although it may have gone unrecognized); problems at birth; and possibly some kind of early emotional trauma that had an effect on the processing mechanisms of the brain.

In some ways, children with ADHD are no different from their peers. One key diagnostic feature noted in children with ADHD is the intense, often frantic quality of their activity. These children are on the move most of the time: climbing the cupboards, tearing about the room, turning over every object that isn’t nailed down — an unending streak of activity and mischief. They quickly wear out their clothes and toys, and usually have more than their share of accidents.

Short Attention Spans
Children with ADHD also have extremely short attention spans. They seem to have difficulty sitting still or waiting their turn. This may be because they are so easily distracted. It often seems that they fail to remember instructions given by a parent or teacher in the time it takes to get from one end of the room to the other. They appear to live only in the present. They don’t seem to think about future consequences. They sometimes can’t remember what they did only moments earlier.

The behavior of a child with ADHD is qualitatively different from the occasional episodes of increased activity in children who do not have ADHD. Every child fidgets or misbehaves from time to time. Children with ADHD, however, are a constant challenge. Their behaviors cause frustration and anger for those around them. Without proper help, these children can become sad or even depressed due to their very accurate perception that the people around them disapprove of everything they do.

Ironically, these very same overactive children can become completely absorbed in a specific activity or task. They sometimes become so over-focused that being asked to shift their attention causes great upset and anger. It is as if the mechanism in the brain that controls their impulsiveness has now gone into overdrive. Once engaged, they can’t let go. Another theory is that these children have learned to compensate for their distractibility by focusing so completely on an activity that they cannot easily alter the track of their attention. They find change initiated by others to be threatening and difficult. This is very confusing for adults because it seems inconsistent with the general stereotypes about ADHD. Puzzled parents often ask things like: “How is it he can remember every arcane move in a video game but can’t remember to take out the garbage?” or “Why can she sit still to watch MTV for hours but can’t sit still through one classroom lesson?”

Friendships and ADHD
Children with ADHD also wear out friendships. Their behavior can be so thoughtless and aggravating, even exhausting, that other children start to avoid them. They miss usual social cues and often blurt out what they are thinking whether or not it is at all appropriate or tactful. Usually good-hearted and wanting friends, they are often mystified by others’ negative reactions to them. It is important to understand that children with ADHD are not trying to be annoying or malicious. In fact, they often seem surprised and embarrassed when their behavior results in rejection by others.

Evaluation for ADHD includes a family history, a medical exam, psychological testing, and, very importantly, a compilation of ratings on paper and pencil behavioral scales completed by parents and teachers who know the child well. A skilled neuropsychologist will recognize patterns in all of these data that generally point to a diagnosis of ADHD.

Treatment of ADHD
It is generally believed that children with ADHD benefit most from a multidisciplinary approach that comes at the problem in many ways simultaneously. On the medical front, stimulants such as Cylert (premoline), Dexedrine (dextroamphetamine), and Ritalin (methylphenidate) are the medications most often used to treat ADHD in the United States; antidepressants are sometimes prescribed as well. These medications increase activity in the frontal lobes of the brain where impulsivity is managed.

Parents and teachers of children with ADHD must be educated about how to best manage their particular child. Many adults make the mistake of getting into power struggles with these children, trying to control them with harsh disciplinary methods. Children with ADHD really can’t help being the way they are. Yelling, scolding, nagging, and punishing will only make them feel and behave worse. Even more than most children, these children need clear and kind guidance, with an emphasis on what they are doing right.

Early identification of special services in the schools can be very helpful. These children do better is a less stimulating, more orderly environment. They benefit from small classes that are fairly quiet. Activities need to be short and focused, with many opportunities for small successes. Parents and teachers should ideally keep in close contact with each other, sharing what they find to be effective for the child in question.

Finally, physical activity can sometimes help children with ADHD channel some of their excessive energy. They tend to do better at individual sports like swim team, rock climbing, weight lifting, or figure skating. Team sports (where a great deal is going on at once) can sometimes be overstimulating and frustrating for these children.

The goal, of course, is for children with ADHD to get the most enjoyment, learning and growth from each day of their lives. With teaching, encouragement, and support, these children can learn to monitor and manage their symptoms and move on with life.

Retrieved from: http://www.everydayhealth.com/adhd/add-adhd-facts.aspx?xid=tw_adhdfacts_20120217_ABCs

ADHD drugs do not raise risk of serious heart conditions in children, study shows

In ADHD, ADHD child/adolescent, ADHD stimulant treatment on Thursday, 13 December 2012 at 08:22

ADHD drugs do not raise risk of serious heart conditions in children, study shows

GAINESVILLE, Fla. — Children taking central nervous system stimulants such as Adderall and Ritalin do not face an increased risk of serious heart conditions during treatment, according to a new University of Florida study that confirms findings reported in 2011. Published in the British Medical Journal in August, the study contributes to a decade-long clinical and policy debate of treatment risks for children with attention deficit hyperactivity disorder, or ADHD.

“This is a question that has been lingering for about 10 years,” said Almut Winterstein, a pharmacoepidemiologist and a professor in pharmaceutical outcomes and policy in the UF College of Pharmacy.

Stimulant drugs are one of the most commonly prescribed medications for children — after antibiotics and antidepressants, Winterstein said.

Winterstein’s results show that every year, children have an approximately one in 30,000 risk of suffering a severe cardiac event. She found no increased risk for children who were taking stimulant drugs. A cardiac event includes sudden cardiac death, heart attack or stroke, and is typically caused by underlying heart disease. These results confirm previous study conclusions that there are no serious cardiac events resulting from short-term use of central nervous system stimulant drugs by children and young adults.

In 2007, Winterstein conducted the first large population study to investigate the risk associated with the use of central nervous system stimulants in children and young adults between ages 3 and 20. Published in the journal Pediatrics, her results showed a 20 percent increase in emergency clinic or doctor’s office visits with cardiac-related symptoms, but no increase in death or hospital admission for serious heart conditions.

In that study, she analyzed records from 55,000 children under Medicaid who had ADHD and were undergoing treatment between 1994 to 2004. But this population was still not large enough to determine if these drugs were indeed safe for children, Winterstein said.

The new study, funded by the Agency for Healthcare Research and Quality and in part by the National Center for Advancing Translational Sciences, examines a larger U.S. population of 1.2 million youths eligible for Medicaid programs in 28 states. It follows a similarly large investigation published in December 2011 in The New England Journal of Medicine by Dr. William O. Cooper, who looked primarily at privately insured patients.

“We complemented Dr. Cooper’s study by utilizing Medicaid patients who are typically more vulnerable and at higher risk for serious adverse events,” Winterstein said. “This allowed us to examine patients with severe underlying heart conditions who received stimulants.”

Although the study confirmed there are no short-term effects from central nervous system stimulants, the study did not reveal how these drugs affect patients in the long term.

“Neither of the studies was able to answer what happens in the long term,” Winterstein said. “It’s an important issue to address, but we won’t be able to answer the question until this generation of ADHD children, who began using stimulant drugs in the 1990s, reaches adulthood into their 50s, 60s and 70s.”

Another concern the study raised to UF researchers is related to children who were on continuous stimulant medication for more than 10 years into their adulthood. The effects of even minor increases in blood pressure and heart rate over a sustained period of time are unknown, Winterstein said.

A decade ago, when initial alarms were raised about stimulant use in children, health-care providers were cautious, but now the practice has increased with the knowledge of little risk of serious effects.

Dr. Regina Bussing, a professor in the UF College of Medicine’s division of child and adolescent psychiatry, said concerns about possible serious cardiovascular risks may have resulted in children not getting needed ADHD treatment.

“Dr. Winterstein and her colleagues’ study yields important information for clinicians,” Bussing said.

Recommended evaluation practices should continue for young patients, Bussing said, including cardiovascular monitoring. Parents will still be advised to stop medication and take the child to the emergency room should he or she develop sudden onset of chest pain or shortness of breath, but the study alleviates doctor and parent concerns for the most serious cardiovascular events.

Though her research does cast a positive light on the safety of central nervous system stimulants, Winterstein agrees that parents should continue to seek medical care if symptoms arise. She also has concerns about the increasing use of stimulant drugs for children without weighing the long-term risks and benefits.

Retrieved from: http://news.ufl.edu/2012/10/31/child-stimulant/

ADHD medication could help cut crime rates, Swedish study finds

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Psychiatry, Psychopharmacology on Thursday, 22 November 2012 at 08:32

ADHD medication could help cut crime rates, Swedish study finds

Many ADHD (attention-deficit hyperactivity disorder) sufferers are less likely to commit a crime while on appropriate medication, a Swedish study found.

Freya Petersen

November 22, 2012

Many ADHD (attention-deficit hyperactivity disorder) sufferers are less likely to commit a crime while on appropriate medication, a Swedish study found.

The study, by researchers at the Karolinska Institute in Stockholm, found that while people with ADHD were far more likely to break the law, the use of Ritalin, Adderall and other drugs to curb hyperactivity and boost attention markedly reduced rates of reoffending, the Associated Press reported.

The researchers focused on older teens and adults with ADHD, studying a Swedish registry of more than 25,650 people with ADHD and comparing their medication history with criminal records from 2006 to 2009, WebMD reported.

The number of crimes committed was about a third or more lower in those taking medication, the study found.

Lead author Paul Lichtenstein said in a statement quoted by Reuters:

“It’s said that roughly 30 to 40 percent of long-serving criminals have ADHD. If their chances of recidivism can be reduced by 30 percent, it would clearly affect total crime numbers in many societies.”

Support groups and preventative medicine experts seized on the study results, saying better access to medication could reduce crime.

They also said it demonstrated the efficacy of medications in older patients.

About 5 percent of children in the US and other Western countries reportedly have ADHD, characterized by impulsiveness, hyperactivity and difficulty paying attention.

While children are routinely given medication to help them focus in school, many sufferers retain symptoms into adulthood.

The AP quoted Dr. William Cooper, a pediatrics and preventive medicine professor at Vanderbilt University in Nashville, as saying:

“There definitely is a perception that it’s a disease of childhood and you outgrow your need for medicines. We’re beginning to understand that ADHD is a condition for many people that really lasts throughout their life.”

The findings were published in Thursday’s New England Journal of Medicine.

Retrieved from: http://www.globalpost.com/dispatch/news/health/121122/adhd-attention-deficit-hyperactivity-disorder-crime-sweden-swedish-study?utm_source=twitterfeed&utm_medium=twitter

Girls with ADHD often diagnosed later than boys

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Child/Adolescent Psychology, Psychiatry, School Psychology on Saturday, 10 November 2012 at 11:06

Girls with ADHD often diagnosed later than boys.

The Lab Rat: A Better Way to Diagnose ADHD

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment on Thursday, 18 October 2012 at 08:03

an adhd diagnosis should be made after a number of assessment techniques (tests, questionnaires, observations, reports from others, etc.).  i am wary of any “one” measure that gives a valid diagnosis.  there are MANY disorders that mimic adhd and have the same constellation of symptoms.  while this system appears valid and reliable, i feel it should still be used in conjunction with other sources of information.

The Lab Rat: A Better Way to Diagnose ADHD

By: John Cloud

Does your child have ADHD, or is he merely rambunctious? Few questions divide parents, teachers, and mental-health professionals as often as this one. Some 5.4 million children ages 4 to 17 had ever been diagnosed with ADHD as of 2007, according to the most recent data available from the Centers for Disease Control and Prevention. The previous year, the total was 4.6 million, meaning 17.4% of all recorded ADHD cases were diagnosed in a single calendar year. There is little hard evidence to suggest that the pace of growth since 2007 has slowed.

The surge in ADHD diagnoses has worried mental-health clinicians because diagnosis of the disorder can be highly subjective. And yet between 1992 and 2000, production of the stimulant methylphenidate — which is marketed as Ritalin — increased 730%, according to the British Medical Journal. But there is a better way to diagnose ADHD — an objective, widely available test developed at McLean Hospital, the psychiatric arm of Harvard Medical School. The test is so good that it could settle the ADHD-diagnosis debate.

Diagnosing any mental illness is difficult. Except in rare cases, specific gene mutations causing mental disorders haven’t been discovered (and may not exist). And while physical injuries and illnesses sometimes trigger mental problems, most of the time psychiatrists play guesswork. They use questionnaires and rating scales to try to determine whether symptoms add up to illness.

Most of these questionnaires have been vetted through psychometric analysis to ensure test-retest reliability, meaning your score on one day is about the same as your score two months later. But any questionnaire is only as reliable as the clinician administering it. In one typical diagnostic interview, the Kiddie Schedule for Affective Disorders and Schizophrenia, Present and Lifetime (K-SADS-PL), the clinician is asked to pose the following set of questions to a child:

  • Do your teachers complain that you don’t follow instructions?
  • When your parents or your teacher tell you to do something, is it sometimes hard to remember what they said to do? Does it get you into trouble?
  • Do you lose points on your assignments for not following directions or not completing the work?
  • Do you forget to do your homework or forget to turn it in?
  • Do you get into trouble at home for not finishing your chores or other things your parents ask you to do? How often?

Believe it or not, that’s just one of 29 sets of questions on the K-SADS-PL that can be used to diagnose ADHD. Although not every set of questions is asked of every child, the diagnostic interview can take up to three hours, according to Dr. Martin Teicher, director of the developmental biopsychiatry research program at McLean and a leading ADHD researcher. Never mind that a typical 10-year-old has a difficult time focusing on anything for more than 10 min. except, say, Toy Story 3.

And even if the child can manage to remember with accuracy all the answers, the clinician might be biased before the interview begins by parent or teacher reports that the child is hyperactive, inattentive or impulsive (the three main signs of ADHD). Past studies have shown that parents sometimes over-predict diagnosis of ADHD in their kids because the parents misremember their own childhoods as times of attentive and tranquil learning. Teachers also sometimes over-predict ADHD diagnosis because they expect ADHD treatment to result in quieter classrooms. And children often under-predict ADHD diagnosis because the kids have no reference point beyond their own behavior, which — even if wildly hyperactive — they see as normal. In any given case, the parents, the teacher, and the child rarely agree on whether the kid has ADHD.

Because of these diagnostic shortcomings, Teicher began experimenting 20 years ago with a test that could more objectively diagnose ADHD. At the time, many researchers were already using continuous-performance tests (CPTs) to help diagnose the disorder. CPTs require test subjects to focus on a boring task — say, pressing the space bar when a random shape appears on-screen but not when another random shape appears — for approximately 15 to 20 min.

CPTs accurately capture whether a student is inattentive (meaning he doesn’t focus on the task) or impulsive (meaning he presses the space bar too often). But they don’t measure how much kids fidget when they take the test, and restlessness (a.k.a. hyperactivity) is a key component of an accurate ADHD diagnosis. An older tool called the actigraph was widely used in the 1990s to measure body movements during tests. Actigraphs use sensors attached to body parts (usually wrists and ankles) to quantify movements.

But at a Society for Neuroscience meeting in the mid-’90s, Teicher learned of a far more sophisticated technology for gauging body movements. The new technology used infrared signals to record movements 50 times per sec. to a resolution of 0.002 in. (0.04 mm). By 1996, Teicher and his colleagues had not only developed a device that combined a CPT with the infrared analysis but published the results of a study showing that it could predict with near-perfect accuracy which students would be diagnosed with ADHD and which ones would not.

Today his device is being marketed as the Quotient ADHD System. Pediatric practices and even school districts would be wise to invest in one of the devices if they want to quell bitter debates among parents, teachers, and counselors over whether a child really has ADHD and needs to take potentially dangerous stimulants or simply has another condition known as “being 10 years old.” Although the devices cost $19,500 apiece, peer-reviewed studies have shown that they are far better than parent, teacher, or clinician evaluations alone at determining whether a child is truly disordered.

Not long ago, I visited Teicher at the bosky McLean campus and underwent the Quotient test, which is also used for adults who think they may have attention-deficit problems. A habitual fidgeter, I get bored easily and tend to spend beyond my salary. All these are traits associated with attention-deficit disorders.

The Quotient device is a bit smaller than one of those arcade games in which you get to shoot Nazis or zombies. But instead of a fake gun, there’s just a keyboard. You are asked to press the space bar whenever you see one a five-pointed star but not when you see an eight-pointed one. The test, which takes 20 min. for adults and 15 min. for kids, is excruciatingly dull. By minute 15 or so, my brain was screaming that the test end.

 

For all that, I didn’t do so badly. I scored 90% in accuracy, although I showed significant impulsiveness by pressing the space bar too fast before registering that the star that had just appeared had eight points, not five. My test results coincide with my scores on a diagnostic interview Teicher conducted with me. The interview had picked up my propensity to act before thinking when I’m bored. In the end, I didn’t meet the threshold for an ADHD diagnosis. But the Quotient system confirmed that I fidget a lot. The infrared sensors showed that for many periods during the 20-min. test, I moved incessantly — far more than most of my fellow 40-year-olds.

I was impressed by the Quotient system because it generates such a large body of statistics and because it’s nearly impossible to cheat.

At some point in the future, we will have an ADHD diagnostic test that accurately measures catecholamine transmission and dopamine D2-receptor density, two neurotransmitter gauges that predict an ADHD diagnosis. Until then, the Quotient system is the best diagnostic tool in the psychiatric armamentarium. Parents and teachers should stop squabbling over which kids are ADHD and which are merely unruly. Before any meds are administered, kids should be seated in front of a Quotient device that can settle almost any quarrels with solid data.

Retrieved from: http://healthland.time.com/2011/02/25/the-lab-rat-a-better-way-to-diagnose-adhd/#ixzz29ePyOeUE

fake it ’til you make it???

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment on Thursday, 18 October 2012 at 07:54

one of the reasons it is so important to be evaluated in a comprehensive manner by someone who is specifically trained in the diagnosis of adhd.

Faking it.  Why Nearly 1 in 4 Adults Who Seek Treatment Don’t Have ADHD

By: Meredith Melnick

A new survey of patients’ medical records finds that nearly a quarter of adults who seek treatment for attention deficit hyperactivity disorder may be exaggerating or faking their symptoms. Why would someone fake a psychological disorder? In a word, Adderall.

The authors of the study, published in The Clinical Neuropsychologist, said there were actually a variety of reasons people exaggerated their symptoms: some legitimately had ADHD, but just wanted to make sure their doctor gave them the diagnosis; others really thought they had ADHD, but didn’t (rather they were stressed or depressed). But in many cases, the reason for claiming symptoms of ADHD was to obtain the drugs — like Adderall and Ritalin — that are used to treat it.

These drugs are stimulants, which work by boosting levels of the neurotransmitters dopamine and norepinephrine in the brain. In people who have ADHD, the drugs calm behavior and help maintain focus. In healthy people, the drugs serve as performance enhancers. College students, journalists, scientists and baseball players, amongothers, have been known to use the drugs to increase their ability to concentrate, improve attention, memory and learning, and get ahead.

