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Archive for the ‘ADHD’ Category

School Testing and the Rising Rate of ADHD

In ADHD, ADHD child/adolescent, Common Core, School Psychology on Tuesday, 1 April 2014 at 05:36

School Testing and the Rising Rate of ADHD

by Miriam

A new book finds a startling connection

Read the Interview: http://www.nbcnews.com/health/kids-health/could-school-testing-be-driving-adhd-n55661

Is the increased demand for performance behind the increased diagnoses of ADHD? Two University of California professors have released a book this month titled, “The ADHD Explosion.” They call it a “reality check” for parents, providers, educators and politicians.

The Berkeley professors, Dr. Stephen Hinshaw and Dr. Richard Scheffler, are noted researchers on ADHD. Their research tells them that federal policy issues may be behind the recent explosion in cases of ADHD.

“When you look at that [national testing policy], you get the
closest thing there is to a smoking gun,” says Dr.Scheffler.

The Journal of the American Medical Association (JAMA) Pediatrics, found that rates of ADHD in California have jumped by 24% since 2001. Additionally, the Center for Disease Control (CDC) reports increases from 7.8 percent in 2003 to
9.5 percent in 2007 and to 11 percent in 2011— a rate of 5 percent a year.

It looks for all the world like a growing epidemic. But ADHD wasn’t even something people noticed until recently,” says Hinshaw.

“It started about the same time in history that we made kids go to school,” Hinshaw told NBC News in an interview.

Then come the 1990s, and a crisis of falling test scores. “What happened is that a number of states began to pass accountability laws,” Hinshaw said.

Hinshaw and Scheffler examined the correlation between diagnoses of ADHD and maps of states that had passed accountability laws.

According to NBC News, by the turn of the century, 30 states had passed accountability laws. They tended to be Republican-leaning states in the South, such as North Carolina. In 2007, 15.6 percent of all children in North Carolina had been diagnosed with ADHD at some point, including nearly one in three teenage boys.

Two things happening together don’t prove a correlation. Is it coincidence? Hinshaw and Scheffler were persuaded to look further.

AN NBC News article reports that the professors then examined date related to the No Child Left Behind federal policy enacted in 2002. It was one of the first official acts of President George W. Bush after he took office. NCLB required standardized testing to show if schools were, in fact, educating students. A truly salient aspect of NCLB was that it held teachers and principals directly responsible for the results and removed federal and state bureaucrats who mandate curriculum and educational policy.

According to the NBC News article:

“Now what happens is a natural experiment,” says Hinshaw. The other states raced to write accountability laws, requiring schools to show they are actually educating children.

“When you incentivize test scores above all else, there is probably pressure to get kids diagnosed with ADHD.”

Hinshaw and Scheffler compared ADHD rates in the 30 states that had been requiring testing with the 20 states that had to play catchup.

Rates of ADHD diagnoses soared.

“Children ages 8 to 13, living in low-income homes and in states without previous consequential accountability laws, went from a 10 percent to a 15.3 percent rate of ADHD diagnoses once No Child Left Behind started,” they wrote. That’s a 53 percent increase over four years.

California’s current rate, post-testing? It’s 7.3 percent. North
Carolina’s rate actually fell slightly, to 14.4 percent in 2011.

“When you incentivize test scores above all else, there is probably pressure to get kids diagnosed with ADHD,” Hinshaw said. “We know from our own research that medication not only makes you less fidgety but also can bump up your test scores.”

That would be the benign interpretation, that testing has
encouraged parents to get their kids in to see specialists for
much-needed medical care. But there’s also a more sinister
possibility and one that Hinshaw and Scheffler say is at work in
some states.

“If you can identify the children with ADHD, you can take them out of the pool that measures how schools are doing,” says Scheffler.

He says some districts — he won’t say where — do seem to have been doing so. State school officials and the federal Department of Education did not respond when contacted by NBC News.

No Child Left Behind ties federal funding to test scores, Scheffler points out.“You can see the incentive for schools to get kids diagnosed with ADHD,” he says.

Either way, Scheffler and Hinshaw say the increase in ADHD cases is real, and it’s not just affecting kids. Recent studies show adult diagnoses are on the rise, too.

“Although often ridiculed, ADHD represents a genuine medical
condition that robs people of major life chances,” they write in the book.

“You can see the incentive for schools to get kids diagnosed with ADHD.”

Scheffler doesn’t see the increase in adult ADHD diagnoses as
surprising. “This has nothing to do with the schools. This has to do with global competition and performance,” he says. People are under pressure to perform better at work.

And news about adult ADHD in turn sends more people to their doctors, and diagnoses spike even more, Hinshaw adds. “Here are we are in 2014 with evidence that medications can benefit. Adult ADHD clinics spring up,” he says.

“That’s not necessarily a bad thing,” says Hinshaw.

What is bad is if ADHD is not being diagnosed with the proper care, Hinshaw says. A 10-minute pediatrician visit is not adequate for an ADHD diagnosis and certainly not as the basis for writing a prescription for a powerful stimulant, such as Ritalin or Adderall, to treat it.

“Many pediatricians are not trained in the emotional disorders of childhood, or not reimbursed for the time it takes,” Hinshaw said.

“It is easy to pull out prescription pad at the end of a visit.”

He calls the book a “reality check” and says parents, providers, educators and politicians should take note, and make sure the right kids are being diagnosed, and helped, properly.

Rertieved from: http://www.playattention.com/school-testing-rising-rate-adhd/

 

Could School Testing Be Driving ADHD?

BY MAGGIE FOX

All it took was a map to convince health economists Stephen Hinshaw and Richard Scheffler that it must be some kind of policy issue driving a recent explosion in cases of ADHD.

And a convenient natural experiment — in the form of the federal government’s No Child Left Behind — provided the answer, the two experts argue in a new book. It’s school testing, they say.

“When you look at that, you get the closest thing there is to a smoking gun,” says Richard Scheffler, of the University of California Berkeley who co-authored the book, “The ADHD Explosion”, which was just published this month.

“You get the closest thing there is to a smoking gun.”

But it’s not necessarily a bad thing, the authors say, if children are being diagnosed properly, and if they’re getting the right treatments.

There’s no question there’s been a huge increase in the number of kids diagnosed with Attention Deficit/Hyperactivity Disorder, or ADHD. The Centers for Disease Control and Prevention found that about 6.4 million kids aged 4 to 17, or 11 percent of that age group, were diagnosed with ADHD as of 2011.

And CDC documents a steady increase, from 7.8 percent in 2003 to 9.5 percent in 2007 and to 11 percent in 2011— a rate of 5 percent a year.

It looks for all the world like a growing epidemic, says Stephen Hinshaw, a professor of psychology at Berkeley who wrote the book with Hinshaw. But ADHD wasn’t even something people noticed until recently, he says.

“It started about the same time in history that we made kids go to school,” Hinshaw told NBC News in an interview.

Then come the 1990s, and a crisis of falling test scores. “What happened is that a number of states began to pass accountability laws,” Hinshaw said.

In the early 2000s, the CDC began tracking ADHD diagnoses. Hinshaw and Scheffler looked at the maps showing the rates of ADHD, and compared them to a map that showed which states had passed accountability laws.

By the turn of the century, 30 states had passed accountability laws. They tended to be Republican-leaning states in the South, such as North Carolina. In 2007, 15.6 percent of all children in North Carolina had been diagnosed with ADHD at some point, including nearly one in three teenage boys.

This was more than twice the rate in California, with a 6 percent rate.

But this was just a correlation, Hinshaw says. Just because two things happen together in time doesn’t mean one caused the other. They looked at differences in culture, ethnicity, in the number of doctors per capita and at possible other causes. Nothing really explained the different rates of ADHD in different states.

Then No Child Left Behind became federal policy in 2002. One of the first official acts of President George W. Bush after he took office was to ask Congress to write and pass the law.

It called for standardized testing to show if schools were, in fact, educating students. Local state laws often held teachers and principals directly responsible for the results.

“Now what happens is a natural experiment,” says Hinshaw. The other states raced to write accountability laws, requiring schools to show they are actually educating children.

“When you incentivize test scores above all else, there is probably pressure to get kids diagnosed with ADHD.”

Hinshaw and Scheffler compared ADHD rates in the 30 states that had been requiring testing with the 20 states that had to play catchup. Rates of ADHD diagnoses soared.

“Children ages 8 to 13, living in low-income homes and in states without previous consequential accountability laws, went from a 10 percent to a 15.3 percent rate of ADHD diagnoses once No Child Left Behind started,” they wrote. That’s a 53 percent increase over four years.

California’s current rate, post-testing? It’s 7.3 percent. North Carolina’s rate actually fell slightly, to 14.4 percent in 2011.

“When you incentivize test scores above all else, there is probably pressure to get kids diagnosed with ADHD,” Hinshaw said. “We know from our own research that medication not only makes you less fidgety but also can bump up your test scores.”

That would be the benign interpretation, that testing has encouraged parents to get their kids in to see specialists for much-needed medical care. But there’s also a more sinister possibility and one that Hinshaw and Scheffler say is at work in some states.

“If you can identify the children with ADHD, you can take them out of the pool that measures how schools are doing,” says Scheffler. He says some districts — he won’t say where — do seem to have been doing so. State school officials and the federal Department of Education did not respond when contacted by NBC News.

No Child Left Behind ties federal funding to test scores, Scheffler points out.“You can see the incentive for schools to get kids diagnosed with ADHD,” he says.

Either way, Scheffler and Hinshaw say the increase in ADHD cases is real, and it’s not just affecting kids. Recent studies show adult diagnoses are on the rise, too.

“Although often ridiculed, ADHD represents a genuine medical condition that robs people of major life chances,” they write in the book.

“You can see the incentive for schools to get kids diagnosed with ADHD.”

Scheffler doesn’t see the increase in adult ADHD diagnoses as surprising. “This has nothing to do with the schools. This has to do with global competition and performance,” he says. People are under pressure to perform better at work.

And news about adult ADHD in turn sends more people to their doctors, and diagnoses spike even more, Hinshaw adds. “Here are we are in 2014 with evidence that medications can benefit. Adult ADHD clinics spring up,” he says.

“That’s not necessarily a bad thing,” says Hinshaw.

What is bad is if ADHD is not being diagnosed with the proper care, Hinshaw says. A 10-minute pediatrician visit is not adequate for an ADHD diagnosis and certainly not as the basis for writing a prescription for a powerful stimulant, such as Ritalin or Adderall, to treat it.

“Many pediatricians are not trained in the emotional disorders of childhood, or not reimbursed for the time it takes,” Hinshaw said. “It is easy to pull out prescription pad at the end of a visit.”

He calls the book a “reality check” and says parents, providers, educators and politicians should take note, and make sure the right kids are being diagnosed, and helped, properly.

Retrieved from: http://www.nbcnews.com/health/kids-health/could-school-testing-be-driving-adhd-n55661

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Adult ADHD And Women: Many Fall Through The Cracks!

In ADHD, ADHD Adult, General Psychology, Psychiatry on Sunday, 30 March 2014 at 04:30

http://www.adultadhdblog.com/2014/03/28/adult-adhd-and-women-2/

Phillip Seymour Hoffman did not have choice or free will and neither do you.

In ADHD, Anxiety, Brain imaging, Brain studies, Child/Adolescent Psychology, General Psychology, Medicine, Mood Disorders, Neuropsychology, Neuroscience, Psychiatry on Tuesday, 11 March 2014 at 12:37

one of the best things about this subject that i’ve read in a long time.  give it a read. it makes you think.

Phillip Seymour Hoffman did not have choice or free will and neither do you..

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 coming to a computer near you…

In ADHD, ADHD Adult, ADHD child/adolescent, School Psychology on Tuesday, 20 August 2013 at 15:11

http://ieeexplore.ieee.org/xpl/login.jsp?tp=&arnumber=6480160&url=http%3A%2F%2Fieeexplore.ieee.org%2Fxpls%2Fabs_all.jsp%3Farnumber%3D6480160

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

what they eyes say about adhd…

In ADHD, ADHD Adult, ADHD child/adolescent, Child/Adolescent Psychology, General Psychology, Neuropsychology, Psychiatry on Tuesday, 21 May 2013 at 06:51

Eye May Be Key to More Accurate ADHD Diagnosis

Megan Brooks

SAN FRANCISCO — Examining the retina may aid in the diagnosis of attention-deficit/hyperactivity disorder (ADHD), new research suggests.

A small study by investigators at Albert-Ludwigs University of Freiburg, Germany, showed that patients with ADHD displayed significantly elevated “background noise” on a pattern electroretinogram (PERG) compared with their healthy peers.

Altered visual signal processing may be a “neuronal correlate for ADHD,” study presenter Emanuel Bubl, MD, told Medscape Medical News. “If we can replicate this finding, it would be of great clinical importance because it would be an objective marker of ADHD.”

Dr. Bubl presented the study here at the American Psychiatric Association’s 2013 Annual Meeting.

PERG — which is a kin to an electrocardiogram of the retina — provides an electrophysiologic measurement of the activity of the retinal ganglion cells.

“This technique is an easy-to-apply and already well-established instrument in ophthalmology. With adaption, it could be widely used,” Dr. Bubl said.

Inattention and distractability are core symptoms of ADHD, but a “clearcut neuronal correlate is missing. Any attempt to find objective markers of ADHD would be very helpful in this context,” Dr. Bubl said.

Dr. Bubl and colleagues used PERG to measure the response of the retina to a checkerboard visual stimuli in 20 patients with ADHD and 20 healthy control participants.

“An elevated neuronal noise or background firing has been proposed as an underlining pathophysiological mechanism and treatment target. We found evidence for an early alteration in visual perception or signal transmission in patients with ADHD, with significantly elevated neuronal noise (P < .014),” said Dr. Bubl. In particular, neuronal noise significantly correlated with inattention, as measured with the Conners’ Adult ADHD Rating Scale.

“The results might explain why patients with ADHD are easily distracted,” Dr. Bubl added.

With more study, the results could have potentially important clinical implications. “With ADHD, there is a debate about the existence of the disease on the one hand and a growing concern about overdiagnosing ADHD and prescription of medication on the other,” he said.

With PERG, the diagnosis of ADHD could be “objectified by measurable signals, and this would be dramatically helpful in the controversial public discussion.” Use of PERG might also help in determining the effects of methylphenidate or psychotherapy on ADHD.

The authors report no relevant financial relationships.

The American Psychiatric Association’s 2013 Annual Meeting. Abstract SCR02-2. Presented May 18, 2013.

Retrieved from: http://www.medscape.com/viewarticle/804409?src=nl_topic&uac=184795PG

ADHD into adulthood

In ADHD, ADHD Adult, ADHD child/adolescent, Neuropsychology, Psychiatry on Sunday, 7 April 2013 at 07:39

Kids’ ADHD May Continue Into Adulthood

By Crystal Phend, Senior Staff Writer, MedPage Today

Published: March 04, 2013

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Childhood attention deficit-hyperactivity disorder (ADHD) may carry over into adulthood in 29% of cases, with a higher risk of other psychiatric disorders, a population-based study showed.

Almost 60% of kids diagnosed with ADHD in the study had at least one other psychiatric disorder at around age 30, which was nearly three times the odds seen among other children followed (P<0.01), according to a report in the April issue of Pediatrics.

Suicide by that age was substantially more common with childhood ADHD as well, although overall mortality wasn’t, wrote William Barbaresi, MD, of Boston Children’s Hospital, and colleagues.

“It is concerning that only a minority of children with ADHD reaches adulthood without suffering serious adverse outcomes, suggesting that the care of childhood ADHD is far from optimal,” they wrote. “Our results also indicate that clinicians, insurers, and healthcare systems must be prepared to provide appropriate care for adults with ADHD.”

The key message is that ADHD shouldn’t be ignored in childhood or adulthood, Rachel Fargason, MD, of the University of Alabama at Birmingham, commented in an interview with MedPage Today.

“There has always been the question of whether childhood ADHD persists into adulthood,” she noted.

Previous studies from the 1980s suggested it did, but by looking at the worst cases — people who presented in psychiatric clinics — rather than the typical child in the general population, Fargason explained.

The study included 5,718 individuals from the same birth cohort in the area around Rochester, Minn., where the Mayo Clinic is based. They were followed to an average age of 27 to 29 years using school and medical records to look for ADHD and other outcomes.

The prospective portion of the study included 367 adults who had childhood ADHD and could have their vital status confirmed.

Seven (1.9%) had died by the time of follow-up, yielding a standardized mortality ratio 1.88-fold higher than seen in the rest of the cohort that didn’t have childhood ADHD.

Although that overall survival impact didn’t reach statistical significance, the difference in suicide did.

The standardized mortality ratio was 3.83 for suicide among childhood ADHD cases versus others (P=0.032).

Notably, five of the seven deaths in the childhood ADHD group occurred in the setting of comorbid substance use and psychiatric disorders.

“This finding suggests the psychiatric comorbidities associated with ADHD may place patients at risk for early death, although the relatively small number of cases precludes a statistical analysis,” the researchers noted.

Childhood ADHD was associated with a 57% rate of one or more other psychiatric disorders at follow-up compared with 35% among controls, for an odds ratio of 2.6 (95% CI 1.8 to 3.8).

The rate was higher for those whose ADHD persisted into adulthood, with an OR 4.8-fold higher than in those whose ADHD didn’t persist (81% versus 47%).

The most common adult psychiatric problems after childhood ADHD were:

  • Alcohol dependence or abuse (26%)
  • Antisocial personality disorder (17%)
  • Substance dependence or abuse (16%)
  • Current or past history of hypomanic episode (15%)
  • Generalized anxiety disorder (14%)
  • Current major depressive episode (13%)

Altogether, only 38% of individuals who had ADHD as a child experienced no mental health problems in adulthood.

Study limitations included use of administrative and school record data to determine childhood ADHD as well as the relatively small number of deaths, which may have limited ability to detect differences in early death risk.

The population studied is primarily a white, middle-class community, which might impact generalizability, Barbaresi’s group added.

“It is possible, if not likely, that the magnitude of the adverse outcomes in this cohort would be even greater in populations with additional challenges such as higher rates of poverty,” they noted.

Retrieved from: http://www.medpagetoday.com/Pediatrics/ADHD-ADD/37637?goback=%2Egde_985117_member_219365690

Barbaresi WJ, et al “Mortality, ADHD, and psychosocial adversity in adults with childhood ADHD: a prospective study” Pediatrics 2013; DOI: 10.1542/peds.2012-2354.

increase in adhd diagnoses…

In ADHD, ADHD Adult, ADHD child/adolescent, Neuropsychology, Neuroscience, School Psychology, Special Education on Tuesday, 12 March 2013 at 11:59

is this because of increased awareness, greater recognition of adhd, better diagnostics and screening, etc. or is it because of the heightened demands put upon all of us in today’s society?  i do believe adhd is a very real diagnosis and can have deleterious effects on the brain if left untreated.  what i can tell you i do see in my work as a school psychologist is some children with a true disability and some very savvy parents (or kids, in some instances) who know that a stimulant will help them meet any increased demands and are able to “get” an adhd diagnosis by going to certain doctors or knowing what to say and what “symptoms” to report.  a comprehensive adhd diagnosis is not an easy one to make and takes way more than a ten-minute session with a pediatrician.  this is one of the reasons i am such a proponent of  the advancements in genome wide association studies, neuroanatomy, neurobiology, etc. that can effectively show differences between a brain with adhd and a brain without adhd, thus, one day hopefully being able to diagnose with more than parent and self-report and some testing.  and, with the large population of untreated adhd or late-diagnosed adhd (so, no treatment until adulthood), we are able to see the effects of no treatment, then getting proper treatment.  

i am a fan of a new book on adhd by cecil reynolds, et al.  it is a comprehensive look at adhd by one of the foremost neuropsychologists today.  http://www.amazon.com/Energetic-Brain-Understanding-Managing-ADHD/dp/0470615168 

there’s my two-cents.  here is the article:

Study Suggests Increased Rate of Diagnosis of Attention-Deficit/Hyperactivity Disorder at Health Plan

EMBARGOED FOR RELEASE: 3 P.M. (CT), MONDAY, JANUARY 21, 2013

Media Advisory: To contact study author Darios Getahun, M.D., Ph.D., call Sandra Hernandez-Millett at 626-405-5384 or email sandra.d.hernandez-millett@kp.org or call Vincent Staupe at 415-318-4386 or email vstaupe@golinharris.com.


CHICAGO – A study of medical records at the Kaiser Permanente Southern California health plan suggests the rate of attention-deficit/hyperactivity disorder (ADHD) diagnosis increased from 2001 to 2010, according to a report published Online First by JAMA Pediatrics, a JAMA Network publication.

ADHD is one of the most common chronic childhood psychiatric disorders, affecting 4 percent to 12 percent of all school-aged children and persisting into adolescence and adulthood in about 66 percent to 85 percent of affected children. The origin of ADHD is not fully understood, but some emerging evidence suggests that both genetic and environmental factors play important roles, the authors write in the study background.

Darios Getahun, M.D., Ph.D., of the Kaiser Permanente Southern California Medical Group, Pasadena, Calif., and colleagues used patient medical records to examine trends in the diagnosis of ADHD in all children who received care at Kaiser Permanente Southern California (KPSC) from January 2001 through December 2010. Of the 842,830 children cared for during that time, 39,200 (4.9 percent) had a diagnosis of ADHD.

“The findings suggest that the rate of ADHD diagnosis among children in the health plan notably has increased over time. We observed disproportionately high ADHD diagnosis rates among white children and notable increases among black girls,” according to the study.

The rates of ADHD diagnosis were 2.5 percent in 2001 and 3.1 percent in 2010, a relative increase of 24 percent. From 2001 to 2010, the rate increased among whites (4.7 percent to 5.6 percent); blacks (2.6 percent to 4.1 percent); and Hispanics (1.7 percent to 2.5 percent). Rates for Asian/Pacific Islanders remained unchanged over time, according to study results.

Boys also were more likely to be diagnosed with ADHD than girls, but the study results suggest that the sex gap for black children may be closing over time. Children who live in high-income households ($70,000 or more) also were at an increased risk of diagnosis, according to the results.

(JAMA Intern Med. Published online January 21, 2013. doi:10.1001/2013.jamapediatrics.401. Available pre-embargo to the media at http://media.jamanetwork.com.)

Retrieved from: http://media.jamanetwork.com/news-item/study-suggests-increased-rate-of-diagnosis-of-attention-deficithyperactivity-disorder-at-health-plan/

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.”

genes, genes…

In ADHD, ADHD Adult, ADHD child/adolescent, Autism Spectrum Disorders, General Psychology, Genes, Neuropsychology, Neuroscience, Personality Disorders, Psychiatry on Friday, 1 March 2013 at 06:15

i love gwas and really feel it will continue to broaden our understanding of psychiatric illnesses and, hopefully, lead to better treatment options.

Five Major Psychiatric Disorders Genetically Linked

By: Caroline Cassels

In the largest genetic study of psychiatric illness to date, scientists have discovered genetic links between 5 major psychiatric disorders.

Investigators from the Cross-Disorder Group of the Psychiatric Genomics Consortium have found that autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia share common genetic risk factors.

Specifically, the results of the genome-wide association study (GWAS) reveal single-nucleotide polymorphisms (SNPs) in 2 genes —CACNA1C and CACNB2 — both of which are involved in the balance of calcium in brain cells, are implicated in several of these disorders, and could provide a potential target for new treatments.

“This analysis provides the first genome-wide evidence that individual and aggregate molecular genetic risk factors are shared between 5 childhood-onset or adult-onset psychiatric disorders that are treated as distinct categories in clinical practice,” study investigator Jordan Smoller, MD, Massachusetts General Hospital, Boston, said in a release.

The study was published online February 28 in the Lancet.

Potential Therapeutic Target

The researchers note that findings from family and twin studies suggest that genetic risks for psychiatric disorders do not always map to current diagnostic categories and that “doubt remains about the boundaries between the syndromes and the disorders that have overlapping foundations or different variants of one underlying disease.”

“The pathogenic mechanisms of psychiatric disorders are largely unknown, so diagnostic boundaries are difficult to define. Genetic risk factors are important in the causation of all major psychiatric disorders, and genetic strategies are widely used to assess potential overlaps,” the investigators write.

The aim of the study was to identify specific variants underlying genetic effects shared between 5 major psychiatric disorders: ASD, ADHD, BD, MDD, and schizophrenia.

The researchers analyzed genome-wide SNP data for the 5 disorders in 33,332 cases and 27,888 control participants of European ancestry. They identified 4 risk loci that have significant and overlapping links with all 5 diseases. These included regions on chromosomes 3p21 and 10q24, and SNPs in the gene CACNA1C,which has previously been linked to bipolar disorder and schizophrenia, and in theCACNB2 gene.

Polygenic risk scores confirmed cross-disorder effects, most strongly between adult-onset disorders BD and MDD and schizophrenia. Further pathway analysis corroborated that calcium channel activity could play an important role in the development of all 5 disorders.

“Significant progress has been made in understanding the genetic risk factors underlying psychiatric disorders. Our results provide new evidence that may inform a move beyond descriptive syndromes in psychiatry and towards classification based on underlying causes.

“These findings are particularly relevant in view of the imminent revision of classifications in the Diagnostic and Statistical Manual of Mental Disorders and the International Classification of Diseases,” said Dr. Smoller.

The investigators add that the study results “implicate a specific biological pathway — voltage-gated calcium-channel signalling — as a contributor to the pathogenesis of several psychiatric disorders, and support the potential of this pathway as a therapeutic target for psychiatric disease.”

In an accompanying editorial, Alessandro Serretti, MD, PhD, and Chiara Fabbri, MD, from the University of Bologna, Italy, assert that “the main innovative contribution of the present study is the combination of qualitative and quantitative analyses of the shared genetic features associated with vulnerability of these 5 disorders.”

They add, “the present study might contribute to future nosographic systems, which could be based not only on statistically determined clinical categories, but also on biological pathogenic factors that are pivotal to the identification of suitable treatments.”

The authors and editorialists have reported no relevant financial relationships.

Retrieved from: http://www.medscape.com/viewarticle/779979?src=nl_topic

Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis

Background

Findings from family and twin studies suggest that genetic contributions to psychiatric disorders do not in all cases map to present diagnostic categories. We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia.

Methods

We analysed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders in 33 332 cases and 27 888 controls of European ancestory. To characterise allelic effects on each disorder, we applied a multinomial logistic regression procedure with model selection to identify the best-fitting model of relations between genotype and phenotype. We examined cross-disorder effects of genome-wide significant loci previously identified for bipolar disorder and schizophrenia, and used polygenic risk-score analysis to examine such effects from a broader set of common variants. We undertook pathway analyses to establish the biological associations underlying genetic overlap for the five disorders. We used enrichment analysis of expression quantitative trait loci (eQTL) data to assess whether SNPs with cross-disorder association were enriched for regulatory SNPs in post-mortem brain-tissue samples.

Findings

SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10−8) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2. Model selection analysis supported effects of these loci for several disorders. Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity. Polygenic risk scores showed cross-disorder associations, notably between adult-onset disorders. Pathway analysis supported a role for calcium channel signalling genes for all five disorders. Finally, SNPs with evidence of cross-disorder association were enriched for brain eQTL markers.

Interpretation

Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology. These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.

Funding-National Institute of Mental Health.

Retrieved from: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)62129-1/abstract

Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis
Cross-Disorder Group of the Psychiatric Genomics Consortium
The Lancet – 28 February 2013
DOI: 10.1016/S0140-6736(12)62129-1

Large study shows substance abuse rates higher in teenagers with ADHD

In ADHD, ADHD Adult, ADHD child/adolescent, Fitness/Health, Psychiatry, School Psychology on Sunday, 24 February 2013 at 10:03

Large study shows substance abuse rates higher in teenagers with ADHD.

adhd, 504, private schools, and provision of services…

In ADHD, ADHD child/adolescent, Education, Education Law, School Psychology on Friday, 25 January 2013 at 07:00

District Not Required to Serve ADHD Student Attending Private School

(January 16, 2013) A school district does not have an obligation to provide services to an ADHD child enrolled in a private religious school under current federal disability-rights law.

The United States Court of Appeals for the Fourth Circuit held that Baltimore City Public Schools had no obligation to provided special education services under Section 504 to an 8th grade ADHD student who attended a private Jewish school in Maryland.

D.L., the student around whom the law suit swirled, was diagnosed with ADHD and anxiety as a fifth grade student in 2007. Two years later, Baltimore City Board of School Commissioners (BCBSC) determined that while D.L. did not qualify for services under the Individuals with Disabilities Educational Act (IDEA), he was eligible under Section 504. Upon making this determination though, BCBSC notified D.L.’s parents that it could not provide the student services unless D.L. was enrolled in one of its schools. Since Maryland is a state that does not allow dual enrollment in a private and public school, D.L. would have to withdraw from his Yeshiva and enroll at the local public school.

D.L.’s parents challenged this decision, arguing that Section 504 creates an affirmative duty for school districts to provide services to eligible students enrolled in private schools. The parents’ arguments failed before a hearing officer so they filed suit in the United States District Court of Maryland. BCBSC filed a motion for summary judgment (a motion which basically says that even if D.L.’s parents were to prove all the facts they assert, they would still lose the case as a matter of law) and the parents filed a motion for partial summary judgment. The lower court granted BCBSC’s summary judgment motion and denied the parent’s partial summary judgment motion. The parents filed an appealed that decision to the U.S. Court of Appeals.

In the case, D.L. v. Baltimore City Board of School Commissioners, the parents argued two main points: 1) that Section 504 regulation mandate that BCBSC provide D.L. with afree and appropriate education (FAPE), and 2) that BCBSC’s requirement that the family enroll D.L. in a public school violates their constitutional rights under the First Amendment’s Freedom of Religion clause.

With regard to the first contention, the court recognized that the plain language of Section 504 leaves unclear whether public schools are required to provide services to students enrolled in private schools. 34 C.F.R. § 104.33(a) states in relevant part that districts must “provide each Section 504 eligible student within its jurisdiction with a [FAPE].” The parents contend this language means that public schools have a greater obligation that simply making such education available.

The court reasoned that while the plain language is ambiguous, that further clarification in Appendix A of the regulations where it states in relevant part, “[i]f . . . a recipient offers adequate services and if alternate placement is chosen by a student’s parent or guardian, the recipient need not assume the cost of the outside services.” In looking at this, the court noted that while this shows that a district need not pay for services obtained outside the public school, it leaves open the question of whether such services can be obtained from the school.

Here, the court relied upon a clarification letter by the Department of Education entitled OCR Response to Veir Inquire Re: Various Matters which offers a direct clarification of the disputed regulation. The court noted that where a regulation is ambiguous, courts must grant deference to an agency’s interpretation of its own regulation. In the Vier letter, the DOE stated that “[w]here a district has offered an appropriate education, a district is not responsible under Section 504, for the provision of educational services to students not enrolled in the public education program based on the personal choice of the parent or guardian.” The court applied this language to hold that BCBSC had no responsibility to provide services to D.L. in his private school placement.

In reaching its holding, the court also rejected the parents’ arguments that Section 504′s language should be interpreted broadly since it is a remedial statute. While noting that turth of the parent’s contention that remedial statutes should be broadly construed, the court noted,

“The purpose of Section 504 does not, however, extend as far as Appellants [parents] assert that it should. Section 504 and its implementing regulations prohibit discrimination on the basis of disability, not on the basis of school choice.”

The court next tackled the First Amendment issues raised by the suit. The parents’ suit tried to persuade the court that the Supreme Court’s rulings in Pierce, 268 U.S. 510, andYoder, 406 U.S. 205, show that requiring D.L. to attend Baltimore public schools was a violation of his First Amendment rights.

The court easily distinguished these cases in that both involved parents being charged under criminal statutes for failure to educate their children in public schools. Here, the parents face no such sanctions and retain free choice as to where their child go to school. The issue was one of payment of services. While it is true that the parents would need to pay additional services that would be free were they to attend public schools, such increased economic burden does not meet the standard of a First Amendment violation. The court noted, “The Supreme Court has explained that a statute does not violate the Free Exercise Clause [First Amendment] merely because it causes economic disadvantage on individuals who choose to practice their religion in a specific manner.

Retrieved from: http://www.ocspecialedattorney.com/district-not-required-to-serve-adhd-student-attending-private-school/

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

#trending now…adhd.

In ADHD, ADHD Adult, ADHD child/adolescent on Tuesday, 22 January 2013 at 17:33

Recent Trends In Childhood ADHD

Darios Getahun, MD, PhD; Steven J. Jacobsen, MD, PhD; Michael J. Fassett, MD; Wansu Chen, MS; Kitaw Demissie, MD, PhD; George G. Rhoads, MD, MPH

JAMA Pediatr. 2013;():1-7. doi:10.1001/2013.jamapediatrics.401.

 

Objective  To examine trends in attention-deficit/hyperactivity disorder (ADHD) by race/ethnicity, age, sex, and median household income.

Design  An ecologic study of trends in the diagnosis of ADHD using the Kaiser Permanente Southern California (KPSC) health plan medical records. Rates of ADHD diagnosis were derived using Poisson regression analyses after adjustments for potential confounders.