“There are big cultural pressures to get these drugs,” Dr. Anjan Chatterjee, a professor of neurology at the University of Pennsylvania, told MSNBC. “That’s because everyone is in an arms race of accomplishment.”
For the new study, lead researcher Paul Marshall, a clinical neuropsychologist at Hennepin Faculty Associates in Minneapolis, and colleagues analyzed patients’ responses in in-person interviews and questionnaires. Within the questionnaires were inserted certain red-flag-raising tests specifically designed to pinpoint fakers and exaggerators.Reported MSNBC:

Ultimately, Marshall and his colleagues found patients who not only exaggerated their symptoms but also scored much more poorly on the embedded tests than people with actual ADHD symptoms would have.

A doctor in [an MSNBC-commissioned] Truth On Call poll summarized the fakers like this: “Patients try to describe typical symptoms with a request for specific ADHD drugs. With standard symptom questionnaires, they will push the responses to the extreme and try to request specific medications when prescribed alternatives.”

The problem is that there is no single guaranteed test for ADHD. Diagnoses depend on individual physicians’ assessments. So how reliable are doctors — and the measures they use — generally?

A study by University of Kentucky psychologists, published in June 2010 in Psychological Assessment, sought an answer by asking college kids to try to fake ADHD symptoms on a series of tests. There were actually three groups of students who took the tests: some who legitimately had ADHD and were temporarily off their medication, others who didn’t have ADHD and weren’t asked to fake it, and those who didn’t have ADHD but were told they’d get $45 if they could convince the assessor they did. To prepare, they were given five minutes to look over ADHD information obtained from Google.

 

Regarding the assessment measures, Psychology Today reported:

Tests for detecting ADHD fall into two broad categories. Firstly, and most simply, there is self-report, where the patient describes their symptoms in response to structured questioning. Second there are neuropsychological tests, where the patient is asked to perform a particular task. These often appear much like a simple computer game and are structured such that persons with ADHD will make certain types of mistakes on the game due to impulsivity, inattention or other ADHD symptoms.

The self-reports couldn’t tell the real ADHD sufferers from the fakers, and the computer tests weren’t much more effective either, the study found.

ADHD diagnoses in adults may be trickier than in kids. For children, there are at least multiple sources of information and observation — parents, teachers, doctors. With adults, physicians can rely only on self-reporting. The Centers for Disease Control and Prevention estimates that 2% to 4% of adults actually have ADHD, many of whom were initially diagnosed as children.

If healthy adults continue to exaggerate symptoms for personal gain, the fallout could affect those who really need help, should doctors become increasingly wary of handing out diagnoses. Worse, legitimate patients are having a hard enough time getting their medication as it is, without fakers filching pills for performance enhancement. Finally, as the MSNBC story points out, if misused the medications could become habit forming — and a surefire way to ruin performance is misusing prescription drugs.

Retrieved from: http://healthland.time.com/2011/04/28/faking-it-why-nearly-1-in-4-adults-who-seek-treatment-dont-have-adhd/#ixzz29eOxxERR

adhd…a longitudinal follow-up

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Brain imaging, Brain studies, Neuropsychology, Neuroscience, Psychiatry, School Psychology on Tuesday, 16 October 2012 at 07:34

Men Diagnosed with ADHD as Children had Worse Outcomes as Adults, Study Says

ScienceDaily (Oct. 15, 2012) — Men who were diagnosed as children with attention-deficit/hyperactivity disorder (ADHD) appeared to have significantly worse educational, occupational, economic and social outcomes in a 33-year, follow-up study that compared them with men without childhood ADHD, according to a report published Online First by Archives of General Psychiatry, a JAMA Network publication.

ADHD has an estimated worldwide prevalence of 5 percent, so the long-term outcome of children with ADHD is a major concern, according to the study background.

Rachel G. Klein, Ph.D., of the Child Study Center at NYU Langone Medical Center in New York, and colleagues report the adult outcome (follow-up at average age of 41 years) of boys who were diagnosed as having ADHD at an average age of 8 years. The study included 135 white men with ADHD in childhood, free of conduct disorder (probands), and a comparison group of 136 men without childhood ADHD.

“On average, probands had 2½ fewer years of schooling than comparison participants … 31.1 percent did not complete high school (vs. 4.4 percent of comparison participants) and hardly any (3.7 percent) had higher degrees (whereas 29.4 percent of comparison participants did). Similarly, probands had significantly lower occupational attainment levels,” the authors note. “Given the probands’ worse educational and occupational attainment, their relatively poorer socioeconomic status at [follow-up at average age of 41 years] is to be expected. Although significantly fewer probands than comparison participants were employed, most were holding jobs (83.7 percent). However, the disparity of $40,000 between the median annual salary of employed probands and comparisons is striking.”

In further comparisons of the two groups, the men who were diagnosed with ADHD in childhood also had more divorces (currently divorced, 9.6 percent vs. 2.9 percent, and ever been divorced 31.1 percent vs. 11.8 percent); and higher rates of ongoing ADHD (22.2 percent vs. 5.1 percent, the authors suspect the comparison participants’ ADHD symptoms might have emerged during adulthood), antisocial personality disorder (ASPD, 16.3 percent vs. 0 percent) and substance use disorders (SUDs, 14.1 percent vs. 5.1 percent), according to the results.

During their lifetime, the men who were diagnosed with ADHD in childhood (the so-called probands) also had significantly more ASPD and SUDs but not mood or anxiety disorders and more psychiatric hospitalizations and incarcerations than comparison participants. And relative to the comparison group, psychiatric disorders with onsets at 21 years of age or older were not significantly elevated in the probands, the study results indicate.

The authors note the design of their study precludes generalizing the results to women and all ethnic and social groups because the probands were white men of average intelligence who were referred to a clinic because of combined-type ADHD.

“The multiple disadvantages predicted by childhood ADHD well into adulthood began in adolescence, without increased onsets of new disorders after 20 years of age. Findings highlight the importance of extended monitoring and treatment of children with ADHD,” the study concludes.

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121015162407.htm

 

                                                                                             

Brain Gray Matter Deficits at 33-Year Follow-up in Adults With Attention-Deficit/Hyperactivity Disorder Established in Childhood

Erika Proal, PhD; Philip T. Reiss, PhD; Rachel G. Klein, PhD; Salvatore Mannuzza, PhD; Kristin Gotimer, MPH; Maria A. Ramos-Olazagasti, PhD; Jason P. Lerch, PhD; Yong He, PhD; Alex Zijdenbos, PhD; Clare Kelly, PhD; Michael P. Milham, MD, PhD; F. Xavier Castellanos, MD

Arch Gen Psychiatry. 2011;68(11):1122-1134. doi:10.1001/archgenpsychiatry.2011.117.

 

Context  Volumetric studies have reported relatively decreased cortical thickness and gray matter volumes in adults with attention-deficit/hyperactivity disorder (ADHD) whose childhood status was retrospectively recalled. We present, to our knowledge, the first prospective study combining cortical thickness and voxel-based morphometry in adults diagnosed as having ADHD in childhood.

Objectives  To test whether adults with combined-type childhood ADHD exhibit cortical thinning and decreased gray matter in regions hypothesized to be related to ADHD and to test whether anatomic differences are associated with a current ADHD diagnosis, including persistent vs remitting ADHD.

Design  Cross-sectional analysis embedded in a 33-year prospective follow-up at a mean age of 41.2 years.

Setting  Research outpatient center.

Participants  We recruited probands with ADHD from a cohort of 207 white boys aged 6 to 12 years. Male comparison participants (n = 178) were free of ADHD in childhood. We obtained magnetic resonance images in 59 probands and 80 comparison participants (28.5% and 44.9% of the original samples, respectively).

Main Outcome Measures  Whole-brain voxel-based morphometry and vertexwise cortical thickness analyses.

Results  The cortex was significantly thinner in ADHD probands than in comparison participants in the dorsal attentional network and limbic areas (false discovery rate < 0.05, corrected). In addition, gray matter was significantly decreased in probands in the right caudate, right thalamus, and bilateral cerebellar hemispheres. Probands with persistent ADHD (n = 17) did not differ significantly from those with remitting ADHD (n = 26) (false discovery rate < 0.05). At uncorrected P < .05, individuals with remitting ADHD had thicker cortex relative to those with persistent ADHD in the medial occipital cortex, insula, parahippocampus, and prefrontal regions.

Conclusions  Anatomic gray matter reductions are observable in adults with childhood ADHD, regardless of the current diagnosis. The most affected regions underpin top-down control of attention and regulation of emotion and motivation. Exploratory analyses suggest that diagnostic remission may result from compensatory maturation of prefrontal, cerebellar, and thalamic circuitry.

Retrieved from: http://archpsyc.jamanetwork.com/article.aspx?articleid=1107429

adhd… a “made up” disorder, redux

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Psychiatry, Psychopharmacology on Friday, 12 October 2012 at 17:38

and here we go, folks! on the heels of my post, 10 October 2012, regarding the good doctor anderson (http://wp.me/p2IpfL-9p), the debate is starting yet once again.  sigh.  you know, this gets a bit boring after a while.   but i do believe we have vastly improved mechanisms of study (fmri, genomic medicine…fantastic stuff!) and robust set of data and literature to support that it’s a valid disorder.  and, i hesitate to even take a stand as to which i ascribe to.  in the end, you are allowed to believe what you want, as long as you aren’t hurting anybody else (if you are hurting yourself) by holding those beliefs.  i would just like to see the actual data that these people base their opinions on.  i don’t believe there is a place for opinions is science.  and diagnosing and prescribing is done based mostly on quantitative data.  

the data (quantitative) speaks for itself , imo.  and to me, the best decisions are made when examining QUANTITATIVE data.  but, as i’ve told you in something i wrote at some point (one musing or another…), i am a ‘quantoid.’  i will always be biased towards quantifiable data.  that’s me.  come to your own conclusions.  i just prefer to come to mine quantifiably.    and that’s a WHOLE other post!  at any rate, as you see below, the debate continues…pick a side.

Should Children Take ADHD Drugs — Even If They Don’t Have The Disorder?

Emily Willingham, Contributor

The discussion is at least twice as old as my 10-year-old son with attention deficit/hyperactivity disorder (ADHD): Should we medicate children with ADHD drugs just to keep order in the classroom or help the child be competitive among peers? I know it’s at least 20 years old, this argument, because it was a subject of almost daily discussion in teachers’ lounges when I taught middle school in the ’90s, and because the tension among teachers, parents, and the children taking the drugs often spilled into the hallways. And this all was in private schools. I can only imagine that the intensity was multifold in the public school setting.

The age of a controversy, as anyone in public health can tell you, doesn’t necessarily diminish its relevance or the passions it inspires. That’s why this piece by Alan Schwarz in the New York Times has yielded some serious angst in many circles. It takes as its center a doctor who, Schwarz writes, prescribes ADHD drugs off-label for children he avers don’t have ADHD, saying that because the schools won’t do what they should to help low-income kids learn, we “have to modify the kid.”

This physician, Dr. Michael Anderson, also happens to be among those who dismiss ADHD is a “made-up” disorder, in spite of considerable evidence linking specific gene variants to ADHD and suggesting a large genetic component [PDF]. He’s another contributor to the ever-present backlash against ADHD as a diagnostic entity, but instead of blaming lazy parents this time, he blames the school system, one that neglects children whose behaviors in a classroom might be ameliorated by an appropriate environment, in the absence of which, medications have to do the job. He certainly has a point … to a point.

His attitude about ADHD, though, is what’s fueled the concerns I’ve seen about this article, particularly from people who love someone with ADHD. ADHD, you see, has a terrible reputation, one that suffers in large part because of abuse of drugs used to treat the condition. Many, many drugs exist that people use off-label to self medicate or boost performance. But I can’t think of drugs whose abuse stigmatizes the disorder for which they’re actually used as much as ADHD drugs do. And abuse of ADHD meds is inextricably linked with skepticism about the ADHD diagnosis: neurobiological conditions that overlap with the typical zones of behavior suffer from this kind of skepticism, but ADHD stands out. Blame for the drug abuse and diagnostic overuse heaps on doctors, parents, teachers, society, and people diagnosed with it. Are any of these groups to blame for the existence of ADHD? Generally, no. But some are to blame for its bad reputation and the abuse of the drugs used to treat it.

Drugs to treat ADHD work, as I’ve written before, but they carry known risks, and we still won’t know for some years what the long-term outcomes are following their use in childhood. Schwarz describes in his article a child taking the medication Adderallwho begins see people and hear voices that aren’t there, a rare side effect of the drug. That child is no longer on Adderall and instead is now takingRisperdal, a psychotropic medication with indications for schizophrenia and irritability associated with autism. It is not an “ADHD drug,” and it too carries potential risks that need to underweigh its benefits to warrant its use. One of the primary benefits of ADHD medications for children with the condition, in addition to the academic, is that the perceived improvement in behavior can translate into better social relationships and a reduction in the constant messages that they receive that they are a “bad person.” Whether or not they ultimately absorb that message as an inherent part of themselves remains to be seen.

In addition to prescribing Adderall to this boy, Anderson also prescribed it to two of the child’s siblings. In the article, the parents think that this prescription is an off-label use of Adderall, and the article holds up these two children as examples of using this drug to improve behavior and classroom performance in the absence of an ADHD indication. Yet Anderson then is reported as saying that all of the children for whom he has prescribed ADHD medications have met the criteria for ADHD, including these two children, whose parents don’t seem to know that. In other words, this story is about children who meet the ADHD criteria receiving drugs to treat ADHD and experiencing benefits, not about a broader use of ADHD drugs off-label to level the classroom playing field.

Forbes writer Matthew Herper blogged today that the NYT piece “hits the problem with ADHD drugs: they work.” Yes, they do. They work for ADHD, based on the only examples provided in this article, not more broadly for low-income children who just need more drug-induced focus in the classroom. Whether the doctor “rails” against the diagnostic criteria or not, the children taking–and responding to–Adderall in this article all met the criteria for an ADHD diagnosis. Indeed, low-income children are most likely to meet the diagnostic criteria for ADHD yet least likely to receive appropriate pharmaceutical intervention for it.  So whether he likes it or not, the doctor, by applying existing criteria, might have appropriately identified and treated children with ADHD who otherwise would have fallen through the cracks.

That doesn’t mean that we’re not still facing a brave new world in which college students pop Adderall for exams or driven high-school students are torn between the med boost and simply making it on their own, as they are. As Herper notes, there’s an important national conversation to be had around ADHD drugs and their off-label use to level the field or give an advantage. In his post, Herper asks, “Can we avoid a world in which thinkers are forced into brain-doping in the same way athletes have been pushed to chemically modify their bodies?” In neither case do we know the long-term positive or negative outcomes for the individuals being doped, whether for brain or brawn. I can’t speak about athletes, but as someone who has taught thousands of students from ages 5 to 65, I can say this: What we, in our short-sightedness, view as a childhood deficit because of its interference with classroom function can often yield our most beautiful manifestations of human thought and diversity later in life. Do medications help children with ADHD? Yes, they do. But … and I think this is the real point of the Schwarz piece, even as the examples simply bear out efficacy of ADHD meds for ADHD: We can’t look to the children for what needs “fixing.” For that, we must look to ourselves, and the depth and breadth of our problems with education in this country aren’t something even a full-scale, population-wide pill can fix.

Retrieved from: http://www.forbes.com/sites/emilywillingham/2012/10/09/adhd-drugs-for-children-who-dont-have-adhd-is-it-ok/

 

ADHD…a “made up” disorder???

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Neuropsychology, Psychiatry, Psychopharmacology, School Psychology on Thursday, 11 October 2012 at 10:37

while i do think adhd is the “diagnosis of the day” and it may be over-diagnosed, i DO NOT agree that it is a “made up”  disorder or “an excuse.”  you only have to look at the latest studies that compare treated and untreated brains of those diagnosed with adhd to see that there are real neurological and neuroanatomical deficits that can arise if adhd is left untreated (for one example, see: Adult ADHD: New Findings in Neurobiology and Genetics ; Scott H. Kollins, Ph.D.  http://www.medscape.org/viewarticle/765528).  

if you think you or someone you know has adhd, the following lists suggestions to make sure you receive a valid diagnosis and what to help to facilitate that*:

A good evaluation may consist of many of the following:

  • Collection of rating scales and referral information before or during the evaluation  
  • An interview with the student and parents
  • A review of previous records that may document impairments (i.e. problems in school, socially, or at home that you believe can be attributed to ADHD.  A good doctor knows exactly what questions to ask.
  • A general medical examination when medication might be part of treatment or coexisting medical conditions need to be evaluated (if the physician hasn’t already done this). 

 What to take along to facilitate these steps:  

  • Any records from schools you.your child attended and any other documentation of problems that could be related to ADHD or another disorder 
  • A list of family members with mental health known disorders
  • A description of impairments during childhood (i.e. elementary school), as well as more recent ones (i.e. middle school).  This can be done via SST notes, progress reports, psychological evaluations, IEP’s, etc.

*adapted from: Barkley, Russell A. (2011-04-04). Taking Charge of Adult ADHD (Kindle Locations 464-483). Guilford Press. Kindle Edition.

Attention Disorder or Not, Pills to Help in School

Alan Schwarz

CANTON, Ga. — When Dr. Michael Anderson hears about his low-income patients struggling in elementary school, he usually gives them a taste of some powerful medicine: Adderall.

The pills boost focus and impulse control in children with attention deficit hyperactivity disorder. Although A.D.H.D is the diagnosis Dr. Anderson makes, he calls the disorder “made up” and “an excuse” to prescribe the pills to treat what he considers the children’s true ill — poor academic performance in inadequate schools.

“I don’t have a whole lot of choice,” said Dr. Anderson, a pediatrician for many poor families in Cherokee County, north of Atlanta. “We’ve decided as a society that it’s too expensive to modify the kid’s environment. So we have to modify the kid.”

Dr. Anderson is one of the more outspoken proponents of an idea that is gaining interest among some physicians. They are prescribing stimulants to struggling students in schools starved of extra money — not to treat A.D.H.D., necessarily, but to boost their academic performance.

It is not yet clear whether Dr. Anderson is representative of a widening trend. But some experts note that as wealthy students abuse stimulants to raise already-good grades in colleges and high schools, the medications are being used on low-income elementary school children with faltering grades and parents eager to see them succeed.

“We as a society have been unwilling to invest in very effective nonpharmaceutical interventions for these children and their families,” said Dr. Ramesh Raghavan, a child mental-health services researcher at Washington University in St. Louis and an expert in prescription drug use among low-income children. “We are effectively forcing local community psychiatrists to use the only tool at their disposal, which is psychotropic medications.”

Dr. Nancy Rappaport, a child psychiatrist in Cambridge, Mass., who works primarily with lower-income children and their schools, added: “We are seeing this more and more. We are using a chemical straitjacket instead of doing things that are just as important to also do, sometimes more.”

Dr. Anderson’s instinct, he said, is that of a “social justice thinker” who is “evening the scales a little bit.” He said that the children he sees with academic problems are essentially “mismatched with their environment” — square pegs chafing the round holes of public education. Because their families can rarely afford behavior-based therapies like tutoring and family counseling, he said, medication becomes the most reliable and pragmatic way to redirect the student toward success.

“People who are getting A’s and B’s, I won’t give it to them,” he said. For some parents the pills provide great relief. Jacqueline Williams said she can’t thank Dr. Anderson enough for diagnosing A.D.H.D. in her children — Eric, 15; Chekiara, 14; and Shamya, 11 — and prescribing Concerta, a long-acting stimulant, for them all. She said each was having trouble listening to instructions and concentrating on schoolwork.

“My kids don’t want to take it, but I told them, ‘These are your grades when you’re taking it, this is when you don’t,’ and they understood,” Ms. Williams said, noting thatMedicaid covers almost every penny of her doctor and prescription costs.

Some experts see little harm in a responsible physician using A.D.H.D. medications to help a struggling student. Others — even among the many like Dr. Rappaport who praise the use of stimulants as treatment for classic A.D.H.D. — fear that doctors are exposing children to unwarranted physical and psychological risks. Reported side effects of the drugs have included growth suppression, increased blood pressure and, in rare cases, psychotic episodes.

The disorder, which is characterized by severe inattention and impulsivity, is an increasingly common psychiatric diagnosis among American youth: about 9.5 percent of Americans ages 4 to 17 were judged to have it in 2007, or about 5.4 million children, according to the Centers for Disease Control and Prevention.

The reported prevalence of the disorder has risen steadily for more than a decade, with some doctors gratified by its widening recognition but others fearful that the diagnosis, and the drugs to treat it, are handed out too loosely and at the exclusion of nonpharmaceutical therapies.

The Drug Enforcement Administration classifies these medications as Schedule II Controlled Substances because they are particularly addictive. Long-term effects of extended use are not well understood, said many medical experts. Some of them worry that children can become dependent on the medication well into adulthood, long after any A.D.H.D. symptoms can dissipate.

According to guidelines published last year by the American Academy of Pediatrics, physicians should use one of several behavior rating scales, some of which feature dozens of categories, to make sure that a child not only fits criteria for A.D.H.D., but also has no related condition like dyslexia or oppositional defiant disorder, in which intense anger is directed toward authority figures. However, a 2010 study in the Journal of Attention Disorders suggested that at least 20 percent of doctors said they did not follow this protocol when making their A.D.H.D. diagnoses, with many of them following personal instinct.

On the Rocafort family’s kitchen shelf in Ball Ground, Ga., next to the peanut butter and chicken broth, sits a wire basket brimming with bottles of the children’s medications, prescribed by Dr. Anderson: Adderall for Alexis, 12; and Ethan, 9; Risperdal (an antipsychotic for mood stabilization) for Quintn and Perry, both 11; and Clonidine (a sleep aid to counteract the other medications) for all four, taken nightly.

Quintn began taking Adderall for A.D.H.D. about five years ago, when his disruptive school behavior led to calls home and in-school suspensions. He immediately settled down and became a more earnest, attentive student — a little bit more like Perry, who also took Adderall for his A.D.H.D.

When puberty’s chemical maelstrom began at about 10, though, Quintn got into fights at school because, he said, other children were insulting his mother. The problem was, they were not; Quintn was seeing people and hearing voices that were not there, a rare but recognized side effect of Adderall. After Quintn admitted to being suicidal, Dr. Anderson prescribed a week in a local psychiatric hospital, and a switch to Risperdal.

While telling this story, the Rocaforts called Quintn into the kitchen and asked him to describe why he had been given Adderall.

“To help me focus on my school work, my homework, listening to Mom and Dad, and not doing what I used to do to my teachers, to make them mad,” he said. He described the week in the hospital and the effects of Risperdal: “If I don’t take my medicine I’d be having attitudes. I’d be disrespecting my parents. I wouldn’t be like this.”

Despite Quintn’s experience with Adderall, the Rocaforts decided to use it with their 12-year-old daughter, Alexis, and 9-year-old son, Ethan. These children don’t have A.D.H.D., their parents said. The Adderall is merely to help their grades, and because Alexis was, in her father’s words, “a little blah.”

”We’ve seen both sides of the spectrum: we’ve seen positive, we’ve seen negative,” the father, Rocky Rocafort, said. Acknowledging that Alexis’s use of Adderall is “cosmetic,” he added, “If they’re feeling positive, happy, socializing more, and it’s helping them, why wouldn’t you? Why not?”

Dr. William Graf, a pediatrician and child neurologist who serves many poor families in New Haven, said that a family should be able to choose for itself whether Adderall can benefit its non-A.D.H.D. child, and that a physician can ethically prescribe a trial as long as side effects are closely monitored. He expressed concern, however, that the rising use of stimulants in this manner can threaten what he called “the authenticity of development.”

“These children are still in the developmental phase, and we still don’t know how these drugs biologically affect the developing brain,” he said. “There’s an obligation for parents, doctors and teachers to respect the authenticity issue, and I’m not sure that’s always happening.”

Dr. Anderson said that every child he treats with A.D.H.D. medication has met qualifications. But he also railed against those criteria, saying they were codified only to “make something completely subjective look objective.” He added that teacher reports almost invariably come back as citing the behaviors that would warrant a diagnosis, a decision he called more economic than medical.

“The school said if they had other ideas they would,” Dr. Anderson said. “But the other ideas cost money and resources compared to meds.”

Dr. Anderson cited William G. Hasty Elementary School here in Canton as one school he deals with often. Izell McGruder, the school’s principal, did not respond to several messages seeking comment.

Several educators contacted for this article considered the subject of A.D.H.D. so controversial — the diagnosis was misused at times, they said, but for many children it is a serious learning disability — that they declined to comment. The superintendent of one major school district in California, who spoke on the condition of anonymity, noted that diagnosis rates of A.D.H.D. have risen as sharply as school funding has declined.

“It’s scary to think that this is what we’ve come to; how not funding public education to meet the needs of all kids has led to this,” said the superintendent, referring to the use of stimulants in children without classic A.D.H.D. “I don’t know, but it could be happening right here. Maybe not as knowingly, but it could be a consequence of a doctor who sees a kid failing in overcrowded classes with 42 other kids and the frustrated parents asking what they can do. The doctor says, ‘Maybe it’s A.D.H.D., let’s give this a try.’ ”

When told that the Rocaforts insist that their two children on Adderall do not have A.D.H.D. and never did, Dr. Anderson said he was surprised. He consulted their charts and found the parent questionnaire. Every category, which assessed the severity of behaviors associated with A.D.H.D., received a five out of five except one, which was a four.

“This is my whole angst about the thing,” Dr. Anderson said. “We put a label on something that isn’t binary — you have it or you don’t. We won’t just say that there is a student who has problems in school, problems at home, and probably, according to the doctor with agreement of the parents, will try medical treatment.”

He added, “We might not know the long-term effects, but we do know the short-term costs of school failure, which are real. I am looking to the individual person and where they are right now. I am the doctor for the patient, not for society.

Retrieved from: http://www.nytimes.com/2012/10/09/health/attention-disorder-or-not-children-prescribed-pills-to-help-in-school.html?pagewanted=all&pagewanted=print

The Energetic Brain…a great reference for ADHD

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Neuropsychology, Psychiatry, Psychopharmacology, School Psychology on Sunday, 7 October 2012 at 09:27

everything you ever wanted to know about adhd. a wonderful reference!

http://www.amazon.com/The-Energetic-Brain-Understanding-ebook/dp/B006RDCF0M/ref=sr_1_1?s=digital-text&ie=UTF8&qid=1349616011&sr=1-1&keywords=the+energetic+brain

FDA approves liquid, extended-release ADHD medication

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Psychiatry, Psychopharmacology on Sunday, 7 October 2012 at 07:14

FDA Approves Liquid, Extended-Release ADHD Med

Caroline Cassels

October 1, 2012 — The US Food and Drug Administration (FDA) has approved a once-daily liquid medication for the treatment of attention-deficit/hyperactivity disorder (ADHD).

In a news release, drug manufacturer NextWave Pharmaceuticals announced FDA approval of its drug Qullivant XR (methylphenidate hydrochloride), the first once-daily, oral-suspension medication for the treatment of ADHD.

According to the company, the central nervous system stimulant is the first extended-release, once-daily liquid ADHD medication on the market. It helps control ADHD symptoms within 45 minutes of administration and lasts for 12 hours.

“The approval of Quillivant XR fills a void that has long existed in the treatment of ADHD. We routinely see the struggles of patients who have difficulty swallowing pills or capsules. Having the option of a once-daily liquid will help alleviate some of these issues while still providing the proven efficacy of methylphenidate for 12 hours after dosing,” said Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, Nevada, who was also an investigator in a clinical trial that tested the drug.

The company notes that the drug’s efficacy was evaluated in a randomized, double-blind , placebo-controlled, crossover, multicenter classroom study of 45 children with ADHD.

Quillivant XR is a federally controlled substance (CII) because of its potential for abuse and/or dependence.

The drug is expected to be available in pharmacies in January 2013.

Retrieved from: http://www.medscape.com/viewarticle/771878?src=nl_topic

 

Psychostimulant treatment and the developing cortex

In ADHD, ADHD child/adolescent, ADHD stimulant treatment, Medication, Psychiatry, Psychopharmacology on Wednesday, 3 October 2012 at 06:19

a brief report on stimulant treatment in children and adolescents.  2008 publication but still useful information.

Psychostimulant Treatment and the Developing Cortex in Attention Deficit Hyperactivity Disorder

Shaw P, Sharp WS, Morrison M, et al
Am J Psychiatry. 2008 Sep 15.

http://www.medscape.org/viewarticle/583251

This study examined whether stimulants for attention-deficit/hyperactivity disorder (ADHD) were associated with differences in cerebral cortex development.

Study Design: Neuroanatomic MRI was used to assess the change in cortical thickness in 43 youths with ADHD; mean age at the first scan was 12.5 years, mean age at the second scan was 16.4 years. Of the 43 adolescents, 24 were treated with stimulants between scans while 19 were not treated between scans. Investigators included an additional comparison to a large sample of (n=294) of typically developing control youths.

Results: The rate of change of the cortical thickness in the right motor strip, the left middle/inferior frontal gyrus, and the right parieto-occipital region was different between the adolescents taking stimulants as compared with those not taking stimulants. Specifically, the study found more rapid cortical thinning in the group of patients not taking stimulants (mean cortical thinning of 0.16 mm/year [SD=0.17], compared with 0.03 mm/year [SD=0.11] in the group taking stimulants). Furthermore, comparison against the controls without ADHD showed that cortical thinning in the group not taking stimulants was in excess of age-appropriate rates.

Conclusion: These findings show no evidence that stimulant treatment is associated with slowing of overall growth of the cortical mantle.

Commentary: This is a remarkable paper from the Child Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland, and the Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. The authors suggest that psychostimulant-induced improvements in cognition and action might foster cortical development within the normative range, as an example of activity-dependent neuroplasticity. The authors note that a randomized trial would be a better scientific design, but in the interim, this study shows the importance of comparisons with controls/normative data.

an interesting look at adhd…

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Mindfulness on Thursday, 27 September 2012 at 04:06

Of ADHD and Lord Ganesha (A Tale of the Differently-Headed)

By ZOË KESSLER, BA, B.ED.

I was a happy little thing as a child. Then, I started feeling like a freak. People called me names. I didn’t know why.

Sometimes, they‘d push me, or punch me. Once, I ended up face down in gravel in the schoolyard.

I looked into the mirror to see if I was bleeding. Tears streamed down my eyes, clouding my vision. Finally, my tears dried. That’s when I saw it.

My eyes opened wide. I jumped back in shock. My head was so very strange. I didn’t look anything like any of my friends.

No wonder they didn’t like me. No wonder they all made fun of me. No wonder they wouldn’t let me play games with them, instead calling me names as I walked away.

“Freak!”

“Weirdo!”

“Loser!”

I was grotesque.

I ran home crying. Mom! Mom!

But mom couldn’t do anything. Reluctantly, she told me that this was my head and I would have to live with it.

No! I cried, running out of the house. I ran and ran and ran. I couldn’t believe it. Why would my mom lie to me? Of course we could fix my head. Of course we could. She just didn’t know how, so she was lying to me.

I ran to my school’s library. I sat tucked away in a corner where no one could find me. Mom was right! I would have this head for ever and ever. It was true: no one could save me. I hung my head.

My teardrops formed dark circles and spread on the page. The wet paper bubbled, each drop coming alive, the words rising up to mock me. I cried and cried. I would always have this head.

Always.

344/365. Deva Shree Ganesha.Creative Commons License photo credit: Anant N S (www.thelensor.tumblr.com)

This is the story of many with ADHD. This is also what vividly came to my imagination as I meditated on Lord Ganesha, the Hindu elephant God, one of Hinduism’s major deities.

There are several versions of Lord Ganesha’s story, but he’s generally accepted as the son of Shiva and Parvati, themselves Hindu deities. Still a babe, Lord Ganesha suffers a terrible tragedy: through a misunderstanding, his head is lopped off by dad.

Mom Parvati is of course grief-stricken, so dad thinks fast and replaces the babe’s head with that of a young elephant.

And the little trooper turns it all around, conquering adversity to become Lord Ganesha, inspiring millions of followers. Metaphorically speaking, his many qualities can also inspire those of us with ADHD.

Symbols as sources of inspiration

The symbolism of Lord Ganesha is singularly relevant to those of us with ADHD. For example, his large ears remind us to listen; his small eyes, to focus and concentrate; and his tiny mouth, to speak less.

Lord Ganesha rose above his misfortunes, becoming revered as the Remover of Obstacles. You think you’ve got challenges? Think about what Lord Ganesha had to overcome with his strange, unusual head.

Now think about what you’ve had to overcome with your unusual head. Lord Ganesha can inspire us to keep fighting to overcome our own obstacles, which, let’s face it, are as small as mice when compared to having the head of an elephant.

Count your blessings.

Annual celebration

As India celebrates its annual Ganesh Chaturthi festival in honor of Lord Ganesha (September 19 – 29, 2012), I’m offering gratitude for Lord Ganesha as a source of inspiration and insight in my daily meditations.

What inspires you?

I’d like to invite you to contemplate your own sources of strength and inspiration. Look closely: you might find more than initially meets the eye. I began to pray to Lord Ganesha to remove obstacles, and found myself relating to having a very different head.

When you look deeply into the face of the Divine, you too may find yourself reflected back.

Namaste.

Retrieved from: http://blogs.psychcentral.com/adhd-zoe/2012/09/of-adhd-and-lord-ganesha-a-tale-of-the-differently-headed/

ADHD medication and cardiovascular risk

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Psychiatry, Psychopharmacology on Wednesday, 26 September 2012 at 07:20

i believe many people may hold some misconceptions related to stimulant medication in treating ADHD.  in fact, i have a personal story related to that.  a friend of mine needed to go to the emergency room for a cut that needed stitches.  while in triage, the nurse took her blood pressure and it was quite elevated.  the nurse questioned her about her bp and asked if she was diagnosed with high blood pressure (this person is an avid athlete and has never had issues with high bp).  once the nurse saw on her intake form that she took 10mg. of adderall a day for adult ADHD, she told my friend that that medicine was “toxic” and the she needed to stop it “right away” and go to her doctor immediately for a cardiac assessment.  she repeatedly stated that the adderall she was taking was going to do her harm and she MUST stop taking it right away!  my friend was somewhat startled at the nurse’s vehement opinions regarding the adderall.  what i do know is that, when i am hurt or in a tense situation (i.e. the emergency room and in pain), my blood pressure might temporarily go up.  i also know that i DO NOT have high blood pressure.  no mention of being anxious or in pain was made in relation to my friend’s high bp at that time.  on a side note, once my friend was out of the ER and we had gone to the pharmacy to get a prescription, she took it again and it was well within the normal range, showing she was just anxious/worried/in pain and her higher bp was a residual effect of that.  but…this does illustrate that there are times people believe that something is fact because of popular opinion, their own biases, etc., even when the literature may not support their belief/s.  so, in light of that, i wanted to share a post on stimulant medication and cardiovascular risk.  as you can see, it is not as clear-cut as our opinionated nurse thought it was.

ADHD Medications in Adults Yield Mixed Cardiovascular Risk Results

Deborah Brauser & Hien T. Nghiem, MD

In the United States, roughly 1.5 million adults use medications for attention-deficit/hyperactivity disorder (ADHD). These medications include amphetamines, atomoxetine, and methylphenidate. ADHD medications are known to increase both blood pressure (< 5 mm Hg) and heart rate (< 7 bpm). Given these effects, there are concerns regarding serious cardiovascular events related to taking ADHD medications.

The aim of this study by Hennessy and colleagues was to determine whether use of methylphenidate in adults is associated with elevated rates of serious cardiovascular events compared with rates in nonusers.

Study Synopsis and Perspective

Although adults prescribed the ADHD medication methylphenidate may be at increased risk for adverse cardiovascular events, this association may not be causal, new research suggests.

In a cohort study of almost 220,000 individuals, new users of methylphenidate had almost twice the risk for sudden death or ventricular arrhythmia than age-matched control participants had. They also had a significantly higher risk for all-cause death.

However, the medication dosage “was inversely associated with risk,” meaning it lacked a dose-response relationship, report the investigators.

“We were surprised by the risk findings. But the inverse associations leads us to be somewhat skeptical,” coinvestigator Sean Hennessy, PharmD, PhD, associate professor of epidemiology and pharmacology at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia, told Medscape Medical News.

“Ordinarily, if a drug increases the risk of adverse outcomes, that increase is going to be dose-dependent. We didn’t see that, and in fact, found an inverse relationship for death and other outcomes,” he explained.

Dr. Hennessy said that this could be due to “frail, elderly patients who have other things going on” and who are prescribed low-dose methylphenidate.

“Maybe baseline differences in those patients that aren’t captured in the medical claims data are responsible for the elevated risk of adverse outcomes we were seeing rather than it being a causal effect of the methylphenidate itself,” he opined.

“So I would say to wait for these findings to be replicated and clarified in other research before they are acted on clinically.”

The study is published in the February issue of the American Journal of Psychiatry.

Mixed Findings

According to the investigators, methylphenidate and other ADHD medications are used by almost 1.5 million adults in the United States — even though these medications have been shown to raise blood pressure and heart rate.

“Given these effects, case reports of sudden death, stroke, and myocardial infarction have led to regulatory and public concern about the cardiovascular safety of these drugs,” write the researchers.

However, in May 2011, and reported by Medscape Medical News at that time, the same group of researchers published a study in Pediatrics that showed no increased risk for cardiovascular events in children treated with ADHD medications.

In addition, researchers from Kaiser Permanente Northern California published a study in December 2011 in the Journal of the American Medical Association that examined risks in adults younger than age 65 years who were taking methylphenidate, amphetamine, atomoxetine, or pemoline.

The combined group of ADHD medication users showed no increased risk for serious cardiovascular events, including myocardial infarction, sudden cardiac death, or stroke, compared with the group of nonusers.

For this analysis, investigators examined records from Medicaid and commercial databases, representing 19 states, for adults in a broader age range. Included were 43,999 new users of methylphenidate and 175,955 individuals who did not use methylphenidate, amphetamines, or atomoxetine (for both groups, 55.4% were women).

In each group, 67.3% of the participants were between the ages of 18 and 47 years, 23.2% were between the ages of 48 and 64 years, and 9.5% were aged 65 years or older.