Setting  Kaiser Permanente Southern California, Pasadena.

Participants  All children who received care at the KPSC from January 1, 2001, through December 31, 2010 (n = 842 830).

Main Exposure  Period of ADHD diagnosis (in years).

Main Outcome Measures  Incidence of physician-diagnosed ADHD in children aged 5 to 11 years.

Results  Rates of ADHD diagnosis were 2.5% in 2001 and 3.1% in 2010, a relative increase of 24%. From 2001 to 2010, the rate increased among whites (4.7%-5.6%; relative risk [RR] = 1.3; 95% CI, 1.2-1.4), blacks (2.6%- 4.1%; RR = 1.7; 95% CI, 1.5-1.9), and Hispanics (1.7%-2.5%; RR = 1.6; 95% CI, 1.5-1.7). Rates for Asian/Pacific Islander and other racial groups remained unchanged over time. The increase in ADHD diagnosis among blacks was largely driven by an increase in females (RR = 1.9; 95% CI, 1.5-2.3). Although boys were more likely to be diagnosed as having ADHD than girls, results suggest the sex gap for blacks may be closing over time. Children living in high-income households were at increased risk of diagnosis.

Conclusions  The findings suggest that the rate of ADHD diagnosis among children in the health plan notably has increased over time. We observed disproportionately high ADHD diagnosis rates among white children and notable increases among black girls.

Retrieved from: http://archpedi.jamanetwork.com/article.aspx?articleid=1558056#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

is in utero oxygen deprivation a risk factor for adhd?

In ADHD, ADHD Adult, ADHD child/adolescent on Wednesday, 9 January 2013 at 06:49

In Utero Exposure to Ischemic-Hypotoxic Conditions and Attention-deficit/Hyperactivity Disorder

 Darios Getahun, MD, PhD, George G. Rhoads, MD, MPH, Kitaw Demissie, MD, PhD, Shou-En Lu, PhD, Virginia P. Quinn, PhD, Michael J. Fassett, MD, Deborah A. Wing, MD, and Steven J. Jacobsen, MD, PhD.

ABSTRACT

OBJECTIVE: To examine the association between ischemic-hypoxic conditions (IHCs) and attention-deficit/hyperactivity disorder (ADHD) by gestational age and race/ethnicity.

METHODS: Nested case-control study using the Kaiser Permanente Southern California (KPSC) medical records. The study cohort included children aged 5 to 11 years who were delivered and cared for in the KPSC between 1995 and 2010 (N = 308 634). Case children had a diagnosis of ADHD and received ≥2 prescriptions specific to ADHD during the follow-up period. For each case, 5 control children were matched by age at diagnosis. Exposures were defined by using International Classification of Diseases, Ninth Revision codes. A conditional regression model was used to estimate adjusted odds ratios (ORs).

RESULTS: Among eligible children, 13 613 (4.3%) had a diagnosis of ADHD. Compared with control children, case children were more likely to be male and of white or African American race/ethnicity. Case children were more likely to be exposed to IHCs (OR = 1.16, 95% confidence interval [CI] 1.11–1.21). When stratified by gestational age, cases born at 28 to 33, 34 to 36, and 37 to 42 weeks of gestation, were more likely to be exposed to IHCs (ORs, 1.6 [95% CI 1.2–2.1], 1.2 [95% CI 1.1–1.3], and 1.1 [95% CI 1.0–1.2], respectively) compared with controls. IHC was associated with increased odds of ADHD across all race/ethnicity groups.

CONCLUSIONS: These findings suggest that IHCs, especially birth asphyxia, respiratory distress syndrome, and preeclampsia, are independently associated with ADHD. This association was strongest in preterm births.

Retrieved from: http://pediatrics.aappublications.org/content/early/2012/12/05/peds.2012-1298

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

the cost of ADHD…

In ADHD, ADHD Adult, ADHD child/adolescent on Wednesday, 21 November 2012 at 13:17

ADHD Takes Heavy Economic Toll

By: Megan Brooks

Attention-deficit/hyperactivity disorder (ADHD) has a “substantial” economic impact in the United States, with overall incremental costs ranging from $143 to $266 billion annually, a new study suggests.

Surprisingly, researchers note, the cost burden is 3-fold higher in adults ($105 to $194 billion) than in children and adolescents ($38 to $73 billion).

For adults, the largest cost drivers are workplace productivity and income losses ($87 to $138 billion). For children, the largest cost categories are healthcare costs ($21 to $44 billion) and education costs ($15 to $25 billion).

“ADHD is often perceived as a childhood disease, but this analysis demonstrates that at a national level, the economic impact of ADHD on adults may be larger than that on children,” study investigator Peter Neumann, ScD, director, Center for the Evaluation of Value and Risk in Health at the Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, Massachusetts, said in a statement.

“ADHD is not only a pediatric disorder,” coinvestigator Paul Hodgkins, PhD, senior director, Global Health Economics and Outcomes Research at Shire Specialty Pharmaceuticals, added in an email to Medscape Medical News. “Adult ADHD has serious implications — for the adult patient, his family, and the workplace. More emphasis has to be given to identifying and appropriately treating adult ADHD,” he said.

“Striking” Finding

The study, which was funded by Shire, is published in the October issue of the Journal of the American Academy of Child and Adolescent Psychiatry.

“Particularly striking is the finding that the lion’s share of overall costs (almost 75%) is attributable to adults with ADHD and adult family members of individuals with ADHD rather than to children,” A. Reese Abright, MD, director, Child and Adolescent Psychiatry, Mount Sinai School of Medicine–Elmhurst Hospital Center, in New York City, writes in an editorial in the journal.

The findings stem from a review of the literature from 1990 to 2011 on the economic impact of ADHD. The study team identified and included in their analysis 19 US-based studies that reported annual incremental (excess) costs per ADHD individual above non-ADHD control participants or from which these costs could be calculated.

They calculated per-person incremental costs adjusted to 2010 US dollars and converted to annual national incremental costs of ADHD based on 2010 US census population estimates, ADHD prevalence rates, number of household members, and employment rates by age group.

Dr. Abright says that this “timely article” is notable for its findings and the clarity with which the authors describe their methodology and how they calculated ADHD-related costs in children and adults, as well as spillover costs borne by the family members of individuals with ADHD. These spillover costs range from $33 to $43 billion.

The analysis, she notes, “consolidates and extends” previous findings and “adds to the growing literature on the burden associated with psychiatric disorders that begin in childhood.”

Impact of Treatment Unclear

Estimates of cost naturally lead to questions about the effectiveness of prevention and treatments in lowering costs. The current analysis did not evaluate the impact of treatment interventions on excess costs due to the lack of available data.

On this front, Dr. Abright noted that the incorporation of assessments of the comparative cost-effectiveness of treatment arms in large multisite studies such as the National Institute of Mental Health’s Multimodal Study of Treatment of Children with ADHD (MTA) and the Treatment of Adolescents with Depression Study (TADS) has been a “promising development.”

Dr. Neumann and colleagues note that the “substantial and multifaceted societal costs of ADHD” call for the development of public policies to address the burden of the condition.

This analysis was funded by Shire Development LLC. Several of the authors have financial relationships with the company. The original article has a complete list of the authors’ disclosures. Dr. Abright has disclosed no relevant financial relationships.

J Am Acad Child Adolesc Psychiatry. 2012;51:987-988,990-1002. Abstract

Retrieved from: http://www.medscape.com/viewarticle/774298?src=rsshttp://www.medscape.com/viewarticle/774298?src=rss

***

Economic Impact of Childhood and Adult Attention-Deficit/Hyperactivity Disorder in the United States

Jalpa A. Doshi, Ph.D.,  Paul Hodgkins, Ph.D., Jennifer Kahle, Ph.D., Vanja Sikirica, Pharm.D., Michael J. Cangelosi, M.P.H., Juliana Setyawan, Pharm.D., M. Haim Erder, Ph.D., & Peter J. Neumann, Sc.D.\

Accepted 17 July 2012. published online 23 July 2012.

Objective

Attention-deficit/hyperactivity disorder (ADHD) is one of the most prevalent mental disorders in children in the United States and often persists into adulthood with associated symptomatology and impairments. This article comprehensively reviews studies reporting ADHD-related incremental (excess) costs for children/adolescents and adults and presents estimates of annual national incremental costs of ADHD.

Method

A systematic search for primary United States-based studies published from January 1, 1990 through June 30, 2011 on costs of children/adolescents and adults with ADHD and their family members was conducted. Only studies in which mean annual incremental costs per individual with ADHD above non-ADHD controls were reported or could be derived were included. Per-person incremental costs were adjusted to 2010 U.S. dollars and converted to annual national incremental costs of ADHD based on 2010 U.S. Census population estimates, ADHD prevalence rates, number of household members, and employment rates by age group.

Results

Nineteen studies met the inclusion criteria. Overall national annual incremental costs of ADHD ranged from $143 to $266 billion (B). Most of these costs were incurred by adults ($105B−$194B) compared with children/adolescents ($38B−$72B). For adults, the largest cost category was productivity and income losses ($87B−$138B). For children, the largest cost categories were health care ($21B−$44B) and education ($15B−$25B). Spillover costs borne by the family members of individuals with ADHD were also substantial ($33B−$43B).

Conclusion

Despite a wide range in the magnitude of the cost estimates, this study indicates that ADHD has a substantial economic impact in the United States. Implications of these findings and future directions for research are discussed.

stability balls…not just for fitness!

In ADHD, ADHD child/adolescent, Attention, Education, Special Education on Wednesday, 21 November 2012 at 12:59

http://wittfitt.com/wittfittmedia/AJOTstudy.pdf

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.

Gargling Sugar Water Can Boost Your Self-Control

In ADHD, ADHD Adult, ADHD child/adolescent, Alternative Health, Psychiatry on Saturday, 10 November 2012 at 10:54

Gargling Sugar Water Can Boost Your Self-Control.

sensory defensiveness can be a gift!

In ADHD, ADHD Adult, ADHD child/adolescent, Autism Spectrum Disorders, Sensory defensiveness on Friday, 2 November 2012 at 06:57

Five Gifts of Being Highly Sensitive

By THERESE J. BORCHARD

Today I have the pleasure of interviewing Douglas Eby, M.A./Psychology, who is a writer and researcher on the psychology of creative expression, high ability and personal growth. He is creator of the Talent
Development Resources series of sites (includingHighlySensitive.org) at http://talentdevelop.com. I know many of you are “highly sensitive” and enjoy articles on that topic, so I am excited to pique his highly-sensitive brain today!

Question: If you had to name the top five gifts of being highly sensitive, what would they be?

Douglas:

1. Sensory detail

One of the prominent “virtues” of high sensitivity is the richness of sensory detail that life provides. The subtle shades of texture in clothing, and foods when cooking, the sounds of music or even traffic or people talking, fragrances and colors of nature. All of these may be more intense for highly sensitive people.

Of course, people are not simply “sensitive” or “not sensitive” — like other qualities and traits, it’s a matter of degree.

Years ago, I took a color discrimination test to work as a photographic technician, making color prints. The manager said I’d scored better, with more subtle distinctions between hues in the test charts, than anyone he had evaluated.

That kind of response to color makes visual experience rich and exciting, and can help visual artists and designers be even more excellent.

2. Nuances in meaning

The trait of high sensitivity also includes a strong tendency to be aware of nuances in meaning, and to be more cautious about taking action, and to more carefully consider options and possible outcomes.

3. Emotional awareness

We also tend to be more aware of our inner emotional states, which can make for richer and more profound creative work as writers, musicians, actors or other artists.

A greater response to pain, discomfort, and physical experience can mean sensitive people have the potential, at least, to take better care of their health.

4. Creativity

Psychologist Elaine Aron, author of The Highly Sensitive Person,estimates about twenty percent of people are highly sensitive, and seventy percent of those are introverted, which is a trait that can also encourage creativity.

As examples, there are many actors who say they are shy, and director Kathryn Bigelow, who recently won an Academy Award, has said, “I’m kind of very shy by nature.” The star of her movie The Hurt Locker, Jeremy Renner (who was reportedly shy as a child), has commented that “in social situations she can be painfully shy.”

5. Greater empathy

High sensitivity to other people’s emotions can be a powerful asset for teachers, managers, therapists and others.

Question: And, if you had to name five curses, what would they be? And how best do we overcome them or co-exist with them?

Douglas:

1. Easily overwhelmed, overstimulated

The biggest challenge in high sensitivity is probably being vulnerable to sensory or emotional overwhelm. Taking in and processing so much information from both inner and outer worlds can be “too much” at times and result in more pain, fatigue, stress, anxiety and other reactions.

An intriguing neuroscience research study I came across that may explain some of this said people with nervous systems having decreased latent inhibition are more open to incoming stimuli. Which can be a good thing, or not so good.

Actor Amy Brenneman once commented, “I’m too sensitive to watch most of the reality shows. It’s so painful for me.”

That kind of pain or discomfort can mean we don’t choose to experience some things that might actually be fun or enriching. Though I don’t mean reality shows.

2. Affected by emotions of others

Another aspect of sensitivity can be reacting to the emotions — and perhaps thoughts — of others. Being in the vicinity of angry people, for example, can be more distressing.

As actor Scarlett Johansson once put it, “Sometimes that awareness is good, and sometimes I wish I wasn’t so sensitive.”

3. Need lots of space and time to ourselves

We may need to “retreat” and emotionally “refresh” ourselves at times that are not always best for our goals or personal growth. For example, being at a professional development conference, it may not be the most helpful thing to leave a long presentation or workshop in order to recuperate from the emotional intensity of the crowd.

4. Unhealthy perfectionism

There can also be qualities of thinking or analyzing that lead to unhealthy perfectionism, or stressful responses to objects, people or situations that are “too much” or “wrong” for our sensitivities.

5. Living out of sync with our culture

Living in a culture that devalues sensitivity and introversion as much as the U.S. means there are many pressures to be “normal” — meaning extroverted, sociable and outgoing.

Dr. Ted Zeff, author of The Highly Sensitive Person’s Survival Guide, points out that other cultures, such as Thailand, have different attitudes, with a strong appreciation of sensitive or introverted people.

Jenna Avery, a “life coach for sensitive souls,” counsels people to accept or even pursue being “out of sync” with mainstream society, and be aware of other’s judgments of people as too sensitive, too emotional, or too dramatic.

And if we are sensitive, we may use those kinds of judgments against ourselves, and think, as Winona Ryder said she did at one time, “Maybe I’m too sensitive for this world.”

Certainly, there are extremes of emotions that are considered mood disorders, for example, and should be dealt with as a health challenge.

But “too emotional” or “too sensitive” are usually criticisms based on majority behavior and standards.

Overall, I think being highly sensitive is a trait we can embrace and use to be more creative and aware. But it demands taking care to live strategically, even outside popular values, to avoid overwhelm so we can better nurture our abilities and creative talents.

Retrieved from: http://psychcentral.com/blog/archives/2010/03/28/5-gifts-of-being-highly-sensitive/

adhd and exercise…more positive evidence of benefits

In ADHD, ADHD Adult, ADHD child/adolescent, Education, Fitness/Health, School Psychology on Friday, 2 November 2012 at 06:49

A Little Exercise May Help Kids With ADHD to Focus

Published November 01, 2012

Reuters

Twenty minutes of exercise may help kids with attention-deficit hyperactivity disorder (ADHD) settle in to read or solve a math problem, new research suggests.

The small study, of 40 eight- to 10-year-olds, looked only at the short-term effects of a single bout of exercise. And researchers caution that they are not saying exercise is the answer to ADHD.

But it seems that exercise may at least do no harm to kids’ ability to focus, they say. And further studies should look into whether it’s a good option for managing some children’s ADHD.

“This is only a first study,” said lead researcher Matthew B. Pontifex, of Michigan State University in East Lansing.

“We need to learn how long the effects last, and how exercise might combine with or compare to traditional ADHD treatments” like stimulant medications, Pontifex explained.

He noted that there’s been a lot of research into the relationship between habitual exercise and adults’ thinking and memory, particularly older adults’. But little is known about kids, even though some parents, teachers and doctors have advocated exercise for helping children with ADHD.

So for their study, Pontifex and his colleagues recruited 20 children with diagnosed or suspected ADHD, and 20 ADHD-free kids of the same age and family-income level.

All of the children took a standard test of their ability to ignore distractions and stay focused on a simple task at hand – the main “aspect of cognition” that troubles kids with ADHD, Pontifex noted. The kids also took standard tests of reading, spelling and math skills.

Each child took the tests after either 20 minutes of treadmill exercise or 20 minutes of quiet reading (on separate days).

Overall, the study found, both groups of children performed better after exercise than after reading.

On the test of focusing ability, the ADHD group was correct on about 80 percent of responses after reading, versus about 84 percent after exercise. Kids without ADHD performed better – reaching about a 90 percent correct rate after exercise.

Similarly, both groups of kids scored higher on their reading and math tests after exercise, versus post-reading.

It’s hard to say what those higher one-time scores could mean in real life, according to Pontifex, who published his results in The Journal of Pediatrics.

One of the big questions is whether regular exercise would have lasting effects on kids’ ability to focus or their school performance, he said.

And why would exercise help children, with or without ADHD, focus? “We really don’t know the mechanisms right now,” Pontifex said.

But there is a theory that the attention problems of ADHD are related to an “underarousal” of the central nervous system. It’s possible that a bout of exercise helps kids zero in on a specific task, at least in the short term.

Parents and experts alike are becoming more and more interested in alternatives to drugs for ADHD, Pontifex noted. It’s estimated that 44 percent of U.S. children with the disorder are not on any medication for it.

And even when kids are using medication, additional treatments may help them cut down their doses. Pontifex said future studies should look at whether exercise fits that bill.

“We’re not suggesting that exercise is a replacement, or that parents should pull their kids off of their medication,” Pontifex said.

But, he added, they could encourage their child to be active for the overall health benefits, and talk with their doctor about whether exercise could help manage ADHD specifically.

“Exercise is beneficial for all children,” Pontifex noted. “We’re providing some evidence that there’s an additional benefit on cognition.”

Retrieved from: http://www.foxnews.com/health/2012/11/01/little-exercise-may-help-kids-with-adhd-focus/?utm_source=twitterfeed&utm_medium=twitter#ixzz2B3qU8bOp

Homework Help, Timing is Vital: Setting Yourself and Your Child Up for Success

In ADHD, ADHD child/adolescent, Education, School Psychology, Special Education on Friday, 2 November 2012 at 05:59

Homework Help, Timing is Vital: Setting Yourself and Your Child Up for Success

Every household and every student is different so we ask that when you are reviewing these guidelines think about what might need to be adjusted in your household to be sure that we are setting up for success! First off, if you are reading this you are already on your way because step 1 is being committed to improving. Whether this is the first year of homework or a teen or college student, creating new habits takes consistency and commitment; if this sounds like too much work or not the easy answer you were hoping keep reading, it is still a start!

Timing is key:  Most people with ADHD are pros at putting off things that are more difficult or take longer to complete. You will hear and may have heard almost every excuse, this isn’t about excuses, this is about accomplishment.We work on upfront contracting and positive reinforcement and reward systems. Work with the student to set the intention in advance and then stick to it. Discuss with the student the expectations of homework such as how and when you  will review daily assignments before and after they are completed. Then set a time frame for which they need to be completed by. It has to be specific and it has to fit your household. Try to use events that occur daily rather than a specific time on the clock to ensure the child has a clear understanding of what that timeframe means.

Here is one example: Child arrives home from school and they show you their work from the day and what assignments they have as soon as they walk in the door. They then have 20 minutes for snack and free time. Once the 20 minutes is up all work  must be completed before any extra activities or electronics are used including cell phone, TV and video games.

Dinner is typically not a priority for most children and even teens/adults, it is a necessity, so avoid using the “finish your homework before dinner” because that affects you and the family time not the students needs, wants or desires. Most often this upsets the person making dinner and turns into an argument and dinner time a negotiation rather than much-needed family time.

During the childs snack/free time try to estimate in your mind what they will need help with more than other things and prepare yourself to be an active observer and helper as needed so that they feel both supported and monitored. Let them  know that you are there if they need help with a certain area and if you have something to accomplish discuss that with the student before their snack.

Example: Student has some geography work that you know they typically struggle with and some reading and math that looks like they should handle with minimal guidance and you have dinner to make. “It looks like the countries you have to identify and the geography assignment is something that might be new to you. I have to make dinner, but am happy to work with you on it or be here for questions if you need, would this help? Could we work on that assignment first so then I can get dinner going while you finish up the rest of your work?”

If a child has something going on that you are aware of in the evening, remind them in the morning that because of the event they will have to skip free time and have their snack while they do their homework so that they can still make the special event.Giving them a heads up helps them to prepare rather than meltdown or feel unexpectedly rushed.

We talked about removing electronics before homework is completed, YOU HAVE TO STICK TO THIS! Set up the students space or their launch pad is vital. We will talk more about how to accomplish this in future posts but the key is to stick with it!

If your child is completing homework at after school or a relatives house be sure and still have guidelines set up for when they walk in the door at home. Is there remediation of a particular subject that they should do a few times a week? Be sure you are at least reviewing the work first thing and then coming up with your strategies from there. The more consistent your expectations and behavior the less likely you will have blow ups and missed work. Your child wants to please you and be successful even if they don’t let you know that!

Retrieved from: http://focusmdblog.com/2012/10/18/homework-help-timing-is-vital-setting-yourself-and-your-child-up-for-success/

 

adhd…under and over diagnosed.

In ADHD, ADHD Adult, ADHD child/adolescent, Psychiatry, School Psychology on Sunday, 21 October 2012 at 09:47

Attention Deficit Hyperactivity Disorder is Both Under and Over Diagnosed, Study Suggests

ScienceDaily (Oct. 19, 2012)

Attention Deficit Hyperactivity Disorder is both under and over diagnosed. That’s the result of one of the largest studies conducted on ADHD in the United States, published in the Journal of Attention Disorders.

A substantial number of children being treated for ADHD may not have the disorder, while many children who do have the symptoms are going untreated, according to the 10-year Project to Learn about ADHD in Youth (PLAY) study funded by the National Center on Birth Defects and Developmental Disabilities of the Centers of Disease Control and Prevention

“Childhood ADHD is a major public health problem. Many studies rely on parent reporting of an ADHD diagnosis, which is a function of both the child’s access to care in order to be diagnosed, and the parent’s perception that there is a problem,” said Robert McKeown, of the University of South Carolina’s Arnold School of Public Health, who led the South Carolina portion of the study.

“Further complicating our understanding of the prevalence of ADHD and its treatment is that the diagnosis often is made by a clinician who has little experience assessing and diagnosing mental disorders. As a result, ADHD is both under and over diagnosed,” said McKeown, distinguished professor emeritus in the department of epidemiology and biostatistics.

The study, conducted between 2002-2012, was a collaborative research project with the University of South Carolina’s Arnold School and School of Medicine and the University of Oklahoma’s Health Sciences Center.

“To our knowledge, this is the largest community-based epidemiologic study of ADHD to date,” McKeown said.

The study found that 8.7 percent of children in the community sample in South Carolina had enough symptoms to fit the ADHD diagnosis at the time of the initial assessment. The percentage was 10.6 in Oklahoma.

The report also revealed that the number of parents in the community sample who reported that their children were taking ADHD medication was 10.1 percent in South Carolina and 7.4 percent in Oklahoma. Yet, of the children taking ADHD medication, only 39.5 percent in South Carolina and 28.3 percent in Oklahoma actually met the case definition of ADHD.

“ADHD is not a snap diagnosis. It requires data from several sources and across several domains and considerable expertise to diagnose accurately and differentiate from other possible problems,” McKeown said.

The CDC reports that ADHD is one of the most common neurobehavioral disorders of childhood. Often first diagnosed in childhood, ADHD affects a child’s ability to do well in school and his or her ability to make and keep friends. While many children “outgrow” the disorder, ADHD can continue into adulthood, impacting the individual’s ability to work and function in society.

McKeown said the study found that many children taking ADHD medication did not meet the ADHD diagnostic criteria.

“These children had more ADHD symptoms, on average, than the other comparison children. Many children meeting case criteria had not been previously identified and were not receiving medication treatment, suggesting that the condition remains underdiagnosed,” he said.

The study was designed to follow children from elementary school through adolescence (ages 5 — 13) and investigate the short- and long-term outcomes of children with ADHD. Teachers screened 10,427 children in four school districts across the two states where the study was conducted. ADHD ratings by teacher and parent reports of diagnosis and medication treatment were used to determine whether children were high or low risk for ADHD.

Study questions focused on the prevalence and treated prevalence of ADHD in children; the existence of other health problems in children with ADHD, and the types and rates of health risk behaviors in children with ADHD. The study also looked at treatment patterns, both past and current, of children with ADHD.

“The findings of our study suggest that a fair number of children are being treated who do not meet case criteria and that there are children who do meet criteria but are not being treated,” McKeown said. “ADHD is not a snap diagnosis. It requires data from several sources and across several domains and considerable expertise to diagnose accurately and differentiate from other possible problems.”

Children and adolescents with ADHD also were found to have high rates of other disorders, including oppositional defiant disorder and conduct disorder. They also were more likely to engage in risky or impulsive behaviors, he said.

“We will follow up on these initial reports as the children age to determine what, if any, changes have occurred in the symptom patterns, as well as in the types of health risk behaviors,” McKeown said.

“We hope that this will shed light on the prevalence and the treatment of ADHD and will lead practitioners to seek consultation if they are not trained to assess, diagnose and treat ADHD,” he said. “We also hope it will lead parents and practitioners to assess all the treatment options to determine what works best for each child.”

USC researchers involved in the study included Dr. Steven Cuffe of the University of Florida College of Medicine-Jacksonville, formerly of the USC School of Medicine; Arnold School doctoral student Lorie L. Geryk; and Matteo Botai of the Karolinska Institutet in Sweden and Joseph R. Holbrook of the CDC, both formerly at the Arnold School.

University of South Carolina (2012, October 19). Attention deficit hyperactivity disorder is both under and over diagnosed, study suggests.ScienceDaily. Retrieved October 21, 2012, from http://www.sciencedaily.com­ /releases/2012/10/121019141124.htm

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121019141124.htm

exercise and adhd…

In ADHD, ADHD Adult, ADHD child/adolescent, Fitness/Health, Neuropsychology, Psychiatry, School Psychology, Special Education on Sunday, 21 October 2012 at 09:43

Exercise May Lead to Better School Performance for Kids with ADHD

ScienceDaily (Oct. 16, 2012)

A few minutes of exercise can help children with attention deficit hyperactivity disorder perform better academically, according to a new study led by a Michigan State University researcher.

The study, published in the current issue of the Journal of Pediatrics, shows for the first time that kids with ADHD can better drown out distractions and focus on a task after a single bout of exercise. Scientists say such “inhibitory control” is the main challenge faced by people with the disorder.

“This provides some very early evidence that exercise might be a tool in our nonpharmaceutical treatment of ADHD,” said Matthew Pontifex, MSU assistant professor of kinesiology, who led the study. “Maybe our first course of action that we would recommend to developmental psychologists would be to increase children’s physical activity.”

While drugs have proven largely effective in treating many of the 2.5 million school-aged American children with ADHD, a growing number of parents and physicians worry about the side effects and costs of medication.

In the study, Pontifex and colleagues asked 40 children aged 8 to 10, half of whom had ADHD, to spend 20 minutes either walking briskly on a treadmill or reading while seated. The children then took a brief reading comprehension and math exam similar to longer standardized tests. They also played a simple computer game in which they had to ignore visual stimuli to quickly determine which direction a cartoon fish was swimming.

The results showed all of the children performed better on both tests after exercising. In the computer game, those with ADHD also were better able to slow down after making an error to avoid repeat mistakes — a particular challenge for those with the disorder.

Pontifex said the findings support calls for more physical activity during the school day. Other researchers have found that children with ADHD are less likely to be physically active or play organized sports. Meanwhile, many schools have cut recess and physical education programs in response to shrinking budgets.

“To date there really isn’t a whole lot of evidence that schools can pull from to justify why these physical education programs should be in existence,” he said. “So what we’re trying to do is target our research to provide that type of evidence.”

Pontifex conducted the study for his doctoral dissertation at the University of Illinois before joining the MSU faculty. His co-investigators included his adviser, kinesiology professor Charles Hillman, and Daniel Picchietti, a pediatrician at the Carle Foundation Hospital in Champaign, Ill. The research was funded by the National Institute of Child Health and Human Development.

Michigan State University (2012, October 16). Exercise may lead to better school performance for kids with ADHD. ScienceDaily. Retrieved October 21, 2012, from http://www.sciencedaily.com­ /releases/2012/10/121016132109.htm

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121016132109.htm

Homework Help, Timing is Vital: Setting Yourself and Your Child Up For Success!

In ADHD, ADHD Adult, ADHD child/adolescent, Education, School Psychology, Special Education on Friday, 19 October 2012 at 15:52

Homework Help, Timing is Vital: Setting Yourself and Your Child Up For Success!.

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

more on men and adhd…

In ADHD, ADHD Adult, ADHD child/adolescent, Psychiatry on Thursday, 18 October 2012 at 07:49

Men Diagnosed with Childhood ADHD Struggle More with Jobs, Relationships

ADHD can have lingering effects among men

By: Alexandra Sifferlin

Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobehavioral disorder among children, and as incidence of the condition continue to rise, parents and patients are asking what happens next. How does ADHD affect children as they become teens and adults and start to form relationships, find jobs and establish families of their own? Does the condition put them at a disadvantage for coping with life’s inevitable challenges?

With 5.4 million children ever diagnosed with ADHD in the U.S., and 3% to 7% of school-aged children currently struggling with the condition, it’s worth considering how ADHD affects their adult lives. Rachel Klein of the Child Study Center at New York University Langone Medical Center and her colleagues studied the potentially long-term effects of ADHD among men who were diagnosed as kids. In their 33-year follow-up study, Klein and her team looked at 135 middle-aged men with childhood ADHD who were referred to the study by their teachers when they were between six to 12 years old. The researchers compared this group to 136 men without ADHD and found that  men with ADHD struggled more in occupational, educational, economic and social arenas later in life compared to men without the diagnosis.

At the 33-year follow-up, when the men were in their forties, those with childhood-diagnosed ADHD without conduct disorders had about 2.5 years fewer years of education compared to the other men; only 3.7% had higher degrees compared to nearly 30% of the control group. The majority (84%) were holding jobs, but at significantly lower positions than peers without ADHD and were therefore at a financial disadvantage. On average, the researchers say, the ADHD group earned $40,000 less in salary than their unaffected counterparts.

Socially, men with ADHD also struggled with higher divorce rates, more antisocial personality disorders and substance abuse. On the positive side, however, they did not have higher rates of mood and anxiety disorders, like depression.

Overall, the ADHD adults showed higher rates of psychiatric hospitalizations and incarcerations, which the authors conclude supports a continued need for monitoring and treatment of kids with ADHD, even when a conduct disorder is not present. Dr. Klein says even when children with ADHD are not disruptive, they may still be at a higher risk for developing antisocial behaviors later on, like lying, stealing and cheating.
But addressing the needs of children with ADHD, by providing academic support in school to help them overcome their frustrations and challenges in paying attention and retaining what they learn, and by giving them emotional support from the family, can given these students the coping skills they need to meet their adult challenges — in the workplace, in relationships and in social interactions —as well.

“One of the very important messages [from our findings] is that most kids [with ADHD] do OK, and some do very well. As a group they did well,” says Klein. While ADHD’s effect can linger into adulthood, it doesn’t have to be either debilitating or inevitable. “It does affect their lives, but not to the point that they’re very badly off,” she says.

The study was published online in the journal Archives of General Psychiatry.

Retrieved from: http://healthland.time.com/2012/10/16/men-diagnosed-with-childhood-adhd-struggle-more-with-jobs-relationships/#ixzz29eNljos5

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

Mixed Signals on Eating Fish While Pregnant

In ADHD, ADHD Adult, ADHD child/adolescent on Wednesday, 10 October 2012 at 15:46

 

Mixed Signals on Eating Fish While Pregnant

 

By Janice Wood Associate News Editor

 

Reviewed by John M. Grohol, Psy.D. on October 9, 2012

 

New research has linked low-level mercury exposure in pregnant women to an increased risk of attention deficit hyperactivity disorder (ADHD) in their children.

 

But the same research also found that eating fish during pregnancy can help reduce the risk of ADHD-related behaviors in children.

 

The scientists who led the study, Susan Korrick, M.D., M.P.H., of Brigham and Women’s Hospital, and Sharon Sagiv, Ph.D., M.P.H., of Boston University School of Public Health, said this “duality” is possible because many types of fish have low levels of mercury, so it is possible for a pregnant woman to eat nutritionally beneficial fish without being exposed to much mercury.

 

“These findings underscore the difficulties pregnant women face when trying to balance the nutritional benefits of fish intake with the potential detriments of low-level mercury exposure,” said Korrick.

 

“Women need to know that nutrients in fish are good for the brain of a developing fetus, but women need to be aware that high mercury levels in some fish pose a risk,” added Sagiv.