Primary cardiac events assessed included sudden death or ventricular arrhythmia, myocardial infarction, stroke, and a combination of stroke/myocardial infarction. All-cause death was a secondary measure.

Unexpected Results

Results showed that the adjusted hazard ratio (HR) for sudden death/ventricular arrhythmia for the methylphenidate users compared with the nonusers was 1.84 (95% confidence interval [CI], 1.33 – 2.55). For all-cause death, the HR was 1.74 (95% CI, 1.60 – 1.89).

Adjusted HRs for myocardial infarction and stroke (alone or in combination) were not statistically different between the 2 treatment groups.

For the participants who experienced a cardiovascular event, the median treatment dosage was 20 mg/day. No significant association was found for sudden death/ventricular arrhythmia between the patients who took more or less than 20 mg/day of methylphenidate.

“However, there were unexpected inverse associations” between high methylphenidate dosage and stroke, myocardial infarction, stroke/myocardial infarction, and all-cause death compared with low dosage, report the researchers. They add that this lack of a dose-response association discredits a causal relationship.

“Furthermore, the inverse relationships…may suggest that lower dosages were prescribed to the frailest patients, who might have had a greater risk of all-cause death and sudden death — that is, the results may have been affected by unmeasured confounding,” write the investigators.

Other limitations cited included the fact that the study was not randomized and that administrative databases do not include potential confounders such as smoking, blood pressure, substance use, and exercise use/nonuse.

Dr. Hennessy reported that the investigators also assessed cardiovascular risks in their study participants who were also taking amphetamines or atomoxetine. They will be publishing those results soon.

Findings “Generally Reassuring”

Christopher J. Kratochvil, MD, from the University of Nebraska Medical Center in Omaha, writes in an accompanying editorial that this and other studies are “generally reassuring and demonstrate movement in the right direction, with systematic retrospective analyses better informing us of issues related to cardiovascular safety with ADHD pharmacotherapy.”

“While gaps persist in the methodical and comprehensive assessments of the safety of ADHD medications, these studies add valuable information to our already large repository of safety and efficacy data…and better inform the risk-benefit analysis of their use,” writes Dr. Kratochvil, who was not involved with this research.

He adds that establishing a “robust” national electronic health records system containing detailed data elements will also offer considerable help to clinicians.

These large and more accessible databases “will allow us to improve our identification and understanding of rare but serious adverse effects and better address these questions of public health significance,” he concludes.

The study was funded through a sponsored research agreement with Shire Development, Inc., and by a Clinical and Translational Science Award from the National Institutes of Health. The study authors all receive salary support from Shire through their employers. All financial disclosures for the study authors and Dr. Kratochvil are listed in the original article.

Am J Psychiatry. 2012;169:112-114;178-185. Abstract, Editorial

Study Highlights

■This study was a nonrandomized cohort study of new users of methylphenidate based on administrative data from a 5-state Medicaid database (1999-2003) and a 14-state commercial insurance database (2001-2006).

■All new methylphenidate users with at least 180 days of prior enrollment were identified.

■Users were matched on data source, state, sex, and age to as many as 4 comparison participants who did not use methylphenidate, amphetamines, or atomoxetine.

■A total of 43,999 new methylphenidate users were identified and were matched to 175,955 nonusers.

■The main outcome measures were (1) sudden death or ventricular arrhythmia; (2) stroke; (3) myocardial infarction; and (4) a composite endpoint of stroke or myocardial infarction.

■Secondary outcomes included all-cause death and nonsuicide death.

■Results demonstrated that the age-standardized incidence rate per 1000 person-years of sudden death or ventricular arrhythmia was 2.17 (95% CI, 1.63 – 2.83) in methylphenidate users and 0.98 (95% CI, 0.89 – 1.08) in nonusers, for an adjusted HR of 1.84 (95% CI, 1.33 – 2.55).

■Dosage was inversely associated with the risks for stroke, myocardial infarction, stroke/myocardial infarction, and all-cause death.

■Adjusted HRs for stroke, myocardial infarction, and the composite endpoint of stroke or myocardial infarction did not differ statistically from one another.

■For the secondary outcome of all-cause death, methylphenidate demonstrated a positive association (adjusted HR, 1.74; 95% CI, 1.60 – 1.89). Nonsuicide deaths were nearly identical.

■Limitations of this study include the potential for unmeasured confounders (ie, smoking, blood pressure, nonprescribed aspirin use, substance misuse, and level of physical activity) because the study was not randomized.

Clinical Implications

■ADHD medications raise blood pressure by less than 5 mm Hg and heart rate by less than 7 bpm.

■Although initiation of methylphenidate was associated with a 1.8-fold increase in the risk for sudden death or ventricular arrhythmia, the lack of a dose-response relationship suggests that this association may not be a causal one.

Retrieved from: http://www.medscape.org/viewarticle/759069

The state of sleep in the U.S.

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Anxiety, Fitness/Health, Medication, Well-being on Tuesday, 18 September 2012 at 05:04

stress, anxiety, and depression are but three related etiologies for insomnia.  people with ADHD also suffer from insomnia, either as a side-effect of psychostimulants or because of the ADHD itself.  insomnia can have significant effects on quality of life, work/school life, and health.  statistics show that insomnia is a growing problem in the U.S. today and sleep aids are being prescribed at an increasing rate.  the following are some statistics related to insomnia as well as a case-study/research article on insomnia. 

to be followed by an article about hypnotic use and associated risk-factors.

***

General Insomnia Statistics

  • People today sleep 20% less than they did 100 years ago.
  • More than 30% of the population suffers from insomnia.
  • One in three people suffer from some form of insomnia during their lifetime.
  • More than half of Americans lose sleep due to stress and/or anxiety.
  • Between 40% and 60% of people over the age of 60 suffer from insomnia.
  • Women are up to twice as likely to suffer from insomnia than men.
  • Approximately 35% of insomniacs have a family history of insomnia.
  • 90% of people who suffer from depression also experience insomnia.
  • Approximately 10 million people in the U.S. use prescription sleep aids.
  • People who suffer from sleep deprivation are 27% more likely to become overweight or obese. There is also a link between weight gain and sleep apnea.
  • A National Sleep Foundation Poll shows that 60% of people have driven while feeling sleepy (and 37% admit to having fallen asleep at the wheel) in the past year.
  • A recent Consumer Reports survey showed the top reason couples gave for avoiding sex was “too tired or need sleep.”

Financial Implications of Insomnia

Insomnia statistics aren’t confined to the relationship between insomnia and health. This sleep disorder costs government and industry billions of dollars a year.

  • The Institute of Medicine estimates that hundreds of billions of dollars are spent annually on medical costs that are directly related to sleep disorders.
  • The National Highway Traffic Safety Administration statistics show that 100,000 vehicle accidents occur annually drowsy driving. An estimated 1,500 die each year in these collisions.
  • Employers spend approximately $3,200 more in health care costs on employees with sleep problems than for those who sleep well.
  • According to the US Surgeon General, insomnia costs the U.S. Government more than $15 billion per year in health care costs.
  • Statistics also show that US industry loses about $150 billion each year because of sleep deprived workers. This takes into account absenteeism and lost productivity.

These sobering insomnia statistics underscore the importance of enhancing sleep disorder awareness and why individuals need to seek immediate treatment for the health and the well-being of others.

Sources: National Sleep Foundation, Better Sleep Council, Gallup Polls, Institute of Medicine, National Highway Traffic Safety Administration, US Surgeon General’s Office

http://www.better-sleep-better-life.com/insomnia-statistics.html

Manifestations and Management of Chronic Insomnia: NIH State-of-the-Science Conference Findings and Implications

Authors: William T. Riley, PhD; Carl E. Hunt, MD

http://www.medscape.org/viewarticle/517618

Introduction

The Problem of the Inadequate Identification and Treatment of Chronic Insomnia

Despite considerable advances in the understanding of and treatments for chronic insomnia, this condition remains inadequately identified and treated. Approximately one third of US adults report difficulty sleeping, and 10% to 15% have the clinical disorder of insomnia.[1] Among primary care patients, approximately half have sleep difficulties, but these difficulties often are undetected by health professionals.[2,3] Even if detected and appropriately diagnosed, these patients are more likely to receive treatments of questionable safety and efficacy rather than treatments with substantial, evidence-based support for safety and efficacy.

The inadequate identification and treatment of chronic insomnia has serious medical and public health implications. Chronic insomnia results in impaired occupational performance and diminished quality of life.[4,5] Insomnia is associated with higher healthcare usage and costs, including a 2-fold increase in hospitalizations and physician visits.[6] Insomnia is also a risk factor for a number of other disorders, particularly psychiatric disorders, such as depression, and an important sign or symptom for a range of medical and other psychiatric disorders.[7]

In a recent review, Benca[8] identified the following 5 barriers to the recognition, diagnosis, and treatment of insomnia in primary care settings:

  • Inadequate knowledge base: In the 1990s, about one third of medical schools had no formal sleep medicine training. A majority of practitioners rate their knowledge of sleep medicine as only “fair.”
  • Office visit time constraints: Unless sleep difficulties are the presenting complaint, visit time may be inadequate for sleep difficulties to be addressed.
  • Lack of discussion about sleep: Less than half of patients with insomnia have discussed this problem with their physicians, and most of these discussions were patient-initiated.
  • Misperceptions regarding treatment: Health professionals may have greater concerns than warranted about the safety and efficacy of pharmacologic treatments, and they may not be aware of or have access to effective nonpharmacologic approaches.
  • Lack of evidence for functional outcomes: Although treatments for insomnia reduce symptoms in the short term, there is inadequate evidence for long-term efficacy, improvements in daytime functioning, or the impact on comorbid disorders.

Addressing these barriers could lead to improved recognition and treatment of chronic insomnia and may substantially reduce the personal and public health burden of this disorder.

The Importance of Appropriate Recognition and Treatment of Chronic Insomnia: NIH State-of-the-Science Conference Statement

The purpose of this Clinical Update is to emphasize the importance of appropriate recognition of and treatment for chronic insomnia based on the recently published statement from the National Institutes of Health (NIH) State-of-the-Science Conference on the Manifestations and Management of Chronic Insomnia in Adults.[9] An independent panel of health professionals convened in June 2005 to evaluate the evidence from (1) systematic literature reviews prepared by the Agency for Health Research and Quality, (2) presentations by insomnia researchers over a 2-day public session, (3) questions and comments by conference attendees during the public sessions, and (4) closed deliberations by the panel. This process resulted in a State-of-the-Science (SOS) Conference Statement on chronic insomnia, including implications for clinical and research efforts.

The SOS Conference proceedings and statement were organized around the following 5 questions, which serve as the outline for this Clinical Update:

  • How is chronic insomnia defined, diagnosed, and classified, and what is known about its etiology?
  • What are the prevalence, natural history, incidence, and risk factors for chronic insomnia?
  • What are the consequences, morbidities, comorbidities, and public health burden associated with chronic insomnia?
  • What treatments are used for the management of chronic insomnia, and what is the evidence regarding their safety, efficacy, and effectiveness?
  • What are important future directions for insomnia-related research?

The SOS Conference focused on adults with chronic insomnia, not acute or episodic manifestations, which typically resolve in a few weeks, often without intervention. Although secondary or comorbid insomnia (insomnia associated with other conditions) was considered with respect to diagnosis and classification, the conference focused on the treatment of primary insomnia, not on any existing comorbid conditions. This Clinical Update, therefore, follows the scope of the SOS Conference and focuses on chronic primary insomnia in adults. Information in the SOS Conference Statement is augmented by the research literature, including a number of excellent, recent reviews on the clinical management of insomnia.[8,10-14]

How Is Chronic Insomnia Defined, Diagnosed, and Classified, and What Is Known About Its Etiology?

Case Study: Part 1

A 56-year-old woman presents for routine monitoring of postmenopausal symptoms and bone density, following a 2-year course of hormone replacement therapy that was initiated 5 years ago when she began experiencing hot flashes and depressive symptoms. During the visit, she is asked about her sleep and reveals that she has difficulty falling asleep most nights and sometimes awakens in the middle of the night, and is unable to go back to sleep. She notes frustration at her inability to get a good night’s sleep, particularly because she often feels tired and has difficulty concentrating at work. She reports that her insomnia began about the time of her menopausal symptoms, but has continued even though her other menopausal symptoms have resolved.

What steps should be taken to diagnose her condition?

Detecting Sleep Difficulties

The patient in the case above has a distinct advantage over many patients who suffer with insomnia because her healthcare professional specifically asked about her sleep. As early as Hippocrates, sleep has been an important indicator of patient health. “Disease exists, if either sleep or watchfulness be excessive”: Hippocrates, Aphorism LXXI.[12] In a recent study of adult primary care patients with insomnia, only about half reported discussing insomnia with their physicians.[15] Other studies have found that only 10% to 30% of those with insomnia discussed this problem with their physicians,[16] and most healthcare providers fail to ask about sleep.[2] Asking a simple question, such as “How have you been sleeping?” can lead to the detection of insomnia and a range of other sleep-related conditions.[17]

Definitions and Diagnostic Criteria for Chronic Insomnia. Insomnia is a sleep disturbance that most often manifests as difficulty initiating sleep, but also manifests as difficulty maintaining sleep or experiencing early-morning awakenings.

How much sleep disruption is sufficient for the diagnosis of insomnia? Normal sleep needs vary greatly from individual to individual. Moreover, the degree of sleep disturbance in those with insomnia can be quite variable from night to night, including nights without any sleep disturbance. Although quantitative indices for sleep-onset latency (≥ 30 minutes) and for sleep efficiency (percentage of total time asleep over total time in bed ≤ 85%) have been used for research purposes,[18] these indices do not correlate well with the patient’s experience of insomnia.[19] Therefore, the subjective experience of inadequate sleep is frequently more important than quantitative sleep indices in diagnosing insomnia.

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) defines primary insomnia as a difficulty initiating or maintaining sleep or experiencing nonrestorative sleep that results in clinically significant distress or impairment in functioning.[20] Based on these criteria, someone who does not appear to have objective manifestations of sleep disturbance but whose sleep is sufficiently inadequate or nonrestorative to produce distress or dysfunction would meet the criteria for insomnia. In contrast, someone who gets only a few hours of sleep each night but feels rested and without associated distress or dysfunction does not meet the criteria for insomnia. Therefore, subjective impressions of nonrestorative sleep with associated distress or dysfunction are important symptoms of insomnia.

These complaints of disturbed sleep also must occur in the context of adequate opportunity and circumstances for sleep. Although disruption of sleep from environmental perturbations may place someone at risk for insomnia, sleep disruption is not classified as insomnia unless there is adequate opportunity to sleep. Resident physicians on call or mothers of newborns commonly experience sleep disturbances, nonrestorative sleep, and daytime distress or impairment from inadequate sleep, but these problems are not diagnosed as insomnia because they are the result of having an inadequate opportunity to sleep.

Many people experience insomnia on occasion, but most of these “acute” or “episodic” forms of insomnia are transient and typically resolve without treatment. The duration required for insomnia to be “chronic” has varied from as little as 1 month to as long as 6 months. Based primarily on recent Research and Diagnostic Criteria (RDC) for insomnia,[21] the SOS Conference Statement concluded that insomnia lasting 1 month or more is clinically important and indicates the need for professional attention.

The SOS Conference Statement concluded that insomnia lasting 1 month or more is clinically important and indicates the need for professional attention.

RDC for insomnia. The Academy of Sleep Medicine recently developed RDC for insomnia[21] in an effort to merge different nosologies and improve the diagnostic reliability of insomnia. The RDC criteria also provide 3 subclassifications of primary insomnia: Psychophysiologic Insomnia, Paradoxical Insomnia (Sleep State Misperception), and Idiopathic Insomnia, which may facilitate research on potential etiologies of this disorder. These diagnostic criteria will be included in the second edition of the International Classification of Sleep Disorders (ICSD-2) and will likely be adopted in the next International Classification of Diseases (ICD) version. The RDC diagnostic scheme first delineates the criteria for an insomnia disorder and then specifies the exclusion criteria for primary insomnia. Compared with the DSM-IV criteria, the RDC insomnia criteria specify the requirement for adequate opportunity or circumstances for sleep and provide greater detail of the distress or functional impairment criteria. The RDC criteria for primary insomnia also clarify that the presence of a comorbid disorder does not exclude the diagnosis of primary insomnia unless the insomnia can be attributed exclusively to the comorbid disorder.

Comorbid insomnia. Primary insomnia is a diagnosis of exclusion. Numerous other conditions can contribute to the onset or maintenance of insomnia, including psychiatric disorders, substance abuse, other sleep disorders, or medical conditions/treatments. In the past, insomnia was considered “secondary” if it appeared due to another condition, but this was often difficult to determine clinically.[22] In addition, the relationship between insomnia and various comorbid disorders is complex and multidirectional. For example, insomnia may be a symptom of comorbid depression, but it may also be a separate and predisposing condition for depression.[23]

Given these complexities, the SOS Conference Panel recommended that “comorbid insomnia” replace the term “secondary insomnia.” The practical implication of this terminology for clinicians is that insomnia should not be relegated to secondary status whenever a comorbid disorder exists. The presence of comorbid disorders needs to be evaluated, and temporal relationships between the course of the comorbid disorder and the insomnia may shed light on possible etiologic relationships between them,[7] but it cannot be assumed that treating only the comorbid disorder will result in resolution of the insomnia as well.

The SOS Conference Panel recommended that “comorbid insomnia” replace the term “secondary insomnia.”

Clinical assessment of insomnia. The diagnosis of insomnia is based primarily on the patient’s history. Reports by family members, particularly the bed partner, can augment the assessment of sleep behavior and daytime functioning. Medical history and physical examination are also useful for determining the presence of possible comorbid syndromes.[7]

Sleep diaries are frequently used to document sleep-and-wake behaviors. In addition to providing data to support a diagnosis, these data are often used to devise treatment plans and to monitor treatment outcomes. Patients are typically instructed to complete the diary each morning after awaking and provide their best estimates of variables, such as time in bed, time of sleep onset, awakenings, and wake time. These data are only estimates by patients and tend to underestimate actual sleep time, but they are useful for assessing individual sleep patterns, possible factors associated with poor sleep, and changes in sleep over time. There are also a number of self-report instruments, a few of which have been adequately standardized and validated for monitoring outcomes.[24]

To provide more objective measures of sleep behavior, actigraphs or accelerometers have been used in research trials to infer sleep-and-wake behaviors from changes in the amount of movement. Although useful, actigraphs have not been fully validated and may underestimate sleep time if sleep is restless or fitful (eg, with comorbid restless legs syndrome). Actigraphs and other automated measures of sleep behavior have not typically been used in routine practice, but can provide more objective measures of sleep patterns, especially when the patient’s report is in question (eg, sleep-state misperception).[25]

Polysomnography remains the gold standard for measuring sleep-wake states; however, the American Academy of Sleep Medicine does not recommend polysomnography for the assessment of insomnia except when needed to rule out a comorbid disorder, such as sleep apnea.[26] In addition to expense, polysomnography is unlikely to provide an accurate representation of an insomnia patient’s sleep difficulties given the night-to-night variability of sleep behavior and influence of the sleep environment on insomnia symptoms.

The American Academy of Sleep Medicine does not recommend polysomnography for the assessment of insomnia except when needed to rule out a comorbid disorder, such as sleep apnea.

Etiology of insomnia. Although there is growing consensus about the appropriate diagnostic criteria and procedures for insomnia, the possible etiologic factors for insomnia remain poorly understood. Spielman’s 3 Ps — predisposing, precipitating, and perpetuating factors — is a useful model for organizing various etiologic factors.[27]

Very little is known about possible predisposing factors for insomnia. Other than some limited research suggesting familial aggregation,[28,29] there are no data on genetic predisposition for insomnia. There is considerable research on the neurobiology of sleep-wake states, including the inhibitory feedback loop involving the GABA and galanin neurons in the ventrolateral preoptic nucleus of the hypothalamus and the orexin or hypocretin neurons in the posterior hypothalamus, which serve as a “flip-flop” switch of major cortical arousal systems.[30,31] It remains unclear, however, how these systems are dysfunctional in insomnia. Deficiencies in endogenous melatonin or benzodiazepine receptors and hyperactivity of corticotropin-releasing factor neurons are possible etiologic factors, but further research is needed to better understand these potential etiologies for insomnia.[32]

The possible etiologic factors for insomnia remain poorly understood, and little is known about possible predisposing factors for insomnia.

Hyperarousal appears to be an important mechanism for insomnia. Research has shown increased brain glucose metabolism when awake or asleep, increased beta and decreased theta and delta during sleep, and increased adrenocorticotropic hormone activity.[33,34] Results from recent functional imaging studies provide additional support for the central nervous system hyperarousal hypothesis.[35]

Potential precipitating factors for insomnia are numerous and include many of the possible disorders that are comorbid with insomnia, such as psychiatric disturbance, sleep-wake schedule changes, medical conditions and their treatments, other sleep disorders, and substance use. Substances, including caffeine, theophylline and other stimulants, steroids, antihypertensives, and antidepressants, can also precipitate insomnia.[12] A recent study found that family, health, and work-school-related events were the most common precipitating factors for insomnia, and that even positive events can precipitate insomnia.[36]

There is general agreement that insomnia, regardless of how it is precipitated, is perpetuated by cognitive and behavioral mechanisms. Cognitive factors involved in perpetuating insomnia include misconceptions about normal sleep needs and stability, misattributions about the causes of sleep disturbance, and catastrophic worry about the daytime effects of inadequate sleep.[18,37] These dysfunctional beliefs often promote behaviors that are intended to improve sleep but are disruptive to sleep homeostasis and a consistent sleep-wake cycle (eg, taking naps and sleeping in late to “catch up” on sleep). These sleep-disruptive behaviors are further perpetuated by behavioral conditioning, which produces conditioned arousal to stimuli that would normally be associated with sleep.[38] It is important to recognize that these cognitive and behavioral perpetuating factors may be present in both comorbid and primary

What Are the Prevalence, Course, Incidence, and Risk Factors for Chronic Insomnia?

Prevalence of Chronic Insomnia

Estimates of the prevalence of insomnia vary depending on the definition used. Approximately one third of the general population complains of sleep disruption, and 9% to 15% of the population report associated daytime impairment consistent with the diagnosis of insomnia.[1] However, the proportion of those reporting sleep disturbance with daytime impairment who would meet the diagnostic criteria for insomnia is unclear. Among patients in primary care, the prevalence rates for insomnia are much higher, as high as 50%.[4] In a large survey of managed care participants, over one third experienced symptoms of insomnia, although less than 1% presented with an insomnia complaint.[39]

Incidence, Natural Course, and Duration of Chronic Insomnia

The SOS Conference Statement noted that there is very little known about the incidence, natural course, and duration of insomnia. Limited evidence suggests that insomnia is a chronic and persisting condition with low rates of spontaneous remission and possible recurrence after a period of remission, but these processes are poorly understood.

There is very little known about the incidence, natural course, and duration of insomnia.

Risk Factors for Chronic Insomnia

Given that most research on risk factors for insomnia is cross-sectional, not longitudinal, it is difficult to know whether potential risk factors are causal or correlational. The prevalence of insomnia is higher in divorced, separated, or widowed adults, and in those with lower education and income levels.[1] Insomnia is also more likely to occur in women, especially postmenopausal women.[1] There is an increased prevalence of insomnia in older adults, but it remains unclear to what extent this is independent of declining health and comorbid influences. Sleep patterns, however, do change with age. Older people experience more awakenings during the night, lower sleep efficiency, less sleep, more variable sleep, and lighter sleep than younger adults.[40]

Several psychiatric and medical disorders are associated with insomnia. As noted earlier, however, these relationships are complex and multidirectional. For example, research on the relationship between insomnia and depression indicates that it is more likely that insomnia is a risk factor for depression than that depression is a risk factor for insomnia. Insomnia appears to be predictive of a number of disorders, including depression, anxiety, alcohol abuse/dependence, drug abuse/dependence, and suicide.[41] Medical and sleep disorders that potentially disrupt sleep (eg, chronic pain conditions, such as arthritis, or sleep apnea) may be precipitants of or risk factors for insomnia. Substance abuse and the use of prescribed medications that can disturb sleep also can be risk factors for insomnia.

It is difficult to know whether potential risk factors are causal or correlational. Several psychiatric and medical disorders are associated with insomnia, but these associations are complex and multidirectional.

What Are the Consequences, Morbidities, Comorbidities, and Public Health Burden Associated With Chronic Insomnia?

Economic Costs of Insomnia

Insomnia is associated with high healthcare utilization. Walsh and Ustun[42] estimated annual direct total costs for insomnia at about $12 billion for healthcare services and $2 billion for sleep-promoting agents. People with insomnia have more medical problems and use more medications than those without insomnia, and they have double the number of office visits and hospitalizations as those without insomnia.[6,43]

The relative contribution of insomnia and comorbid conditions to these costs remains unclear. Indirect costs of insomnia are even less clear. In 1994, the economic costs of insomnia were estimated at $80 billion annually.[44,45] These indirect cost estimates are higher than those for other chronic conditions, such as rheumatoid arthritis,[46] but there are limited data available to reliably estimate the indirect costs of insomnia.

Effects of Insomnia on Functioning and Quality of Life

Sleep loss does result in impaired psychomotor and cognitive functioning, but these impairments are less pronounced for insomnia.[47] Despite the equivocal impact of insomnia on memory and cognitive functioning, insomnia is related to occupational role dysfunction, including increased absenteeism and decreased work performance.[4,43] These daytime impairments, however, may be more related to the chronic hyperarousal state[48] or to perceptions of sleep deprivation[49] than to actual sleep loss from insomnia.

In considering the consequences of insomnia, it is important to differentiate being sleepy from being tired or fatigued. Sleepiness involves recurrent episodes of being drowsy and involuntarily falling asleep in nonstimulating environments (ie, dozing off). Sleepiness is more often associated with other primary sleep disorders, such as narcolepsy, sleep apnea, and periodic limb movement disorder. In contrast, those with insomnia are often tired or fatigued but not sleepy.[48,50]

Insomnia is associated with substantial impairments in quality of life. Although insomnia is often considered more benign than most other chronic medical and psychiatric disorders, the impairments in quality of life in insomnia are comparable to those observed in diabetes, arthritis, and heart disease.[5] Quality of life also improves with treatment for insomnia, although not to the level of the normal population.[51]

Insomnia is associated with substantial impairments in quality of life that are comparable to the impairments observed in other chronic medical disorders.

Comorbidities and Morbidities

Approximately 40% of adults with insomnia also have a diagnosable psychiatric disorder.[16] In addition, approximately three quarters of people presenting to sleep clinics or general medical practices with insomnia have a comorbid psychiatric disorder.[52] Although there are a number of psychiatric disorders that are comorbid with insomnia (eg, generalized anxiety disorder, attention-deficit/hyperactivity disorder, and schizophrenia), depression has received the most attention. Insomnia was once considered only a symptom of depression or secondary to depression. Recent research, however, has consistently shown that insomnia is a predisposing factor for depression. Insomnia often occurs prior to the onset of depression,[53] and often precedes depression relapses.[54,55] Those with persistent insomnia are also much more likely to develop depression at a later time.[16,56] In addition to depression, insomnia is associated with an increased risk for suicide[57] and is a precipitant of manic episodes in those with bipolar disorder.[58]

Insomnia is common in other primary sleep disorders, such as sleep apnea (sleep-disordered breathing [SDB]), restless legs syndrome, and periodic limb movement disorder. In these cases, insomnia may be secondary or fully attributable to the underlying sleep disorder, but often is a comorbid disorder precipitated by the other primary sleep disorder but perpetuated by cognitive and conditioning factors.[59] SDB typically presents clinically with nonrestorative sleep complaints and disturbed sleep maintenance with normal sleep onset. Snoring and/or apnea episodes are often reported by the bed partners, but patients are typically unaware of their sleep-related symptoms. If positive indications of SDB are found during a clinical interview, then overnight sleep recording is typically performed to establish the diagnosis and determine its severity.[7,59] SDB may be exacerbated by benzodiazepines, so it is important to rule out this condition before proceeding with insomnia treatment.

A number of chronic medical conditions are associated with insomnia, including chronic pain syndromes, coronary heart disease, asthma, gastrointestinal disorders, vascular disorders, chronic fatigue, and endocrine and metabolic disorders.[7] In addition, substances, including caffeine, theophylline and other stimulants, steroids, antihypertensives, and antidepressants, can precipitate insomnia.[12]

Although many of the disorders comorbid with insomnia are associated with increased mortality rates, insomnia itself does not appear to be associated with higher mortality. In a recent longitudinal study, neither insomnia nor the use of hypnotics for insomnia increased the risk for mortality over a 6-year period.[60] Higher mortality has been associated with either too much or too little sleep, but not with insomnia disorder per se.[61,62]

Insomnia is frequently comorbid with psychiatric disorders, other primary sleep disorders, and chronic medical conditions.

What Treatments Are Used for the Management of Chronic Insomnia, and What Is the Evidence Regarding Their Safety, Efficacy, and Effectiveness?

Case Study: Part 2

The patient’s medical history reveals menopausal symptoms that were controlled on hormone replacement therapy and did not recur following discontinuation 3 years ago. Her insomnia symptoms, however, have continued and worsened in the past 5 years. The patient is otherwise healthy. She does not report pain at night, snoring or gasping for air during sleep, or restless legs. She does report awakening at least once a night to urinate, but indicates that she is sometimes unable to return to sleep after awakening.

The clinical interview reveals no other psychiatric disorder. She has no history of substance abuse or dependence, but does indicate that she has begun drinking a glass or 2 of wine at night to help her fall asleep. She describes primarily being unable to fall asleep, and says it takes her an hour or 2 to fall asleep most nights. She also describes awakening during the night, sometimes being unable to go back to sleep, and that these sleep-maintenance symptoms have worsened in the past 6 months. She reports hearing that older people can get by on less sleep, but that she feels tired and irritable after nights of inadequate sleep. She is beginning to believe that she is not functioning as well at work because of her sleep difficulties. She reports feeling particularly distressed in the evening as her bedtime approaches and worries whether she will get enough sleep to perform well the next day.

The patient is provided with general information about sleep and insomnia and reassured that her sleep difficulties can be managed. She is provided with a sleep diary and asked to record her sleep-wake patterns for 2 weeks and then to return with her husband to complete the evaluation.

At the second visit, her husband confirms that she does not snore loudly or excessively and does not appear to experience short bouts of not breathing while asleep. He reports that she does have difficulty going to sleep and will toss and turn for an hour or so before falling asleep. On 2-3 mornings each week, he wakes up and finds that she is not in bed but that she got up during the night and later fell asleep while watching television downstairs. On weekends, he usually lets her sleep in late. He reports that she is sometimes so tired after a bad night that she will come home from work and take a nap before dinner. Her sleep diary reveals an average sleep-onset latency of about 45 minutes each night, that she is awake for over an hour during the night on about half the nights, a mean total sleep time of 6 hours and 30 minutes per night, and a mean sleep efficiency of 82%.

Based on this assessment, what treatment approaches should be considered?

Cognitive Behavioral Therapy

Cognitive behavioral therapy for insomnia (CBTI) addresses the hyperarousal, cognitive, and conditioning factors that appear to perpetuate the disorder. CBTI typically consists of 5 major components:[38]

  • Sleep-hygiene strategies to promote a sleep environment and routine that promote sleep.
  • Relaxation therapy (progressive muscle relaxation, visual imagery, etc) to reduce physiologic arousal.
  • Cognitive restructuring to change dysfunctional attitudes about sleep (eg, attempting to will oneself to sleep or excessive worrying about the effects of not sleeping).
  • Stimulus control to reassociate the bed and bedroom with going to sleep instead of staying awake. These instructions include (1) going to bed only when sleepy, (2) establishing a standard wake-up time, (3) getting out of bed whenever awake in bed for 15 minutes or more, (4) avoiding doing sleep-incompatible behaviors (reading or watching television) while in bed, and (5) refraining from daytime napping.
  • Sleep restriction to condense time in bed to the average time typically asleep. For this component, the time to bed is set based on the average time asleep but not less than 5 hours, and then it is gradually increased as sleep efficiencies improve.

The American Academy of Sleep Medicine Task Force on nondrug alternatives for primary chronic insomnia[63] found that CBTI produced reliable and durable improvement in chronic insomnia. Nearly 80% of those treated with CBTI show measurable benefit, but the magnitude of the benefit varies. CBTI produces objective improvements as well as subjective improvements in sleep and appears to improve homeostatic sleep regulation.[64] Although most of the research on CBTI is with primary insomnia, CBTI has been shown to produce benefits for the comorbid condition as well as for the insomnia.[65]

Sleep hygiene is the component of CBTI that is most often provided by healthcare providers,[66] and patients tend to like and adhere to sleep-hygiene strategies.[67] Unfortunately, sleep hygiene appears to be the least effective CBTI component. Stimulus control and sleep restriction are the most effective CBTI components,[68] but patients have the most difficulty adhering to these components.[67]

When CBTI is compared with medications, sedative hypnotics appear to produce more rapid improvements, but the long-term safety and efficacy of sedative hypnotics are less well established than CBTI.[69,70] The efficacy of CBTI, particularly long-term, and the minimal apparent adverse effects of this treatment have resulted in it being considered a first-line treatment for primary insomnia.[70]

Challenges with CBTI. Although CBTI is clearly efficacious, accessibility to this treatment has been severely limited by a general lack of knowledge regarding efficacy, inadequate coverage of this treatment by insurance carriers, and a lack of professionals trained in CBTI, even at certified sleep disorder centers.[38] The treatment is generally well accepted by patients when they are provided this option,[71] and the treatment is relatively short. Although session dosage remains unclear, Edinger and Means[38] have suggested that 4 sessions at 2-week intervals may be optimal based on their review of this treatment approach.

To increase availability, researchers have experimented with alternative methods of CBTI treatment delivery. Treatment delivery in individual, group, or phone-based sessions appears to be equally helpful.[72] Although self-help interventions appear less effective than professional assistance, self-help versions of CBTI still provide modest benefit over controls.[73] Delivery of CBTI via the Internet and other technologies is a promising new approach area for potentially improving the accessibility of this efficacious treatment for insomnia.[74]

Although CBTI is not typically provided by primary care health professionals, recent efforts show this to be another potential strategy for providing this treatment to those with insomnia. Indeed, allied healthcare providers have been trained to deliver CBTI with some success.[75] Recently, Edinger and Sampson[76] devised a “primary care friendly” form of CBTI. This abbreviated form of CBTI involves two 25-minute sessions 2 weeks apart. Session 1 consists of reviewing sleep logs and providing sleep education, stimulus control, and sleep-restriction instructions, such as eliminating activities that are incompatible with sleep, avoiding daytime naps, and setting up a consistent sleep-wake schedule (including sleep restriction). Session 2 consists of reviewing progress, addressing adherence difficulties, and modifying sleep strategies accordingly. This abbreviated treatment was significantly better than sleep-hygiene instructions alone for most insomnia measures and resulted in reductions of insomnia symptoms to normal levels in over half of patients.[76]

Although CBTI is efficacious, accessibility to this treatment has been severely limited by a general lack of knowledge regarding efficacy, inadequate coverage of this treatment by insurance carriers, and a lack of professionals trained in CBTI, even at certified sleep disorder centers.

US Food and Drug Administration-Approved Medications

Benzodiazepine and nonbenzodiazepine hypnotics. Both benzodiazepine and nonbenzodiazepine hypnotics have been approved for the treatment of insomnia.

Benzodiazepine hypnotics. The benzodiazepine hypnotics approved by the US Food and Drug Administration (FDA) for the treatment of insomnia are estazolam, flurazepam, quazepam, temazepam, and triazolam. These medications have been found effective in a number of double-blind, placebo-controlled trials, but these trials have typically been short-term (4-6 weeks).[77] Even with longer term use, there is a reduced effect after 4-8 weeks.[78] Except for triazolam, these benzodiazepine hypnotics have long half-lives, which contribute to their efficacy for maintaining sleep, but also result in higher rates of next-day impairments, such as morning sedation, cognitive impairment, and motor incoordination.[79] Temazepam is the most commonly prescribed benzodiazepine hypnotic,[80] but, despite its long half-life, it appears to have minimal impact on number of awakenings, and produces tolerance, morning sedation, and cognitive impairment.[8] Triazolam, the only short half-life agent in this group, has more of an impact on sleep onset than maintenance, but possible amnestic effects have been a concern.[81,82]

Except in those with a history of substance abuse, abuse liability from these benzodiazepine hypnotics appears to be minimal.[83] However, due to concerns about abuse liability, the FDA has indicated that these medications should be limited to 7-10 days of use with reevaluation if used for more than 2-3 weeks. Some have argued that these limitations were based on now obsolete guidelines,[84] and that longer term use may not increase the risk for abuse liability,[85] but the long-term effects of these medications on tolerance and abuse liability require further study.