 

This study involved approximately 400 children born in New Bedford, Mass., between 1993 and 1998. Shortly after their mothers gave birth, researchers collected hair samples from the mothers and analyzed them for mercury.

 

They also gave the mothers a questionnaire to determine their fish consumption during pregnancy. Eight years later, researchers followed up with the children and administered standardized tests to determine behaviors related to ADHD.

 

Researchers found an increased risk of childhood ADHD-related behaviors with increasing maternal hair mercury levels.

 

These mercury levels were lower than levels shown to be potentially hazardous in previous studies, the researchers noted.

 

Additionally, researchers found a reduced risk of ADHD-related behaviors in children whose mothers reported eating more than two servings of fish per week, which is a higher number of servings than is currently recommended by the United States Food and Drug Administration and Environmental Protection Agency.

 

The study did not examine what types of fish are best for a pregnant woman to eat, but previous studies have shown women should avoid fish that are high in mercury, such as shark, swordfish, king mackerel and fresh tuna.

 

Fish that are low in mercury, such as flounder, haddock, and salmon, are safer to eat and good sources of nutrition, the researchers concluded.

 

The study was published in the online version of the Archives of Pediatrics & Adolescent Medicine.

 

APA Reference
Wood, J. (2012). Mixed Signals on Eating Fish While Pregnant. Psych Central. Retrieved on October 10, 2012, from http://psychcentral.com/news/2012/10/09/mixed-signals-on-eating-fish-while-pregnant/45755.html

 

Retrieved from: http://psychcentral.com/news/2012/10/09/mixed-signals-on-eating-fish-while-pregnant/45755.html

 

 

 

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.

the state of anxiety in the united states

In ADHD, Anxiety, Medication, Psychiatry, Psychopharmacology on Wednesday, 3 October 2012 at 05:51

Some Facts about Anxiety in the United States:

Anxiety disorders are the most common mental illness in the U.S., affecting 40 million adults in the United States age 18 and older (18% of U.S. population).

Anxiety disorders are highly treatable, yet only about one-third of those suffering receive treatment.

Anxiety disorders cost the U.S. more than $42 billion a year, almost one-third of the country’s $148 billion total mental health bill, according to “The Economic Burden of Anxiety Disorders,” a study commissioned by ADAA (The Journal of Clinical Psychiatry,60(7), July 1999).

More than $22.84 billion of those costs are associated with the repeated use of health care services; people with anxietydisorders seek relief for symptoms that mimic physical illnesses.

People with an anxiety disorder are three to five times more likely to go to the doctor and six times more likely to be hospitalized for psychiatric disorders than those who do not suffer from anxiety disorders.

Anxiety disorders develop from a complex set of risk factors, including genetics, brain chemistry, personality, and life events.

 

Facts: Anxiety and Stress-Related Disorders

Generalized Anxiety Disorder (GAD)

GAD affects 6.8 million adults, or 3.1% of the U.S. population.
Women are twice as likely to be affected as men.

Obsessive-Compulsive Disorder (OCD)
2.2 million, 1.0%
Equally common among men and women.
The median age of onset is 19, with 25 percent of cases occurring by age 14. One-third of affected adults first experienced symptoms in childhood.

  • Hoarding is the compulsive purchasing, acquiring, searching, and saving of items that have little or no value.

Panic Disorder

6 million, 2.7%
Women are twice as likely to be affected as men.
Very high comorbidity rate with major depression.

Posttraumatic Stress Disorder (PTSD)
7.7 million, 3.5%
Women are more likely to be affected than men.
Rape is the most likely trigger of PTSD: 65% of men and 45.9% of women who are raped will develop the disorder.
Childhood sexual abuse is a strong predictor of lifetime likelihood for developing PTSD.

Social Anxiety Disorder
15 million, 6.8%
Equally common among men and women, typically beginning around age 13.
According to a 2007 ADAA survey, 36% of people with social anxiety disorder report experiencing symptoms for 10 or more years before seeking help.

Specific Phobias
19 million, 8.7%
Women are twice as likely to be affected as men.

Related Illnesses 

Many people with an anxiety disorder also have a co-occurring disorder or physical illness, which can make their symptoms worse and recovery more difficult. It’s essential to be treated for both disorders.

Children 

Anxiety disorders affect one in eight children. Research shows that untreated children with anxiety disorders are at higher risk to perform poorly in school, miss out on important social experiences, and engage in substance abuse.

Anxiety disorders also often co-occur with other disorders such as depression, eating disorders, and attention-deficit/hyperactivity disorder (ADHD).

Older Adults

Anxiety is as common among older adults as among the young. Generalized anxiety disorder (GAD) is the most common anxiety disorder among older adults, though anxiety disorders in this population are frequently associated with traumatic events such as a fall or acute illness. Read the best way to treat anxiety disorders in older adults.

Treatment Options

Anxiety disorders are treatable, and the vast majority of people with an anxiety disorder can be helped with professional care. Several standard approaches have proved effective:

Retrieved from: http://www.adaa.org/about-adaa/press-room/facts-statistics

 

The United States of Anxiety

By Ben Michaelis, Ph.D.

America is in an acute state of anxiety. For those of you who were concerned during the debt ceiling discussions, have been fearful during the stock market gyrations and are now panicking about your job, family and future, take a moment, take a deep breath and imagine that there is a better way. Because there is.

As human beings, our minds are prewired to react more strongly to negative information than positive information. This makes sense from an evolutionary psychology perspective: Negative information may mean threats to our survival, such as predators who may try to eat us. This is the reason that when a stranger gives you a nasty look it stays on your mind longer than when someone flashes a smile at you. This natural bias towards focusing on the negative becomes even more pronounced during times of uncertainty. When we don’t know where to turn, anything that seems potentially dangerous grabs our attention and activates our primitive survival instincts.

The fight or flight system is quite useful when you are facing a specific physical threat, but it is not helpful when you are facing general uncertainty, which is really what this is about. In fact, our survival instincts actually steer us in the wrong direction and can quickly make the situation worse. What is needed during periods of uncertainty is not this primitive instinct toward biological survival, which drove investors to “sell, sell sell!” on Monday, but rather the capacity to use our higher brain centers to imagine a different future.

As a clinical psychologist, I don’t treat nations, I treat people. In my work, I often see patients who experience intense, runaway anxiety (not unlike what happened on Monday) at just the time of a triumph or when things are about to turn for the better. Giving into the fear of the moment is both psychologically unpleasant and socially contagious. When other people see, or sense, that you are afraid, they focus on their instinctive reaction to seeing your fear and begin to experience terror themselves. Societal fear can quickly create an environment where your fears can come true simply by people behaving as though they are true. Regardless of the headlines suggesting the end is nigh, try taking a beat and doing something different: Imagine that all is not lost. Consider the ways that the future might actually be better than the present or the past.

When I am with a patient who is in the grip of such a panic, I suggest following these three steps in order to shift from fear to faith:

  1. Recognize: If you can recognize that you are in a state of panic, you are, frankly, more than halfway to stopping it. If you are not sure if you are in a state of panic, ask yourself this question: “Can I choose to stop these unpleasant, spiraling thoughts if I want to?” If the answer to the question is, “Yes,” then go ahead and do it. If the answer is “No,” then you have just realized that you are panicking.
  2. Refocus: Focus your energy on your five senses. Ask yourself: “What am I smelling?” “What am I seeing?” “What am I hearing?” “What are the tastes in my mouth?” and “How is my body feeling?” If you intentionally bring your focus away from the scenarios of Armageddon (not the Bruce Willis version) that you are cooking up and unto your present circumstances, you will break the chain of runaway thinking, because you can’t do both simultaneously. Even if you only get a brief respite any break, no matter how small, is enough to change the direction of your anxiety and help you take an active approach to problem solving.
  3. Re-imagine: Take your doomsday scenario and re-write it so that you are not stuck with the same old script. Write a Hollywood ending if you like. If you are scared that you will lose all of your money in the stock market, imagine the opposite. Picture the market changing direction, and that you will have more than you will ever need. If you have been out of work and are afraid that you will never get another job, imagine that you will be inundated with job offers. I am not suggesting that by simply imagining these things that they will happen, only that by doing so you can stop the spiral of anxiety and start thinking and planning for your next steps. That shift can make all of the difference between fueling the contagion of panic and returning to a more balanced state where you can actually effect real change in your life.

Your imagination is your greatest cognitive gift. It is also our greatest national asset. The ability to imagine a different and better future is the first step toward creating one. By recognizing, refocusing and re-imagining your circumstances you will feel better in the moment and shift from fear to faith. Using your mind’s eye to envision a positive outcome can help calm you down and make better momentary decisions. Plus, you might just inspire others to do the same.

Retrieved from: http://www.huffingtonpost.com/ben-michaelis-phd/americans-anxiety-stress_b_925420.html

 

are we over-medicating?

In ADHD, Anxiety, Brain imaging, Brain studies, Medication, Psychiatry, Psychopharmacology on Wednesday, 3 October 2012 at 05:39

this is one author’s opinion on anxiety and “the little blue pill.”  while anxiety is a VERY REAL and often debilitating condition for some, many wonder if anxiety medications (such as xanax and valium) are too readily prescribed and taken.  in my work as a school psychologist, i am asked constantly if i think adhd is over-diagnosed and children are over-medicated.  my answer is based in my belief that most psychological conditions are brain-based (this is becoming especially evident in light of new ways to examine the brain, i.e. genomic medicine, advanced brain imaging, etc.).  not treating those who have a REAL diagnosis has deleterious effects, but do i think that there are many physicians who will prescribe medications without possibly doing a full evaluation?  yes, i do.  but, i also think there are some VERY savvy parents who know what to say to get their kids medication that they *think* will give them an advantage over others.  while stimulants have a paradoxical effect on those with adhd (meaning they are stimulants but do not act as a stimulant behaviorally, i.e. not hyping kids up, but stimulating parts of the brain that are responsible for attending, focus, etc., thus appearing to calm them down), they also act as true stimulants for those that do not have a valid adhd diagnosis.  there are many stories of all-night study sessions in college and kids who use stimulants to stay awake and keep studying (i have even heard about kids who purchase stimulants just as they would marijuana or other drugs and crush it up and snort it for a cocaine-like effect).  the effect of a stimulant on someone without adhd is much like that of someone on cocaine.  they are ‘stimulated.’  so, while i believe the author has some valid points related to medication, i also believe that people who TRULY have a diagnosis of anxiety, adhd, depression, etc., do more harm than good when they do not take medication.  that is my personal opinion based on the many studies of those with treated issues versus those who do not seek treatment or were not treated until adulthood.  the differences in neuroanatomy and structural changes in the brain show that medication does work IF properly prescribed.  my personal opinion is if you think you are suffering from a brain-based disorder (adhd, anxiety, etc.), do yourself a favor and go to a PSYCHIATRIST.  while pediatricians and general practitioners are good at what they do and are knowledgeable about so many things, you wouldn’t go to an ophthalmologist for a broken leg, so why would you go to a pediatrician for a psychiatric issue?  psychiatrists’ entire business is of the mind and it is their job to keep up with the latest research and medications.  why go to anyone BUT a specialist?  once again, this is nothing more than my PERSONAL opinion.  

Valium’s Contribution to the New Normal

OPINION

By Robin Marantz Henig

IT wasn’t funny, really, but everybody laughed at the scene in the 1979 film “Starting Over” when Burt Reynolds’s character had a panic attack in the furniture department of Bloomingdale’s (something to do with terror at the prospect of buying a couch). “Does anyone have a Valium?” his brother called out as Burt hyperventilated. The punch line: Every woman in the store reached into her purse and pulled out a little vial of pills.

Nor was it surprising that all those Bloomie’s shoppers could be so helpful, since by that time Valium, which had been introduced in 1963, was the best-selling prescription drug in America, with billions of blue or yellow or white pills, each stamped with a trademark V, sold every year.

Valium was, significantly, one of the first psychoactive drugs to be used on a large scale on people who were basically fine. It has since been surpassed by other drugs, like the popular tranquilizer Xanax. But with the pharmaceutical giant Roche announcing that it will soon close the Nutley, N.J., plant where Valium and its predecessor, Librium, were developed, it’s a good time to remember how revolutionary these “minor tranquilizers” were half a century ago. These were the drugs that gave us a new way to slay our inner demons, medicating our way to a happier life.

How did Roche convince physicians that it was O.K. to offer their patients a bottled form of serenity? How did the physicians persuade their patients? And how did the company’s success in this venture shape our collective attitudes toward normal versus abnormal, stoic versus foolhardy, and the various ways available to cope with the ups and downs of daily life?

Marketing, essentially — which was first put into action with Librium, one of those evocative drug names that pharmaceutical companies invent. Librium was introduced in 1960 and promptly outsold its predecessors, the barbiturates, because it had fewer side effects. (Barbiturates were serious downers, making people sleepy and zombielike, and they were habit-forming; Marilyn Monroe died from an overdose.)

“A Whole New World … of Anxiety” read one of the early Roche ads for Librium, featuring a young woman with a pageboy hairdo holding an armload of books, wearing a short stadium coat and heading off to college. The copy made it sound as though every step in this “whole new world” called out for a tranquilizer. “The new college student may be afflicted by a sense of lost identity in a strange environment … Her newly stimulated intellectual curiosity may make her more sensitive to and apprehensive about unstable national and world conditions.”

The ad lists other sources of “anxiety” in a college student’s life — new friends, new influences, stiff competition for grades and tests of her moral fiber — that could just as easily be seen as growing pains, or as a healthy response to the turbulent world of the 1960s, when this ad appeared in The Journal of the American College Health Association. But Roche wanted doctors to believe that they were problems, not adventures, and that they warranted a prescription for Librium.

The next step was to develop something better — stronger, faster acting, less toxic. The Roche chemist who had originally stumbled upon Librium, Leo Sternbach, went back to the lab and tweaked the compound. Then he tested the drug on humans — in this case, the mothers-in-law of a few Roche executives. The executives thought that the new drug, Valium, rendered their mothers-in-law significantly less annoying.

In retrospect, Librium turned out to be a great first act, teaching Roche how to pitch a psychoactive drug to doctors of healthy patients who just needed a little something to unjangle their nerves. By the time Valium arrived, Roche was poised to dominate the field. In 1974, Americans filled nearly 60 million prescriptions for Valium.

Taking a pill to feel normal, even a pill sanctioned by the medical profession, led to a strange situation: it made people wonder what “normal” really was. What does it mean when people feel more like themselves with the drug than without it? Does the notion of “feeling like themselves” lose its meaning if they need a drug to get them there?

At the same time that Valium became famous for being in everyone’s medicine chest (or in every department store shopper’s purse), it also became famous for ruining lives. Elizabeth Taylor said she was addicted to Valium plus whiskey, Jack Daniel’s in particular. Tammy Faye Bakker said she was addicted to Valium plus nasal spray. Elvis Presley’s personal poison was Valium mixed with an assortment of other prescriptions. And Karen Ann Quinlan, the young woman languishing in a chronic vegetative state while her parents fought all the way to the New Jersey Supreme Court for the right to remove her from life support, originally lapsed into a coma in 1975 from a combination of Valium and gin.

Nearly 50 years after Valium was introduced and aggressively marketed, we’ve learned its lessons well. My generation of aging baby boomers does its brain styling, by and large, with antidepressantsProzac, Wellbutrin, CelexaPaxilZoloft. And for my daughters’ generation, the millennials, the pills of choice tend to be Ritalin and Adderall, for mental focus.

But when Americans are feeling out of sorts, we are still more likely to turn to anti-anxiety drugs than to any other kind. The leading successor to Valium, Xanax, outsells every other psychiatric drug on the market (48.7 million prescriptions last year). And even Valium is still out there, the classic little-black-dress of tranquilizers. In 2011, 14.7 million prescriptions were written for the drug that first made its cultural mark as a Rolling Stones song (“Mother’s Little Helper”) back in 1966.

As Roche closes its New Jersey headquarters, it plans to open a smaller research facility in Manhattan in late 2013, part of a wave that city officials hope will turn New York into a biotech mecca. The company’s transition reminds us of a phenomenon that’s become so common we no longer even think of it as weird: the oxymoronic attainment, through using drugs to make you feel more like yourself, of an artificially induced normal.

Robin Marantz Henig is a contributing writer for The New York Times Magazine and the co-author, with her daughter Samantha Henig, of the forthcoming “Twentysomething: Why Do Young Adults Seem Stuck?”

Retrieved from: http://www.nytimes.com/2012/09/30/sunday-review/valium-and-the-new-normal.html?ref=opinion&_r=0

Schools and ADHD…an “F” grade

In ADHD, ADHD Adult, ADHD child/adolescent, Education, School Psychology, Special Education on Thursday, 27 September 2012 at 07:25

How schools (even great ones) fail kids with ADHD

By Valerie Strauss

 There’s a group of students struggling through school rd to navigate that gets little attention in the media or in the debate about how to fix schools: Children with ADHD.

ADHD, or Attention Deficit Hyperactivity Disorder, is a brain condition that makes it especially hard for children to focus and concentrate in school and has a number ofother symptoms. It is too often misunderstood by teachers, parents and even the students themselves. According to the Centers for Disease Control, about 9.5% or 5.4 million children 4-17 years of age, had been diagnosed with ADHD, as of 2007. Many others who have the disorder haven’t had the benefit of a diagnosis.

Here is a powerful post by David Bernstein, a nonprofit executive who lives in Gaithersburg, Md., writing about the difficulties that his two sons, ages 7 and 15, have confronted in school as a result of ADHD.

By David Bernstein

When I was in fourth grade in the mid-1970s, my teacher pronounced that I was going to be an artist. The truth was that she didn’t think I had any academic talent to speak of. I was an “ADHD” boy who couldn’t follow directions, figure out what page we were on in the book, or turn my work in on time. With a severely limited understanding of the mind, the teacher simultaneously overestimated my artistic talent and underestimated my intellectual gifts.

School, particularly elementary school, was not for boys like me. And, 25 years later, even the very best schools have only changed slightly.
Like so many others who deviated from the norm, I learned much more from exploring my passions than I ever did from a structured school setting. With the help of numerous mentors, I taught myself how to write op-eds, lead teams, speak, and advocate. I actually cared about ideas, not primarily because of school, but despite it.  The Washington area, alive with political discourse, was the perfect place to give expression to my passions, and I moved here in my early twenties to take a job in the world of advocacy.

Now I have two boys of my own, neither of whom possesses a normative learning style. My teenage son goes to what is widely considered an excellent private school in the area with numerous wonderful, committed teachers. But like nearly every other educational institution in America, it’s built on an outmoded educational model.

Ironically, I first began to question the current model of education when the headmaster of my son’s school showed a video clip at a graduation ceremony of creativity guru Ken Robinson discussing how education kills creativity. Robinson maintains that we are using a model of education left over from the industrial revolution, where schools are organized along factory lines, complete with ringing bells and separate facilities.  “We educate kids in batches, as if the most important thing about them is their date of manufacture,” he states in another video on the topic.

Influenced by Robinson, best-selling author Seth Godin recently published a manifesto , “Stop Stealing Dreams,” on the need for radical education reform. He lays out the need for a post-industrial educational model that caters to diverse learning styles, passion for ideas and what individual students really care about. In such a school, teachers are coaches who help students in a journey of self-discovery. Students have a great deal of choice to determine what they study and how they study it, in stark contrast to the one-size-fits-all system of today.

Your child is right that he or she will never use trigonometry (unless so inclined). Exposing them to variety is one thing, but forcing the same subject for 13 years is another. In the modern marketplace, depth is just as important, if not more so, than breadth. Schools are all about breadth.

In today’s schools, the “good” students end up conforming, diminishing their own prospects for greatness, and the rest end up in an excruciating battle with themselves, their parents (trust me on this), their teachers and the endless tutors. My job as a parent, I’m reminded over and over again by the school, is to enforce the absurdity of the current system — make them turn everything in on time — which I do faithfully because there seems to be no other choice.

My youngest child, a rising second grader, rambunctious and restless as any you’ll find, has “fallen behind” in reading. He is “not sufficiently available for learning,” we are told. The teachers and guidance counselors, loving and well-meaning though they are, insist on ADHD meds so he can amp up his reading and catch up with his classmates. He’s a creative, bright, independent child, who will, there’s not a doubt in my mind, learn to read well and become highly successful. But he’s just not on their timetable for reading.

We are forced, in the words of Ken Robinson, to “anesthetize” him so he can function in today’s antiquated classroom setting. The Ritalin will do nothing to make him a more successful human being, a better thinker, or a more productive member of society. It will simply help him keep up with the masses and potentially drain him of some of his creative juices. By forcing him and so many other children like him to take thesepowerful drugs , schools deprive the future economy and society of precisely the creative talent they will need the most.

Greg Selkoe, the 36-year-old CEO of Karmaloop, a growing hipster media company with revenue of more than $130 Million a year, stated in a recent interview in Inc.: “I was diagnosed with ADHD in elementary school and actually got kicked out of several schools before landing in one for kids with learning issues. What made me not do well in school has actually been very beneficial in business, because I can focus on something very intensely for a short while and then move on to the next thing.”

Yet today’s schools insist that we prescribe our kids drugs to rid them of their hyper-focus.

I’ve talked with a number of educators, who see the writing on the wall for the current education system. They know that the economic reality of the day demands that schools change. But they also know that college-obsessed parents would balk at such changes, fearful that it might detract from their kids’ chances to go to the best college possible.
It will take monumental leadership to change the current educational mindset and model. In the meantime, my kids will struggle through school, battered along the way, and, like their father, be forced to discover most of their talents and passions on their own, outside of school.

Retrieved from: http://www.washingtonpost.com/blogs/answer-sheet/post/how-schools-even-great-ones-fail-kids-with-adhd/2012/09/23/8e81c83c-f828-11e1-8253-3f495ae70650_blog.html

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

First Direct Genetic Evidence for ADHD Discovered-2010

In ADHD, ADHD Adult, ADHD child/adolescent, Genes, Genomic Medicine, Neuropsychology, Psychiatry, School Psychology on Tuesday, 25 September 2012 at 06:20

an older article, but one i thought worthy of posting.

First Direct Genetic Evidence for ADHD Discovered

Caroline Cassels

September 29, 2010 — New research provides the first direct evidence that attention-deficit/hyperactivity disorder (ADHD) is genetic.

In a study published online September 30 in The Lancet, investigators from the University of Cardiff in the United Kingdom say their findings, which show that ADHD has a genetic basis, suggest it should be classified as a neurodevelopmental and not a behavioral disorder.

“We’ve known for many years that ADHD may well be genetic because it tends to run in families in many instances. What is really exciting now is that we’ve found the first direct genetic link to ADHD,” principal investigator Anita Thapar, MD, told reporters attending a press conference to unveil the study results.

In the genomewide analysis, 366 children 5 to 17 years of age who met diagnostic criteria for ADHD but not schizophrenia or autism and 1047 matched controls without the condition were included. Researchers found that compared with the control group without ADHD, children with the disorder were twice as likely — approximately 15% vs 7% — to have copy number variants (CNVs).

CNVs, explained study investigator Nigel M. Williams, PhD, are sections of the genome in which there are variations from the usual 2 copies of each chromosome, such that some individuals will carry just 1 (a deletion) and others will have 3 or more (duplications).

“If a gene is included in one of these copy number variants, it can have deleterious consequences,” said Dr. Williams.

Shared Biological Link

The study authors note that the increased rate of CNVs was particularly high among children with a combination of ADHD and learning disabilities but “there was also a significant excess in cases with no such disability.”

The researchers also found that CNVs overlap with chromosomal regions that have previously been linked to autism and schizophrenia. Although these disorders are thought to be completely separate, there is some overlap between ADHD and autism in terms of symptoms and learning difficulties.

We’ve looked at only 1 class of variation, but it’s an important one because it has been linked to other brain disorders.

This finding suggests there may be a shared biological basis for the 2 conditions and, according to investigators, provides the first direct evidence that ADHD is a neurodevelopmental condition.

“We found that the most significant excess of these types of copy number variants was on a specific region of chromosome 16. This chromosomal region includes a number of genes, including one that affects brain development,” said Dr. Thapar.

The team’s research marks the start of the “unraveling of the genetics” of ADHD, according to Dr. Thapar.

“We’ve looked at only 1 class of variation, but it’s an important one because it has been linked to other brain disorders,” she said.

Implications for DSM-5?

Dr. Thapar added that the study results also have direct implications for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), which is currently under development by the American Psychiatric Association.

A “huge debate” about whether ADHD should be classified as a behavioral or neurodevelopmental disorder is ongoing. However, she said, these findings should help put this controversy to rest.

“Our results clearly show that ADHD should be considered a neurodevelopmental disorder,” she said.

In fact, Dr. Thapar noted that the study findings have been submitted to one of the DSM-5 work groups for consideration in the development of the new manual.

The investigators note that despite epidemiologic evidence derived from twin studies showing high heritability and the fact that ADHD is often accompanied by learning disabilities, there is still a great deal of public misunderstanding about the disorder.

Some people say this is not a real disorder, that it is the result of bad parenting. Children and parents can encounter much stigma because of this. So this finding of a direct genetic link to ADHD should help clear this misunderstanding and help address the issue of stigma.

“Some people say this is not a real disorder, that it is the result of bad parenting. Children and parents can encounter much stigma because of this. So this finding of a direct genetic link to ADHD should help clear this misunderstanding and help address the issue of stigma,” said Dr. Thapar.

Although there are no immediate treatment implications, Dr. Thapar said she hopes the research will have an immediate impact in terms of shifting public perception about ADHD and fuel further research into the biological basis of the disorder with a view to developing better, more effective therapies for affected individuals.

In an accompanying editorial, Peter H. Burbach, PhD, from the Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, the Netherlands, writes, “The first gains beyond today’s study might be initial insights into the pathogenesis and neurobiology of brain development as influenced by these genetic variants. This knowledge will eventually enter the clinic and might affect the way people think about and treat neurodevelopmental disorders by accounting for the biological consequence of the specific patient’s genotype.”

Lancet. Published online September 30, 2010.

Retrieved from: http://www.medscape.com/viewarticle/729652

coming soon to a bookstore near you!

In ADHD, ADHD Adult, ADHD child/adolescent, Neuropsychology, School Psychology, Uncategorized on Monday, 24 September 2012 at 16:47

Psychometric Analysis of the New ADHD DSM-V Derived Symptoms

Ahmad Ghanizadeh

BMC Psychiatry. 2012;12(21) © 2012 BioMed Central, Ltd.

Abstract and Introduction

AbstractBackground Following the agreements on the reformulating and revising of ADHD diagnostic criteria, recently, the proposed revision for ADHD added 4 new symptoms to the hyperactivity and Impulsivity aspect in DSM-V. This study investigates the psychometric properties of the proposed ADHD diagnostic criteria.
Method ADHD diagnosis was made according to DSM-IV. The parents completed the screening test of ADHD checklist of Child Symptom Inventory-4 and the 4 items describing the new proposed symptoms in DSM-V.
Results The confirmatory factor analysis of the ADHD DSM-V derived items supports the loading of two factors including inattentiveness and hyperactivity/impulsivity. There is a sufficient reliability for the items. However, confirmatory factor analysis showed that the three-factor model is better fitted than the two-factor one. Moreover, the results of the exploratory analysis raised some concerns about the factor loading of the four new items.
Conclusions The current results support the two-factor model of the DSM-V ADHD diagnostic criteria including inattentiveness and hyperactivity/impulsivity. However, the four new items can be considered as a third factor.

Background

Attention-deficit/hyperactivity disorder (ADHD) is one of the most common behavioral disorders in children and adolescents. Its rate in community samples is variably reported. A study reported the rate of 5.29%.[1] Meanwhile, the rate of its screening symptoms is much higher, reaching up to 10.1% in school age children.[2] This high rate of ADHD prevalence emphasizes the need for accurate identification and diagnosis of ADHD.[3]

There has been a recent significant argument or controversy regarding the necessity of reformulating and revising ADHD criteria.[1,4,5] For example, recent criticism of the current ADHD subtypes and the suggestion of including age-specific ADHD criteria in DSM V should be considered.[6] In addition, the current ADHD subtypes are frequently criticized.[3] Some researchers are interested in introducing ADHD-inattentive type as a learning disorder.[7] Furthermore, there is a debate whether oppositional defiant disorder should be considered as a type of ADHD.[8,9] Girls with ADHD are underdiagnosed in the community.[6] Moreover, the impact of the change in the age of the onset has been investigated.[10]

Given that the proposed DSM-V criteria for ADHD are available and would be implemented in the near future,[11] it is advised that their psychometric properties and modifications be studied before their clinical application. To the best of the author’s knowledge, there are no published studies investigating the psychometric properties of the proposed ADHD diagnostic criteria for DSM-V.

DSM-IV defines ADHD as a cluster of symptoms; the patient must have at least six or more out of the 9 symptoms of inattention and/or six or more out of the 9 symptoms of hyperactivity/impulsivity.[12] The proposed revision of ADHD by American Psychiatric Association added 4 new symptoms to the Hyperactivity and Impulsivity aspect in DSM- V. These four symptoms are: “Tends to act without thinking, such as starting tasks without adequate preparation or avoiding reading or listening to instructions, may speak out without considering consequences or make important decisions on the spur of the moment, such as impulsively buying items, suddenly quitting a job, or breaking up with a friend”, “Is often impatient, as shown by feeling restless when waiting for others and wanting to move faster than others, wanting people to get to the point, speeding while driving, and cutting into traffic to go faster than others”, “Is uncomfortable doing things slowly and systematically and often rushes through activities or tasks”, and “Finds it difficult to resist temptations or opportunities, even if it means taking risks (A child may grab toys off a store shelf or play with dangerous objects; adults may commit to a relationship after only a brief acquaintance or take a job or enter into a business arrangement without doing due diligence)”.[11]

The aim of this study was to investigate the psychometric properties of the proposed ADHD symptoms in DSM-V. In the first step, factor analyses were conducted to assess the loadings for the symptoms. Then, the convergent and discriminative validity of the categories of inattentiveness and hyperactivity-impulsivity of DSM-V ADHD symptoms were assessed. Finally, the internal reliability of the inattentiveness and hyperactivity- impulsivity was calculated.

Methods

106 children, who were consecutive referrals to a university affiliated Child and Adolescent Psychiatry Clinic in Shiraz, Iran, participated in this study. All of the children and adolescents were interviewed face to face by a board certified Child and Adolescent psychiatrist. In addition, at least one of their parents or caregivers was interviewed face to face as a collateral information resource.

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, DSM-IV diagnostic criteria was used to make psychiatric diagnoses.[12] Interviews were conducted according to the Farsi version of the Schedule for Affective Disorders and Schizophrenia for School-Age Children.[13]

Parents reported ADHD symptoms by completing the ADHD checklist of child symptom inventory-4.[14–16] The ADHD checklist of child symptom inventory-4 includes 18 symptoms. The symptoms are categorized into two groups of inattentiveness and hyperactive/impulsivity symptoms. The inattentiveness symptoms category consists of 9 symptoms according to DSM-IV. The category of hyperactive/impulsivity symptoms consists of 9 symptoms according to DSM-IV as well. In fact, the symptoms are the DSM-IV diagnostic criteria. There is a 5-point Likert response scale for the symptoms. The responses ranged from “never,” “sometimes,” “often,” to “almost always”. Scores 0 and 1 were assigned to the categories of “never” and “sometimes”, respectively. The categories of “often” and “almost always” were assigned to 2 and 3, respectively. The range of scoring for each of inattentiveness and hyperactivity-impulsivity categories was from 0 to 9. The Farsi version of this checklist has enough reliability, convergent and discrimination validity[15] and has been used in many studies.[17–19] The internal reliability of this checklist for ADHD-inattentive type, ADHD-Hyperactive impulsive type, and combined type of ADHD is 0.81, 0.85, and 0.83, respectively.[14]

The four new items proposed by DSM-V to be added to ADHD diagnostic criteria were translated into Farsi and back translated into English by a bilingual child and adolescent psychiatrist and a psychologist. Every effort was made to preserve the concept of each symptom. After a pilot study on children referred to the clinic, the final version was used in the current study. The responses to these symptoms were in the Likert scale ranging from “never,” “sometimes,” “often,” to “almost always”.

The children and parents or caregivers gave their assent or informed written consent for voluntary participation in this study. This study was approved by the Ethics Committee of Shiraz University of Medical Sciences.

Analysis

SPSS statistical software was used to analyze the data. A factor analysis with varimax rotation was conducted to examine the factor structure of the ADHD DSM-V symptoms. The Kaiser-Meyer-Olkin Measure and the Bartlett’s test of sphericity were conducted. Internal consistency was examined using Cronbach’s tests.

One-, two-, three-factor models of confirmatory factor analysis were also conducted using LISREL 8.54 software. The convergent and discriminative validity of ADHD symptoms were analyzed using Pearson’s r correlation coefficient.

Another factor analysis was also conducted including the four newly proposed symptoms to examine item loading of the 13 symptoms of DSM-V derived hyperactivity- impulsivity symptoms. Here, the symptoms of inattentiveness were not included in the analysis. This analysis was conducted to examine whether the 13 items could be divided into two categories of hyperactivity and impulsivity.

Another factor analysis was conducted including the DSM-IV derived inattentiveness symptoms and the four new symptoms proposed in DSM-V. The symptoms of hyperactivity-impulsivity of DSM-IV were not included.

Results

The sample included 84 (79.2%) boys and 22 (20.8%) girls. The age range of the children and adolescents was 5.5 to 17years. Their mean age was 9.1(SD = 2.5) years.

The Kaiser-Meyer-Olkin Measure was 0.76. It shows the adequacy of sampling. The Bartlett’s test of sphericity was less than 0.001. These results indicate that the data are suitable for factor analysis. The factor loading of the principal component analysis is indicated in Table 1. The factor of Hyperactivity-Impulsivity explained 30.4% (eigenvalue = 6.7) of the total variance. The factor of Inattentiveness accounted for 12.1% (eigenvalue = 2.6). Nearly all of the symptoms of inattentiveness were loaded in one factor. All of the Hyperactivity-Impulsivity symptoms were loaded on another factor. Three out of the four newly proposed ADHD separate symptoms were loaded on the factor including inattentiveness symptoms.

[ CLOSE WINDOW ]

Table 1. Principal component analysis of the ADHD DSM-V checklist by rotated method of varimax

Component DSM-V symptoms Hyperactivity- Impulsivity
Inattentiveness
ADHD- item 1- makes careless mistakes −.049 .600
ADHD- item 2- sustaining attention .032 .731
ADHD- item 3- listening when spoken to .323 .319
ADHD- item 4- follows instructions .354 .515
ADHD- Item 5- organizing tasks .164 .775
ADHD-Item 6 – sustained mental effort −.097 .784
ADHD- item 7- loses things .185 .527
ADHD- item 8- distracted by extraneous stimuli .223 .536
ADHD- item 9- forgetful in daily activities .157 .486
ADHD- item10- fidgets with hands .532 .227
ADHD- item11- leaves seat in classroom .657 .206
ADHD- item 12- runs about .638 .178
ADHD- item 13- playing or leisure activities .864 −.013
ADHD- item 14- often “on the go” .800 −.008
ADHD- item 15- talks excessively .726 .152
ADHD- item 16- blurts out answers .663 .134
ADHD- item 17- awaiting turn .625 .335
ADHD- item 18- interrupts or intrudes on others .713 .086
ADHD- item 19- act without thinking .272 .412
ADHD- item 20- impatient .431 .330
ADHD- item 21- uncomfortable doing things slowly and systematically .358 .430
ADHD- item 22- difficult to resist temptations or opportunities .236 .399

Extraction Method: Principal Component Analysis. Rotation Method: Varimax with Kaiser Normalization.

In order to test which of the various models gives the best fit to the data, three confirmatory factor analyses were conducted. A one-factor model was not a good fit (Chi- square = 384.65, df = 209, P value 0.0001, Root Mean Square Error of Approximation (RMSEA) = 0.098, Non-normed Fit index (NNFI) = 0.96, Comparative Fit index = 0.96.).

A two-factor model fit well. The results of two-factor model confirmatory factor analysis showing the correlation between inattentiveness and hyperactivity/impulsivity factors that was .56 are displayed in Table 2.

Table 2. The two-factor model of Confirmatory Factor Analysis of the ADHD DSM- V Checklist

Component DSM-V symptoms Hyperactivity- Impulsivity
Inattentiveness
ADHD- item 1- makes careless mistakes .49
ADHD- item 2- sustaining attention .71
ADHD- item 3- listening when spoken to .53
ADHD- item 4- follows instructions .73
ADHD- Item 5- organizing tasks .81
ADHD-Item 6 – sustained mental effort .66
ADHD- item 7- loses things .57
ADHD- item 8- distracted by extraneous stimuli .63
ADHD- item 9- forgetful in daily activities .56
ADHD- item10- fidgets with hands .64
ADHD- item11- leaves seat in classroom .72
ADHD- item 12- runs about .71
ADHD- item 13- playing or leisure activities .84
ADHD- item 14- often “on the go” .81
ADHD- item 15- talks excessively .76
ADHD- item 16- blurts out answers .69
ADHD- item 17- awaiting turn .76
ADHD- item 18- interrupts or intrudes on others .72
ADHD- item 19- act without thinking .49
ADHD- item 20- impatient .62
ADHD- item 21- uncomfortable doing things slowly and systematically .58
ADHD- item 22- difficult to resist temptations or opportunities .51

Chi-square = 384.65, df = 209, P valu < 0.0001, Root Mean Square Error of Approximation (RMSEA) = 0.098, Non-normed Fit index (NNFI) = 0.96, Comparative Fit index = 0.96.

However, a three-factor model of confirmatory factor analysis also fit well and it was better than the two-factor model (Table 3).

Table 3. The three-factor model of Confirmatory Factor Analysis of the ADHD DSM-V Checklist

Component Newly DSM-V symptoms Hyperactivity- Impulsivity
Inattentiveness added items
ADHD- item 1- makes careless mistakes .49
ADHD- item 2- sustaining attention .71
ADHD- item 3- listening when spoken to .52
ADHD- item 4- follows instructions .72
ADHD- Item 5- organizing tasks .82
ADHD-Item 6 – sustained mental effort .67
ADHD- item 7- loses things .57
ADHD- item 8- distracted by extraneous stimuli .63
ADHD- item 9- forgetful in daily activities .56
ADHD- item10- fidgets with hands .65
ADHD- item11- leaves seat in classroom .74
ADHD- item 12- runs about .73
ADHD- item 13- playing or leisure activities .86
ADHD- item 14- often “on the go” .83
ADHD- item 15- talks excessively .78
ADHD- item 16- blurts out answers .71
ADHD- item 17- awaiting turn .78
ADHD- item 18- interrupts or intrudes on others .74
ADHD- item 19- act without thinking .63
ADHD- item 20- impatient .80
ADHD- item 21- uncomfortable doing things slowly and systematically .78
ADHD- item 22- difficult to resist temptations or opportunities .66

Chi-square = 31.84, df = 206, P valu < 0.0001, Root Mean Square Error of Approximation (RMSEA) = 0.077, Non-normed Fit index (NNFI) = 0.99, Comparative Fit index = 0.99.

The factor loading of the second component analysis including only the symptoms of hyperactivity-impulsivity of DSM-V is displayed in Table 4. The Kaiser-Meyer-Olkin Measure was 0.83. Bartlett’s test of sphericity was less than 0.001. It shows that all of the symptoms of the ADHD DSM-IV derived are loaded in one factor. Meanwhile, the four new symptoms proposed in DSM-V are loaded in another factor.

Table 4. Principal components analysis of the hyperactivity-impulsivity symptoms of ADHD DSM-V Checklist

Hyperactivity-impulsivity symptoms
Component
1 2
ADHD- item10- fidgets with hands .566 .123
ADHD- item11- leaves seat in classroom .666 .214
ADHD- item 12- runs about .629 .225
ADHD- item 13- playing or leisure activities .834 .111
ADHD- item 14- often “on the go” .771 .157
ADHD- item 15- talks excessively .753 .154
ADHD- item 16- blurts out answers .682 .112
ADHD- item 17- awaiting turn .574 .396
ADHD- item 18- interrupts or intrudes on others .717 .132
ADHD- item 19- act without thinking .207 .496
ADHD- item 20- impatient .208 .794
ADHD- item 21- uncomfortable doing things slowly and systematically .187 .755
ADHD- item 22- difficult to resist temptations or opportunities .022 .781

Extraction Method: Principal Component Analysis. Rotation Method: Varimax with Kaiser Normalization.

The principal component analysis including the DSM-IV derived inattentiveness symptoms and the four new symptoms proposed in DSM-V indicated the two factor loading (Table 5). This analysis indicates that all of the inattentiveness symptoms are loaded in one factor and the new symptoms proposed in DSM-V are loaded in another factor.

Table 5. Principal component analysis including the DSM-IV derived inattentiveness symptoms and the four new symptoms proposed in DSM-V

Inattentiveness symptom of DSM-IV and new proposed symptoms in DSM-V
Component
1 2
ADHD- item 1- makes careless mistakes .676 −.045
ADHD- item 2- sustaining attention .780 .079
ADHD- item 3- listening when spoken to .486 .122
ADHD- item 4- follows instructions .551 .322
ADHD- Item 5- organizing tasks .686 .386
ADHD-Item 6 – sustained mental effort .667 .192
ADHD- item 7- loses things .414 .341
ADHD- item 8- distracted by extraneous stimuli .450 .367
ADHD- item 9- forgetful in daily activities .579 .057
ADHD- item 19- act without thinking .275 .565
ADHD- item 20- impatient .069 .785
ADHD- item 21- uncomfortable doing things slowly and systematically .136 .793
ADHD- item 22- difficult to resist temptations or opportunities .058 .750

Extraction Method: Principal Component Analysis. Rotation Method: Varimax with Kaiser Normalization.

The convergent and discriminative validity for the whole 22 symptoms proposed for ADHD in DSM-V were calculated. The range of convergent validity for the symptoms of inattentiveness was from 0.504 to 0.772 and that of discriminative validity for the symptoms of inattentiveness was from 0.017 to 0.427. Also, the range of convergent validity for the symptoms of hyperactivity-impulsivity was from 0.42 to 0.770 and that of discriminative validity for the symptoms of hyperactivity-impulsivity was from 0.12 to 0.39.

The alpha coefficient for the whole 24 symptoms of ADHD in DSM-V was 0.88. The alpha for the DSM-V hyperactivity-impulsivity was 0.87. It was 0.80 for DSM-IV inattention.

Discussion

To the best of the author’s knowledge, this is the first study investigating psychometric and factor structure of ADHD DSM-V derived symptoms. So, it is not possible to compare the current results with those of other studies. Confirmatory factor analysis confirmed the proposed two-factor loading of inattentiveness and hyperactivity/impulsivity for the new ADHD DSM-V criteria. However, the three-factor model of confirmatory factor analysis showed that the four new items can be considered as the third factor.

The results indicate that convergent and discriminative validity for ADHD DSM-V derived inattention symptoms are sufficient. Although the symptoms of hyperactivity- impulsivity are discriminated from inattentiveness symptoms, the convergent validity of the four newly proposed symptoms in DSM-V is not as high as that of the 9 symptoms derived from DSM-IV. The three new criteria for hyperactivity/impulsivity were loaded in inattentiveness factor rather than in hyperactivity-impulsivity factor. These may not support the fact that the 4 proposed symptoms for revision of ADHD exactly describe hyperactivity-impulsivity symptoms. However, the internal consistency and reliability of the inattentiveness and hyperactive/impulsivity symptoms are high.\

Considering the factor loading of the four newly proposed symptoms added to DSM-V, there is a concern that inattentiveness symptoms may falsely increase the diagnosis of ADHD-hyperactive/impulsive type or combined type of ADHD. It means that the symptoms which are loaded as inattentive symptoms may lead to subthreshold ADHD- hyperactive/impulsive type using DSM-IV, while fulfilling criteria of ADHD- hyperactive/impulsive type using DSM-V.

With respect to the fact that the better diagnoses and classification of children with ADHD could lead to a better treatment, more discussion and justification about the new items are required. Probably, future studies should investigate the neuropsychological functioning of children with ADHD for the classification of the subtypes of ADHD. The current results indicated that continued research is required to reach accurate diagnostic criteria for making accurate ADHD diagnoses.

There is some overlap between ADHD symptoms and ODD in DSM-IV.[20] ODD symptoms are properly differentiated from ADHD. However, two items of the ADHD including “Often has trouble organizing activities” and “Often runs about or climbs when and where it is not appropriate” are loaded in the oppositional defiant disorder component rather than ADHD component.[20] Another concern is whether the new added symptoms in DSM-V are well differentiated from ODD symptoms. This needs further studies.

There are some limitations in this study which need to be considered. This study was conducted on a clinical sample of children and adolescents with ADHD. Further studies with larger sample size including community sample with a wider age rage are recommended. The children and their parents were the sources of information. Including other informants such as teachers is also recommended. This study is based on one sample in a specific geographical area. In addition, the use of translation instead of the actual questionnaire is another limitation. A multi-site approach with a more limited age range would be required to appropriately assess the psychometric properties of the proposed items of a classification used worldwide.

Despite the above-mentioned limitations, this is the first study that assesses psychometric properties of ADHD DSM-V derived symptoms. In addition, the children, adolescents and parents were interviewed face to face using a well known semi- structured interview. Moreover, all the interviews were conducted by a Board-certified child and adolescent psychiatrist.

Conclusion

The findings of present study support the two-factor model of the DSM-V ADHD diagnostic criteria including inattentiveness and hyperactivity/impulsivity. Nevertheless, the four new items can be considered as a third factor.

References

  1. Rohde LA: Is there a need to reformulate attention deficit hyperactivity disorder criteria in future nosologic classifications? Child Adolesc Psychiatr Clin N Am 2008, 17(2):405–420.
  2. Ghanizadeh A: Distribution of symptoms of attention deficit-hyperactivity disorder in schoolchildren of Shiraz, south of Iran. Arch Iran Med 2008, 11(6):618–624.
  3. Bell AS: A Critical Review of ADHD Diagnostic Criteria: What to Address in the DSM-V. J AttenDisord 2010.
  4. Ghanizadeh A: Is it time to revise the definition of attention deficit hyperactivity disorder? Ann Acad Med Singapore 2010, 39(2):155–156.
  5. Swanson JM, Wigal T, Lakes K: DSM-V and the future diagnosis of attention- deficit/hyperactivity disorder. Curr Psychiatry Rep 2009, 11(5):399–406.
  6. Ramtekkar UP, Reiersen AM, Todorov AA, Todd RD: Sex and age differences in attention- deficit/hyperactivity disorder symptoms and diagnoses: implications for DSM-V and ICD-11. J Am Acad Child Adolesc Psychiatry 2010, 49(3):217–228. e211–213
  7. Milich R, Balentine AC, Lynam DR: ADHD combined type and ADHD predominantly inattentive type are distinct and unrelated disorder. Clinical Psychology: Science and Practice 2001, 8:463–488.
  8. Poulton AS: Time to redefine the diagnosis of oppositional defiant disorder. J Paediatr Child Health 2010.
  9. Ghanizadeh A: Should ADHD broaden diagnostic classification to include oppositional defiant disorder? Journal of Paediatrics and Child Health 2011, 47(6):396–397.
  10. Polanczyk G, Caspi A, Houts R, Kollins SH, Rohde LA, Moffitt TE: Implications of extending the ADHD age-of-onset criterion to age 12: results from a prospectively studied birth cohort. J Am Acad Child Adolesc Psychiatry 2010, 49(3):210–216.
  11. DSM-5 development [http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=383]
  12. American Psychiatric Association. Diagnostic and statistical manual of mental disorders Fourth edition. Washington, DC: American Psychiatric Association; 1994.
  13. Ghanizadeh A, Mohammadi MR, Yazdanshenas A: Psychometric properties of the Farsi translation of the Kiddie Schedule for Affective Disorders and Schizophrenia-Present and Lifetime Version. BMC Psychiatry 2006, 6:10.
  14. Ghanizadeh A, Jafari P: Cultural structures of the Persian parents’ ratings of ADHD. J Atten Disord 2010, 13(4):369–373.
  15. Alipour A, Esmaile EM (Eds): Studying of Validity, Reliability, and Cutoff points of CSI-14 in the School Children Aged 6 to 14 in Tehran In Tehran Exceptional students’ Research Center 2004.
  16. Sprafkin J, Gadow KD, Salisbury H, Schneider J, Loney J: Further evidence of reliability and validity of the Child Symptom Inventory-4: parent checklist in clinically referred boys. J Clin Child Adolesc Psychol 2002, 31(4):513–524.
  17. Ghanizadeh A, Mohammadi MR, Moini R: Comorbidity of psychiatric disorders and parental psychiatric disorders in a sample of Iranian children with ADHD. J Atten Disord 2008, 12(2):149–155.
  18. Ghanizadeh A: Psychiatric comorbidity differences in clinic-referred children and adolescents with ADHD according to the subtypes and gender. J Child Neurol 2009, 24(6):679–684.
  19. Ghanizadeh A, Khajavian S, Ashkani H: Prevalence of psychiatric disorders, depression, and suicidal behavior in child and adolescent with thalassemia major. J Pediatr Hematol Oncol 2006, 28(12):781–784.
  20. Ghanizadeh A: Overlap of ADHD and oppositional defiant disorder DSM-IV derived criteria. Arch Iran Med 2011, 14(3):179–182.

Retrieved from: http://www.medscape.com/viewarticle/764516

Perinatal Risk Factors for ADHD Confirmed

In ADHD, ADHD Adult, Psychiatry, School Psychology on Monday, 24 September 2012 at 16:06

important info!

Perinatal Risk Factors for ADHD Confirmed

Megan Brooks

September 13, 2012 — The combination of maternal gestational diabetes mellitus (GDM) and low socioeconomic status (SES) is a strong risk factor for childhood attention-deficit/hyperactivity disorder (ADHD), a study from Germany confirms.

Perinatal health problems, maternal smoking during pregnancy, and atopic eczema also raise the risk for ADHD, whereas fully breastfeeding appears to protect against ADHD, regardless of the duration of breastfeeding, the study showed.

“Modification of these environmental risk factors by evidence-based prevention programs may help to decrease the burden of ADHD,” write coinvestigators Jochen Schmitt, MD, MPH, of Technical University Dresden, and Marcel Romanos, MD, from the University Hospital of Würzburg, in Germany.

The study was published online September 10 in Archives of Pediatrics and Adolescent Medicine.

It follows a study published in the same journal earlier this year by Yoko Nomura, PhD, MPH, from the Department of Psychology, Queens College, City University of New York, and colleagues. That study, which included 212 preschool-age children, linked maternal GDM and low SES, especially in combination, to a heightened risk for childhood ADHD.

Nationwide Study

These latest findings from Dr. Schmitt and Dr. Romanos replicate this finding in a large nationwide representative sample of 3- to 17-year-olds who participated in the German Health Interview and Examination Survey for Children and Adolescents (n = 13,488).

The outcome of interest was childhood ADHD, and the primary exposures of interest were self-reported physician-diagnosed GDM (absent or present) and SES, classified as low, medium, or high on the basis of parental education, professional qualification, professional status, and family income.

The authors also considered age, sex, and a broad set of environmental exposures in the prenatal and perinatal period and in infancy as competing risk factors in multivariate analysis.

A total of 660 children (4.9%) had ADHD; the prevalence of GDM and low SES was 2.3% (n = 280) and 25.5% (n = 3420), respectively, the authors report.

Both maternal GDM and low SES were significantly related to ADHD. In multivariate regression modeling (based on 11,222 observations without any missing data), GDM and low SES were independent risk factors for childhood ADHD. The same was true for perinatal health problems, maternal smoking during pregnancy, and atopic eczema, whereas breastfeeding was protective.

Table: Risk for ADHD With Outcomes of Interest

Characteristic/Exposure aOR (95% CI)
Maternal GDM 1.91 (1.21 – 3.01)
Low SES 2.04 (1.56 – 2.68)
Smoking 1.48 (1.19 – 1.84)
Perinatal health problems 1.69 (1.40 – 2.03)
Atopic eczema 1.62 (1.30 – 2.02)
Breastfeeding 0.83 (0.69 – 0.996)

aOR = adjusted odds ratio; CI = confidence interval

The investigators note that their findings confirm those of Dr. Nomura and colleagues by showing an association between low SES, maternal GDM, and ADHD “and their additive interaction as risk factors for ADHD in a large population-based sample.”

The researchers say their study also extends previous research by showing that fully breastfeeding may have protective effects on childhood ADHD.

Fetus a “Captive Audience”

Dr. Nomura told Medscape Medical News that “being able to duplicate our findings in a different sample and a much larger sample is important.”

“I’m not sure if most doctors know that GDM is a risk factor for ADHD; biological and environmental risk factors for ADHD is a fairly new scientific field,” she added.

“ADHD is a highly hereditary illness, but it’s not only hereditary; we are beginning to gather information about environmental or biological causes and beginning to focus on perinatal risk factors for ADHD,” said Dr. Nomura.

“The fetus is a captive audience,” she noted, “and it seems like in utero exposure to a variety of things like excessive insulin, smoking, plastic materials, food dyes, toxic chemicals may cause epigenetic changes in brain development that may show up later in life.”

Arch Pediatr Adolesc Med. Published online September 10, 2012. Abstract

 

Tailoring Antidepressant Treatment

In ADHD, ADHD Adult, ADHD child/adolescent, Anxiety, Medication, Psychiatry, Psychopharmacology on Monday, 24 September 2012 at 07:13

Tailoring Antidepressant Treatment: Factors to Individualize Medication Selection Thomas L. Schwartz, MD; Daniel Uderitz, MD

In the realm of psychopharmacology, we often declare medications within their respective therapeutic classes as being equal. This is a byproduct related to the way medications achieve their indications for treatment for specific psychiatric disorders. In the case of antidepressant treatments, the US Food and Drug Administration (FDA) indicates that if a study can obtain a majority of patients improved by 50% compared with placebo, then a drug may become an antidepressant treatment. There are no standards for differentiating antidepressant treatments beyond this. Clinicians often note that all antidepressant treatments are not created equal, especially when applied to clinical situations and patients who are often complex and have comorbid conditions. The goal of this article is to sort out regimens that may convey certain advantages during the treatment in an individualized manner. This involves conceptualizing and utilizing monotherapies, combination therapies, and adjunctive treatments.

Monotherapies

The first-line treatment of patients with major depressive disorder (MDD) should start with an aggressive monotherapy. This occurs in clinical practice and is supported by many guidelines and reviews. The various antidepressant medications have unique properties that can be used to individualize treatments. Most psychiatrists can easily name their “favorite” antidepressant to use in certain situations. This is sometimes based on a simple bias, but often has evidence to back up clinical practice. Let us start with the mechanistically simple and move toward more complex ways to think about these medications. This includes thinking about FDA approvals, available guidelines, comorbidities, side effects, and more complex pharmacodynamic receptor-based neuropsychiatry.

A patient rarely comes to a psychiatrist without having a combination of psychiatric symptoms. Typically, clinicians screen patients and find that they often meet criteria for more than 1 Diagnostic and Statistical Manual of Mental Disorders Fourth Edition-Text Revision (DSM IV-TR) criteria.[1] At a minimum, the individual patient raises suspicion for various problem areas, even if they do not meet criteria for a specific disorder. In reviewing FDA guidelines, clinicians may quickly make simple decisions regarding treatment regimens that are more individualized based on these comorbidities and predominant symptoms. Of note, additional FDA approval or lack of approval for various indications does not necessarily mean that evidence does not support efficacy for other disorders. For example, the manufacturer may not have pursued FDA approval for other indications, or may have decided not to support randomized controlled trials to study another indication.

Single Indication

The first group of antidepressants approved by the FDA for the single indication of MDD include amitriptyline, citalopram, desipramine, desvenlafaxine, mirtazipine, nortriptyline, protriptyline, trazodone, trimipramine, vilazodone, and the monoamine oxidase inhibitor (MAOI) class.[2-4] Clinicians should know that these medications have only the 1 indication, and this clearly supports their use in MDD. However, many practitioners recognize that there are multiple other factors that allow these medications to be used in an off-label manner for various individuals. In a pure model, these antidepressants have regulatory data suggesting use only in patients with MDD but, as discussed, a lack of approval for other indications does not necessarily indicate a lack of supportive data or lack of efficacy.

Multiple Indications

Unlike those listed above, many antidepressants have other labeled or approved indications. These span a variety of comorbidities including anxiety disorders, seasonal affective disorder, sleep disorders, pain disorders, premenstrual dysphoric disorder, bulimia nervosa, and other miscellaneous indications. Given this, and assuming MDD is often complicated by comorbidity, let us evaluate a few comorbidities where data-driven decisions may help in individualizing treatments in patients who are depressed and simultaneously experience other psychiatric conditions.

Posttraumatic Stress Disorder

Patients with posttraumatic stress disorder often have comorbid depression. Only 2 antidepressants, the selective serotonin reuptake inhibitors (SSRI) sertraline and paroxetine, are approved for this indication.[2] Multiple other medications have been recognized as effective off-label treatments for posttraumatic stress disorder, however; these include amitriptyline, fluoxetine, fluvoxamine, imipramine, and venlafaxine.[5-7] If a patient presents with MDD and posttraumatic stress disorder, these antidepressants may be considered if necessary to achieve efficacy for both conditions.

Obsessive-Compulsive Disorder

Several medications are approved for obsessive-compulsive disorder, including the tricyclic antidepressant clomipramine, and the SSRIs fluoxetine, fluvoxamine, paroxetine, and sertraline.[2] Venlafaxine, a serotonin norepinephrine reuptake inhibitor (SNRI),[8] and the SSRI citalopram have shown some promise in obsessive compulsive disorder,[9] but have not yet received that indication from the FDA.

Panic Disorder

The SSRIs fluoxetine, paroxetine, and sertraline are approved for treatment of panic disorder, as is the SNRI venlafaxine.[2,10] Other antidepressants with an evidence base for use that are not approved include the TCAs clomipramine and imipramine, and the SSRI fluvoxamine.[6]

Anxiety Disorders

Social anxiety disorder. The SSRIs paroxetine and sertraline, and the SNRI, venlafaxine extended-release (ER) have been approved for the treatment of social anxiety disorder.[2] The SSRI fluoxetine is sometimes used for treatment of social anxiety disorder.

Generalized anxiety disorder. Four antidepressants have been indicated for the treatment of generalized anxiety disorder. These include the SSRI escitalopram and paroxetine, and the SNRI duloxetine and venlafaxine ER.[2,11]

Insomnia

Although sleep difficulties are a nearly universal symptom of depression, few antidepressants have an official indication for insomnia. Doxepin, a TCA, is the sole antidepressant labeled with this indication, when it is used at subtherapeutic antidepressant doses of 3 to 6 mg per day.[12] However, clinicians often use sedating antidepressants to induce sleep in those patients with MDD and insomnia (Schwartz TL. Novel hypnotics: moving beyond positive allosteric modulation of the GABA-A receptor. Manuscript submitted). These medications include the TCA amitriptyline, the tetracyclic mirtazapine, and the serotonin modulator trazodone.

Pain Syndromes

Duloxetine, an SNRI, is the only antidepressant medication that has official indications for treatment of pain syndromes.[2,10] These include chronic musculoskeletal pain, neuropathic pain (diabetic neuropathy in particular), and fibromyalgia. Alternatively, many of the TCAs, as well as other SNRI, have been studied for the treatment of pain syndromes, primarily involving neuropathic or chronic pain conditions.[13,14] Amitriptyline also is often used for migraine headaches. Unfortunately these other medications have not received official indications for these psychosomatic comorbidities.

Attention-Deficit/Hyperactivity Disorder

Some antidepressants have shown promise for the treatment of attention-deficit/hyperactivity disorder, but not enough to warrant a specific FDA indication. Nonetheless, these medications are used for the treatment of attention-deficit/hyperactivity disorder, particularly in patients with substance use disorder. Bupropion, desipramine, imipramine, nortriptyline, and venlafaxine have some evidence base to support their use.[15-19]

Other Comorbid Considerations

Premenstrual dysphoric disorder. The SSRI fluoxetine, paroxetine, and sertraline have been FDA approved for the treatment of premenstrual dysphoric disorder.[2]

Smoking cessation. Many patients who receive mental health treatment are also addicted to nicotine. Bupropion SR has received the indication for nicotine addiction.[2] Nortriptyline also has been shown to be helpful for smoking cessation efforts, but has not received an official indication.[20]

Miscellaneous. Bupropion XL carries a specific indication for prophylaxis of seasonal affective disorder and often is used off-label for the treatment of bipolar depression.[19,21,22] Fluoxetine is indicated for treatment of bulimia nervosa and sometimes is used for the treatment of Raynaud’ phenomenon.[2,19,23] Venlafaxine and paroxetine have data supporting use for the treatment of vasomotor hot flashes.[24,25] Finally, imipramine may be used in the treatment of enuresis.[26]

Take-Home Point

Clinicians should be aware of FDA approvals and the evidence base supporting the use of antidepressants in patients with MDD, who are often complex and suffering with other medical and psychiatric comorbidities. Choosing agents with indications that match the patient’s comorbid symptoms is one way to tailor and individualize treatment to each patient.

Beyond the simplistic but labor-intensive role of delineating specific comorbidities and focusing on antidepressant indications, is the imperative to develop a more complex individualized antidepressant treatment plan. If it were as simple as following the FDA labels and simple algorithms to make decisions, then much psychiatric education could be eliminated. A review of antidepressant mechanisms of action will allow us to further distinguish these medications, thus allowing more individualized treatments for MDD.

SSRI Class

The first and most commonly prescribed class of antidepressant is the SSRI. At the most basic understanding, these medications increase serotonin in the synapse and function ultimately to down-regulate serotonin receptors. However, as the science behind these medications is further explored, there is much more to these agents. When looking at the SSRI class as a whole, and in comparison with other antidepressant classes, a few general characteristics can be considered. The SSRI medications as a group are thought of as having fewer side effects than most other classes of antidepressants, and particularly the older classes of drugs. The most common and clinically relevant consideration for these medications is the development of gastrointestinal upset, sexual side effects, and weight gain.[27] The following delineates some of the subtle differences for each medication in this class and describes the benefits and drawbacks of treatment with each to help refine treatment selection.

Citalopram. Citalopram is one of the most widely used antidepressants today, and has a few properties that make it desirable. The medication has a long half-life of 23-45 hours, second only to fluoxetine,[2] and it is typically well tolerated in medically ill patients and the elderly.[19,28] Citalopram has weak H1 receptor antihistamine properties, and these properties provide anxiolytic and positively sedating effects.[27] Citalopram is made up of 2 mirror image enantiomers, each of which have different properties [27] that may lead to some inconsistencies in the property or function of the medication at lower doses. Citalopram is a weak inhibitor of CYP 2D6, with minimal drug-drug interactions.[30] Finally, recent FDA warnings have changed prescribing practices of this medication because of potential QTc prolongation at daily doses higher than 40 mg[29]; daily doses of 60 mg should no longer be used.

Benefits.Citalopram is a well-tolerated medication with mild antihistamine effects that may help with insomnia or mild anxieties. The longer half-life results in less withdrawal or discontinuation side effects.[31]

Drawbacks.Structural enantiomers result in this medication having less predictable effects at lower doses, and higher doses are contrary to FDA recommendations related to the potential for QTc prolongation. It has fewer FDA approvals for comorbid psychiatric disorders than other drugs in the SSRI class; as discussed earlier, this may simply reflect the manufacturer’s failure to seek approval for other indications.

Escitalopram. In contrast to the parent drug citalopram, escitalopram is separated and includes only the left enantiomer.[27] This results in the removal of much of the antihistamine and CYP 2D6 inhibitory properties.[19,27] It also results in more effective and predictable dose responses of the medication at the lower doses.

Benefits.Escitalopram has the benefit of better tolerability with less drug interactions. It may have less sedating effects, and is approved for generalized anxiety disorder as well as MDD.[2]

Drawbacks.Currently this is the only SSRI still on patent, and is thus more expensive than other, generic SSRI.

Fluoxetine. The first member of the SSRI class, fluoxetine has a few characteristics that make it desirable. Fluoxetine has mild serotonin 2C receptor antagonistic actions. This may result in the disinhibition of dopamine and norepinephrine release to the prefrontal cortex, which likely helps to improve concentration, energy, and executive functioning.[19,27] Furthermore, the serotonin 2C effects of this medication may contribute to the initial anorexic and ongoing anti-bulimic effects of this medication.[27] More recently, the effects of fluoxetine on the serotonin system have been combined with those of olanzapine, a second-generation antipsychotic, for the treatment of depression in patients with bipolar disorder and for treatment resistant unipolar depression.[19,27] Fluoxetine also may be a mild norepinephrine reuptake inhibitor, particularly at higher doses.

Fluoxetine significantly affects CYP 2D6 and 3A4 inhibition, and thus is highly likely to interact with other medications.[19,27] Finally, this medication has the longest half-life of the SSRIs, at 2-3 days, with an active metabolite that exists for 2 weeks.[2]

Benefits.Fluoxetine has action at the serotonin 2C receptor, and may affect norepinephrine levels at higher doses. The drug has the longest half-life among the SSRI, making it least likely to cause withdrawal. It is available as a once weekly dosing formulation and is approved for MDD, panic disorder, premenstrual dysphoric disorder, obsessive compulsive disorder, and bulimia nervosa.[2] It also has positive combination effects with the second generation antipsychotic olanzapine, and a combination formulation has been approved by the FDA for treating treatment-resistant and bipolar depression.*[19]

Drawbacks.The medication is likely to be activating in some patients, making it a more difficult option for those with insomnia, agitation, and intense anxiety.[19,27] Slower dose titration is warranted in these cases. Fluoxetine has a high degree of CYP 2D6 inhibition, resulting in significant drug-drug interactions.[19]

*Multiple trials of other second generation antipsychotics combined with various antidepressants including SSRI and SNRI have shown antidepressant efficacy for these combinations in patients with refractory depression.[32]

Paroxetine. The action of paroxetine is more complex than the previously described SSRI medications. In addition to serotonin reuptake inhibition, paroxetine functions with mild anticholinergic properties, mild norepinephrine reuptake inhibition (NRI), inhibition of nitric oxide synthetase, and potent inhibition of CYP 2D6 (similar to fluoxetine).[19,27] It has anticholinergic and antihistaminergic properties that may lend to its being calming and sedating, but also may increase dry mouth, blurred vision, and short term memory problems.[19,27] The NRI effects of the medication may contribute to clinical effectiveness. The effects on nitric oxide synthetase may cause sexual dysfunction.