Nonbenzodiazepine hypnotics. Nonbenzodiazepine hypnotics are a new class of hypnotics that act on specific benzodiazepine receptor subtypes, but have a nonbenzodiazepine structure. Three nonbenzodiazepine hypnotics — zaleplon, zolpidem, and eszopiclone — have been approved by the FDA for the treatment of insomnia. As a class, these medications generally have shorter half-lives than their benzodiazepine predecessors, which results in greater effects on sleep onset than sleep maintenance and minimal morning sedation and other daytime impairments. Nonbenzodiazepine hypnotics also may have less abuse liability potential than benzodiazepine hypnotics, although further research is needed.[86]

Zolpidem is the most commonly prescribed agent for insomnia,[80] and due to its rapid onset and short half-life (1.5-4 hours), it has more of an effect on sleep onset than sleep maintenance.[87] Modified-release formulations may provide better sleep-maintenance effects, but data on these formulations are still needed.[88] Efficacy data do not extend beyond 1-2 months, so the effects of longer term use are unknown.[89]

Zaleplon has a very short half-life of only about 1 hour and, therefore, affects primarily sleep onset.[90] Higher doses may affect sleep maintenance and may increase the risk for side effects.[91] Although studies of zaleplon have been of longer duration than zolpidem, long-term safety and efficacy beyond 1-3 months have not been established.[92,93]

Eszopiclone is the newest medication in this group, and it has the longest half-life (5-6 hours). Studies show that this half-life appears adequate to produce effects on sleep maintenance as well as sleep onset while also resulting in minimal morning sedation.[94,95] Eszopiclone does not have a limitation on duration of use, and recent findings have shown efficacy and safety with minimal tolerance or abuse liability over 12 months of use.[96]

As a group, these medications appear to produce minimal sedation effects or psychomotor impairment.[97,98] These reduced side effects relative to benzodiazepine hypnotics appear to be due to their short half-lives more so than their selective receptor agonist effects.[99] Nonbenzodiazepine hypnotics also may produce potentially fewer or less severe drug interactions than many of the benzodiazepine hypnotics because they rely less exclusively on CYP3A4 metabolism.[100] Substantial proportions of these medications, however, are still metabolized through CYP3A4; so these medications, as is the case with the most traditional benzodiazepine hypnotics, should be carefully monitored if CYP inducers (rifampicin) or CYP3A4 inhibitors (ketoconazole, erythromycin, and cimetidine) are also being prescribed.[100] Alcohol also potentiates the effects of all hypnotics, so patients should be instructed not to drink, and if they do, to understand that they will feel more sedated the next morning, potentially affecting their ability to drive.

Medications for insomnia are typically taken every night on a prophylactic basis to manage insomnia. Due to the rapid onset and minimal abuse liability of nonbenzodiazepine hypnotics, nonnightly or as-needed use has been considered and appears safe and efficacious in preliminary trials.[101] Further trials, however, are needed to substantiate the safety and efficacy of long-term, nonnightly administration.

Nonbenzodiazepine hypnotics have shorter half-lives, which result in greater effects on sleep onset than sleep maintenance and minimal morning sedation and other daytime impairments. They may also be associated with fewer or less severe drug interactions, and may have less abuse liability than benzodiazepine hypnotics.

Discontinuation of hypnotics. Little research has been conducted on the persistence or reappearance of symptoms after prescription therapy is discontinued. Discontinuation of hypnotics, whether benzodiazepine or nonbenzodiazepine, generally results in relapse of symptoms. Many of the benzodiazepines also produce rebound insomnia, insomnia that is worse than pretreatment levels, for a few days. Rebound insomnia also may be reduced with the newer nonbenzodiazepine hypnotics, although further research is needed.[78] CBTI has been used to reduce relapse rates after benzodiazepine discontinuation.[102]

Melatonin receptor agonists. The FDA recently approved ramelteon for the treatment of chronic insomnia. Ramelteon is a selective melatonin receptor agonist (MT1, MT2) that is rapidly absorbed (< 1 hour) and has a relatively short half-life (2-5 hours). Initial studies of ramelteon have shown reduced sleep-onset latency compared with placebo, with a low rate of side effects and adverse events.[103] Abuse liability also appears to be minimal. Ramelteon should not be prescribed concomitantly with strong CYP1A2 inhibitors, such as fluvoxamine. Although ramelteon is a promising alternative to sedative-hypnotics, further research on its safety and efficacy, particularly long-term, is needed.

Prescription Drugs Without FDA Approval for Insomnia

Trazodone is one of the most commonly prescribed medications for the treatment of insomnia, comparable to zolpidem.[80] The low cost of antidepressant medications along with unrestricted long-term use and minimal abuse liability may be factors leading to the increased use of these medications for insomnia.

Trazodone is sedating, but there is a paucity of data on its effects on insomnia. Research has usually been performed with small, comorbid, depressed samples with short and equivocal effects on sleep.[104,105] Trazodone can have significant side effects, including orthostatic hypotension, blurred vision, nausea, dry mouth, constipation, drowsiness, headache, and (rarely) priapism. These side effects also increase the risk for falls and accidents, which can have serious consequences in the elderly. Although these risks are less pronounced at the lower doses typically used for insomnia, the risk-benefit ratio may be too great in some situations to use trazodone for insomnia.[106] There are also limited data on the short-term effects of doxepin[107] for insomnia. The potential adverse effects from trazadone, doxepin, and other antidepressants overshadow the limited efficacy data on these medications. Dose-response relationships of antidepressants for insomnia also are poorly understood.[108,109]

The SOS Conference Statement notes that various other medications have been used in the treatment of insomnia, including barbiturates (phenobarbital) and antipsychotics (quetiapine and olanzapine). These medications, however, have serious side effects and adverse risks with little to no data supporting their efficacy. Therefore, these medications are not recommended for the treatment of insomnia.

According to the SOS Conference Statement, the risk-benefit ratio may be too great in some situations to use trazodone or other antidepressants for the treatment of insomnia. In addition, barbiturates (phenobarbital) and antipsychotics are not recommended for the treatment of insomnia.

Over-the-Counter Medications

Over-the-counter (OTC) medications are frequently used for insomnia. About one fourth of US adults with sleep difficulties use OTC sleep aids.[110]

Antihistamines (H1 receptor agonists, such as diphenhydramine) are the most commonly used OTC medications for insomnia. There is, however, no systematic evidence of efficacy for insomnia, and there are significant side effects, including dry mouth, blurred vision, urinary retention, constipation, and a risk for increased intraocular pressure in patients with narrow angle glaucoma.[111]

Alcohol is often used to reduce sleep-onset latency. Although alcohol does reduce sleep latency, it also results in poorer quality sleep and nighttime awakening. Alcohol also is clearly not appropriate for someone with a risk for substance use. Therefore, alcohol cannot be recommended as a sleep aid.[112]

Melatonin is a natural hormone that is produced by the pineal gland that has a role in circadian rhythm control. Melatonin may be helpful for reducing symptoms of jet lag, but there is minimal evidence of efficacy for insomnia. Melatonin appears to be safe for short-term use, but long-term safety is unknown. Except for the recently FDA-approved ramelteon, melatonin compounds are unregulated, and preparations may vary.[113]

L-tryptophan is an endogenous amino acid sometimes used as a hypnotic. Evidence of efficacy for insomnia, however, is extremely limited and there are possible toxic interaction effects with some psychiatric medications.[114]

Valerian is derived from the valeriana plant root and thought to promote sleep, but there is no proven benefit for insomnia. Valerian is unregulated and possibly associated with hepatotoxicity. Other herbal products are sometimes used for insomnia, but there are no data supporting their efficacy and there are similar concerns about safety and drug interactions.[115]

Other alternative treatments, such as tai chi, yoga, acupuncture, and light therapy, have been used to treat insomnia, but they have not been adequately evaluated.[114,116]

OTC products, alternative treatments, and complementary therapies are often used to treat insomnia. These therapies, however, have not been systematically evaluated; efficacy data are lacking; and there are concerns about side effects.

Case Study: Part 3

Following the clinical assessment, the patient is advised regarding treatment approaches. Although menopausal symptoms appear to have been a precipitant of the insomnia, these symptoms have resolved and no longer appear to be related to the insomnia. The patient is counseled about cognitive behavioral and sedative-hypnotic approaches for insomnia. Given the minimal risks, she would prefer to try CBTI first, but the nearest specialist with expertise in CBTI is 2 hours away. Therefore, she agrees to try one of the newer sedative-hypnotics and to obtain an abbreviated form of CBTI from the nurse practitioner who has some limited training in this approach.

Because she presents with both sleep-onset and sleep-maintenance difficulties, and may require long-term medication use to control her insomnia, she is started on an agent appropriate for long-term administration immediately before bed each night, and advised that it may be necessary to increase her prescription if her sleep difficulties, particularly sleep maintenance difficulties, persist.

The patient meets with the nurse practitioner who provides information about sleep hygiene and instructs her to refrain from using alcohol to fall asleep, particularly in combination with her medication. A consistent wake time of 7:00 am is agreed to and a time to bed of 12:30 am is determined based on her average time asleep from her sleep diaries. The patient is concerned that she may be more tired than usual if she goes to bed this late, but is reassured that she will be getting the same amount of sleep as she usually does, just more consolidated. She is also instructed to get out of bed if she does not fall asleep within 15 minutes, to do something restful, and then return to bed when she feels sleepy again. She is assured that she can function adequately the next day if she does not get much sleep, which she has been doing for years, and that she can only control getting in and out of bed, not if and when she falls asleep while in bed. She is encouraged not to take naps and to maintain her regular wake time even if she did not sleep well the night before or can sleep later that morning.

After 2 weeks, the patient’s sleep diary shows that she has generally adhered to her new sleep schedule and that her sleep efficiencies are above 90% as a result of her bedtime restrictions. She is instructed to adjust her bedtime 15 minutes earlier and to readjust her bedtime earlier each week if her sleep efficiencies average above 90%. She is encouraged to continue the strategies that appear to be working, particularly maintaining a consistent bedtime, not taking naps, and getting out of bed if she is unable to fall asleep.

At a follow-up visit 1 month later, the patient reports sleeping well and feeling rested although her total sleep time is only 7.5 hours, less than she thought was adequate. She is reassured that sleep needs change over time and that her sense of feeling rested and restored is more important than how much sleep she gets. She is encouraged to continue the CBTI strategies that she has found helpful thus far. She wonders whether the medication is still needed to control her sleep. She is instructed to shift from taking it every night to taking it as needed after getting out bed if she is unable to fall asleep within 15 minutes.

At a follow-up visit 3 months later, the patient reports that she no longer takes the medication for sleep, that she continues to get about 7.5 hours of sleep per night with little to no difficulty initiating or maintaining sleep, and that she feels rested and refreshed most mornings.

What Are Important Directions for Insomnia-Related Research?

Based on what is known about the manifestations and management of insomnia, the SOS Conference Panel made a number of recommendations for future research needs:[9]

  1. Developing and validating instruments to assess chronic insomnia, particularly measures of outcome and diurnal consequences;
  2. Conducting more research on possible genetic and neural mechanisms of insomnia;
  3. Conducting longitudinal observational studies to better understand the incidence, course, and correlates of insomnia, including the adoption of sleep-disturbance items in national health survey research;
  4. Obtaining more information on the impact of insomnia on quality of life and the indirect and direct impact on individuals, caregivers, and society as a whole;
  5. Providing better estimates of the cost of illness to determine cost-effectiveness of treatments;
  6. Obtaining more long-term outcome data, particularly following discontinuation of treatment;
  7. Performing large-scale, multisite comparative treatment trials, including studies of the efficacy of combined or sequenced administration of medications and CBTI;
  8. Conducting more research on OTC and alternative remedies for insomnia;
  9. Conducting efficacy trials in subpopulations, such as children, nursing home residents, and postmenopausal women, and in those with comorbid as well as primary chronic insomnia; and
  10. Assessing clinician decision making with insomnia patients; although much is known that can inform clinical decision making, much more research is needed in this area.

Conclusions

Insomnia is a major public health problem affecting millions of individuals, their families, and their communities. Little is known about etiologic mechanisms, but hyperarousal, cognitive processes, and behavioral conditioning have some support as possible factors. Current evidence supports the efficacy of CBTI and sedative-hypnotics for the treatment of insomnia. Despite widespread use, there is very little evidence supporting the use of other treatments, such as antidepressants and OTC agents, for the treatment of insomnia.

Although there are a number of efficacious medications for insomnia, the SOS Conference Panel noted concern about the mismatch between the chronic, long-term nature of the disorder and the short duration of most clinical trials. Only eszopiclone has been evaluated in trials lasting 6-12 months. Newer medications not yet approved, such as indiplon (a short-acting nonbenzodiazepine hypnotic), provide additional options for the treatment of chronic insomnia, but there remains a clear need for new and more targeted drug therapies that can be used safely and effectively long-term. CBTI shows promising long-term effects with minimal safety concerns, and accessibility to this treatment option should be expanded.

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Managing Adverse Effects to Optimize Treatment for ADHD

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Medication, Psychiatry, School Psychology on Sunday, 16 September 2012 at 10:35

Managing Adverse Effects to Optimize Treatment for ADHD

http://www.medscape.org/viewarticle/583252

Introduction

Attention-deficit/hyperactivity disorder (ADHD) begins in early childhood, and at least 50% of children will go on to have symptoms and impairment in adulthood.[1] Treatment requires a combination of medication and counseling, and adherence to medication therapy is essential for good outcomes. Managing adverse effects is a key component of effective treatment. Diagnosis and treatment of psychiatric comorbidity, which is common, is another essential aspect of care. This review will examine common adverse effects, prescribing medication successfully, deciding when to switch to an alternative medication, and some aspects of using concomitant medication.

Initiating Treatment

Diagnosis

According to the text revision of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), the diagnosis of ADHD requires symptom onset before age 7 years. When evaluating children, parent and teacher input is essential and easy to obtain. Although some investigators have suggested that adult-onset ADHD is possible,[2] a full evaluation of an adult involves attempts to document symptoms and impairment in childhood. Interviews with parents and examination of school or medical records are often helpful.

Monitoring treatment success requires documentation of baseline functional impairment. In adults, collateral interviews with partners or even coworkers, with the patient’s permission, may be illuminating. Adults with ADHD experience important consequences from their impaired functioning. In a case-control study of 500 adults, those with ADHD had lower educational attainment, less job stability, lower incomes, and less successful relationships.[3] The evaluating clinician should investigate all of these areas.

The other essential aspect of evaluation is screening for comorbidity. In many cases, ADHD is not the chief complaint but comes to light during evaluation of another symptom. The most prevalent comorbid conditions are depression, bipolar disorder, and anxiety disorders.[4] Substance-use disorders including nicotine dependence are also more common in people with ADHD than in the general population.

Patient Education

Once the diagnosis is established, the physician should explain the implications and the proposed treatment plan. Educating patients and families about both the therapeutic and adverse effects of pharmacotherapy will help them know what to expect. Describing the benefits of treatment, including possible improvements in psychosocial outcomes, will allow a fully informed decision.

After learning about the side-effect profile of psychostimulants, a few patients who are ambivalent about medication may reject that treatment option. Nonstimulants should also be discussed to provide the full range of options, but the clinician should mention the trade-off of lower efficacy of nonstimulants compared with psychostimulants.[5] Once a patient has consented to a specific medication, the physician should explain the minimum trial duration necessary to determine a response and the dose-adjustment schedule. Clearly worded written information about the medication is usually appreciated by patients and their families. The informed-consent process should be documented.

Managing Adverse Effects

The common adverse effects of treatment are inherent in the pharmacodynamics of stimulant medication. Enhanced catecholamine neurotransmission in the central and autonomic nervous systems can cause insomnia, anorexia, and increased heart rate and blood pressure. These effects are most noticeable at the outset of treatment and after increases in dose. Patients often adjust to them during the ensuing weeks but may require encouragement during that interval.

Insomnia

Studies show that adults and children with untreated ADHD experience sleep anomalies compared with control subjects. A review of sleep studies of unmedicated children found evidence of more nocturnal motor activity and daytime somnolence compared with controls.[6] An actigraphic study of 33 adults with ADHD and 39 control subjects found similar differences between the groups at baseline, and sleep latency was prolonged in the ADHD subjects.[7] After treatment with methylphenidate, the adult patients continued to experience prolonged sleep latency and less total sleep duration, but sleep efficiency improved.

In a study that used the most comprehensive method of evaluating sleep, polysomnography in a sleep lab, 34 untreated adults with ADHD had increased nocturnal activity, reduced sleep efficiency, more awakenings, and reduced REM sleep compared with control subjects.[8] For 10 patients who were treated with open-label methylphenidate, repeat polysomnography showed better sleep efficiency, and the patients also reported improved restorative value of sleep.

Clinicians can conclude from these studies that the effect of medication on sleep may be beneficial in at least some patients, but further research with more subjects and with a variety of medications is needed. The fact remains that many patients treated with psychostimulants complain of initial insomnia, so an approach to manage this problem is necessary. Clinicians should document sleep patterns and complaints before treatment to help interpret problems that may arise after medication is prescribed.

Sleep hygiene, consisting of simple behavioral approaches to promote sound sleep (eg, creating a restful environment and avoiding caffeine), is an inexpensive intervention for all patients with insomnia. In a study of initial insomnia in 27 children 6-14 years treated for ADHD with psychostimulants, the researchers provided a sleep hygiene intervention to which 5 of the children responded.[9] They randomly assigned the nonresponders to either 5 mg of melatonin or placebo. Adverse effects of placebo and melatonin were not significantly different. The investigators found the combination of sleep hygiene and melatonin to be safe and effective, with an effect size of 1.7.

Although comparable randomized, controlled trial data do not exist for adults, mirtazapine has been reported as safe and effective for adults taking psychostimulants.[10]

Atomoxetine may have an effect on sleep that is different from that of psychostimulants, including reduced sleep latency but less efficiency. In a randomized, double-blinded, crossover trial, methylphenidate treatment for children with ADHD caused more initial insomnia but fewer awakenings compared with atomoxetine treatment.[11] Switching to atomoxetine may be considered for patients who prefer it or who do not respond to adjunctive interventions for stimulant-associated insomnia.

Appetite and Growth

Appetite reduction is common with psychostimulants and also can occur with nonstimulants, including atomoxetine and bupropion. This may be accompanied by nausea and abdominal pain in some patients. Some adults treated with psychostimulants may regard appetite suppression with resultant weight loss as beneficial. With long-acting stimulants, appetite returns later in the day.

Simple approaches to this problem include eating breakfast before taking medication. Having food in the stomach may also help reduce abdominal symptoms. Children in particular should have a nutritious, high-calorie snack in the evening if their food intake has been low since breakfast. However, parents should be warned to monitor evening intake of empty calories, such as candy and chips.

Weight loss or a downward shift of weight percentile is typical in children treated with psychostimulants. Short-term reduction in height growth rate during the initial 1-3 years of treatment with psychostimulants is well documented. In a literature review article, Poulton[12] concluded that a mean 1 cm/year deficit in height occurs during that interval. Less conclusive findings included a possible negative correlation between dose and growth, greater growth effect from dextroamphetamine than from methylphenidate, and rebound in growth of height and weight after discontinuation of stimulants.

More controversial is the effect on final stature. According to Poulton, “It would appear that most children achieve a satisfactory adult height, but there may be an important subgroup whose growth is permanently attenuated.”[12] Clinicians must discuss this with parents, many of whom will already have some concerns about the issue, and monitor children’s height and weight, ideally at each visit.

Research on atomoxetine is less comprehensive, but available evidence suggests a short-term downward shift in height and weight percentile. The effect on height may be minimal,[13] but longer-term studies are needed.

In a child or adult with worrisome weight loss, or if a child’s parents are anxious about growth deceleration, switching to another medication should be considered. Substituting methylphenidate for amphetamine would be more rational than substituting amphetamine for methylphenidate, but a nonstimulant is more likely to be ameliorative.