Benefits.In addition to major depression, paroxetine is approved for various anxiety disorders, with possible calming/sedating effects. It is available in immediate- and slow-release preparations.

Drawbacks.Paroxetine has the potential for anticholinergic side effects[31] Its shorter half-life may result in more and more severe withdrawal side effects than other SSRI; paroxetine is also most strongly associated with weight changes, compared with other SSRI.[2] This medication also has a higher drug-drug interaction probability.

Sertraline. This SSRI may have dual mechanisms that distinguish it from other SSRIs. At higher doses, it acts as both a dopamine transporter inhibitor and a sigma 1 receptor binder.[27] The effects of dopamine transporter inhibition may result in improved energy, motivation, and concentration. Sigma 1 implications are not yet well understood, but some hypothetical benefit is attributed to their mild anxiolytic effects in psychotic and delusional depressions.[27]

Benefits.Sertraline is approved for MDD, many anxiety disorders, eating disorders, and premenstrual dysphoric disorder.[2] This medication has very little CYP 2D6 inhibition and therefore few drug-drug interactions.[19] It has a moderate half-life and thus the possibility of some withdrawal symptoms.

Drawbacks.Sertraline can be activating in patients with anxiety disorders, which may require slowly titrating doses; it is often associated with gastrointestinal distress.

Take-Home Point

The SSRI class is considered a homogeneous class of antidepressants because all are held to the same standard of passing FDA regulatory norms. However, a pharmacodynamic look into their wider mechanisms of action may suggest that each drug is actually different in ways that may foster unique advantages or disadvantages for any given patient. This type of finding would not be apparent in a typical 300-subject regulatory trial, but is often noted in clinical practice, where the sample size comprises the one unique subject that the clinician is treating.

SNRI Class

The next most common class of medications used for the treatment of MDD is the SNRI. This group of medications has a dual mechanism of action, increasing synaptic norepinephrine as well as serotonin.[19,27] In addition to increasing norepinephrine and serotonin levels throughout the brain, these medications may also boost dopamine in the prefrontal cortex, resulting in additional benefits.[27] In the prefrontal cortex, no dopamine transporters are there to recycle dopamine out of the synapse. Typically norepinephrine transporters remove dopamine in these areas, but with the inhibition of these, the dopamine effect in the dorsal lateral prefrontal cortex is more robust.[27] This activation in the brain has been correlated with antidepressant effects.

On the other hand, as the additional norepinephrine boost is added to the brain, it is not contained there. Norepinephrine effects are seen throughout the body, including the spinal cord, peripheral autonomic nervous system, heart, and bladder.[19,27] In the spinal cord this may reduce pain, but may also lead to side effects such as tremor, motor activation, and increased blood pressure and heart rate.[27] Also, these effects may allow a pseudo-anticholinergic effect resulting in such things as dry mouth, constipation, and urinary retention. However, these norepinephrine-related side effects do not rival those of the tricyclic antidepressant class.[31] Generally, the SNRIs are well tolerated, but the subtle increase in side effect burden needs to be considered.

Venlafaxine. Venlafaxine was the first SNRI and was initially approved in an immediate-release preparation. This medication is a substrate of CYP 2D6, and is converted into desvenlafaxine, an SNRI that was developed subsequently.[19,27] Unfortunately, the absorption of immediate-release venlafaxine is rapid, affording it remarkable side effects; this has been mitigated with an extended-release formulation that appears to be much better tolerated in practice. The medication also has a unique character, causing a varying ratio of serotonin to norepinephrine effects.[19,27] At low doses, there are fewer NRI properties (and more SRI properties) available and only at higher doses do the norepinephrine transporter inhibition properties increase more robustly.

Benefits.Compared with the SSRI, this medication has effects at both serotonin and norepinephrine receptors leading to its antidepressant effectiveness. The medication is very effective in the treatment of anxiety disorders, with multiple approved uses, likely comparable to sertraline and paroxetine.[2]

Drawbacks.The norepinephrine effects of the medication are much more robust only at higher doses and must be titrated. The medication has a short half-life resulting in many withdrawal side effects. There may be higher rates of nausea and dry mouth in comparison to some other antidepressants.[31] This medication may cause hypertension in some patients, and thus, blood pressure should be monitored.[19]

Desvenlafaxine. Desvenlafaxine is the active metabolite of venlafaxine,[19] and has the added benefit of a greater effect on norepinephrine transporter inhibition than its precursor at the initial dose levels. However, the effects on norepinephrine are less than those on serotonin.[27] Because it is the active metabolite of venlafaxine, it is less subjected to the genetic and drug-induced differences of CYP 2D6, which allows more consistent plasma levels of the medication.[27] It may be one of the “cleanest” antidepressant medications, given its extremely low vulnerability to cytochrome P450 metabolism, renal excretion, and low protein binding. The role of desvenlafaxine in the regulation of vasomotor symptoms (night sweats, hot flashes, insomnia, and related depression) in perimenopausal women is being investigated.[27]

Benefits.Although similar to extended-release venlafaxine, desvenlafaxine has a more balanced ratio of norepinephrine/serotonin properties, and it has one of the most favorable drug-drug interaction profiles.

Drawbacks.This medication has a short half-life and significant withdrawal side effects.[31]

Duloxetine. Duloxetine is unique among the SNRI class of drugs because, in addition to MDD, it is approved for treating a variety of pain syndromes.[2] This is related to the SNRI effect on the descending spinal norepinephrine pathways that reduce afferent pain fiber activity.[27] The increase in norepinephrine activity in spinal areas results in less thalamic input to the sensory cortex and therefore less perceived pain. The norepinephrine-facilitating effects in the prefrontal cortex also may show some benefit in treatment of cognitive symptoms prevalent in geriatric depression.[27]. Compared with venlafaxine, duloxetine has a lower incidence of treatment-related hypertension and milder withdrawal reactions. It is approved for MDD, generalized anxiety disorder, musculoskeletal pain, neuropathic pain, and fibromyalgia-related pain.[2]

Benefits.One of the only antidepressants approved for management of pain syndromes, duloxetine also has a more balanced norepinephrine to serotonin ratio at its initial doses.[28]

Drawbacks.Duloxetine is a mild to moderate CYP 2D6 inhibitor, which results in some drug-drug interactions.[19] In addition, it should not be used in alcoholic patients or those with renal and/or liver impairment.

Take-Home Point

The SNRI class is considered a homogeneous class of antidepressants because all are held to the same standard of passing FDA regulatory norms. As with the SSRI, a pharmacodynamic look into their wider mechanisms of action suggests that each drug is actually different in ways that may foster unique advantages or disadvantages for any given patient. This is clear when one considers the diverse FDA approvals for each and different potencies related to facilitating distinct ratios of serotonin to norepinephrine transporter inhibition. Again, this type of finding would not be apparent in a typical 300-subject regulatory trial, but is often noted in clinical practice, where the sample size comprises the one unique subject that the clinician is treating.

TCA Class

This class is one of the oldest and still highly utilized classes of antidepressant in the history of psychopharmacology, and includes amitriptyline, imipramine, clomipramine, desipramine, trimipramine, and nortriptyline. The TCAs are often overlooked because of their relatively high level of side effects when compared with other classes of antidepressant, and because of high lethality in overdose. The TCAs have significant effects on the norepinephrine, serotonin, and to some extent dopamine activity in the brain.[19,27] The higher incidence of side effects are likely mediated through blockade of anticholinergic receptors (M1/M3), histamine receptors (H1), alpha 1 adrenergic receptors, and voltage-sensitive sodium channels.[19,27] Histamine blockade causes sedation and weight gain. Muscarinic blockade causes dry mouth, blurred vision, urinary retention, and constipation. Alpha 1 blockade causes orthostatic hypotension and dizziness. Sodium channel blockade affects the heart significantly, resulting in arrhythmias and conduction changes at higher doses.[27] This latter side effect results in significant risk of successful suicide with overdose, and renders TCAs difficult to use in medically comorbid patients.

Benefits.Overall, TCAs are very effective antidepressants. Indeed, early studies comparing TCA with SSRI medications found significantly higher remission rates with TCA than with SSRI in depressed, endogenous and inpatients samples.[33-36] However, in less severely depressed patients, there is not conclusive evidence of benefit of either class of antidepressant over another. Off-label, the use of TCAs in the treatment of pain, enuresis, and insomnia is widespread.[19] Availability of plasma level monitoring helps to guarantee therapeutic trials while minimizing toxicity.

Drawbacks.The significant adverse event profile causes an array of side effects that are often poorly tolerated and lead to medication noncompliance. Because of cardiac side effects, TCAs carry significant risk of death with overdose.

MAOI Class

This class of antidepressants has its own unique mechanism of action. MAOI has fallen into the realm of rarely used antidepressants in modern day psychopharmacology. This is related to the risks and side effects inherent to MAOI use. On the other hand, MAOI are among the most clinically powerful classes of antidepressant treatments. This class interferes with MAO enzyme subtypes A and B. The inhibition of these enzymes results in higher levels of serotonin and norepinephrine due to reduced catabolism of these neurotransmitters.[27] Moreover, by specifically lowering MAO-B activity, dopamine levels in the brain increase as well. Thus, all 3 monoamine neurotransmitter levels are robustly increased, which, in turn, affects a broad array of depressive symptoms.

The use of these medications may come at the cost of difficulty in using them. The most well-known drawback is that patients need to maintain a specific diet that is free of high tyramine foods, or risk the likelihood of hypertensive crisis related to the acute elevation of systemic norepinephrine, which also may result in stroke.[19,27] Foods to be avoided include tap beers, smoked meat or fish, fava beans, aged cheeses, sauerkraut, and soy. However, certain beers, wines, and cheeses are not contraindicated. These items need to be researched and discussed prior to starting a patient on the medication.

Drug-drug interactions are plentiful; combining an MAOI with other norepinephrine medications may increase blood pressure, and combining with a serotonin-based medication can cause serotonin syndrome.[19,27] Patients are also advised to avoid decongestants, stimulants, antidepressants, certain opioids, and appetite suppressants.[19,27]

The MAOI tranylcypromine may act similarly to an amphetamine in the frontal cortex, affording it some additional benefits.[27] Likewise, selegiline also involves breakdown into an amphetamine metabolite. Selegiline is more often used for Parkinson disease than depression.

Benefits.MAOIs are recognized as among the most potent of antidepressants in monotherapy, with effects on serotonin, dopamine, and norepinephrine. This class of antidepressant is often used for the patient who is refractory to other antidepressant trials.

Drawbacks.The MAOIs are associated with risks of hypertensive crisis and serotonin syndrome. There is a need to maintain a tyramine free diet except when using the low dose transdermal selegiline. Because of potential for drug-drug interactions, careful, ongoing monitoring of all additional medications (including over-the-counter medications) is essential.

Miscellaneous Antidepressants

Several other well-known antidepressant medications do not fit discretely into the 4 main antidepressant classes. Each has unique mechanisms that will be discussed similarly below.

Bupropion. This norepinephrine-dopamine receptor inhibitor (NDRI) medication is of particular use in a few subsets of patients. As the class name indicates, bupropion facilitates effects on norepinephrine and dopamine, blocking norepinephrine transporter and dopamine transporter activity at a moderate level, likely in the frontal cortex.[27] The unique properties of bupropion as an antidepressant may be related to its lack of serotonin activity. It is approved for smoking cessation and is used off-label to reduce craving for substances of abuse. Clinicians contend that the dopamine actions of this medication help to improve the loss of positive affect in MDD. Thus, it effectively increases joy, interest, pleasure, energy, enthusiasm, alertness, and self-confidence.[27] The norepinephrine and dopamine facilitation helps patients with attention-deficit/hyperactivity disorder as well.[19]

Several cases of psychosis and paranoia have been reported in patients taking bupropion, likely related to the dopamine effects of the drug.[37] Limited data suggest that this medication, like all antidepressants, may activate depressed patients with bipolar disorder, causing manic episodes. However, it is widely accepted that bupropion and the SSRI class may be less likely to activate mania compared with the TCA class of medications. Because it does not act on serotonin, this is one of the few antidepressants that does not cause sexual side effects or weight gain.[19,27] The medication is uniquely approved for the treatment of seasonal affective disorder.[2]

Benefits.Bupropion is indicated for the treatment of MDD, seasonal affective disorder, and nicotine dependence. It has very low sexual and weight gain side effect liability.

Drawbacks.There is limited serotonin activity with bupropion and less evidence for the treatment of anxiety. Bupropion lowers the seizure threshold in patients predisposed to these events (including patients with eating disorders and those with epilepsy).

Trazodone. Trazodone is a serotonin antagonist/reuptake inhibitor (SARI). It blocks serotonin 2A and 2C receptors and also acts as a mild serotonin reuptake inhibitor.[19,27] This medication typically is used at lower doses because of its properties as a strong antihistamine (H1) and alpha-1 adrenergic blocking medication. The blockade of these receptors causes significant sedation, which may help with insomnia, but may cause excessive somnolence and dizziness in the daytime. The blockade of serotonin also may explain trazodone’s properties as a hypnotic, providing more efficient sleep.[27] Although higher doses of this medication provide excellent benefit related to the synergistic effects of blocking serotonin 2A and 2C and by acting as a serotonin reuptake inhibitor, this medication is not typically given in full divided doses because of excessive side effects.[19,27] A new slow-release preparation has been approved to allow a better tolerated, full dose range.

Benefits.Trazodone is often called a sedating antidepressant. It helps insomnia, improves sleep efficiency, and has its action even at low doses. Sexual side effects and activating side effects are low.[19,27]

Drawbacks. Significant sedation may limit its use.

Mirtazapine. This medication is also considered to be sedating and is typically either avoided or sought because of its side effect profile. Side effects include sedation/hypnotic effects and appetite stimulation, but not sexual side effects. The lack of sexual side effects is again related to serotonin in that mirtazapine is not a serotonin reuptake inhibitor, but in this case acts as a serotonin 2A/2C receptor antagonist.[19,27] The blockade of these receptors may result in more dopamine and norepinephrine release in the prefrontal cortex. The histamine blockade (H1) results in sedation, anxiolytic/hypnotic effects, and weight gain.[19,27] Mirtazapine also acts as a 5HT3 receptor antagonist, resulting in reduction of gastrointestinal problems.[19,27] The primary mechanism of antidepressant action is through alpha 2/norepinephrine receptor antagonism. Through this antagonism, inhibition of norepinephrine is disinhibited through auto receptor blockade. This allows downstream effects on several pathways and may result in overall release of serotonin and norepinephrine. This effect can often be combined with an SNRI to obtain synergistic effects.[27]

Benefits.Mirtazapine has many unique mechanisms of actions that make it beneficial in particular populations. It lacks sexual side effects, reduces gastrointestinal upset, and is not activating. The sedating qualities of this medication are typically used to the medication’s and the patient’s benefit.

Drawbacks.Mirtazapine has significant weight gain/appetite stimulation effects, which could lead to metabolic disorders.

This review is both practical and factual. Clinicians ideally should be aware of regulatory approvals and appropriate use of them in certain patient populations. When used this way, clinicians may expect results comparable to those noted in the evidence base of regulatory trials. However, those who treat patients understand that not all are identical to those enrolled in research trials. What follows will provide some practical clinical approaches when responses do not meet expectations.

As noted, only one third of patients will fully remit on their first antidepressant trial.[38] These numbers hold true for patients who are fully treated with moderate to high dose SSRI for as long as 12 weeks. In clinical practice, patients may not even have such a rigorous dosing profile and failure rates are likely higher. What approaches should be taken when a patient is not responding to treatment?

Adherence and Dosing

First, ask and attempt to ensure adherence to the antidepressant treatment. This questioning should be nonjudgmental and empathic, as most patients will likely say they are compliant even when they are not. Oftentimes suggesting that most people tend to naturally miss a few doses and that you as the clinician are just checking up will diffuse the situation. As dosing becomes divided throughout the day and polypharmacy increases, compliance usually diminishes, making assessment for compliance and adherence to medical regimens even more important.

Tolerability

An important area to address to improve adherence to a regimen relates to side effects and antidepressant tolerability. Sometimes patients cease taking their antidepressant or fail to escalate the dose as advised when adverse effects are not well tolerated. Many mild side effects will dissipate over time and this should be discussed directly with the patient.[39] Patients should be instructed to inform prescribers of any moderate to severe side effects and the drug can then be safely stopped. Patients should also be told that there are many antidepressants, and these have different side effects.[2,39] For example, SSRI, SNRI, and NDRI may be activating, and thus cause insomnia or nervousness upon initiation of treatment. Patients may be switched to a less activating SARI or noradrenergic antagonist-selective serotonin antagonist mechanism-based product, as these tend to be less activating and more sedating.[2]

Some patients may experience drug-drug interactions depending upon their genetic make-up.[2] Switching away from hepatic inhibiting medications towards medications that are less likely to interact with other drugs may be warranted. Typical side effects of headaches, stomachaches, or even insomnia often can be treated very effectively with over the counter or prescription medications. Later onset side effects such as weight gain or sexual dysfunction may be more difficult to mitigate or treat. Open discussions with patients about these longer term risks are warranted because patients often have to stay on their antidepressants for a year or more to maintain remission and avoid a depressive relapse.[38] Because certain antidepressants may have a more, or less favorable weight or sexual side effect profile, they should be chosen based on a discussion about patient preference when possible.

Assuming adherence is adequate, the next step is to confirm that the antidepressant dose was at the moderate to high end of the approved range and has been taken for at least 4 to 6 weeks. If dosing is confirmed to be reasonable, consider a final maximization of dose or switch to a new antidepressant monotherapy.[39]

Switching Monotherapies

If it is necessary to consider switching monotherapies, no clear benefit has been attributed to any particular strategy.[38] Many experts agree, however, that a switch away from an SSRI is warranted if the fully dosed SSRI therapy has failed to improve the patient’s symptoms.[27,39] The theoretical implication is that the patient’s current depressive symptoms have been treated with aggressive serotonergic facilitation and that repeating this mechanism may not be fruitful. This suggests that, pharmacodynamically, the depression may not be entirely serotonin-based in regards to its etiology.[27,39] Given this, a cross titration on to an SNRI such as venlafaxine XR or duloxetine, a NDRI such as bupropion XL, a noradrenergic antagonist-selective serotonin antagonist such as mirtazapine, or a more aggressive serotonergic facilitating agent like a SARI such as trazodone ER or a serotonin partial agonist-reuptake inhibitor such as vilazodone theoretically may be warranted.[2]

One final concern regarding switching involves the use of generic vs brand-name drugs. The FDA ensures that the bioavailability between a brand name and its generic counterpart is approximately between 20% weaker and 20% stronger.[40,41] Most generics are highly comparable, but occasionally when a patient actually changes from one generic to another, the bioavailability could change from a 20% stronger to a 20% weaker generic drug and symptom relapse may occur. By contrast, going from a weaker to a stronger generic might actually improve depression outcomes but may also create new-onset side effects after months of stable treatment as the newer generic preparation is more potent, raising blood levels higher than previously. These types of events should be monitored and dosing adjusted as needed.

Finally, a generic drug may possess a different slow-release mechanism compared with the parent brand-name drug. Oftentimes the generic, despite being a slow-release drug itself may actually release active drug more quickly than the original brand’s slow-release technology. There may be no evidence of a clinical problem; however, some patients may develop side effects when taking the faster release preparation. In this case, the dose may need to be lowered while monitoring for relapse or a switch back to the brand-name slow-release product may be warranted.

In conclusion, this article seeks to identify treatments that match patients with MDD and their common comorbidities, as a first line approach to MDD management. Secondarily and more theoretically, patients’ MDD symptoms may be effectively treated if clinicians are aware of the neurotransmitters and receptors that each antidepressant modulates. Finally, patients may suffer issues with nonefficacy, noncompliance, and tolerability. Each patient is unique and these clinical situations may interfere with optimal depression outcomes. Each patient must be educated and given informed consent about the myriad effective antidepressant treatment options available.

Supported by an independent educational grant from Valeant Pharmaceuticals.

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Retrieved from:

Tailoring Antidepressant Treatment: Factors to Individualize Medication Selection Thomas L. Schwartz, MD; Daniel Uderitz, MD

In the realm of psychopharmacology, we often declare medications within their respective therapeutic classes as being equal. This is a byproduct related to the way medications achieve their indications for treatment for specific psychiatric disorders. In the case of antidepressant treatments, the US Food and Drug Administration (FDA) indicates that if a study can obtain a majority of patients improved by 50% compared with placebo, then a drug may become an antidepressant treatment. There are no standards for differentiating antidepressant treatments beyond this. Clinicians often note that all antidepressant treatments are not created equal, especially when applied to clinical situations and patients who are often complex and have comorbid conditions. The goal of this article is to sort out regimens that may convey certain advantages during the treatment in an individualized manner. This involves conceptualizing and utilizing monotherapies, combination therapies, and adjunctive treatments.

Monotherapies

The first-line treatment of patients with major depressive disorder (MDD) should start with an aggressive monotherapy. This occurs in clinical practice and is supported by many guidelines and reviews. The various antidepressant medications have unique properties that can be used to individualize treatments. Most psychiatrists can easily name their “favorite” antidepressant to use in certain situations. This is sometimes based on a simple bias, but often has evidence to back up clinical practice. Let us start with the mechanistically simple and move toward more complex ways to think about these medications. This includes thinking about FDA approvals, available guidelines, comorbidities, side effects, and more complex pharmacodynamic receptor-based neuropsychiatry.

A patient rarely comes to a psychiatrist without having a combination of psychiatric symptoms. Typically, clinicians screen patients and find that they often meet criteria for more than 1 Diagnostic and Statistical Manual of Mental Disorders Fourth Edition-Text Revision (DSM IV-TR) criteria.[1] At a minimum, the individual patient raises suspicion for various problem areas, even if they do not meet criteria for a specific disorder. In reviewing FDA guidelines, clinicians may quickly make simple decisions regarding treatment regimens that are more individualized based on these comorbidities and predominant symptoms. Of note, additional FDA approval or lack of approval for various indications does not necessarily mean that evidence does not support efficacy for other disorders. For example, the manufacturer may not have pursued FDA approval for other indications, or may have decided not to support randomized controlled trials to study another indication.

Single Indication

The first group of antidepressants approved by the FDA for the single indication of MDD include amitriptyline, citalopram, desipramine, desvenlafaxine, mirtazipine, nortriptyline, protriptyline, trazodone, trimipramine, vilazodone, and the monoamine oxidase inhibitor (MAOI) class.[2-4] Clinicians should know that these medications have only the 1 indication, and this clearly supports their use in MDD. However, many practitioners recognize that there are multiple other factors that allow these medications to be used in an off-label manner for various individuals. In a pure model, these antidepressants have regulatory data suggesting use only in patients with MDD but, as discussed, a lack of approval for other indications does not necessarily indicate a lack of supportive data or lack of efficacy.

Multiple Indications

Unlike those listed above, many antidepressants have other labeled or approved indications. These span a variety of comorbidities including anxiety disorders, seasonal affective disorder, sleep disorders, pain disorders, premenstrual dysphoric disorder, bulimia nervosa, and other miscellaneous indications. Given this, and assuming MDD is often complicated by comorbidity, let us evaluate a few comorbidities where data-driven decisions may help in individualizing treatments in patients who are depressed and simultaneously experience other psychiatric conditions.

Posttraumatic Stress Disorder

Patients with posttraumatic stress disorder often have comorbid depression. Only 2 antidepressants, the selective serotonin reuptake inhibitors (SSRI) sertraline and paroxetine, are approved for this indication.[2] Multiple other medications have been recognized as effective off-label treatments for posttraumatic stress disorder, however; these include amitriptyline, fluoxetine, fluvoxamine, imipramine, and venlafaxine.[5-7] If a patient presents with MDD and posttraumatic stress disorder, these antidepressants may be considered if necessary to achieve efficacy for both conditions.

Obsessive-Compulsive Disorder

Several medications are approved for obsessive-compulsive disorder, including the tricyclic antidepressant clomipramine, and the SSRIs fluoxetine, fluvoxamine, paroxetine, and sertraline.[2] Venlafaxine, a serotonin norepinephrine reuptake inhibitor (SNRI),[8] and the SSRI citalopram have shown some promise in obsessive compulsive disorder,[9] but have not yet received that indication from the FDA.

Panic Disorder

The SSRIs fluoxetine, paroxetine, and sertraline are approved for treatment of panic disorder, as is the SNRI venlafaxine.[2,10] Other antidepressants with an evidence base for use that are not approved include the TCAs clomipramine and imipramine, and the SSRI fluvoxamine.[6]

Anxiety Disorders

Social anxiety disorder. The SSRIs paroxetine and sertraline, and the SNRI, venlafaxine extended-release (ER) have been approved for the treatment of social anxiety disorder.[2] The SSRI fluoxetine is sometimes used for treatment of social anxiety disorder.

Generalized anxiety disorder. Four antidepressants have been indicated for the treatment of generalized anxiety disorder. These include the SSRI escitalopram and paroxetine, and the SNRI duloxetine and venlafaxine ER.[2,11]

Insomnia

Although sleep difficulties are a nearly universal symptom of depression, few antidepressants have an official indication for insomnia. Doxepin, a TCA, is the sole antidepressant labeled with this indication, when it is used at subtherapeutic antidepressant doses of 3 to 6 mg per day.[12] However, clinicians often use sedating antidepressants to induce sleep in those patients with MDD and insomnia (Schwartz TL. Novel hypnotics: moving beyond positive allosteric modulation of the GABA-A receptor. Manuscript submitted). These medications include the TCA amitriptyline, the tetracyclic mirtazapine, and the serotonin modulator trazodone.

Pain Syndromes

Duloxetine, an SNRI, is the only antidepressant medication that has official indications for treatment of pain syndromes.[2,10] These include chronic musculoskeletal pain, neuropathic pain (diabetic neuropathy in particular), and fibromyalgia. Alternatively, many of the TCAs, as well as other SNRI, have been studied for the treatment of pain syndromes, primarily involving neuropathic or chronic pain conditions.[13,14] Amitriptyline also is often used for migraine headaches. Unfortunately these other medications have not received official indications for these psychosomatic comorbidities.

Attention-Deficit/Hyperactivity Disorder

Some antidepressants have shown promise for the treatment of attention-deficit/hyperactivity disorder, but not enough to warrant a specific FDA indication. Nonetheless, these medications are used for the treatment of attention-deficit/hyperactivity disorder, particularly in patients with substance use disorder. Bupropion, desipramine, imipramine, nortriptyline, and venlafaxine have some evidence base to support their use.[15-19]

Other Comorbid Considerations

Premenstrual dysphoric disorder. The SSRI fluoxetine, paroxetine, and sertraline have been FDA approved for the treatment of premenstrual dysphoric disorder.[2]

Smoking cessation. Many patients who receive mental health treatment are also addicted to nicotine. Bupropion SR has received the indication for nicotine addiction.[2] Nortriptyline also has been shown to be helpful for smoking cessation efforts, but has not received an official indication.[20]

Miscellaneous. Bupropion XL carries a specific indication for prophylaxis of seasonal affective disorder and often is used off-label for the treatment of bipolar depression.[19,21,22] Fluoxetine is indicated for treatment of bulimia nervosa and sometimes is used for the treatment of Raynaud’ phenomenon.[2,19,23] Venlafaxine and paroxetine have data supporting use for the treatment of vasomotor hot flashes.[24,25] Finally, imipramine may be used in the treatment of enuresis.[26]

Take-Home Point

Clinicians should be aware of FDA approvals and the evidence base supporting the use of antidepressants in patients with MDD, who are often complex and suffering with other medical and psychiatric comorbidities. Choosing agents with indications that match the patient’s comorbid symptoms is one way to tailor and individualize treatment to each patient.

Beyond the simplistic but labor-intensive role of delineating specific comorbidities and focusing on antidepressant indications, is the imperative to develop a more complex individualized antidepressant treatment plan. If it were as simple as following the FDA labels and simple algorithms to make decisions, then much psychiatric education could be eliminated. A review of antidepressant mechanisms of action will allow us to further distinguish these medications, thus allowing more individualized treatments for MDD.

SSRI Class

The first and most commonly prescribed class of antidepressant is the SSRI. At the most basic understanding, these medications increase serotonin in the synapse and function ultimately to down-regulate serotonin receptors. However, as the science behind these medications is further explored, there is much more to these agents. When looking at the SSRI class as a whole, and in comparison with other antidepressant classes, a few general characteristics can be considered. The SSRI medications as a group are thought of as having fewer side effects than most other classes of antidepressants, and particularly the older classes of drugs. The most common and clinically relevant consideration for these medications is the development of gastrointestinal upset, sexual side effects, and weight gain.[27] The following delineates some of the subtle differences for each medication in this class and describes the benefits and drawbacks of treatment with each to help refine treatment selection.

Citalopram. Citalopram is one of the most widely used antidepressants today, and has a few properties that make it desirable. The medication has a long half-life of 23-45 hours, second only to fluoxetine,[2] and it is typically well tolerated in medically ill patients and the elderly.[19,28] Citalopram has weak H1 receptor antihistamine properties, and these properties provide anxiolytic and positively sedating effects.[27] Citalopram is made up of 2 mirror image enantiomers, each of which have different properties [27] that may lead to some inconsistencies in the property or function of the medication at lower doses. Citalopram is a weak inhibitor of CYP 2D6, with minimal drug-drug interactions.[30] Finally, recent FDA warnings have changed prescribing practices of this medication because of potential QTc prolongation at daily doses higher than 40 mg[29]; daily doses of 60 mg should no longer be used.

Benefits.Citalopram is a well-tolerated medication with mild antihistamine effects that may help with insomnia or mild anxieties. The longer half-life results in less withdrawal or discontinuation side effects.[31]

Drawbacks.Structural enantiomers result in this medication having less predictable effects at lower doses, and higher doses are contrary to FDA recommendations related to the potential for QTc prolongation. It has fewer FDA approvals for comorbid psychiatric disorders than other drugs in the SSRI class; as discussed earlier, this may simply reflect the manufacturer’s failure to seek approval for other indications.

Escitalopram. In contrast to the parent drug citalopram, escitalopram is separated and includes only the left enantiomer.[27] This results in the removal of much of the antihistamine and CYP 2D6 inhibitory properties.[19,27] It also results in more effective and predictable dose responses of the medication at the lower doses.

Benefits.Escitalopram has the benefit of better tolerability with less drug interactions. It may have less sedating effects, and is approved for generalized anxiety disorder as well as MDD.[2]

Drawbacks.Currently this is the only SSRI still on patent, and is thus more expensive than other, generic SSRI.

Fluoxetine. The first member of the SSRI class, fluoxetine has a few characteristics that make it desirable. Fluoxetine has mild serotonin 2C receptor antagonistic actions. This may result in the disinhibition of dopamine and norepinephrine release to the prefrontal cortex, which likely helps to improve concentration, energy, and executive functioning.[19,27] Furthermore, the serotonin 2C effects of this medication may contribute to the initial anorexic and ongoing anti-bulimic effects of this medication.[27] More recently, the effects of fluoxetine on the serotonin system have been combined with those of olanzapine, a second-generation antipsychotic, for the treatment of depression in patients with bipolar disorder and for treatment resistant unipolar depression.[19,27] Fluoxetine also may be a mild norepinephrine reuptake inhibitor, particularly at higher doses.

Fluoxetine significantly affects CYP 2D6 and 3A4 inhibition, and thus is highly likely to interact with other medications.[19,27] Finally, this medication has the longest half-life of the SSRIs, at 2-3 days, with an active metabolite that exists for 2 weeks.[2]

Benefits.Fluoxetine has action at the serotonin 2C receptor, and may affect norepinephrine levels at higher doses. The drug has the longest half-life among the SSRI, making it least likely to cause withdrawal. It is available as a once weekly dosing formulation and is approved for MDD, panic disorder, premenstrual dysphoric disorder, obsessive compulsive disorder, and bulimia nervosa.[2] It also has positive combination effects with the second generation antipsychotic olanzapine, and a combination formulation has been approved by the FDA for treating treatment-resistant and bipolar depression.*[19]

Drawbacks.The medication is likely to be activating in some patients, making it a more difficult option for those with insomnia, agitation, and intense anxiety.[19,27] Slower dose titration is warranted in these cases. Fluoxetine has a high degree of CYP 2D6 inhibition, resulting in significant drug-drug interactions.[19]

*Multiple trials of other second generation antipsychotics combined with various antidepressants including SSRI and SNRI have shown antidepressant efficacy for these combinations in patients with refractory depression.[32]

Paroxetine. The action of paroxetine is more complex than the previously described SSRI medications. In addition to serotonin reuptake inhibition, paroxetine functions with mild anticholinergic properties, mild norepinephrine reuptake inhibition (NRI), inhibition of nitric oxide synthetase, and potent inhibition of CYP 2D6 (similar to fluoxetine).[19,27] It has anticholinergic and antihistaminergic properties that may lend to its being calming and sedating, but also may increase dry mouth, blurred vision, and short term memory problems.[19,27] The NRI effects of the medication may contribute to clinical effectiveness. The effects on nitric oxide synthetase may cause sexual dysfunction.

Benefits.In addition to major depression, paroxetine is approved for various anxiety disorders, with possible calming/sedating effects. It is available in immediate- and slow-release preparations.

Drawbacks.Paroxetine has the potential for anticholinergic side effects[31] Its shorter half-life may result in more and more severe withdrawal side effects than other SSRI; paroxetine is also most strongly associated with weight changes, compared with other SSRI.[2] This medication also has a higher drug-drug interaction probability.

Sertraline. This SSRI may have dual mechanisms that distinguish it from other SSRIs. At higher doses, it acts as both a dopamine transporter inhibitor and a sigma 1 receptor binder.[27] The effects of dopamine transporter inhibition may result in improved energy, motivation, and concentration. Sigma 1 implications are not yet well understood, but some hypothetical benefit is attributed to their mild anxiolytic effects in psychotic and delusional depressions.[27]

Benefits.Sertraline is approved for MDD, many anxiety disorders, eating disorders, and premenstrual dysphoric disorder.[2] This medication has very little CYP 2D6 inhibition and therefore few drug-drug interactions.[19] It has a moderate half-life and thus the possibility of some withdrawal symptoms.

Drawbacks.Sertraline can be activating in patients with anxiety disorders, which may require slowly titrating doses; it is often associated with gastrointestinal distress.

Take-Home Point

The SSRI class is considered a homogeneous class of antidepressants because all are held to the same standard of passing FDA regulatory norms. However, a pharmacodynamic look into their wider mechanisms of action may suggest that each drug is actually different in ways that may foster unique advantages or disadvantages for any given patient. This type of finding would not be apparent in a typical 300-subject regulatory trial, but is often noted in clinical practice, where the sample size comprises the one unique subject that the clinician is treating.

SNRI Class

The next most common class of medications used for the treatment of MDD is the SNRI. This group of medications has a dual mechanism of action, increasing synaptic norepinephrine as well as serotonin.[19,27] In addition to increasing norepinephrine and serotonin levels throughout the brain, these medications may also boost dopamine in the prefrontal cortex, resulting in additional benefits.[27] In the prefrontal cortex, no dopamine transporters are there to recycle dopamine out of the synapse. Typically norepinephrine transporters remove dopamine in these areas, but with the inhibition of these, the dopamine effect in the dorsal lateral prefrontal cortex is more robust.[27] This activation in the brain has been correlated with antidepressant effects.

On the other hand, as the additional norepinephrine boost is added to the brain, it is not contained there. Norepinephrine effects are seen throughout the body, including the spinal cord, peripheral autonomic nervous system, heart, and bladder.[19,27] In the spinal cord this may reduce pain, but may also lead to side effects such as tremor, motor activation, and increased blood pressure and heart rate.[27] Also, these effects may allow a pseudo-anticholinergic effect resulting in such things as dry mouth, constipation, and urinary retention. However, these norepinephrine-related side effects do not rival those of the tricyclic antidepressant class.[31] Generally, the SNRIs are well tolerated, but the subtle increase in side effect burden needs to be considered.

Venlafaxine. Venlafaxine was the first SNRI and was initially approved in an immediate-release preparation. This medication is a substrate of CYP 2D6, and is converted into desvenlafaxine, an SNRI that was developed subsequently.[19,27] Unfortunately, the absorption of immediate-release venlafaxine is rapid, affording it remarkable side effects; this has been mitigated with an extended-release formulation that appears to be much better tolerated in practice. The medication also has a unique character, causing a varying ratio of serotonin to norepinephrine effects.[19,27] At low doses, there are fewer NRI properties (and more SRI properties) available and only at higher doses do the norepinephrine transporter inhibition properties increase more robustly.

Benefits.Compared with the SSRI, this medication has effects at both serotonin and norepinephrine receptors leading to its antidepressant effectiveness. The medication is very effective in the treatment of anxiety disorders, with multiple approved uses, likely comparable to sertraline and paroxetine.[2]

Drawbacks.The norepinephrine effects of the medication are much more robust only at higher doses and must be titrated. The medication has a short half-life resulting in many withdrawal side effects. There may be higher rates of nausea and dry mouth in comparison to some other antidepressants.[31] This medication may cause hypertension in some patients, and thus, blood pressure should be monitored.[19]

Desvenlafaxine. Desvenlafaxine is the active metabolite of venlafaxine,[19] and has the added benefit of a greater effect on norepinephrine transporter inhibition than its precursor at the initial dose levels. However, the effects on norepinephrine are less than those on serotonin.[27] Because it is the active metabolite of venlafaxine, it is less subjected to the genetic and drug-induced differences of CYP 2D6, which allows more consistent plasma levels of the medication.[27] It may be one of the “cleanest” antidepressant medications, given its extremely low vulnerability to cytochrome P450 metabolism, renal excretion, and low protein binding. The role of desvenlafaxine in the regulation of vasomotor symptoms (night sweats, hot flashes, insomnia, and related depression) in perimenopausal women is being investigated.[27]

Benefits.Although similar to extended-release venlafaxine, desvenlafaxine has a more balanced ratio of norepinephrine/serotonin properties, and it has one of the most favorable drug-drug interaction profiles.

Drawbacks.This medication has a short half-life and significant withdrawal side effects.[31]

Duloxetine. Duloxetine is unique among the SNRI class of drugs because, in addition to MDD, it is approved for treating a variety of pain syndromes.[2] This is related to the SNRI effect on the descending spinal norepinephrine pathways that reduce afferent pain fiber activity.[27] The increase in norepinephrine activity in spinal areas results in less thalamic input to the sensory cortex and therefore less perceived pain. The norepinephrine-facilitating effects in the prefrontal cortex also may show some benefit in treatment of cognitive symptoms prevalent in geriatric depression.[27]. Compared with venlafaxine, duloxetine has a lower incidence of treatment-related hypertension and milder withdrawal reactions. It is approved for MDD, generalized anxiety disorder, musculoskeletal pain, neuropathic pain, and fibromyalgia-related pain.[2]

Benefits.One of the only antidepressants approved for management of pain syndromes, duloxetine also has a more balanced norepinephrine to serotonin ratio at its initial doses.[28]

Drawbacks.Duloxetine is a mild to moderate CYP 2D6 inhibitor, which results in some drug-drug interactions.[19] In addition, it should not be used in alcoholic patients or those with renal and/or liver impairment.

Take-Home Point

The SNRI class is considered a homogeneous class of antidepressants because all are held to the same standard of passing FDA regulatory norms. As with the SSRI, a pharmacodynamic look into their wider mechanisms of action suggests that each drug is actually different in ways that may foster unique advantages or disadvantages for any given patient. This is clear when one considers the diverse FDA approvals for each and different potencies related to facilitating distinct ratios of serotonin to norepinephrine transporter inhibition. Again, this type of finding would not be apparent in a typical 300-subject regulatory trial, but is often noted in clinical practice, where the sample size comprises the one unique subject that the clinician is treating.

TCA Class

This class is one of the oldest and still highly utilized classes of antidepressant in the history of psychopharmacology, and includes amitriptyline, imipramine, clomipramine, desipramine, trimipramine, and nortriptyline. The TCAs are often overlooked because of their relatively high level of side effects when compared with other classes of antidepressant, and because of high lethality in overdose. The TCAs have significant effects on the norepinephrine, serotonin, and to some extent dopamine activity in the brain.[19,27] The higher incidence of side effects are likely mediated through blockade of anticholinergic receptors (M1/M3), histamine receptors (H1), alpha 1 adrenergic receptors, and voltage-sensitive sodium channels.[19,27] Histamine blockade causes sedation and weight gain. Muscarinic blockade causes dry mouth, blurred vision, urinary retention, and constipation. Alpha 1 blockade causes orthostatic hypotension and dizziness. Sodium channel blockade affects the heart significantly, resulting in arrhythmias and conduction changes at higher doses.[27] This latter side effect results in significant risk of successful suicide with overdose, and renders TCAs difficult to use in medically comorbid patients.

Benefits.Overall, TCAs are very effective antidepressants. Indeed, early studies comparing TCA with SSRI medications found significantly higher remission rates with TCA than with SSRI in depressed, endogenous and inpatients samples.[33-36] However, in less severely depressed patients, there is not conclusive evidence of benefit of either class of antidepressant over another. Off-label, the use of TCAs in the treatment of pain, enuresis, and insomnia is widespread.[19] Availability of plasma level monitoring helps to guarantee therapeutic trials while minimizing toxicity.

Drawbacks.The significant adverse event profile causes an array of side effects that are often poorly tolerated and lead to medication noncompliance. Because of cardiac side effects, TCAs carry significant risk of death with overdose.

MAOI Class

This class of antidepressants has its own unique mechanism of action. MAOI has fallen into the realm of rarely used antidepressants in modern day psychopharmacology. This is related to the risks and side effects inherent to MAOI use. On the other hand, MAOI are among the most clinically powerful classes of antidepressant treatments. This class interferes with MAO enzyme subtypes A and B. The inhibition of these enzymes results in higher levels of serotonin and norepinephrine due to reduced catabolism of these neurotransmitters.[27] Moreover, by specifically lowering MAO-B activity, dopamine levels in the brain increase as well. Thus, all 3 monoamine neurotransmitter levels are robustly increased, which, in turn, affects a broad array of depressive symptoms.

The use of these medications may come at the cost of difficulty in using them. The most well-known drawback is that patients need to maintain a specific diet that is free of high tyramine foods, or risk the likelihood of hypertensive crisis related to the acute elevation of systemic norepinephrine, which also may result in stroke.[19,27] Foods to be avoided include tap beers, smoked meat or fish, fava beans, aged cheeses, sauerkraut, and soy. However, certain beers, wines, and cheeses are not contraindicated. These items need to be researched and discussed prior to starting a patient on the medication.

Drug-drug interactions are plentiful; combining an MAOI with other norepinephrine medications may increase blood pressure, and combining with a serotonin-based medication can cause serotonin syndrome.[19,27] Patients are also advised to avoid decongestants, stimulants, antidepressants, certain opioids, and appetite suppressants.[19,27]

The MAOI tranylcypromine may act similarly to an amphetamine in the frontal cortex, affording it some additional benefits.[27] Likewise, selegiline also involves breakdown into an amphetamine metabolite. Selegiline is more often used for Parkinson disease than depression.

Benefits.MAOIs are recognized as among the most potent of antidepressants in monotherapy, with effects on serotonin, dopamine, and norepinephrine. This class of antidepressant is often used for the patient who is refractory to other antidepressant trials.

Drawbacks.The MAOIs are associated with risks of hypertensive crisis and serotonin syndrome. There is a need to maintain a tyramine free diet except when using the low dose transdermal selegiline. Because of potential for drug-drug interactions, careful, ongoing monitoring of all additional medications (including over-the-counter medications) is essential.

Miscellaneous Antidepressants

Several other well-known antidepressant medications do not fit discretely into the 4 main antidepressant classes. Each has unique mechanisms that will be discussed similarly below.

Bupropion. This norepinephrine-dopamine receptor inhibitor (NDRI) medication is of particular use in a few subsets of patients. As the class name indicates, bupropion facilitates effects on norepinephrine and dopamine, blocking norepinephrine transporter and dopamine transporter activity at a moderate level, likely in the frontal cortex.[27] The unique properties of bupropion as an antidepressant may be related to its lack of serotonin activity. It is approved for smoking cessation and is used off-label to reduce craving for substances of abuse. Clinicians contend that the dopamine actions of this medication help to improve the loss of positive affect in MDD. Thus, it effectively increases joy, interest, pleasure, energy, enthusiasm, alertness, and self-confidence.[27] The norepinephrine and dopamine facilitation helps patients with attention-deficit/hyperactivity disorder as well.[19]

Several cases of psychosis and paranoia have been reported in patients taking bupropion, likely related to the dopamine effects of the drug.[37] Limited data suggest that this medication, like all antidepressants, may activate depressed patients with bipolar disorder, causing manic episodes. However, it is widely accepted that bupropion and the SSRI class may be less likely to activate mania compared with the TCA class of medications. Because it does not act on serotonin, this is one of the few antidepressants that does not cause sexual side effects or weight gain.[19,27] The medication is uniquely approved for the treatment of seasonal affective disorder.[2]

Benefits.Bupropion is indicated for the treatment of MDD, seasonal affective disorder, and nicotine dependence. It has very low sexual and weight gain side effect liability.

Drawbacks.There is limited serotonin activity with bupropion and less evidence for the treatment of anxiety. Bupropion lowers the seizure threshold in patients predisposed to these events (including patients with eating disorders and those with epilepsy).

Trazodone. Trazodone is a serotonin antagonist/reuptake inhibitor (SARI). It blocks serotonin 2A and 2C receptors and also acts as a mild serotonin reuptake inhibitor.[19,27] This medication typically is used at lower doses because of its properties as a strong antihistamine (H1) and alpha-1 adrenergic blocking medication. The blockade of these receptors causes significant sedation, which may help with insomnia, but may cause excessive somnolence and dizziness in the daytime. The blockade of serotonin also may explain trazodone’s properties as a hypnotic, providing more efficient sleep.[27] Although higher doses of this medication provide excellent benefit related to the synergistic effects of blocking serotonin 2A and 2C and by acting as a serotonin reuptake inhibitor, this medication is not typically given in full divided doses because of excessive side effects.[19,27] A new slow-release preparation has been approved to allow a better tolerated, full dose range.

Benefits.Trazodone is often called a sedating antidepressant. It helps insomnia, improves sleep efficiency, and has its action even at low doses. Sexual side effects and activating side effects are low.[19,27]

Drawbacks. Significant sedation may limit its use.

Mirtazapine. This medication is also considered to be sedating and is typically either avoided or sought because of its side effect profile. Side effects include sedation/hypnotic effects and appetite stimulation, but not sexual side effects. The lack of sexual side effects is again related to serotonin in that mirtazapine is not a serotonin reuptake inhibitor, but in this case acts as a serotonin 2A/2C receptor antagonist.[19,27] The blockade of these receptors may result in more dopamine and norepinephrine release in the prefrontal cortex. The histamine blockade (H1) results in sedation, anxiolytic/hypnotic effects, and weight gain.[19,27] Mirtazapine also acts as a 5HT3 receptor antagonist, resulting in reduction of gastrointestinal problems.[19,27] The primary mechanism of antidepressant action is through alpha 2/norepinephrine receptor antagonism. Through this antagonism, inhibition of norepinephrine is disinhibited through auto receptor blockade. This allows downstream effects on several pathways and may result in overall release of serotonin and norepinephrine. This effect can often be combined with an SNRI to obtain synergistic effects.[27]

Benefits.Mirtazapine has many unique mechanisms of actions that make it beneficial in particular populations. It lacks sexual side effects, reduces gastrointestinal upset, and is not activating. The sedating qualities of this medication are typically used to the medication’s and the patient’s benefit.

Drawbacks.Mirtazapine has significant weight gain/appetite stimulation effects, which could lead to metabolic disorders.

This review is both practical and factual. Clinicians ideally should be aware of regulatory approvals and appropriate use of them in certain patient populations. When used this way, clinicians may expect results comparable to those noted in the evidence base of regulatory trials. However, those who treat patients understand that not all are identical to those enrolled in research trials. What follows will provide some practical clinical approaches when responses do not meet expectations.

As noted, only one third of patients will fully remit on their first antidepressant trial.[38] These numbers hold true for patients who are fully treated with moderate to high dose SSRI for as long as 12 weeks. In clinical practice, patients may not even have such a rigorous dosing profile and failure rates are likely higher. What approaches should be taken when a patient is not responding to treatment?

Adherence and Dosing

First, ask and attempt to ensure adherence to the antidepressant treatment. This questioning should be nonjudgmental and empathic, as most patients will likely say they are compliant even when they are not. Oftentimes suggesting that most people tend to naturally miss a few doses and that you as the clinician are just checking up will diffuse the situation. As dosing becomes divided throughout the day and polypharmacy increases, compliance usually diminishes, making assessment for compliance and adherence to medical regimens even more important.

Tolerability

An important area to address to improve adherence to a regimen relates to side effects and antidepressant tolerability. Sometimes patients cease taking their antidepressant or fail to escalate the dose as advised when adverse effects are not well tolerated. Many mild side effects will dissipate over time and this should be discussed directly with the patient.[39] Patients should be instructed to inform prescribers of any moderate to severe side effects and the drug can then be safely stopped. Patients should also be told that there are many antidepressants, and these have different side effects.[2,39] For example, SSRI, SNRI, and NDRI may be activating, and thus cause insomnia or nervousness upon initiation of treatment. Patients may be switched to a less activating SARI or noradrenergic antagonist-selective serotonin antagonist mechanism-based product, as these tend to be less activating and more sedating.[2]

Some patients may experience drug-drug interactions depending upon their genetic make-up.[2] Switching away from hepatic inhibiting medications towards medications that are less likely to interact with other drugs may be warranted. Typical side effects of headaches, stomachaches, or even insomnia often can be treated very effectively with over the counter or prescription medications. Later onset side effects such as weight gain or sexual dysfunction may be more difficult to mitigate or treat. Open discussions with patients about these longer term risks are warranted because patients often have to stay on their antidepressants for a year or more to maintain remission and avoid a depressive relapse.[38] Because certain antidepressants may have a more, or less favorable weight or sexual side effect profile, they should be chosen based on a discussion about patient preference when possible.

Assuming adherence is adequate, the next step is to confirm that the antidepressant dose was at the moderate to high end of the approved range and has been taken for at least 4 to 6 weeks. If dosing is confirmed to be reasonable, consider a final maximization of dose or switch to a new antidepressant monotherapy.[39]

Switching Monotherapies

If it is necessary to consider switching monotherapies, no clear benefit has been attributed to any particular strategy.[38] Many experts agree, however, that a switch away from an SSRI is warranted if the fully dosed SSRI therapy has failed to improve the patient’s symptoms.[27,39] The theoretical implication is that the patient’s current depressive symptoms have been treated with aggressive serotonergic facilitation and that repeating this mechanism may not be fruitful. This suggests that, pharmacodynamically, the depression may not be entirely serotonin-based in regards to its etiology.[27,39] Given this, a cross titration on to an SNRI such as venlafaxine XR or duloxetine, a NDRI such as bupropion XL, a noradrenergic antagonist-selective serotonin antagonist such as mirtazapine, or a more aggressive serotonergic facilitating agent like a SARI such as trazodone ER or a serotonin partial agonist-reuptake inhibitor such as vilazodone theoretically may be warranted.[2]

One final concern regarding switching involves the use of generic vs brand-name drugs. The FDA ensures that the bioavailability between a brand name and its generic counterpart is approximately between 20% weaker and 20% stronger.[40,41] Most generics are highly comparable, but occasionally when a patient actually changes from one generic to another, the bioavailability could change from a 20% stronger to a 20% weaker generic drug and symptom relapse may occur. By contrast, going from a weaker to a stronger generic might actually improve depression outcomes but may also create new-onset side effects after months of stable treatment as the newer generic preparation is more potent, raising blood levels higher than previously. These types of events should be monitored and dosing adjusted as needed.

Finally, a generic drug may possess a different slow-release mechanism compared with the parent brand-name drug. Oftentimes the generic, despite being a slow-release drug itself may actually release active drug more quickly than the original brand’s slow-release technology. There may be no evidence of a clinical problem; however, some patients may develop side effects when taking the faster release preparation. In this case, the dose may need to be lowered while monitoring for relapse or a switch back to the brand-name slow-release product may be warranted.

In conclusion, this article seeks to identify treatments that match patients with MDD and their common comorbidities, as a first line approach to MDD management. Secondarily and more theoretically, patients’ MDD symptoms may be effectively treated if clinicians are aware of the neurotransmitters and receptors that each antidepressant modulates. Finally, patients may suffer issues with nonefficacy, noncompliance, and tolerability. Each patient is unique and these clinical situations may interfere with optimal depression outcomes. Each patient must be educated and given informed consent about the myriad effective antidepressant treatment options available.

Supported by an independent educational grant from Valeant Pharmaceuticals.

References:

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Text revision. Washington, DC: American Psychiatric Association; 2000.
  2. Stahl SM. Essential Psychopharmacology: The Prescriber’s Guide. Cambridge, Mass: Cambridge University Press; 2005.
  3. FDA Package Insert. Pristiq. Pfizer Inc. 2011.
  4. FDA Package Insert. Viibryd. Forest Laboratories, Inc. 2011.
  5. Davidson J, Baldwin D, Stein DJet al.Treatment of posttraumatic stress disorder with venlafaxine extended release: a 6-month randomized controlled trial. Arch Gen Psychiatry. 2006;63:1158-1165. Abstract
  6. Bandelow B, Zohar J, Hollander E, et al. World federation of societies of biological psychiatry (WFSBP) guidelines for the pharmacological treatment of anxiety, obsessive-compulsive and post-traumatic stress disorders — first revision. World J Biol Psychiatry. 2008;9:248-312. Abstract
  7. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder.
  8. Phelps NJ, Cates ME, The role of venlafaxine in the treatment of obsessive-compulsive disorder. Ann Pharmacother. 2005;39:136-140. Abstract
  9. Gartlehner G, Hansen RA, Reichenpfader U, et al. Drug class review: second-generation antidepressants: final update 5 report [internet].Portland, Ore: Oregon Health & Science University; March 2011.
  10. Effexor Prescribing Information. http://labeling.pfizer.com/showlabeling.aspx?id=100
  11. FDA Package Insert. Cymbalta. Lilly USA LLC. 2004/2011.
  12. FDA Package Insert. Silenor. Somaxon Pharmaceuticals Inc. 1969.
  13. Hsu, ES. Acute and chronic pain management in fibromyalgia: updates on pharmacotherapy. Am J Ther. 2011;18:487-509. Abstract
  14. Verdu B, Decosterd I, Buclin T, et al. Antidepressants for the treatment of chronic pain. Drugs. 2008;68:2611-2632. Abstract
  15. Prince JB, Wilens TE, Biederman J, et al. A controlled study of nortriptyline in children and adolescents with attention deficit hyperactivity disorder. J Child Adolesc Psychopharmacol. 2000;10:193-204. Abstract
  16. Pliszka SR. Non-stimulant treatment of attention-deficit/hyperactivity disorder. CNS Spectr. 2003;8:253-258. Abstract
  17. Wilens TE, Prince JB, Spencer T, et al, An open trial of bupropion for the treatment of adults with attention-deficit/hyperactivity disorder and bipolar disorder. Biol Psychiatry. 2003;54:9-16. Abstract
  18. Olvera RL, Pliszka SR, Luh J, et al. An open trial of venlafaxine in the treatment of attention-deficit/hyperactivity disorder in children and adolescents. J Child Adolesc Psychopharmacol. 1996;6:241-250. Abstract
  19. Sadock BJ, Sadock VA, et al. Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. Tenth ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2007:977-1126.
  20. Prochazka AV, Kick S, Steinbrunn C, et al. A randomized trial of nortriptyline combined with transdermal nicotine for smoking cessation. Arch Intern Med. 2004;164:2229-2233. Abstract
  21. FDA Package Insert. Wellbutrin XL. GlaxoSmithKline. 2008.
  22. McIntyre RS, Mancini DA, McCann S, et al, Topiramate versus bupropion SR when added to mood stabilizer therapy fpr the depressive phase of bipolar disorder: a preliminary single-blind study. Bipolar Disord. 2002;4:207-213. Abstract
  23. Coleiro B, Marshall SE, Denton CP, et al. Treatment of raynaud’s phenomenon with the selective serotonin reuptake inhibitor fluoxetine. Rheumatology. 2001;40:1038-1043. Abstract
  24. Stearns V, Beebe KL, Iyengar M, et al. Paroxetine controlled release in the treatment of menopausal hot flashes: a randomized controlled trial. JAMA. 2003;289:2827-2834. Abstract
  25. Evans ML, Pritts E, Vittinghoff E, et al. Management of postmenopausal hot flushes with venlafaxine hydrochloride: a randomized, controlled trial. Obstet Gynecol. 2005;105:161-166. Abstract
  26. Muller D, Roehr CC, Eggert P. Comparative tolerability of drug treatment for nocturnal enuresis in children. Drug Saf. 2004;27:717-727. Abstract
  27. Stahl SM. Stahl’s Essential Psychopharmacology: Neuroscientific Basis and Practical Applications. 3rd ed. Cambridge, Mass: Cambridge University Press; 2008:511-666.
  28. Spina E, Scordo MG. clinically significant drug interactions with antidepressants in the elderly. Drugs Aging. 2002;19:299-320. Abstract
  29. FDA Packet Insert. Celexa. Forest Laboratories, Inc. 2010/2011.
  30. Spina E, Santoro V, D’Arrigo C. Clinically relevant pharmacokinetic drug interactions with second-generation antidepressants: an update. Clin Ther. 2008;30:1206-1227. Abstract
  31. Cipriani A, Furukawa TA, Salanti G, et al. Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis. Lancet. 2009;373:746-758. Abstract
  32. Nelson JC, Papakostas GI. Atypical antipsychotic augmentation in major depressive disorder: a meta-analysis of placebo-controlled randomized trials. Am J Psychiatry. 2009;166:980-991. Abstract
  33. Danish University Antidepressant Group. Citalopram: clinical effect profile in comparison with clomipramine. A controlled multicenter study. Psychopharmacology (Berl). 1986;90:131-138. Abstract
  34. Danish University Antidepressant Group.Paroxetine: a selective serotonin reuptake inhibitor showing better tolerance, but weaker antidepressant effect than clomipramine in a controlled multicenter study. J Affect Disord. 1990;18:289-299. Abstract
  35. Roose SP, Glassman AH, Attia E, Woodring S. Comparative efficacy of selective serotonin reuptake inhibitors and tricyclics in the treatment of melancholia. Am J Psychiatry. 1994;151:1735-1739. Abstract
  36. Beasley CM Jr, Holman SL, Potvin JH. Fluoxetine compared with imipramine in the treatment of inpatient depression. A multicenter trial. Ann Clin Psychiatry. 1993;5:199-207. Abstract
  37. Bailey J. Acute psychosis after bupropion treatment in a healthy 28-year-old woman. J Am Board Fam Med. 2008;21:244.
  38. Rush AJ, Trivedi MH, Wisnewlski Sr, et al. Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. Am J Psychiatry. 2006; 163:1905-1917. Abstract
  39. Zajecka JM, Goldstein C. Combining medication to achieve remission. In: Schwartz T, Petersen T, eds. Depression: Treatment Strategies and Management. 2nd ed. New York: Informa; 2009.
  40. Park K, ed. Controlled Drug Delivery: Challenges and Strategies. Washington, DC: American Chemical Society; 1997.
  41. Orange book annual preface, statistical criteria for bioequivalence. In: Approved Drug Products with Therapeutic Equivalence Evaluations. 29th ed. US Food and Drug Administration Center for Drug Evaluation and Research; 2009-06-18, update 3-01-11. http://www.fda.gov/Drugs/DevelopmentApprovalProcess/ucm079068.htm

Retrieved from: http://www.medscape.org/viewarticle/755180

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 and Sensory Defensiveness

In ADHD, ADHD Adult, ADHD child/adolescent, School Psychology on Sunday, 16 September 2012 at 10:30

ADD and Hypersensitivity:
Is There A Connection?

Follow Up Report by Mary Jane Johnson

from http://www.oneaddplace.com

It has been several months now since I reported on ADHD and hypersensivity. Since that time I have heard from several ADD adults who suffer some of the same symptoms. One person sent me an article entitled “Social and Emotional Issues of Adults with Sensory Defensiveness “from the Sensory Integration Newsletter published by The American Occupational Therapy Assoc.

Many of these same hypersensitivities are mentioned in this article and I will quote from the article as well as what was shared by the readers who wrote to me. Sensory Integration Newsletter states, “Adults with tactile defensiveness commonly report strong clothing preferences and avoidances, and aversions to clothes with tags, jewelry….may also feel uncomfortable with wool or synthetic materials against the skin….and may be bothered by these aversions to an extreme degree….

“Along those same lines K. wrote in that, “I have to keep my shoes tied tight on my feet… If they are not tight I get frustrated… I find that I constantly re-tie my shoes as tight as possible, during the day.” And D. relates, “I agree completely about the elastic… I also do not like sleeves, high collars, knee socks that fall down, tags on the inside of shirts, anything touching my skin that isn’t soft or cottony, slacks too tight in the crotch… I hate panty hose… I don’t wear my coat in the car, I have a nice thin vest with lots of pockets that I wear while shopping.

“In regards to sensitivity to food textures M. shares, “My dad as a child couldn’t stand different foods to touch, so my grandmother bought him a compartmentalized plate… I had to do the same for my son… He stopped picking up wet finger foods or food that made his hands sticky… He wanted a different spoon or fork for each food… He wanted only bland soft foods and to this day there are very few foods he likes… My taste is more sensitive than the others in my family.” D. says, “I am also a picky eater, but I love spicy food. I can’t stand browned scrambled eggs and my fried eggs must be perfect.”

When it comes to heat and cold sensitivity, M. writes, “If it gets around 70 degrees I’m cold… That’s why we live in the desert… my hands and feet seem to always have had poor circulation… My hands get cold inside good leather gloves.” K. states, “…especially cold… I need to dress and keep the house warm as soon as cool weather moves in… If I didn’t love New England so much I would probably live in a warm climate year round.

“The remarks about hearing sensitivity includes: M., “clock in the living room because he could hear it ticking all the way in his room…My son can sleep through noises but certain frequencies hurt or upset him…I travel with a Sears ‘sleepmate’ white noise machine. I can’t sleep without masking the noise. I annoy the heck out of my husband by my ability to hear the TV at the other end of the house… I can’t have a ticking clock in the room where I sleep… My dad also has a noise machine.

” K., “…when trying to focus on things I can’t filter out noises…While typing this letter I can hear water dripping in the next room, the refrigerator turning on and off, and a car engine idling outside. “And D., “I enjoy loud music, but only when I feel like it. I think that’s why people think we are selfish at times.”

Sensory Integration Newsletter reports, “Social events… puts the person with defensiveness in an uncomfortable situation… Almost all subjects described the discomfort experienced when someone’s touch takes them by surprise… Many subjects describe shaking hands as unpleasant… When the touch or hug from comes from behind, it’s effect is multiplied because of the element of surprise… and many need to exert self-control to avoid striking out at the person who touched them.

“M. shares, “I don’t like being touched… even shaking hands is difficult… It’s taken my husband years to learn how to touch me without provoking a negative response… Touching my head or hair is a no no!” A twist on this particular hypersensitivity comes from D. who says, “I am happy to say the hypersensitivity to touch, in the romantic sense, is more often a plus than a minus.” And K. adds, “I don’t mind shaking someone’s hand, but forget hugging… Whenever someone hugs me, I tense up and my stomach gets tied up in knots… Being married my wife loves to be touched… I get all tied up when she hugs me or wants to be hugged or held… It tears me apart because I love my wife and yet for some reason want my space

“……..”Most subjects described feeling uncomfortable in crowded places such as crowded elevators, buses, or subways, restaurants, stores, malls… Shopping is difficult for them”, states Sensory Integration Newsletter. K. agrees by saying, “I have difficulty going into elevators, and detest having to go to malls, food stores, sporting events, etc… I get very over-stimulated, overwhelmed and irritable until I’m free from crowded areas.” D. states, “I notice that claustrophobia is more evident when I am somewhere I don’t like to be, such as in a car on a trip of more than an hour.” In some individuals there seems to be a connection between having ADD and being hypersensitive, as these cases indicate.

ADULT SENSORY QUESTIONNAIRE (ASQ)

(Kinnealey and Oliver, © 2002)

Circle the item as T – true or F – False as it applies to you.

 

 

 

 

 

1.  T   F

 

I am sensitive and get bothered by smells that don’t seem to bother other people.