Affective Symptoms

Irritability, dysphoria, and (rarely) suicidal ideation can occur during treatment of ADHD.[14] Atomoxetine carries an FDA warning of a 0.4% incidence of suicidal ideation that has occurred in children during the first month of therapy.[15] No completed suicides have been reported, but discontinuation of atomoxetine is indicated if suicidal thoughts emerge. Minor mood changes and irritability occur with both psychostimulants and atomoxetine. Little evidence is available to guide intervention, but if the symptom is severe, the clinician may consider dose reduction, switching to an alternative psychostimulant, or trying an antidepressant nonstimulant such as bupropion or nortriptyline.

Psychosis and Mania

As dopamine transmission agonists, psychostimulants at excessive and prolonged doses would be expected to provoke psychotic symptoms or mania. These are well-reported but uncommon adverse effects during treatment in children, with an incidence estimated at 0.25%.[16] Emergent delusions, hallucinations, mania, or disorganized behavior requires treatment discontinuation. Most such symptoms resolve, but in a few cases, a bipolar disorder may be unmasked, which takes treatment priority.

Cardiovascular Effects

Psychostimulants cause increased heart rate and blood pressure in adults and children. The effect is mild in most cases, but in adults, some patients with borderline baseline blood pressure may develop frank hypertension. In a 24-month study of 223 adults treated with mixed amphetamine salts, 5 subjects developed hypertension and 2 experienced palpitations or tachycardia that required medication discontinuation.[17]

In a manufacturer-sponsored review of clinical-trial data, atomoxetine was found to cause small but clinically insignificant effects on blood pressure and heart rate in children, adolescents, and adults.[18] Treatment discontinuation for these effects was necessary only in a few adults. In managing any patient on psychostimulants or atomoxetine, clinicians should document pulse rate and blood pressure at baseline and every 6 months, with more frequent monitoring of patients with elevated risk for hypertension.

A more controversial aspect of ADHD medications is the effect on cardiac conduction and the rare occurrence of sudden death. In an unpublished review of documented cases of sudden death in children and adults treated with stimulants or atomoxetine through 2005, many of these patients had an underlying cardiac anomaly discovered on autopsy or were taking other medications.[19] Furthermore, psychostimulants have little effect on the QTc interval. Data on atomoxetine are conflicting, with US trials suggesting no QTc effect.[14] A Europe-wide postmarketing surveillance study, however, found a small number of cases of QTc prolongation that resolved with medication discontinuation.[20]

Whether a baseline electrocardiogram (ECG) is necessary for every patient is a matter of debate among specialists. Dr. David Goodman, an ADHD researcher and clinician, recommends specific screening for cardiac risk.[21] The 5 items he inquires about are history of spontaneous syncope, exercise-induced syncope, exercise-induced chest pain, sudden death in family members age 30 years and younger, and a family history of structural or electrical abnormalities. An ECG — and in ambiguous situations, specialist consultation — would be appropriate before initiating medication in older adults or any patient with risk factors.

Complex Psychopharmacology

Because comorbidity is common with ADHD, clinicians may prescribe psychostimulants with other medications, such as antidepressants, mood stabilizers, or antipsychotics. In fact, experienced psychopharmacologists often prescribe psychostimulants adjunctively for adults with treatment-resistant depression. Atomoxetine metabolism and a small portion of amphetamine metabolism involve CYP2D6, so caution is appropriate when combining these medications with fluoxetine, paroxetine, or fluvoxamine, which inhibit the enzyme.

Tricyclic antidepressants have been safely prescribed with psychostimulants, although several case reports exist of increased adverse effects with the combination of imipramine and methylphenidate.[22] Psychostimulants combined with monoamine oxidase inhibitors may cause a hypertensive crisis; coadministration is contraindicated.

The comorbidity of bipolar disorder and ADHD remains an area of active research and controversy. In a recent randomized, controlled trial, 40 children 6-17 years old with bipolar mania or hypomania and ADHD received divalproex for 8 weeks.[23] The 30 whose mood stabilized but who had active ADHD symptoms received mixed amphetamine salts. The researchers reported no significant adverse effects or worsening of mania. Similar controlled trials in adults are lacking, but in a retrospective study of 16 adult patients with bipolar disorder who were receiving methylphenidate, 5 patients had comorbid ADHD.[24] The others received a stimulant for depression. The patients were also taking various mood stabilizers, including divalproex, lithium, carbamazepine, lamotrigine, and second-generation antipsychotics. The investigators concluded that the practice was safe and effective, although “mild to moderate side effects” occurred, the single most common of which was irritability.

Conclusion

Initiating treatment with psychostimulants is no different from initiating other psychiatric medications. The key steps are:

  • Obtaining baseline data and, in exceptional cases, specialist consultation;
  • Educating patients and families about risks and benefits;
  • Documenting informed consent; and
  • Monitoring adverse effects and intervening as needed.

Rare adverse effects, such as jaundice, skin reactions, vasculitis, and thrombocytopenia, are idiosyncratic, and routine testing for them is not cost-effective.[14] Any unusual complaints should prompt further investigation. Regular documentation of pulse and blood pressure (and growth in children) is mandatory. Most adverse effects can be managed by reassurance or dose reduction, but switching to a different agent may at times be necessary. Combining medications for comorbidities is justifiable and often safe if diagnoses and rationale are well documented, but evidence of efficacy is not well established.

 

ADHD into Adolescence

In ADHD, ADHD child/adolescent, ADHD stimulant treatment, Medication, Neuropsychology, School Psychology on Friday, 14 September 2012 at 05:26

Adolescent ADHD: Diagnosis and Initial Treatment

Scott H. Kollins, PhD

http://www.medscape.org/viewarticle/749104_2

ADHD Into Adolescence

Longitudinal studies demonstrate that ADHD is a disorder that children do not simply outgrow as they reach adolescence.[1-5] Follow-up studies of children with ADHD estimate that the diagnosis persists in 50% to 80% of cases.[1,6-10] Studies of clinically referred adolescents with ADHD also indicate that the disorder continues into adolescence and is associated with various functional impairments, particularly when compared with nondiagnosed peers, including social competence, behavioral and emotional adjustment, school performance, and general quality of life.[11,12]

Although ADHD as a disorder is continuous from childhood into adolescence,[13] the persistence of ADHD into adolescence needs to be considered in the context of adolescence as a period of development in which there are many changes at multiple levels, including physical, psychological, and social changes. During this developmental period, adolescents typically experience a growing influence of peers and independence from family members.[14] For adolescents with a disorder like ADHD in which social and emotional impairment is common,[15] this transitional period may be particularly difficult. Cognitive demands increase along with greater independence from adult supervision (eg, multiple teachers with different teaching styles, amount and scope of homework) as children enter into middle and high school,[11] which requires greater self-regulation, a quality that is often impaired in those with ADHD.

Neuronal and hormonal developmental changes during adolescence can further influence how symptoms are expressed.[14] Related to these biologically based changes, adolescence also is a critical period neurobiologically, with more risk-taking behavior and drug and alcohol use, which correspond with notable changes in motivational and reward-related brain regions. Such behaviors can be problematic because adolescents are naturally more sensitive to the positive rewarding properties of various drugs and natural stimuli and less sensitive to the aversive properties of these stimuli.[16] These behavioral and neurobiological developmental changes in concert with social, hormonal, and physiological changes place adolescents at high risk for substance use.[17,18] ADHD is an additional risk factor for such substance use behavior (reviewed in greater detail below) and thus places adolescents with ADHD at greater risk during this critical developmental period.

Given such developmental changes, the presentation of ADHD changes in adolescence as well, including symptom presentation; although inattentive symptoms continue to be involved in the clinical characteristics of most patients, hyperactive symptoms decline in severity for many.[7,19-21] This symptom presentation continues to cause functional impairment in domains typically impaired in childhood, including academics.[22]

Adolescents with ADHD smoke at significantly higher rates than peers without ADHD and start smoking earlier, demonstrate a higher level of nicotine dependence, and have greater difficulty quitting than youth without ADHD. Some studies have estimated that 25% to 75% of adolescents with ADHD meet diagnostic criteria for ODD or CD. Although mood disorders are often seen in adolescents with ADHD, with an incidence of roughly 10% to 20%, they are less common than DBD. ADHD may be evidence of more severe bipolar disease. For example, ADHD is more common in those with childhood-onset bipolar disorder, which suggests that in some cases ADHD may signal an earlier onset, more chronic bipolar disorder.

ADHD and Comorbid Conditions in Adolescence

Comorbidity within populations of adolescents with ADHD is typically the norm rather than the exception. For example, in one clinical sample of patients 6 to 18 years old, more than half met the criteria for at least one comorbid disorder.[23] Disruptive behavior disorders, including ODD and CD, are particularly common.[24] In general population studies, ADHD increases the odds of ODD or CD by 10.7-fold.[25] Some studies have estimated that 25% to 75% of adolescents with ADHD meet the diagnostic criteria for ODD or CD.[14] In another study, ODD was comorbid among 54% to 67% of clinically referred 7- to 15-year-old children with ADHD.[23] In this study, differences in subtypes also emerged. ODD was significantly more common among those with combined and hyperactive-impulsive ADHD subtypes (50.7% and 41.9%, respectively) than with inattentive subtype (20.8%). Such rates are concerning not only because of the characteristics of these comorbid disruptive behavior disorders (eg, delinquency) that are dealt with in adolescence, but also because CD is a precursor to antisocial personality disorder in adulthood. Given that CD is commonly seen in children with ADHD and is a precursor to antisocial personality disorder, it is not surprising that rates of antisocial personality disorder (among additional forms of Axis II psychopathology) are elevated in adults with ADHD.[4,5,10,26,27]

SUDs are also common in adolescents with ADHD. In longitudinal studies of hyperactive children, the risk for SUDs ranges from 12% to 24% into adulthood.[8,10,26] Because adolescence is a time when initial exposure to substances occurs and because adolescence is also a developmental period during which susceptibility to the reinforcing effects of substances is heightened,[16-18] substance use in adolescence is a concern both as an outcome of current use and of continued risk for future use. This risk is further elevated among adolescents with ADHD. Individuals with ADHD engage in experimentation earlier than children without ADHD.[28,29] Although such findings indicate that the relationship between ADHD and SUDs is independent of comorbidity, CD is a strong predictor of risk for SUDs among children with ADHD when they reach adolescence and adulthood.[30-32] In addition, prospective studies indicate that children with ADHD and co-occurring CD or bipolar disorder are at a higher risk for SUDs during adolescence.[33-35]

Adolescents with ADHD smoke at significantly higher rates than peers without ADHD. Prevalence rates range from 10% to 46% for adolescents with ADHD vs 10% to 24% for adolescents without ADHD.[34,36,37] Even among nonclinical patient samples, there is a linear relationship between number of ADHD symptoms, lifetime risk of smoking, and age of onset of regular smoking.[38] Additional studies have demonstrated that youth with ADHD initiate smoking earlier, exhibit a higher level of nicotine dependence, have greater difficulty quitting than youth without ADHD, and are at an increased risk for becoming a regular cigarette smoker.[37,39] In addition, the relationship between ADHD and tobacco use has remained significant as an independent risk factor after accounting for comorbidity, including CD.[40,41]

Mood disorders are also common among adolescents with ADHD.[42] For example, in one study, 21.6% of children 6 to 18 years old who had ADHD also had a depressive disorder.[23] The combination of a major depressive disorder and a comorbid disruptive behavior disorder is a risk factor for suicidal behavior,[43] and both major depressive disorder and disruptive behavior disorder are common comorbidities in those with ADHD. One longitudinal study assessing childhood ADHD reported that the diagnosis of ADHD in children predicted adolescent depression and/or suicide attempts. In addition, female sex, maternal depression, and concurrent symptoms in childhood predicted which children with ADHD were at greatest risk for these outcomes.[44]

Bipolar disorder is another disorder commonly seen in children with ADHD. Studies have estimated that bipolar disorder co-occurs among 10% to 20% of children and adolescents with ADHD.[45-47] Longitudinal studies of hyperactive children indicate a similar prevalence in adulthood,[5,10,26] although another longitudinal study of children with ADHD reported higher rates into adolescence (12%).[48] In some cases, ADHD may be evidence of more severe bipolar disorder. For example, ADHD is more common in cases of childhood-onset bipolar disorder, which suggests that in some cases ADHD may signal an earlier onset, more chronic bipolar disorder.[48] Regarding anxiety disorders, longitudinal studies of hyperactive children do not report significant elevations in comorbid anxiety disorders.[5,10,26] However, anxiety disorders have been reported in 10% to 40% of clinic-referred children and adolescents with ADHD.[23,49-51] Overall, these studies demonstrate that comorbidity is typical among adolescents with ADHD and further complicates its clinical presentation in adolescence. In addition to concerns about prognosis, such comorbidities can easily complicate issues related to assessment.

Assessment of Adolescents With ADHD

An empirically-based assessment of ADHD typically includes structured clinical interviews, standardized questionnaires, and a review of records, all in the context of diagnostic criteria.[14,52] Cognitive test performance may provide additional value when differentiating ADHD subtypes.[53] Although there is diagnostic continuity of ADHD from childhood into adolescence,[13] assessing ADHD during adolescence needs to be considered in the context of complicating factors. One such factor involves comorbidity. Comorbidity is common in adolescents with ADHD, and conditions can co-occur with ADHD or can mimic ADHD symptoms. Regarding the latter, a diminished ability to concentrate can also be a symptom of a major depressive episode, distractibility and being overly talkative can also be symptoms of a manic or hypomanic episode, and restlessness and difficulty concentrating can be symptoms of generalized anxiety disorder or post-traumatic stress disorder.[54] Further, substance use can confound the assessment for ADHD, as alcohol and illicit drug use can create cognitive impairments that are also common in youth with ADHD.[55-57]

An additional factor that emerges in assessments of adolescent ADHD involves reporting source. In childhood ADHD assessments, parents and teachers are the typical reporters.[14] However, adolescents spend more time with peers and less time with parents. Further, in contrast to elementary school, adolescents have multiple teachers who spend less time with them during the school day and thus have fewer opportunities to observe their students’ behavior. Self-report methods can be incorporated into adolescent ADHD assessments as well; however, adolescents with ADHD have a tendency to underreport the severity of their symptoms,[7,58] which should be considered in any assessment. In adolescents with ADHD, concerns about the accuracy of self-report involve not only their account of ADHD symptoms, but of past delinquent behaviors as well. In one study, adolescents and young adults with ADHD were less likely than those without ADHD to report accurately on delinquent behaviors they engaged in 1 year earlier.[59] Such inaccurate reporting of behavior in ADHD is consistent with findings that persons with ADHD have a tendency toward a positive illusory bias view of their behavior[60] and with theories of ADHD that argue that problems with self-awareness emerge from working memory impairments.[61]

Developmental changes in the presentation of ADHD symptoms also have implications for self-report in the assessment of adolescents with ADHD. In particular, the decline in overt hyperactive symptoms into adolescence[7,19,21,22] makes inattentive symptoms more prominent. As a clinical observation, inattentive features common in ADHD may be experienced more subjectively (eg, daydreaming) than more overt hyperactive behaviors (eg, getting out of one’s seat at inappropriate times), thus making self-report more relevant in this age group.

Finally, the appropriateness of diagnostic criteria for ADHD complicates adolescent assessment. Specifically, the Diagnostic and Statistical Manual of Mental Disorders, Fourth edition, Text Revision [54] states that symptom onset must have occurred by age 7 to qualify for an ADHD diagnosis. However, studies addressing the empiric basis for this criterion have called it into question and recommend a revision to include childhood onset at or before age 12.[39,62-64] One study assessing the implications of this diagnostic revision in a large longitudinal sample found that the prevalence estimate, correlates, and risk factors of ADHD would not be affected if this new diagnostic criterion were adopted.[65] Thus, although following diagnostic criteria in adolescent ADHD assessments is recommended, incorporating these more recent findings may be crucial in making a diagnosis.

Treatment of ADHD in Adolescence

Relatively less research has been devoted to efficacious treatments for adolescents with ADHD compared with treatments for children with ADHD.[66] Despite diagnostic continuity, given the physical, social, and psychological changes that occur in adolescents with ADHD, it is somewhat difficult to simply extend childhood treatments to this group. ADHD treatments in this age group are likely to require more extensive and costly interventions. Further, treating adolescents is particularly challenging because they are less likely than children to receive mental health services in the first place.[67]

ADHD treatment is focused on symptom management and the reduction of downstream effects of unmanaged ADHD, such as school failure, automobile accidents, and peer rejection.[68] The more complex academic and social demands during adolescence require a management plan that addresses academic needs throughout the school day and into the evening, as well as weekday and weekend activities including driving, athletic and artistic endeavors, and family and peer relationships. Symptom management should be analogous to symptom management for any lifelong condition, such as nearsightedness, diabetes, or asthma. Such comparisons emphasize that ADHD is not the fault of the person with the disorder but rather a neurobiological condition, and making such comparisons may help the teen deal with any stigma associated with a psychiatric disorder.[69]

For children with ADHD, psychoeducation about ADHD, psychopharmacology (primarily stimulants), parent training in behavior management methods, classroom behavioral modification and academic interventions, and special educational placement are the most effective or promising interventions.[68] The empiric literature regarding extending these treatments into adolescence is much less prevalent, however. Thus, although treatment options for adolescent ADHD may be available, not all are equally effective and in many cases well-controlled studies are lacking. However, some treatments for adolescents with ADHD and their families do have empiric support, particularly pharmacotherapy and specific psychosocial treatment approaches.[68,70]

Although the stimulants and nonstimulants used for the treatment of ADHD can cause minor changes in blood pressure and heart rate, most analyses of studies of cardiac events and sudden death in children, youth, and adults with ADHD treated with stimulants have not found a higher incidence of these events in patients without preexisting structural cardiovascular conditions or a family history of sudden death.[71,72] Therefore, only routine assessment of cardiovascular function, similar to screening for participation in school sports, is recommended.

Current guidelines and consensus statements[71,72] do not recommend specialty cardiovascular screening (including routine electrocardiogram) before initiating treatment for ADHD, either with stimulants or nonstimulants. However, because these medications are known to cause small elevations in blood pressure and pulse (in the case of stimulants and atomoxetine) or hypotensive changes (in the case of the alpha-2 agonists), blood pressure and heart rate should be checked before treatment is started and should be monitored regularly at follow-up visits.