2.  T   F I am sensitive or bothered by sounds that don’t seem to bother other people.
3.  T   F I am bothered by looking down a long flight of stairs or going down an escalator.
4.  T   F I get car sick.
5.  T   F I am sensitive to movement.  I get dizzy very easily.
6.  T   F I am sensitive to and bothered by lights/contrasts/reflections or objects close to my face (that don’t seem to bother others).
7.  T   F I am bothered by some food textures in my mouth (or I avoid them).
8.  T   F It bothers me to be barefoot on grass or sand.
9.  T   F I am bothered by tags and labels in my clothes (or I remove them).
10. T   F I am bothered by turtleneck shirts, tight fitting clothes, elastic, nylons, or synthetic material in clothes (any of the above).
11. T   F I am bothered by the feeling of jewelry (or I never wear it because of this).
12. T   F I am very aware that certain parts of my body are very sensitive.
13. T   F I avoid putting creams and lotions on my skin because of how it feels.
14. T   F I have a sensitive scalp.
15. T   F I do not like being in crowded areas such as elevators, malls, subways, crowded shops or bars (or I never put myself in these situations).
16. T   F Growing up, I did not like to be hugged (except by my mother).
17. T   F I am often uncomfortable with physical intimacy because touching bothers me.
18. T   F I feel bothered when someone touches me from behind or unexpectedly, or stands too close.
19. T   F I was very active as a child (or I am now).
20. T   F I have mood swings more than other people.
21. T   F I do not go to sleep easily and wake up easily and/or I don’t sleep between 6 and 8 hours each night.
22. T   F I consider myself to be anxious.
23. T   F I feel I must mentally prepare myself for situations in which people are apt to touch me.
24. T   F It is important for me to be in control and know what to expect.
25. T   F I am perfectionistic, or compulsive.
26. T   F I avoid if at all possible, situations in which my senses will be stressed.

____________ Total Score (count up the number of “Trues”)

Scoring:           

> 10   = definite sensory defensiveness

6 – 10 = moderate sensory defensiveness

< 6      = not sensory defensive

 

Healthy Diet and ADHD

In ADHD, ADHD Adult, ADHD child/adolescent, Alternative Health, School Psychology on Sunday, 16 September 2012 at 05:16

Healthy vs Western Diet Linked to Better Outcomes in ADHD

Megan Brooks & Penny Murata, MD

http://www.medscape.org/viewarticle/757166

Clinical Context

In children with attention-deficit/hyperactivity disorder (ADHD), the effectiveness of diet and dietary supplements is not clear. Dietary measures that have been proposed include sugar restriction; the additive- and salicylate-free Feingold diet; the oligoantigenic or elimination diet; and ketogenic, megavitamin, and polyunsaturated fatty acid (PUFA) supplements. In the July 2011 issue of the Journal of Attention Disorders, Howard and colleagues reported a link between ADHD and a “Western” diet high in fat, refined sugars, and sodium.

This review of the literature assesses the evidence for dietary treatment in children with ADHD.

Study Synopsis and Perspective

When drug therapy fails to control ADHD or is unacceptable, adopting a “healthy” diet, eliminating items known to predispose to ADHD, and adding omega-3 fatty acid supplementation may be worth trying, new research suggests.

“The recent increase of interest in this form of therapy for ADHD, and especially in the use of omega supplements, significance of iron deficiency, and the avoidance of the ‘Western pattern’ diet, make the discussion timely,” the authors write.

Many parents and physicians continue to be interested in how diet and dietary changes, particularly parents wanting to find an alternative to stimulant medication or a complementary therapy. Nevertheless, it remains a “controversial” topic, the authors note.

For their review, J. Gordon Millichap, MD, and Michelle M. Yee, CPNP, from Children’s Memorial Hospital in Chicago, Illinois, searched PubMed for relevant studies on the role of diet and dietary supplements for the treatment of children with ADHD.

They note that their recommendations on diet and dietary supplements are based on a critical review of the data and their own experience in a neurology clinic for children and adolescents with ADHD.

The study was published online on January 9 in Pediatrics.

Elimination Diets Not Advisable

Perhaps the “most promising and practical” complementary or alternative treatment, write Dr. Millichap and Ms. Yee, is adopting a “healthy” dietary pattern, omitting items shown to predispose to ADHD or to make the condition worse. These items include fast foods, red meat, processed meat, potato chips, high-fat dairy foods, and soft drinks.

They point to a “provocative” study published last year, which found a link between ADHD in adolescents and a “Western-style” dietary pattern that was high in fat, refined sugars, and sodium and low in fiber, folate, and omega-3 fatty acids (Howard et al, J Atten Disord. 2011;15:403-411). ADHD was not associated with a “healthy” dietary pattern rich in fish, vegetables, fruit, legumes, and whole-grain foods.

Adopting a healthy dietary pattern “may offer an alternative method of treatment of ADHD and less reliance on medications,” the authors of the current study write.

They also note that although many parents report worsening of hyperactivity symptoms after consumption of foods and drinks containing sugar or aspartame — and isolated reports support the parents’ observations — most controlled studies have failed to find a significant harmful effect of sugar or aspartame, the authors note.

Additionally, they say that the elimination of sugar and aspartame and adapting additive-free diets are complicated, disruptive, and often impractical; such measures are indicated only in select cases.

Fatty Acid Supplements May Be Helpful

Low levels of long-chain PUFAs have been reported in the plasma and red cells of children with ADHD in comparison with their ADHD-free peers, Dr. Millichap and Ms. Yee note. Some studies have demonstrated a reduction in ADHD symptoms with PUFA supplementation, although no definitive conclusions can be drawn.

However, the authors note that “on the basis of reports of efficacy and safety, we use doses of 300 to 600 mg/day of omega-3, and 30 to 60 mg/day of omega-6 fatty acids, continued for 2 or 3 months, or longer if indicated.”

“As initial or add-on therapy, we have occasional reports of improved school grades and lessening of symptoms of ADHD, without occurrence of adverse effects. Most parents are enthusiastic about trying the diet supplements, despite our explanation of only possible benefit and lack of proof of efficacy,” they note.

They also note that iron and zinc supplementation is advisable when there is a known deficiency in these minerals, and this may “enhance the effectiveness” of stimulant therapy.

Pediatrics. Published online January 9, 2012.

Related Link
The National Institute of Mental Health’s Attention Deficit Hyperactivity Disorder (ADHD) site offers a wide range of information helpful for parent education including a downloadable booklet discussing the condition and its management.

Study Highlights

  • This review study provides an overview of the role diet has in children with ADHD. The following supplements, foods, and diets affect the children’s health outcomes in various ways, according to several studies.
  • Omega-3 and omega-6 fatty acid supplements
    • Low long-chain PUFA levels were reported in children with ADHD vs control patients.
    • Some studies showed that PUFA reduced ADHD symptoms, but other studies did not.
    • Doses of omega-3, 300 to 600 mg/day, and omega-6, 30 to 60 mg/day, for 2 to 3 months or longer have been used.
    • Concurrent ADHD medication is almost always needed.
  • Additive and salicylate-free (Feingold) diet
    • Adherence to the diet is complicated and may be disruptive or impractical.
    • Foods to be avoided are apples, grapes, luncheon meats, sausage, hot dogs, and cold drinks with artificial flavors and coloring agents.
    • Permitted foods are grapefruit, pears, pineapple, bananas, beef, lamb, plain bread, certain cereals, milk, eggs, and color-free vitamins.
    • Controlled trials found a small subgroup of preschool children had an adverse response to challenges of additives and preservatives.
    • Children with ADHD and atopy vs no atopy have a higher response to elimination of foods, artificial colorings, and preservatives.
  • Oligoantigenic (hypoallergenic/elimination) diet
    • Adherence to the diet is complicated and may be disruptive or impractical.
    • The oligoantigenic diet eliminates sensitizing food antigens or allergens, including cow’s milk, cheese, wheat cereals, egg, chocolate, nuts, and citrus fruits.
    • Elimination of some foods appeared to decrease some ADHD symptoms, but plays an uncertain role in ADHD treatment.
    • A 2- to 3-week period of elimination diet is followed by the reintroduction of single items each week until the food sensitivity is identified.
    • Behavior improvements might not occur for up to 2 weeks.
    • Enzyme-potentiated desensitization might enable children to become tolerant of provoking foods.
  • Sugar and aspartame
    • Sugar does not affect behavior or cognitive performance, but might affect a subset.
    • In preschool boys, daily sucrose and total sugar intake correlated with duration of aggression.
    • Reactive hypoglycemia after sugar load might reduce cognitive function.
    • Hypoglycemia is linked with impaired electrical activity of the cerebral cortex and slow rhythms on electroencephalogram.
  • Ketogenic diet
    • A ketogenic diet high in fats and low in carbohydrates for children with intractable seizures helped to control seizures and improve behavior, attention, and social functioning.
  • Iron deficiency
    • Iron deficiency is not consistently linked with ADHD severity or frequency.
    • 1 study showed that low serum ferritin correlated with baseline inattention, hyperactivity, impulsivity, and effective amphetamine dose needed.
  • Zinc deficiency
    • Low zinc levels were found in the serum, red cells, hair, urine, and nails of children with ADHD, but mostly in countries with endemic zinc deficiency.
    • In the United States, low serum zinc was linked with inattention, but not with hyperactivity or impulsivity.
    • Zinc supplements might enhance the effect of d-amphetamine, but are not routinely recommended.
  • Other alternative dietary therapies
    • Orthomolecular medicine and megavitamin therapy refer to combination of minerals and nutrients.
    • A study of megavitamin therapy in children with ADHD showed no improvement in behavior, but 42% had elevated serum transaminase levels.
  • “Healthy” vs “Western” diet pattern
    • A cohort study of children from birth to age 14 years found a “Western” dietary pattern associated with ADHD diagnosis and a “Healthy” diet pattern not associated with ADHD diagnosis.
    • The Western dietary pattern includes fast foods, red and processed meats, potato chips, high-fat dairy products, and soft drinks.
    • The Healthy dietary pattern includes fish, vegetables, tomatoes, fresh fruit, whole grains, and low-fat dairy products.

Clinical Implications

  • Indications for dietary therapy in children with ADHD include medication failure or adverse reactions, patient or parental preference, mineral deficiency, and need for change from an ADHD-linked Western diet to an ADHD-free Healthy diet.
  • In children with ADHD, additive-free and elimination diets are time-consuming and disruptive, but might be indicated in selected patients; iron and zinc are indicated for deficiencies; omega-3 supplements have inconsistent effects; and a Healthy diet rich in fish, vegetables, fruit, legumes, and whole grains might be beneficial vs a Western diet of fast foods, red or processed meats, high-fat dairy products, soft drinks, and potato chips.

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.

 

ADHD in Adults

In ADHD, Anxiety, Brain studies, School Psychology on Thursday, 13 September 2012 at 05:58

Unmasking ADHD in Adults

David W. Goodman, MD

http://www.medscape.org/viewarticle/768677

Adult ADHD

During the past decade, awareness has grown that ADHD is not limited to children and adolescents. Rather, ADHD is now recognized as a chronic neuropsychiatric disorder that persists into adulthood in up to 65% of children with ADHD.[1-3] Data from the National Comorbidity Survey Replication (NCSR) estimate that 4.4% of adults in the United States have ADHD, although as many as 75% have never been diagnosed and 90% remain untreated.[4,5] The many similarities in symptoms and impairments seen in ADHD and mood and anxiety disorders likely account for many of the misdiagnoses.[6] In addition, the rate of comorbidity in ADHD with mood and anxiety disorders, sleep disorders, and substance use disorders is high and further complicates accurate diagnosis.[5]

Current criteria for ADHD in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR) were originally developed and validated for children.[7] Diagnostic criteria require an onset of symptoms before age 7 years; the presence of at least 6 of 9 possible symptoms in 1 or both of the 2 diagnostic clusters of inattentiveness and hyperactivity; and impairment in 2 or more settings (such as home, school, and work).[7] Many similarities exist in the presentations of childhood and adult ADHD; however, adults are more likely to present with symptoms of inattention than hyperactivity.[8] But the presence of childhood symptoms is necessary for a diagnosis of ADHD in an adult.

Clinicians can use several screening tools to help in the ADHD diagnostic process; however, high scores on these tools must be interpreted within a clinical context following a clinical interview. For example, a high score on the ASRS may suggest ADHD[9,10] but may also be the result of acute anxiety, acute depression, or active substance abuse. Patients who take online screeners and self-diagnose ADHD present their symptoms and “diagnosis” to their clinicians in a descriptive rather than a diagnostic context, not understanding how other possible psychiatric disorders may lead to high screening scores. As a result, their self-diagnoses are typically inaccurate.

The clinical interview includes a comprehensive patient history that covers all major psychiatric disorders. The clinician reviews the presenting symptoms in a diagnostic evaluation, inquiring about other possible psychiatric disorders that the patient may not include in the description of symptoms. Through this process, the clinician can rule out primary mood or anxiety disorders (among others), and also ascertain a longitudinal course of symptoms originating during childhood to confirm a diagnosis of ADHD. An accurate account of childhood symptoms of ADHD improves if corroborative historical information can be obtained from an outside informant (for example, a parent). This historical information can be obtained by having a parent complete a childhood ADHD symptom rating scale that can be returned to the PCP. The use of an outside informant also conveys to the patient that third-party information will be used to establish an accurate diagnosis, a disincentive to those who simply seek a prescription for stimulants.

ADHD vs GAD

The cognitive and affective symptoms of ADHD can be similar to those of other psychiatric disorders, most notably mood and anxiety disorders. However, specific distinguishing characteristics can assist with the differential diagnosis. In this case, despite reporting current symptoms that might be consistent with ADHD, the notable absence of ADHD symptoms during Ms Jones’s childhood and adolescence precludes a diagnosis of ADHD. A more accurate diagnosis is generalized anxiety disorder (GAD), which is characterized by excessive anxiety and worry that is difficult to control and is associated with at least 3 of the following symptoms: restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance, which cause clinically significant distress or functional impairments.[7] Significant chronic anxiety exacerbated by an acute, stressful event can produce cognitive symptoms that appear similar to ADHD. Remember: patients use psychological terms descriptively, not diagnostically.

A survey of 400 primary care physicians highlighted the challenges clinicians face when diagnosing ADHD in adults.[11] Approximately two-thirds of the participating respondents referred adults with possible ADHD to specialists for diagnosis and treatment, whereas they felt more competent and confident when diagnosing depression or GAD. Surveys find that only 2% of PCPs refer patients to specialists for the diagnosis and management of depression; for GAD, only 3% refer out.[11,12]

ADHD and Comorbidity

ADHD affects approximately 9 to 10 million adults in the United States (4.4% of the adult population). This makes ADHD in adults the second most prevalent psychiatric disorder after major depressive disorder (MDD), which reportedly affects 6.6% of the US population, and more prevalent than GAD (3%), bipolar disorder (2%), and schizophrenia (1%).[5] Adults with ADHD have a higher percentage of comorbidities than their peers without ADHD.[5] Among the most prevalent psychiatric comorbidities in patients with ADHD are anxiety disorders, mood disorders, and substance use disorders (SUD).[13] Many adults with ADHD present with symptoms of anxiety, MDD, or both. Further, high levels of stress may mimic the symptoms of ADHD.[13] Consequently, the high prevalence rate of ADHD in the adult population makes it essential for clinicians to include ADHD as part of the differential diagnosis in any mental health evaluation or whenever patients present with depression or anxiety.

Data from the NCSR suggest that up to 75% of adults with ADHD were not diagnosed during childhood.[5] Many adults play down a possible diagnosis of ADHD because they do not recall being hyperactive in childhood or because they have not been previously diagnosed with the disorder. Other adults will dismiss the diagnosis because they appear to be functioning well and are successful in their chosen fields, even though they have symptoms such as restlessness, low self-esteem, or poor time-management skills.[14] Exceptionally intelligent individuals or adults who had predominantly inattentive ADHD as children may not have had observable impairments during childhood because disruptive behavior was absent; however, symptoms may surface as demands increase with greater school and work responsibilities.[15] Similarly, clinicians may overlook ADHD among high-functioning patients, not realizing the need to look past a patient’s success to explore whether the patient might have developed strategies to compensate for ADHD-related deficiencies and is working hard to compensate.

PCPs who rely on the accuracy of a psychiatric diagnosis of adult ADHD from mental health clinicians may not serve their patients well. Data from the NCSR indicate that 37% of women and 53% of men later diagnosed with ADHD were currently taking or had been in treatment for other mental disorders or SUDs in the previous year, in contrast to 25% who had been treated for ADHD.[5] From these data, Kessler and colleagues concluded that adult ADHD is often misdiagnosed by mental health providers.[5] Before prescribing medication, the PCP should review the psychiatric presentation and history with the patient to ensure agreement on the diagnosis. Premature prescription of stimulants for ADHD will only cloud the diagnosis, as adults with ADHD, as well as people in general, may report improvements in mood, cognition, and energy when taking stimulants, which does not confirm a diagnosis of ADHD. In addition, undetected psychiatric disorders may worsen in the presence of stimulants prescribed for ADHD.

Strict adherence to the DSM-IV-TR diagnostic criteria might lead to substantial underdiagnosis of ADHD, as these criteria were originally developed for young boys and may not reflect ADHD symptoms in adults.[16] Clinicians may need to examine whether the patient is advancing appropriately in his or her career or has become a workaholic to compensate for disorganization, procrastination, and sloppy errors.[17] Recent research highlights that adults with ADHD often underestimate the degree of ADHD-related impairments.[18] ADHD that persists into adulthood has been associated with many adverse life experiences or outcomes, including divorce, substance abuse, motor vehicle infractions, academic and occupational underachievement, and brushes with the law.[5,16,19-24] Research suggests that although the number of symptoms may decline along the lifespan, the severity of the impairments does not.[25]

Among the numerous medical conditions that may be associated with cognitive symptoms similar to those of ADHD are thyroid disorders, sleep apnea, hypoglycemia, and lead poisoning.[13] The prevalence of psychiatric comorbidity associated with ADHD is high, with 1 large study reporting that 87% of adults with ADHD had at least 1 comorbid psychiatric diagnosis and 56% had at least 2 comorbid psychiatric disorders.[25] Common comorbidities in ADHD include GAD (which occurs in 25% to 43% of the adult population with ADHD), MDD (16% to 31%), bipolar disorder (up to 47%), and SUD (21% to 53%).[26-28]

Differentiating ADHD and Other Psychiatric Disorders

Clinicians often mistake adult ADHD symptoms as manifestations of other psychiatric disorders, especially anxiety, MDD, or bipolar disorder.[29] It is especially important that clinicians attend to the context of the symptoms: when they originated, how long they have persisted, and whether aggravating or alleviating factors exist. Clinicians also need to determine whether the symptoms might be a function of stress or another condition, such as a sleep disorder. Patient misinterpretation of the symptoms may be more prevalent among adults who were not diagnosed with ADHD during childhood, and some adults may be surprised that they did not “outgrow” their childhood ADHD. Other adults may not recall being diagnosed with ADHD during childhood, suggesting that the absence of a self-report of an ADHD diagnosis may not accurately reflect the absence of childhood ADHD.[30] Misdiagnosis and subsequent inappropriate treatment may help to resolve some secondary symptoms (anxiety and minor depression) but will not resolve the core symptoms of inattentiveness, impulsivity, and hyperactivity.

ADHD is historically a disorder of childhood; as such, diagnosis requires evidence of symptoms occurring during childhood. Adults typically present with fewer overt symptoms and different manifestations of hyperactivity, inattention, and impulsivity than children (Table 1).[31] Whereas hyperactive children cannot sit still and are fidgety, adults may feel restless, have difficulty relaxing, and show impatience. Childhood manifestations of inattention include daydreaming, poor reading comprehension, and working slowly; adult manifestations include procrastination, disorganization, forgetfulness, and missing or showing up late for appointments. Making careless mistakes is common among patients of all ages with ADHD. Impulsive symptoms during childhood include blurting out answers, interrupting others, and having temper outbursts; adults will also manifest with temper outbursts and verbal impulsivity, as well as impulsive spending, starting but not necessarily finishing multiple projects, and moving from job to job.[31]

Table 1.

ADHD Symptom Evolution from Childhood to Adulthood

Childhood Adulthood
Inattention
  Difficulty sustaining attention (meetings, reading, paperwork)
Failure to pay attention to details Makes careless errors
Appears not to listen Easily distracted/forgetful
Lacks follow-through Poor concentration
Cannot organize Difficulty finishing tasks
Loses important items Disorganized/misplaces items
Hyperactivity
Squirming/fidgeting Inefficiencies at work
Cannot stay seated Internal restlessness
Cannot wait his/her turn Difficulty sitting through meetings
Runs/climbs excessively Works more than one job
Cannot play/work quietly Works long hours
“On the go”/seems “driven by a motor” Self-selects very active jobs
Talks excessively Overwhelmed
Talks excessively
Impulsivity
Blurts out answers Impulsive job changes
Cannot wait in line Drives too fast
Intrudes/interrupts others Interrupts others
Easily frustrated

The Question of Early Symptoms

A particularly challenging component in diagnosing adult ADHD is obtaining sufficient retrospective information to confirm the presence of ADHD symptoms during childhood. Patients may not remember having ADHD-related symptoms before age 7 (a diagnostic criterion for pediatric ADHD in the DSM-IV-TR), although they may identify problems in late grade school or early middle school that continued throughout high school. A recent study compared 4 groups of adults: those who met all criteria for childhood-onset ADHD; those who met all criteria except the age-at-onset criterion (late-onset ADHD); those with subthreshold ADHD who did not meet full symptom criteria; and those without ADHD.[32] Substantial similarities existed between the adults who met the age-at-onset criterion and those with late-onset ADHD, leading these and other investigators to conclude that the current age-at-onset criterion of 7 years is too stringent and to suggest extending the criterion to age 12 in the next iteration of the DSM.[32,33]

Many adults who were not diagnosed during childhood have developed compensatory mechanisms enabling them to function, albeit less than optimally. Clinicians could ask to speak with the patient’s parents or other family members who may be able to provide insights into the patient’s childhood symptomatology. Similarly, current family members, a spouse, and friends might report clinically relevant ADHD symptoms that have been observed for a long time. While an adult might recognize restlessness as a possible ADHD symptom and admit to receiving numerous driving citations, others might note that the patient overreacts, has difficulty staying with tasks, is easily frustrated, or has held numerous jobs.

No standard for the screening of adults for ADHD currently exists. Among the tools that clinicians can use to help in the diagnostic process are the 18-item World Health Organization’s (WHO) ASRS, which can be freely downloaded from the Internet[34]; the Conners’ Adult ADHD Rating Scale (CAARS); the Brown Attention Deficit Disorder Scale (BADDS); the Wender Utah Rating Scale; and the Wender-Reimherr Adult Attention Deficit Disorder Scale. A recent factor analysis determined that many of these scales are in strong agreement with one another, suggesting that clinicians can choose whichever scale is the most pragmatic, cost efficient, and least time-consuming to use.[35] Patients who screen positive on these assessments should then undergo a full diagnostic evaluation, including a clinical interview that assesses current and lifetime symptoms, a thorough developmental history, and behavioral assessments to identify any functional impairments and symptoms.[31]

Treatment of ADHD in Adults

As yet, no formal guidelines have been developed for the treatment of adult ADHD in the United States. However, guidelines for the treatment of ADHD in children and adolescents, as well as international guidelines for the treatment of adult ADHD, offer recommendations that can be extrapolated to US adults. Considerable concordance exists among the guidelines established by the Canadian ADHD Resource Alliance (CADDRA),[17] the American Academy of Child and Adolescent Psychiatry (AACAP), the National Institutes of Health (NIH), and the British Association for Psychopharmacology on Childhood ADHD.[36] The National Institute for Health and Clinical Excellence (NICE) guidelines address both childhood and adult ADHD.[37] The European Network Adult ADHD consensus statement on the diagnosis and treatment of adult ADHD notes the substantial negative and far-reaching consequences of non-treatment of ADHD.[38] These guidelines recommend a multimodal approach to the treatment of ADHD in adults, beginning with psychoeducation about ADHD and pharmacotherapy for ADHD and any comorbid disorders. Recognizing that pharmacotherapy is often insufficient to address all the problems associated with adult ADHD, the guidelines recommend various symptom-specific coaching programs and cognitive behavior therapy to teach problem solving, coping, and time management skills.[38] Similar multimodal treatment recommendations have been proposed by CADDRA.[17]

Available pharmacologic treatments include short-acting and long-acting stimulant and nonstimulant medications. Psychostimulants, including amphetamines and methylphenidates, are recommended as first-line therapy for both children and adults across all sets of US and international guidelines. Currently, only long-acting agents have been approved for the treatment of ADHD in adults in the United States. Despite this, research suggests that 46% of adults diagnosed with ADHD are prescribed off-label, short-acting stimulants.[39]

Approximately 95% of children who were diagnosed with ADHD during childhood and treated with stimulants do not persist with their medication into adulthood,[40] perhaps because clinicians and patients continue to believe that ADHD is a disorder of childhood. Stimulant medications have been shown to effectively address many of the symptoms of ADHD, including poor attention span, restlessness, short-term memory, and hyperactivity. Some patients may respond preferentially to either amphetamine or methylphenidate compounds, and a small percentage of patients do not respond to stimulants at all.[41,42] Side effects are dose-dependent and can include insomnia, nausea, loss of appetite and weight loss, irritability, mood changes, and clinically nonsignificant increases in heart rate and blood pressure in the majority of patients.[43,44,45] However, clinical practice dictates monitoring vital signs to detect any clinically significant changes that may need to be addressed. A baseline check of vital signs also allows for the detection of undiagnosed hypertension that would require treatment before consideration of stimulant medication. Treatment should be initiated at a low dose and titrated based on symptom reduction and side effects. The dose response in adults is variable; clinicians should not expect that higher doses are needed because the patient is an adult or overweight.

US Food and Drug Administration (FDA)-approved nonstimulants in the ADHD armamentarium include atomoxetine, extended-release (XR) guanfacine, and extended-release (ER) clonidine. Only atomoxetine is currently approved for use in adults, while guanfacine XR and clonidine ER have been approved for use in children and adolescents up to age 18. Other agents that are used off-label include bupropion, tricyclic antidepressants (especially desipramine), and modafinil. The onset of action for atomoxetine is slower than for stimulants, taking to a few weeks to attain the maximum treatment effect. The lack of an abuse potential with nonstimulants may be particularly attractive for use in patients who have SUDs, are at risk for substance abuse, or are potential diverters or sellers of illicit substances.

Atomoxetine is a selective inhibitor of the presynaptic norepinephrine transporter. It has been associated with slightly increased diastolic blood pressure and heart rate, and patients with milder forms of autonomic impairment should be monitored if given this agent.[46] In addition, atomoxetine is predominantly metabolized by the cytochrome P450 2D6 (CYP2D6) isoenzyme, necessitating caution for patients who take medication that inhibits CYP2D6, including fluoxetine, paroxetine, and bupropion.[13] Guanfacine is a direct agonist of the α-2a subtype of norepinephrine receptors. Guanfacine XR can be used as monotherapy or adjunctive therapy with a long-acting psychostimulant.[47,48] Clonidine ER is an α-2a-adrenergic receptor agonist that is considered a second-line agent in the treatment of ADHD, but it may be particularly useful for patients with ADHD and comorbid Tourette syndrome or other tic disorders. As yet, the α-2a agonists have not been studied sufficiently in adults either as monotherapy or as adjunctive treatment in combination with stimulants. Because of the effects of these agents on blood pressure and pulse, monitoring vital signs is recommended, and caution is needed in adults who are being treated for hypertension with other medications.

Monitoring Effects and Side Effects After Initial Treatment

Routine clinical monitoring is necessary throughout the duration of treatment.[13] It is important to meet with the patient on a more frequent basis after medication has been initiated to review tolerability and efficacy and to adjust the dosage (or the medication) as necessary; this typically requires follow-up every 2 to 3 weeks and availability by phone if the patient encounters problems with the medication or dosage. Patients engaged in psychotherapy or skills training will likely be seen on a more frequent, often weekly or biweekly, basis. Once stabilized on an effective and well-tolerated dosage of medication, patients can be seen every 2 to 3 months to monitor the need for dosage adjustments based on tolerability and residual symptoms. Clinicians should assess ADHD symptoms, medication side effects, medication adherence, and comorbid medical/psychiatric conditions at each visit. Similarly, clinicians should monitor caffeine and nicotine intake, as these will further elevate blood pressure and heart rate for all patients on ADHD pharmacotherapies. Although not a common problem, patients with a low body mass index (BMI) should be monitored for suppressed appetite leading to weight loss. Regular assessment of medication utility as measured by daily functional performance should be part of routine monitoring. In the process, you can discuss the continued benefit of medication with the patient. On occasion, a patient may wish to stop the medication to reassess its benefit, and the physician should provide support and oversight in this process. A follow-up reassessment when the patient is off the medication can clarify the re-emergence of ADHD symptoms and impact on daily productivity.

One means for monitoring symptom reduction is through the periodic use of symptom checklists, such as the patient-rated 18-item ASRS. The ASRS is an easy and preferred tool to use because it is standardized, validated, nonproprietary, and readily available on the Internet. It can be administered at baseline and then intermittently, especially with changes to medication dosage, to complement the clinical interview. Patients and their clinicians can get a sense of ADHD symptom improvement with treatment or an increase in symptoms if treatment is suspended or stopped. Patients may forget their ratings of baseline symptoms and find the change in symptom ratings helpful to verify treatment benefit. Although symptom reduction is desirable, the true measure of treatment benefit is the improvement in daily function, such as the ability to initiate and complete more tasks, sustain attention, be less distractible in conversations and meetings, finish tasks on time, reduce careless oversights and errors, and have better, more patient social interactions.

Stimulants, Nonstimulants, and Cardiovascular Risk in Adults

Stimulants are associated with mild elevations in both blood pressure and pulse. It is recommended that patients receiving stimulants have blood pressure and heart rate checked at baseline and regularly throughout treatment.[49] A retrospective database analysis in the United Kingdom found no additional risk of sudden death associated with either stimulants or atomoxetine in children and adolescents 2 to 21 years of age with ADHD.[50] Another retrospective study of adults with new ADHD treatments found that preexisting cardiovascular conditions appeared more likely to reduce prescribing of stimulant treatment in younger vs older patients but did not appear to influence initiation of atomoxetine therapy.[51] In this cohort of 8752 patients, 41% with 1 or more preexisting cardiovascular conditions were prescribed stimulants.[51] Small studies have demonstrated that adults being treated for primary essential hypertension can be safely treated with mixed amphetamine salts[52,53] and methylphenidate.[54] However, stimulant medications for ADHD should not be initiated until the patient is normotensive with a stable antihypertensive medication dose.

In 2008, in response to evidence supporting concerns that the use of stimulants for ADHD could augment the risk of serious cardiovascular events by increasing heart rate and blood pressure, the American Heart Association (AHA) recommended an electrocardiogram (ECG) before initiating treatment in children.[55] This recommendation contradicted recommendations by the AACAP and the American Academy of Pediatrics (AAP), which found that sudden cardiac death in persons taking stimulants was a rare event that could not be prevented or predicted by routine screening with ECG.[56] The AAP recommends an ECG only in those patients with the following risk factors: previously detected cardiac disease, palpitations, syncope, or seizures; a family history of sudden death in children or young adults; hypertrophic cardiomyopathy; or long QT syndrome.[56] Two recent large studies found no significant additional risk of sudden death, myocardial infarction, or stroke in children, young adults, or middle-age adults who were receiving stimulants or atomoxetine.[45,57]

Clinical trials of ADHD medications demonstrate short-term efficacy and safety; however, the majority of patients require chronic long-term treatment.[58-60] Recent studies have demonstrated the safety and efficacy of stimulants, atomoxetine, and guanfacine XR over 24-month treatment periods in children and adolescents.[61] Significant differences between stimulants regarding efficacy or risk of cardiac or cerebrovascular events are not apparent.[62] If clinicians observe any cardiovascular changes, they should determine whether these changes are directly related to the ADHD medication or might instead be related to cardiovascular risks and changes associated with normal aging — for example, weight gain as a cause of hypertension. Nevertheless, long-term studies addressing adverse events are warranted.[59]

Approaches to Improve Executive Function in Adults With ADHD

ADHD can be associated with executive function impairments that can compromise occupational functioning.[63] Executive function is broadly defined as the ability to organize, sequence, prioritize, and hold information in your memory as you consider multiple factors (working memory). Executive function can be defined behaviorally (symptoms observed by patient or others) or by specific neuropsychological measures. Most ADHD symptom checklists enumerate executive function symptoms because they are part of the ADHD symptom criteria. By this definition, all patients with ADHD have executive dysfunction. Executive function may improve with ADHD medication such that inattention, distractibility, and sustained attention improve. In this case, executive dysfunction may be an epiphenomenon of inattention, distractibility, and restlessness. Adults with ADHD may notice improvements in many of their symptoms of impulsivity, inattention, and restlessness but may still struggle with difficulties in organization, developing timelines, planning, and making and initiating decisions.

If the definition of executive function is based on abnormalities that appear on specific neuropsychological tests, then approximately one-third of ADHD patients have executive dysfunction, not 100% as the behavioral definition demands.[64] The clinical relevance of these distinctions is that patients with ADHD may have improved attention and less distractibility and restlessness but still be disorganized. If the clinician believes the disorganization is a residual ADHD symptom, the clinician may respond by increasing the dose of ADHD medication, only to find no further benefit but more side effects. These residual executive dysfunction symptoms tend not to improve with escalating medication dosing.

Results from 2 large trials indicate that adults with ADHD who experienced improvements in executive function with stimulant treatment also experienced improvements in health-related quality of life, particularly in the domains of performance and function.[65] However, a clinical trial of adults with ADHD found that the presence of executive function deficits, as assessed by standardized neuropsychological testing, did not affect clinical response to treatment with osmotic controlled-release oral delivery system (OROS) methylphenidate, and that measures of executive function were not affected by treatment response.[66] The need to better define executive function deficits so that an accurate assessment can be determined is critical; the means to minimize such impairments can be challenging.