Pharmacotherapy

Stimulant medications. Stimulants and noradrenergic agonists are psychotropic treatments approved by the US Food and Drug Administration (FDA) for use in adolescents. Stimulants include methylphenidates and amphetamine compounds; these medications have a long-standing history in the treatment of ADHD and are considered the first-line therapies for ADHD.[73] The 2 classes of stimulants have slightly differing mechanisms of action. Whereas both block the reuptake of dopamine and norepinephrine into the presynaptic neuron and thereby increase neurotransmitter concentrations, amphetamine compounds also increase the release of dopamine from presynaptic cytoplasmic storage vesicles.[74]

Stimulants are effective in approximately 70% of adolescents with ADHD.[75-77] At least 7 randomized controlled trials have been conducted among adolescents with ADHD and all but one support the efficacy of stimulants for ADHD in adolescence.[74] Consistent with findings of diagnostic continuity of ADHD from childhood into adolescence, the efficacy of stimulants (specifically, methylphenidate) is largely equal from childhood into adolescence.[78] In a meta-analysis of children and adolescents comparing the efficacy of the methylphenidates and amphetamine compounds, amphetamine compounds had a small yet statistically significant advantage over a standard-release form of methylphenidate for parent and clinicians ratings of ADHD symptoms and global ratings (but not for teacher ratings).[79] Although stimulants are effective in acutely reducing ADHD symptoms, common medication side effects (eg, decreased appetite) have prompted consideration of other pharmacologic interventions.[80]

Nonstimulant medications. Noradrenergic agonists approved by the FDA for use in children and adolescents with ADHD include guanfacine extended release (XR), clonidine modified release (MR),[81] and atomoxetine. Although the precise mechanism of action for treating ADHD is unclear, these medications likely facilitate dopamine and noradrenaline neurotransmission thought to play a role in the pathophysiology of ADHD.[81,82]

In 2009, guanfacine XR was the first alpha-2 agent to be approved by the FDA for use in the treatment of ADHD in children and adolescents. According to one randomized controlled trial in children and adolescents with ADHD, guanfacine XR performed better than placebo in reducing teacher-rated ADHD symptoms but not parent-rated ADHD symptoms.[83] In several double-blind, placebo-controlled trials involving child and adolescent participants, guanfacine XR performed significantly better than placebo in reducing ADHD symptoms.[84,85] A 2-year, open-label, follow-up study of guanfacine XR in children and adolescents, with or without co-administration of stimulants, demonstrated continued efficacy as that seen in short-term randomized controlled trials.[86] Such findings emerged in a similar study,[87] although the attrition rate in both studies was greater than 75%, limiting generalizability.

Two randomized, double-blind, placebo-controlled studies evaluating the efficacy of clonidine MR in children and adolescents with ADHD have been conducted. One assessed clonidine MR as a monotherapy, and another studied it as an add-on agent in patients on a non-optimal stimulant drug regimen. In both trials, clonidine MR significantly reduced ADHD symptoms from baseline and was well tolerated.[88,89]

Atomoxetine is another noradrenergic agonist approved for use in adolescents with ADHD,[90-92] and it has comparable efficacy with methylphenidate in reducing core ADHD symptoms in children and adolescents.[93] In one randomized, placebo-controlled, dose-response study of atomoxetine in children and adolescents with ADHD, atomoxetine was consistently associated with a significant reduction of ADHD symptoms.[94] Social and family functioning also improved among those taking atomoxetine with statistically significant improvements in measures of ability to meet psychosocial role expectations and parental impact. In a randomized, placebo-controlled study of atomoxetine among children and adolescents with ADHD, atomoxetine-treated participant reductions in ADHD symptoms were superior to those of the placebo treatment group as assessed by investigator, parent, and teacher ratings.[95] Additional trials have demonstrated the efficacy and tolerability of this medication in children and adolescents with ADHD.[96-101] In addition, acute atomoxetine treatment appears to be equally effective and equally tolerated in children and adolescents.[102] Such findings suggest that pharmacologic differences in tolerability or ADHD symptom response are negligible between children and adolescents.

Treatment Discontinuation in Adolescence

When considering pharmacotherapy, one issue relevant to adolescents with ADHD involves treatment discontinuation. The prevalence of prescribing by general practitioners to adolescent patients with ADHD drops significantly.[103] Further, this decline is greater than the reported age-related decline in symptoms, indicating that treatment is prematurely discontinued in many cases when symptoms persist.[104] In one longitudinal study,[105] 48% of children between the ages of 9 and 15 had discontinued ADHD medication. Age was a significant moderator of medication adherence such that adolescents were less likely to continue their medication.[105] Thus, in addition to a need for continued research devoted to effective treatments for adolescents with ADHD,[66] unique barriers to treatment such as premature discontinuation need to be addressed.

Psychosocial Treatments

In terms of psychosocial treatments for adolescents with ADHD, the empiric literature is sparse compared with the literature on pharmacotherapy options. In addition, because of the many developmental and environmental changes that occur during the transition into adolescence, childhood treatments are not easily translated for this age group. Developmental changes with implications for treatment include that adolescents have a greater cognitive capacity for abstraction, they have more behavioral self-awareness, adolescents are undergoing identity formation and have a need for independence, there is peer influence, there is variability in daily school routines, and adolescents are undergoing physiologic changes (eg, development of secondary sex characteristics).[66] Thus, treatment approaches are recommended that include increased involvement of the teenager, behavioral contingencies that involve more opportunities to socialize with peers and exert independence, collaboration with multiple teachers, homework issues (particularly time management and organizational skills), and self-monitoring strategies.[44] Among studies that have considered psychosocial treatments for adolescents with ADHD, family-based and school-based approaches are the most promising.[44,106]

Family-Based Interventions

Three studies have examined family-based interventions. Barkley and colleagues[107] randomly assigned 12- to 18-year-olds to 8 to 10 sessions of behavior management training, problem-solving and communication training, or structural family therapy. All strategies resulted in significant improvement in negative communication, conflict, anger during conflicts, school adjustment, internalizing and externalizing symptoms, and maternal depressive symptoms at post-treatment, and improvements were largely maintained at a 3-month follow-up visit. However, only 5% to 20% in each treatment group demonstrated clinically significant reliable change following treatment.

Another study compared parent behavior management training with parent behavior management training/problem solving and communication therapy.[108] Both treatments resulted in significant improvement in parent-teen conflicts but were not statistically different from each other. Although such group-level analysis and normalization rates supported the efficacy of these treatments, reliable change indices were similar to those reported by Barkley and colleagues.[107]

Another study evaluated behavior management, problem solving, and education groups for parents of adolescents with ADHD.[109] Pretreatment and posttreatment comparisons indicated statistically significant reductions in the frequency and intensity of self-reported parent-adolescent conflict and in parent-reported problem behavior and positive effects on parent skills and confidence.

Although all these studies are promising, they did not produce much clinically significant reliable change or they were limited by methodologic design (ie, lack of a control or alternative treatment group). In terms of clinical implications, multimodal long-term treatment may be useful to assist parents in their interactions with their teens to manage parental and family distress,[110] as opposed to simply reducing ADHD symptom severity.

School-Based Interventions

Academic functioning is one of the most common concerns of parents of adolescents with ADHD.[110] Interventions targeting academic impairment in adolescents with ADHD are promising.[111] One school-based intervention involving directed note taking through group-based didactic and modeling yielded statistically significant improvements in on-task behavior, material comprehension, and daily assignment scores in a sample of adolescents with ADHD.[112] A more comprehensive treatment, called the Challenging Horizons Program,[113] involves after-school academic training incorporating behavioral strategies in a group and individual setting and monthly group parent training. This program has yielded moderate to large effect sizes on parent- and teacher-rated academic functioning and classroom disturbance compared with a community care group among middle school students with ADHD.[114] Although effect sizes were less promising for social functioning, and methodologic design limited the generalizability of these findings (eg, quasi-experimental design, small sample size), a 3-year treatment outcome study of this program indicated cumulative long-term benefits for the treatment group compared with a community care control group for parent ratings of ADHD symptoms and social functioning.[115] However, this latter study did not indicate any academic benefits of the treatment. Single-subject design studies also support the beneficial impact of behavioral techniques (eg, self-monitoring and functional analysis) in improving goal-oriented behavior in the classroom while reducing disruptive behavior among adolescents with ADHD.[116,117] This deserves additional consideration in future research.

A variant of the interventions aimed at academic behavior in adolescents with ADHD is also emerging. The Homework Intervention Program is a behavioral-based parent training program targeting homework in middle school students. In a pilot study of a small sample of middle school students diagnosed with ADHD (n = 11), multiple-baseline design analyses indicated an improvement in parent-reported homework problems and ADHD symptoms, overall grade point average, and teacher-reported productivity.[118]

Overall, comprehensive school-based interventions are promising and, similar to family-based interventions, warrant future research. Psychosocial treatment for adolescents with ADHD is a small, yet developing field of research. Current treatments need to be more thoroughly assessed. For example, social impairment continues into adolescence.[119] Further, social impairment in youth with ADHD increases the risk for substance use and related problems,[120] which demonstrates the need to also target social functioning in adolescent ADHD interventions. Providers also need to consider how to individualize treatment for adolescents with ADHD and the various potential comorbidities that can be present. In addition, treatments that complement existing psychosocial treatment approaches should be considered to target the multidimensional challenges that adolescents with ADHD face.[66] Some potentially complimentary treatments have yielded promising results. For example, attention training in cognitive training programs, mindfulness meditation, and physical exercise to reduce disruptive behaviors have shown potential, although more methodologically rigorous trials are required.[121-123]

Driving and ADHD

In North America, motor vehicle accidents are the leading cause of death among adolescents.[124] Drivers with ADHD are at significantly higher risk for poor driving outcomes, including increased traffic citations (particularly speeding), accidents that are their fault, repeated and more severe accidents, driving-related morbidity, and license suspensions and revocations.[125] Such findings were not better accounted for by comorbidity or intelligence. Given that substance use is not uncommon in persons with ADHD, the risks associated with drug and alcohol use should also be considered.[126] In terms of clinical implications of such findings, stimulant medications have been shown to improve driving performance in drivers with ADHD.[127-129] The method of stimulant delivery is also an important factor. In one study, adolescent drivers with ADHD drove better throughout the day on a driving simulator after taking an extended controlled-release stimulant compared with an immediate-release formulation.[126]

ADHD Pharmacotherapy and Growth

The effects of ADHD medication (especially stimulants) have been an area of considerable debate and controversy. Reviews indicate that treatment with stimulant medication does lead to subsequent delays in height (approximately 1 cm per year during the first 3 years of treatment) and weight.[130,131] These reviews also indicate that the effect of stimulants on growth decline over time, that growth deficits may be dose dependent, that growth suppression effects may not differ between methylphenidate and amphetamine, that stimulant discontinuation may lead to growth normalization, and that ADHD may itself be associated with dysregulated growth.[130,131]

In one longitudinal study, methylphenidate treatment was associated with small yet significant delays in height, weight, and body mass index.[132] Within the ADHD sample, those who had not received prior stimulant therapy and those who entered the study with an above average height, weight, and body mass index were most likely to experience growth deficits while taking stimulants. Further, the impact on all growth indices was most apparent during the first year of treatment and attenuated over time. In another longitudinal study that evaluated the effect of stimulant medication on physical growth, a newly medicated group exhibited reductions in size after 3 years of treatment relative to a nonmedicated group; the newly medicated group was 2.0 cm shorter and weighed 2.7 kg less.[133]

These findings indicate that in clinical settings, the potential benefits in symptom reduction and daily functioning need to be contrasted with the small but significant effects of pharmacotherapy (particularly stimulants) on growth. In most cases, growth suppression effects do not appear to be a clinical concern for most children treated with stimulants.[130] Although future studies are required to clarify the effects of continuous pharmacotherapy into adulthood to attain a better perspective of the long-term impact on growth, these findings suggest that growth rate should be monitored during treatment for ADHD.

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ADHD Medications in Adults Yield Mixed Cardiovascular Risk Results

In ADHD, ADHD stimulant treatment, Medication, School Psychology on Thursday, 13 September 2012 at 06:22

ADHD Medications in Adults Yield Mixed Cardiovascular Risk Results

Deborah Brauser & Hien T. Nghiem, MD

http://www.medscape.org/viewarticle/759069

In the United States, roughly 1.5 million adults use medications for attention-deficit/hyperactivity disorder (ADHD). These medications include amphetamines, atomoxetine, and methylphenidate. ADHD medications are known to increase both blood pressure (< 5 mm Hg) and heart rate (< 7 bpm). Given these effects, there are concerns regarding serious cardiovascular events related to taking ADHD medications.

The aim of this study by Hennessy and colleagues was to determine whether use of methylphenidate in adults is associated with elevated rates of serious cardiovascular events compared with rates in nonusers.

Study Synopsis and Perspective

Although adults prescribed the ADHD medication methylphenidate may be at increased risk for adverse cardiovascular events, this association may not be causal, new research suggests.

In a cohort study of almost 220,000 individuals, new users of methylphenidate had almost twice the risk for sudden death or ventricular arrhythmia than age-matched control participants had. They also had a significantly higher risk for all-cause death.

However, the medication dosage “was inversely associated with risk,” meaning it lacked a dose-response relationship, report the investigators.

“We were surprised by the risk findings. But the inverse associations leads us to be somewhat skeptical,” coinvestigator Sean Hennessy, PharmD, PhD, associate professor of epidemiology and pharmacology at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia, told Medscape Medical News.

“Ordinarily, if a drug increases the risk of adverse outcomes, that increase is going to be dose-dependent. We didn’t see that, and in fact, found an inverse relationship for death and other outcomes,” he explained.

Dr. Hennessy said that this could be due to “frail, elderly patients who have other things going on” and who are prescribed low-dose methylphenidate.

“Maybe baseline differences in those patients that aren’t captured in the medical claims data are responsible for the elevated risk of adverse outcomes we were seeing rather than it being a causal effect of the methylphenidate itself,” he opined.

“So I would say to wait for these findings to be replicated and clarified in other research before they are acted on clinically.”

The study is published in the February issue of the American Journal of Psychiatry

Am J Psychiatry. 2012;169:112-114;178-185.

Mixed Findings

According to the investigators, methylphenidate and other ADHD medications are used by almost 1.5 million adults in the United States — even though these medications have been shown to raise blood pressure and heart rate.

“Given these effects, case reports of sudden death, stroke, and myocardial infarction have led to regulatory and public concern about the cardiovascular safety of these drugs,” write the researchers.

However, in May 2011, and reported by Medscape Medical News at that time, the same group of researchers published a study in Pediatrics that showed no increased risk for cardiovascular events in children treated with ADHD medications.

In addition, researchers from Kaiser Permanente Northern California published a study in December 2011 in the Journal of the American Medical Association that examined risks in adults younger than age 65 years who were taking methylphenidate, amphetamine, atomoxetine, or pemoline.

The combined group of ADHD medication users showed no increased risk for serious cardiovascular events, including myocardial infarction, sudden cardiac death, or stroke, compared with the group of nonusers.

For this analysis, investigators examined records from Medicaid and commercial databases, representing 19 states, for adults in a broader age range. Included were 43,999 new users of methylphenidate and 175,955 individuals who did not use methylphenidate, amphetamines, or atomoxetine (for both groups, 55.4% were women).

In each group, 67.3% of the participants were between the ages of 18 and 47 years, 23.2% were between the ages of 48 and 64 years, and 9.5% were aged 65 years or older.

Primary cardiac events assessed included sudden death or ventricular arrhythmia, myocardial infarction, stroke, and a combination of stroke/myocardial infarction. All-cause death was a secondary measure.

Unexpected Results

Results showed that the adjusted hazard ratio (HR) for sudden death/ventricular arrhythmia for the methylphenidate users compared with the nonusers was 1.84 (95% confidence interval [CI], 1.33 – 2.55). For all-cause death, the HR was 1.74 (95% CI, 1.60 – 1.89).

Adjusted HRs for myocardial infarction and stroke (alone or in combination) were not statistically different between the 2 treatment groups.

For the participants who experienced a cardiovascular event, the median treatment dosage was 20 mg/day. No significant association was found for sudden death/ventricular arrhythmia between the patients who took more or less than 20 mg/day of methylphenidate.

“However, there were unexpected inverse associations” between high methylphenidate dosage and stroke, myocardial infarction, stroke/myocardial infarction, and all-cause death compared with low dosage, report the researchers. They add that this lack of a dose-response association discredits a causal relationship.

“Furthermore, the inverse relationships…may suggest that lower dosages were prescribed to the frailest patients, who might have had a greater risk of all-cause death and sudden death — that is, the results may have been affected by unmeasured confounding,” write the investigators.

Other limitations cited included the fact that the study was not randomized and that administrative databases do not include potential confounders such as smoking, blood pressure, substance use, and exercise use/nonuse.

Dr. Hennessy reported that the investigators also assessed cardiovascular risks in their study participants who were also taking amphetamines or atomoxetine. They will be publishing those results soon.

Findings “Generally Reassuring”

Christopher J. Kratochvil, MD, from the University of Nebraska Medical Center in Omaha, writes in an accompanying editorial that this and other studies are “generally reassuring and demonstrate movement in the right direction, with systematic retrospective analyses better informing us of issues related to cardiovascular safety with ADHD pharmacotherapy.”

“While gaps persist in the methodical and comprehensive assessments of the safety of ADHD medications, these studies add valuable information to our already large repository of safety and efficacy data…and better inform the risk-benefit analysis of their use,” writes Dr. Kratochvil, who was not involved with this research.

He adds that establishing a “robust” national electronic health records system containing detailed data elements will also offer considerable help to clinicians.

These large and more accessible databases “will allow us to improve our identification and understanding of rare but serious adverse effects and better address these questions of public health significance,” he concludes.

The study was funded through a sponsored research agreement with Shire Development, Inc., and by a Clinical and Translational Science Award from the National Institutes of Health. The study authors all receive salary support from Shire through their employers. All financial disclosures for the study authors and Dr. Kratochvil are listed in the original article.

Study Highlights

■This study was a nonrandomized cohort study of new users of methylphenidate based on administrative data from a 5-state Medicaid database (1999-2003) and a 14-state commercial insurance database (2001-2006).

■All new methylphenidate users with at least 180 days of prior enrollment were identified.

■Users were matched on data source, state, sex, and age to as many as 4 comparison participants who did not use methylphenidate, amphetamines, or atomoxetine.

■A total of 43,999 new methylphenidate users were identified and were matched to 175,955 nonusers.

■The main outcome measures were (1) sudden death or ventricular arrhythmia; (2) stroke; (3) myocardial infarction; and (4) a composite endpoint of stroke or myocardial infarction.

■Secondary outcomes included all-cause death and nonsuicide death.

■Results demonstrated that the age-standardized incidence rate per 1000 person-years of sudden death or ventricular arrhythmia was 2.17 (95% CI, 1.63 – 2.83) in methylphenidate users and 0.98 (95% CI, 0.89 – 1.08) in nonusers, for an adjusted HR of 1.84 (95% CI, 1.33 – 2.55).

■Dosage was inversely associated with the risks for stroke, myocardial infarction, stroke/myocardial infarction, and all-cause death.

■Adjusted HRs for stroke, myocardial infarction, and the composite endpoint of stroke or myocardial infarction did not differ statistically from one another.

■For the secondary outcome of all-cause death, methylphenidate demonstrated a positive association (adjusted HR, 1.74; 95% CI, 1.60 – 1.89). Nonsuicide deaths were nearly identical.

■Limitations of this study include the potential for unmeasured confounders (ie, smoking, blood pressure, nonprescribed aspirin use, substance misuse, and level of physical activity) because the study was not randomized.

Clinical Implications

■ADHD medications raise blood pressure by less than 5 mm Hg and heart rate by less than 7 bpm.

■Although initiation of methylphenidate was associated with a 1.8-fold increase in the risk for sudden death or ventricular arrhythmia, the lack of a dose-response relationship suggests that this association may not be a causal one.

 

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