Some patients might benefit from adjunctive therapy to address executive function deficits. Research in children and adolescents suggests that the concurrent use of stimulant and nonstimulant therapies can afford significantly greater improvements in ADHD symptoms than stimulant monotherapy, although some combinations have been associated with an additive adverse effect burden and higher cost.[67;48]

Many clinicians recommend cognitive behavior therapy (CBT) or other forms of psychotherapy once the patient has been stabilized on pharmacotherapy. CBT and other interventions can help the patient address organization skills and self-efficacy that have evolved over many years of insufficient treatment for ADHD; it can help patients develop effective compensatory strategies and improve other functional impairments typically associated with ADHD.[68,69] CBT may also help the subset of patients who choose not to use medications (or for whom medications are not appropriate or intolerable), as well as the large proportion of patients who have comorbid conditions.[70] Research suggests that adding CBT may enhance the response to and benefits of pharmacologic treatments.[68]

Metacognitive therapy uses principles and methods of CBT to teach time management, organization, and planning skills, and to address depressive and anxious thoughts that undermine effective self-management. Solanto and colleagues[71] compared a 12-week course of group metacognitive therapy (N = 41) with supportive therapy (including nonspecific group support and validation, psychoeducation, and therapist attention; N = 38) in adults with ADHD. They found that metacognitive therapy provided significantly more benefit in adults with ADHD “with respect to inattention symptoms that reflect the specific functions of time management, organization, and planning.” These benefits were seen in patients who were receiving medication treatment as well as those who were not.

When appropriate, patients may also benefit from couples or family counseling or both, and life skills training or coaching. A review of studies of group and individual psychosocial treatments for adult ADHD found that various psychosocial therapies, including skills-training and psychoeducation, improved motivation and reduced residual symptoms in adults with ADHD.[72]

ADHD and Substance Use Disorders

Up to 75% of adults with ADHD have had at least one comorbid condition,[13] and 40% of adults with ADHD present with a concurrent comorbidity.[73] The high rate of comorbid psychiatric conditions — particularly anxiety disorders, mood disorders, and SUDs — can influence both diagnosis and treatment of ADHD as well as the other condition(s). A significant number of adults with ADHD have a comorbid mood disorder, and a significant proportion of adults with mood disorders have comorbid ADHD.[74] As many as 50% of adult patients with ADHD have had comorbid SUDs.[23] Consequently, clinicians should maintain a high index of suspicion for ADHD among patients with any mental health concern because of its high prevalence in these subpopulations.[75,13]

Evidence suggests that ADHD is a significant risk factor for the development of both SUDs and cigarette smoking.[76] A recent meta-analysis and meta-regression analysis suggests that nearly 1 in 4 patients with SUD met DSM criteria for comorbid ADHD,[77] and 10% to 30% of adults with ADHD have SUD.[78] Alcohol dependence is associated with higher ADHD prevalence than cocaine dependence.[77] Substance use, including cigarette smoking, begins at an earlier age among adults with ADHD,[79] and SUDs are generally more severe in patients with comorbid ADHD.[16] Moreover, SUD may manifest with self-control, attention, and behavioral symptoms similar to those seen in ADHD. The prognosis for patients with ADHD and SUD worsens with additional comorbidities. Adolescents with ADHD and comorbid major depression generally have more severe substance use at baseline and throughout treatment compared with nondepressed adolescents with ADHD and SUD.[80]

Concerns that children treated for ADHD with stimulants are at elevated risk for developing SUD have not been supported by the research. A naturalistic, controlled, 10-year follow-up study of 112 boys and men over 10 years and found no statistically significant associations between stimulant treatment and alcohol, drug, or nicotine use disorders.[81] The investigators concluded that the risk for subsequent SUD is neither increased nor decreased in individuals treated with stimulants for ADHD during childhood and adolescence.

ADHD Comorbidity

It is estimated that only 25% of adult ADHD cases are uncomplicated.[26] In addition to SUD, ADHD has a high comorbidity with mood and anxiety disorders. Data from the NCSR indicate that 9.4% of adults with MDD have ADHD, as do 22.6% of adults with dysthymia.[5] The lifetime prevalence of anxiety disorders among adult patients with ADHD is 40% to 60%.[23] ADHD has been identified in 21.2% of adults with bipolar disorder,[5] and the presence of ADHD may increase the risk of developing bipolar disorder.[17] Many patients do not have just 1 comorbid diagnosis; diagnosing patients with SUD and comorbid psychiatric disorders can be particularly challenging because of the high rate of symptom overlap.

The numerous similarities in clinical presentation among these psychiatric disorders can interfere with accurate diagnosis. For example, symptoms of both ADHD and depression may include trouble sleeping, eating, and concentrating; patients with MDD, ADHD, or GAD may be restless and fidgety. It is important to obtain a comprehensive evaluation for child and adult symptoms, including the temporal relationship between the various comorbid disorders.[82] A primary complaint of a consistent negative mood for 3 months is more suggestive of MDD than ADHD, whereas a report of persistent poor concentration and lack of motivation dating from childhood is more consistent with ADHD. Poor concentration and anhedonia following a depressive episode suggests MDD; poor concentration, depression, organizational problems, and impulsivity that are long-standing suggest ADHD.[17] The clinical presentation of MDD is not affected by comorbid ADHD.[23] Clinicians need to distinguish between a lack of motivation suggestive of ADHD, dysregulated mood and irritability that might indicate ADHD with comorbid mood disorder, and significantly low affect symptomatic of depression.[17] The psychotic symptoms present in bipolar disorder are not likely to be misdiagnosed as ADHD; patients with ADHD do not report a cyclic pattern to their symptoms.[28] Primary care physicians who suspect bipolar disorder, or a manic or hypomanic episode, may want to refer the patient to a specialist, particularly if the patient is diagnosed with comorbid ADHD.

What to Manage First?

Identifying the primary disorder can be particularly challenging in adults with ADHD, as many comorbidities have an onset in mid-to-late-adolescence and these individuals have had many years of dealing with their disorders. In patients with active substance abuse, experts recommend that SUD be considered the primary diagnosis and treated first, regardless of age; once the SUD is under control, clinicians can then reassess the patient to determine whether the presenting symptoms were caused by the SUD, comorbid ADHD, or a mood disorder.[17,38] This strategy is based on controlled studies suggesting that treatment for ADHD in patients with comorbid active SUDs has little effect on either ADHD symptoms or substance use.[83] Adults with SUD who require treatment for ADHD cannot be treated with stimulants until they are in recovery treatment, as stimulants are contraindicated for patients who are actively using addictive substances. However, in adults with comorbid SUD, ADHD can be treated with FDA-approved nonstimulants such as atomoxetine or off-label bupropion, tricyclic antidepressants, or modafinil.[84] Stimulants, preferably long-acting formulations, can be used once patients are in stable substance use remission.

In adults, severe psychiatric mood or anxiety disorders are treated before treating ADHD, whereas ADHD is typically treated prior to initiating treatment for other psychiatric disorders of mild to moderate severity. In some cases, treating ADHD will help resolve the mild or moderate symptoms of the other psychiatric disorders. Clinicians must perform an adequate screen in adult patients with ADHD suspected of comorbid depression to rule out bipolarity. It is recommended that patients with comorbid bipolar disorder and ADHD be treated with mood stabilizers or atypical antipsychotics before initiating treatment with stimulants, which can destabilize bipolar symptoms.[85] Patients with comorbid ADHD and MDD can be treated with a stimulant and an antidepressant, particularly selective serotonin reuptake inhibitors (SSRIs).[74] Stimulants can be administered with serotonin-norepinephrine reuptake inhibitors (SNRIs), but this combination needs to be closely monitored for sympathomimetic side effects.[13] However, when atomoxetine is co-administered with SSRIs, one should be mindful of potential kinetic interactions through the cytochrome P450 enzyme system.

ADHD Treatment for Patients in Stable Recovery

Guidelines support and encourage treatment of ADHD in patients with SUD.[2,17,37,38] Indeed, optimal treatment for ADHD may improve adherence to treatment for SUD. Pharmacotherapy choices for adult patients in stable recovery can follow usual adult recommendations. Stimulants are more effective than nonstimulants for adult ADHD[86]; however, stimulants may be diverted or abused. These risks are lower for long-acting stimulants approved for adult ADHD (OROS methylphenidate, dexmethylphenidate XR, mixed amphetamine salts, and lisdexamfetamine) than for the short-acting agents.[83] At this time, atomoxetine is the only nonstimulant treatment approved for adult ADHD. The nonstimulant α-2 receptor agonists guanfacine XR and clonidine ER have not been studied in adults; their use is currently off-label in this population.

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Diet and ADHD

In ADHD, Fitness/Health, School Psychology on Wednesday, 12 September 2012 at 07:24

Healthy vs Western Diet Linked to Better Outcomes in ADHD

Megan Brooks & Penny Murata, MD

http://www.medscape.org/viewarticle/757166

Clinical Context

In children with attention-deficit/hyperactivity disorder (ADHD), the effectiveness of diet and dietary supplements is not clear. Dietary measures that have been proposed include sugar restriction; the additive- and salicylate-free Feingold diet; the oligoantigenic or elimination diet; and ketogenic, megavitamin, and polyunsaturated fatty acid (PUFA) supplements. In the July 2011 issue of the Journal of Attention Disorders, Howard and colleagues reported a link between ADHD and a “Western” diet high in fat, refined sugars, and sodium.

This review of the literature assesses the evidence for dietary treatment in children with ADHD.

Study Synopsis and Perspective

When drug therapy fails to control ADHD or is unacceptable, adopting a “healthy” diet, eliminating items known to predispose to ADHD, and adding omega-3 fatty acid supplementation may be worth trying, new research suggests.

“The recent increase of interest in this form of therapy for ADHD, and especially in the use of omega supplements, significance of iron deficiency, and the avoidance of the ‘Western pattern’ diet, make the discussion timely,” the authors write.

Many parents and physicians continue to be interested in how diet and dietary changes, particularly parents wanting to find an alternative to stimulant medication or a complementary therapy. Nevertheless, it remains a “controversial” topic, the authors note.

For their review, J. Gordon Millichap, MD, and Michelle M. Yee, CPNP, from Children’s Memorial Hospital in Chicago, Illinois, searched PubMed for relevant studies on the role of diet and dietary supplements for the treatment of children with ADHD.

They note that their recommendations on diet and dietary supplements are based on a critical review of the data and their own experience in a neurology clinic for children and adolescents with ADHD.

The study was published online on January 9 in Pediatrics.

Elimination Diets Not Advisable

Perhaps the “most promising and practical” complementary or alternative treatment, write Dr. Millichap and Ms. Yee, is adopting a “healthy” dietary pattern, omitting items shown to predispose to ADHD or to make the condition worse. These items include fast foods, red meat, processed meat, potato chips, high-fat dairy foods, and soft drinks.

They point to a “provocative” study published last year, which found a link between ADHD in adolescents and a “Western-style” dietary pattern that was high in fat, refined sugars, and sodium and low in fiber, folate, and omega-3 fatty acids (Howard et al, J Atten Disord. 2011;15:403-411). ADHD was not associated with a “healthy” dietary pattern rich in fish, vegetables, fruit, legumes, and whole-grain foods.

Adopting a healthy dietary pattern “may offer an alternative method of treatment of ADHD and less reliance on medications,” the authors of the current study write.

They also note that although many parents report worsening of hyperactivity symptoms after consumption of foods and drinks containing sugar or aspartame — and isolated reports support the parents’ observations — most controlled studies have failed to find a significant harmful effect of sugar or aspartame, the authors note.

Additionally, they say that the elimination of sugar and aspartame and adapting additive-free diets are complicated, disruptive, and often impractical; such measures are indicated only in select cases.

Fatty Acid Supplements May Be Helpful

Low levels of long-chain PUFAs have been reported in the plasma and red cells of children with ADHD in comparison with their ADHD-free peers, Dr. Millichap and Ms. Yee note. Some studies have demonstrated a reduction in ADHD symptoms with PUFA supplementation, although no definitive conclusions can be drawn.

However, the authors note that “on the basis of reports of efficacy and safety, we use doses of 300 to 600 mg/day of omega-3, and 30 to 60 mg/day of omega-6 fatty acids, continued for 2 or 3 months, or longer if indicated.”

“As initial or add-on therapy, we have occasional reports of improved school grades and lessening of symptoms of ADHD, without occurrence of adverse effects. Most parents are enthusiastic about trying the diet supplements, despite our explanation of only possible benefit and lack of proof of efficacy,” they note.

They also note that iron and zinc supplementation is advisable when there is a known deficiency in these minerals, and this may “enhance the effectiveness” of stimulant therapy.

Pediatrics. Published online January 9, 2012.

Related Link
The National Institute of Mental Health’s Attention Deficit Hyperactivity Disorder (ADHD) site offers a wide range of information helpful for parent education including a downloadable booklet discussing the condition and its management.

Study Highlights

  • This review study provides an overview of the role diet has in children with ADHD. The following supplements, foods, and diets affect the children’s health outcomes in various ways, according to several studies.
  • Omega-3 and omega-6 fatty acid supplements
    • Low long-chain PUFA levels were reported in children with ADHD vs control patients.
    • Some studies showed that PUFA reduced ADHD symptoms, but other studies did not.
    • Doses of omega-3, 300 to 600 mg/day, and omega-6, 30 to 60 mg/day, for 2 to 3 months or longer have been used.
    • Concurrent ADHD medication is almost always needed.
  • Additive and salicylate-free (Feingold) diet
    • Adherence to the diet is complicated and may be disruptive or impractical.
    • Foods to be avoided are apples, grapes, luncheon meats, sausage, hot dogs, and cold drinks with artificial flavors and coloring agents.
    • Permitted foods are grapefruit, pears, pineapple, bananas, beef, lamb, plain bread, certain cereals, milk, eggs, and color-free vitamins.
    • Controlled trials found a small subgroup of preschool children had an adverse response to challenges of additives and preservatives.
    • Children with ADHD and atopy vs no atopy have a higher response to elimination of foods, artificial colorings, and preservatives.
  • Oligoantigenic (hypoallergenic/elimination) diet
    • Adherence to the diet is complicated and may be disruptive or impractical.
    • The oligoantigenic diet eliminates sensitizing food antigens or allergens, including cow’s milk, cheese, wheat cereals, egg, chocolate, nuts, and citrus fruits.
    • Elimination of some foods appeared to decrease some ADHD symptoms, but plays an uncertain role in ADHD treatment.
    • A 2- to 3-week period of elimination diet is followed by the reintroduction of single items each week until the food sensitivity is identified.
    • Behavior improvements might not occur for up to 2 weeks.
    • Enzyme-potentiated desensitization might enable children to become tolerant of provoking foods.
  • Sugar and aspartame
    • Sugar does not affect behavior or cognitive performance, but might affect a subset.
    • In preschool boys, daily sucrose and total sugar intake correlated with duration of aggression.
    • Reactive hypoglycemia after sugar load might reduce cognitive function.
    • Hypoglycemia is linked with impaired electrical activity of the cerebral cortex and slow rhythms on electroencephalogram.
  • Ketogenic diet
    • A ketogenic diet high in fats and low in carbohydrates for children with intractable seizures helped to control seizures and improve behavior, attention, and social functioning.
  • Iron deficiency
    • Iron deficiency is not consistently linked with ADHD severity or frequency.
    • 1 study showed that low serum ferritin correlated with baseline inattention, hyperactivity, impulsivity, and effective amphetamine dose needed.
  • Zinc deficiency
    • Low zinc levels were found in the serum, red cells, hair, urine, and nails of children with ADHD, but mostly in countries with endemic zinc deficiency.
    • In the United States, low serum zinc was linked with inattention, but not with hyperactivity or impulsivity.
    • Zinc supplements might enhance the effect of d-amphetamine, but are not routinely recommended.
  • Other alternative dietary therapies
    • Orthomolecular medicine and megavitamin therapy refer to combination of minerals and nutrients.
    • A study of megavitamin therapy in children with ADHD showed no improvement in behavior, but 42% had elevated serum transaminase levels.
  • “Healthy” vs “Western” diet pattern
    • A cohort study of children from birth to age 14 years found a “Western” dietary pattern associated with ADHD diagnosis and a “Healthy” diet pattern not associated with ADHD diagnosis.
    • The Western dietary pattern includes fast foods, red and processed meats, potato chips, high-fat dairy products, and soft drinks.
    • The Healthy dietary pattern includes fish, vegetables, tomatoes, fresh fruit, whole grains, and low-fat dairy products.

Clinical Implications

  • Indications for dietary therapy in children with ADHD include medication failure or adverse reactions, patient or parental preference, mineral deficiency, and need for change from an ADHD-linked Western diet to an ADHD-free Healthy diet.
  • In children with ADHD, additive-free and elimination diets are time-consuming and disruptive, but might be indicated in selected patients; iron and zinc are indicated for deficiencies; omega-3 supplements have inconsistent effects; and a Healthy diet rich in fish, vegetables, fruit, legumes, and whole grains might be beneficial vs a Western diet of fast foods, red or processed meats, high-fat dairy products, soft drinks, and potato chips.

Taking Charge of Adult ADHD-R. Barkley

In ADHD, Brain studies, School Psychology on Wednesday, 12 September 2012 at 06:38

Here is some general information regarding ADHD in adults.  For an incredibly informative and helpful read, please look to Russell Barkley’s book “Taking Charge of Adult ADHD.”  I highly recommend it for anyone who wants to know more about ADHD, has been diagnosed with ADHD (child or adult), or treats those with ADHD.

***

What the research shows about the causes of ADHD: Studies of twins and families have made it abundantly clear that genetic factors are the major causes of ADHD. If a child has ADHD, nearly one out of three siblings will also have ADHD. A study done at UCLA examined 256 parents of children with ADHD and found that 55% of these families had at least one parent affected by the disorder. An estimated 75–80% of variation in the severity of ADHD traits is the result of genetic factors, and some studies place this figure at over 90%—higher than the genetic contribution to personality traits, intelligence, and other mental disorders such as anxiety and depression and nearly the same as the genetic contribution to individual differences in height. Several recent studies have scanned the entire human genome searching for genes that carry the risk of ADHD and have found at least 20 to 25 sites on chromosomes to be associated with ADHD. It is therefore likely that ADHD arises from a combination of multiple risk genes, with each contributing a small likelihood of risk for the disorder. The more risk genes you inherit, the greater the number and severity of ADHD symptoms, and so the greater the probability you will be impaired by and diagnosed with the disorder. A very small number of cases are caused by early-development (often prenatal) neurological injury, such as alcohol and tobacco exposure during pregnancy, premature delivery, especially with minor brain hemorrhaging, early lead poisoning, stroke, and frank brain trauma, to name just a few. The frontal lobes, basal ganglia, cerebellum, and anterior cingulate cortex are 3–5% smaller in people with ADHD than in others of the same age and substantially less active. Studies show that the brains of those with ADHD react to events more slowly than the brains of those without ADHD. People with ADHD have less blood flow to the right frontal region of the brain than those who don’t have ADHD, and severity of symptoms increases the more blood flow is reduced.

What the research says about popular myths regarding the causes of ADHD: Available evidence suggests that sugar plays no role in the disorder and that fewer than 1 in 20 preschool children with ADHD may have their symptoms worsened by additives and preservatives. No compelling evidence exists to support the claim that ADHD results from watching too much TV or playing too many video games as a child, other than that people growing up with ADHD may be more likely to watch television or play video games. Little evidence has emerged that child-rearing practices can cause ADHD. There is no question that families with children having ADHD show more conflict and stress than other families. But researchers found that this was largely due to the impact of the child’s ADHD in disrupting family functioning and also to the likelihood that the parent also had ADHD.

PREPARE BY KNOWING WHAT TO EXPECT AND WHAT TO TAKE ALONG Here are the typical elements in a diagnostic evaluation:  Collection of rating scales and referral information before or during the evaluation  An interview with you  A review of previous records that may document your impairments  Psychological testing to rule out general cognitive delay or learning disabilities  Interviews with others who know you well to corroborate your reports  A general medical examination when medication might be part of your treatment or coexisting medical conditions need to be evaluated (if your physician hasn’t already done this) What you can take along to facilitate these steps:  Any records you have or can collect in advance from schools you attended and physicians and mental health professionals you’ve seen, any driving and criminal records, and any other documentation of problems that could be related to ADHD or another disorder  The names of a few people who know you well and whom you trust to speak honestly and objectively with the evaluators  Results of a medical exam if you’ve already had one from your physician  A list of family members with mental disorders you know about  A description of impairments during childhood and adolescence, as well as more recent ones

Here’s how the anti-ADHD medications work neurogenetically: Brain imaging, EEGs, and a variety of other testing methods have shown that the brains of those with ADHD are different from those of others in several important ways: Certain regions of the brain are different structurally, mainly being smaller than in those without ADHD: the right prefrontal region, associated with attention and inhibition; the striatal region, associated with pursuing pleasurable or rewarding behavior; the anterior cingulate cortex, which helps you govern or self-regulate your emotional reactions; and the cerebellum, associated with the timing and timeliness of your actions, among other executive functions. People with ADHD have less electrical activity in the brain, particularly in these regions, meaning they don’t react to stimulation in these regions as much as others. Children and adolescents with ADHD also have less metabolic activity in the frontal regions. The brains of those with ADHD seem to be deficient in or show excessive reuptake of norepinephrine and dopamine. Other neurochemicals may also be involved. Scientists believe the structural abnormalities in the ADHD brain underlie the development of the disorder: this is the genetic legacy that causes ADHD to appear in the descendants of those who have ADHD. We don’t know how to restore a typical structure to these brains. We do, however, know how to correct the neurochemical imbalance found in those with ADHD, at least temporarily: medication. When the neurotransmitters dopamine and norepinephrine are not available in the same measure as they are in typical adults, the messages these chemicals are supposed to send don’t get through as they should. Without the help of these neurotransmitters, the brain does not respond to stimulation (any input, like an event or an idea or an emotion) the way it should. Impulse control doesn’t kick in when it should. Memories of the past and visions of the future aren’t triggered to keep you mentally on track. And even when they are, they cannot be sustained for very long, leading you to forget what it is you were planning on doing. The motor-control brakes don’t keep you from fidgeting with restlessness. This is why ADHD medications work (though some operate on other neurochemicals). By causing nerve cells to express more of these neurochemicals, or by keeping the nerve cells from pulling them back in once they’ve been released, they increase communication between nerve cells in regions of the brain linked to ADHD. The two basic categories of drugs approved by the U.S. Food and Drug Administration for use with adults who have ADHD—stimulants and a few nonstimulants—boost your mind’s ability to respond to whatever is going on in your day.

Reference:

Barkley, Russell A. (2011-04-04). Taking Charge of Adult ADHD.  Guilford Press. Kindle Edition.

Mindfulness and ADHD

In ADHD, Mindfulness, School Psychology on Tuesday, 11 September 2012 at 07:55

A mindfulness prescription for adult ADHD

Psychiatrist Lidia Zylowska shares how people with ADHD can manage their restless minds.

www.lidiazylowska.com

 

“My mind is always busy,” exclaimed Carolyn. “If you ask me about one thing, that makes me think of a million other things.” 

“I noticed,” I thought to myself. Carolyn was in my office for an evaluation of possible ADHD, and it was a struggle to keep her focused. Many of my questions were met with long descriptions and too many details. Other times, she veered to another topic. She seemed to be insightful, and her answers were often interesting or humorous—but they didn’t always address the question.

Along with a restless body, a busy or restless mind is common with ADHD. This can be a curse and a blessing. Having a restless mind can make it difficult to focus and follow through on one’s tasks without getting sidetracked or lost in thought. On the other hand, having lots of thoughts and ideas can lead to making unusual and intriguing connections between things. Many adults with ADHD exhibit “out-of-the box” thinking and creativity due to their incessantly curious mind.

(…)

The ADHD Mind

In ADHD, thought flow is often irregular. Ideas can frequently branch out or jump from place to place. On the other hand, there may also be a tendency to get stuck in one way of thinking or to obsess about something—a kind of inflexible flow.

With frequent jumps in thinking, the content of ADHD mind may sometimes look like a disorganized closet and sometimes like a zigzaggy road that ultimately reaches a novel insight. Sometimes the content of the ADHD mind is out of balance or skewed. For example, the thinking may be overly optimistic or overly pessimistic.

Self-Perception and ADHD

Accurate self-perception seems to be difficult in ADHD. For example, positively biased self-perceptions—reporting higher competence than what the actual performance shows—are common in ADHD children. This kind of overestimation in children is found across the board in social, academic, and behavioral domains. It may be in part a result of certain cognitive deficits, and it may have a protective role in early years; however, its full impact is still unknown. (At the same time, children with ADHD are typically accurate in their perceptions of others’ performance.)

The problem with accurate self-perception is also shown in adults with ADHD. In a 2005 study adults with ADHD self reported higher competence as drivers than their observed performance and their driving record showed.3 In contrast, a 2007 study among college-aged students, by contrast, suggested that ADHD students tended to underestimate their academic performance.

In my clinical experience, many adults with ADHD, before even being introduced to mindfulness, are able to notice or joke about their mental process. Perhaps the repeated experience of living with an unruly, frustrating, and skewed mind makes it easier for them to see their thoughts as somewhat separate from themselves. However, despite this general knowledge, it can still be difficult for people with ADHD to notice the very moments when their mind jumps or gets stuck in unbalanced thinking.

Mindfulness of Thinking

The mindfulness-based approach to thinking is different from traditional psychotherapy in that it teaches us to experience a different relationship to our thoughts before attempting to focus on their content. Mindfulness first invites us to watch or witness the flow of thinking. Instead of being caught up in the narrative in our head, we are invited to observe our thinking as an everchanging stream, similar to watching clouds float across the sky. This shift in perspective weakens the grip of unhelpful thinking.

A 2007 study by Norman Farb at the University of Toronto showed that mindfulness training can weaken the tendency to be caught in an inner story and analysis of yourself and promotes focus on direct experience. This is important since habitual self-analysis can make one more vulnerable to unhelpful rumination, anxiety, and depression. In contrast, focus on present-moment experience, as in mindfulness, has been demonstrated to promote well-being.

Exploration 5.1: Mind Like a Sky

  • Sit comfortably and close your eyes. Become grounded in the present moment by noticing your breathing
  • When you feel settled, imagine a spacious blue sky with white clouds floating across it.
  • Sense your awareness as being like the blue sky, vast and spacious, larger than the passing clouds. With such awareness, you can watch your thoughts and feelings asif they were clouds coming and going.
  • As you watch them, label your thoughts and feelings without personalizing them—for example, “oh, there is worry,” “sadness,” “remembering.”
  • Notice that, just like clouds, your thoughts may go by quickly or slowly. They may be linked with each other or floating separately. They may appear light and fluffy or dark and heavy.
  • As you watch your thoughts flow, see if you can sense the space between them. This space—the space of open awareness—is a place where you can observe your mind without being pulled by it. It is the space from which you can note thoughts and feelings but choose to not act on them.
  • As you do this exercise, it is easy to get lost in thinking—to go into the clouds and become enveloped by the content of your thoughts and feelings. Whenever that happens, become aware of your breath and reground yourself in the present moment. Then return to watching your mind.

 

musings on…an open comment.

In ADHD on Monday, 10 September 2012 at 17:26

someone was lamenting (and rightly so, but it’s not really a great agent of change, obviously) about the difficulty of being ‘newly’ diagnosed with adhd as an adult, when, as we all know, this person was adhd as a child and unidentified (you can’t diagnose adhd without there being a developmental component).  so, this person basically said that it kinda sucked that they only NOW have an explanation as to why they felt the way they did then and a kind of, “what if…”  i’m not making ANY value judgments here!  trust me, i can only imagine the “could” and “should haves” (and what does adler say about society’s “shoulds?”  they cause…what???)  that  go through one’s mind.  but…to me the next step seems so simple.  i understand the fright that might go with having to actually go out and confront the idea and accept it.  but…once you do (and this can go for anything, this is certainly not exclusive to adhd), DO SOMETHING!  life isn’t about the moments you wanted to experience.  or thought about experiencing.  and this go round is only once.  if you’re lucky, you’ll have another shot.  it’s all about the karma…

so, this was my drafted response to this person: “ the first step is done, you received an adhd diagnosis!  an explanation, so to speak.  at the very least you obtained an “ah-ha moment.”  Now go inform yourself and DO something!  read the studies.  read barkley’s latest adult adhd book.  it’s a wonderful read about adult adhd and those, like you, who were adhd in childhood and didn’t get diagnosed until adulthood.  i really enjoyed it.  yes, it stunk that, for so many years, you didn’t know and you can extol all the things you could have done…but, where is that going to get you???  take action now that you have an explanation as to why you felt things were so difficult.  there ARE effective treatments that work.  i tend to appreciate all things quantifiable and like to refer to the literature.   as an admitted and proud “quantoid,”  it is pretty clear to me what works.  but, what you decide to do about and how you decide to go about it is personal.  but…just do SOMETHING!”

i’m comin’ out!

sidenote:  consider this post my “coming out.”  while i am ALL ABOUT the oxford comma and all things proper grammar (hello, do we know what an adverb is???  or, at the very least, the difference between “good” and “well???”), when i write freestyle (i.e. non-work or professionally related, i prefer not to use punctuation.  i never learned how to type .  while i have my own way that is efficient for me (i have tried every typing program known to man and can type excellently IN MY HEAD) and i am blaming muscle memory.  i get by just fine.  but, i don’t want to worry about the shift key every other second.  i’m telling you, i’d like to say it’s a “style thing” a ‘la e.e.cummings, but, sadly, i’m not THAT cool.  it’s more of a pragmatic thing.  but…if you prefer to think i’m cool…well, then, you go right ahead!  consider it geek chic and color me flattered!

so, from now on, if i am just posting free-thought, whatever comes to mind (i.e. see everything above), you will, most hopefully, see proper punctuation (albeit quite possibly a liberal use of ALL CAPS, ellipses, parenthesis, and quotation marks) but not proper capitalization.  and i like proper spelling.  hey, it’s just how i roll…

~be love~

ADHD funny comic…

In ADHD, Humor on Monday, 10 September 2012 at 07:52

What ADHD looks like…

Some humor…

In ADHD on Monday, 10 September 2012 at 06:59

This was sent to me in email form a long time ago and the author is unknown to me.  My apologies for the lack of citation.

AAADD- KNOW THE SYMPTOMS…PLEASE READ!

Thank goodness there’s a name for this disorder.
Somehow I feel better, even though I have it!!
Recently, I was diagnosed with AAADD –
Age Activated Attention Deficit Disorder.
This is how it manifests:

I decide to water my garden.

As I turn on the hose in the driveway,
I look over at my car and decide it needs washing.

As I start toward the garage,
I notice mail on the porch table that
I brought up from the mail box earlier.

I decide to go through the mail before I wash the car.

I lay my car keys on the table,
put the junk mail in the garbage can under the table,
and notice that the can is full.

So, I decide to put the bills back
on the table and take out the garbage first.

But then I think,
since I’m going to be near the mailbox
when I take out the garbage anyway,
I may as well pay the bills first.

I take my check book off the table,
and see that there is only one check left.

My extra checks are in my desk in the study,
so I go inside the house to my desk where
I find the can of Coke I’d been drinking.

I’m going to look for my checks,
but first I need to push the Coke aside
so that I don’t accidentally knock it over.
The Coke is getting warm,
and I decide to put it in the refrigerator to keep it cold.

As I head toward the kitchen with the Coke,
a vase of flowers on the counter
catches my eye–they need water.

I put the Coke on the counter and
discover my reading glasses that
I’ve been searching for all morning.

I decide I better put them back on my desk,
but first I’m going to water the flowers

I set the glasses back down on the counter,
fill a container with water and suddenly spot the TV remote.
Someone left it on the kitchen table.

I realize that tonight when we go to watch TV, I’ll be looking for the remote,
but I won’t remember that it’s on the kitchen table,
so I decide to put it back in the den where it belongs,
but first I’ll water the flowers.

I pour some water in the flowers,
but quite a bit of it spills on the floor

So, I set the remote back on the table,
get some towels and wipe up the spill.

Then, I head down the hall trying to
remember what I was planning to do.

At the end of the day:

the car isn’t washed

the bills aren’t paid

there is a warm can of Coke sitting on the counter

the flowers don’t have enough water,

there is still only 1 check in my check book,

I can’t find the remote,

I can’t find my glasses,

and I don’t remember what I did with the car keys.

Then, when I try to figure out why nothing got done today, I’m really baffled because I know I was busy all day,
and I’m really tired.

I realize this is a serious problem,
and I’ll try to get some help for it,
but first I’ll check my e-mail….

 

While true ADHD does not “appear” magically at a later age (as it states in the DSM-IV-TR that onset of symptoms must be around age 7.  Even if they are not diagnosed at that time, there must have been some indications and behaviors present developmentally.  This is why a good history and information on childhood MUST be part of a comprehensive evaluation), but I thought this was humorous and also can give a great scenario for adult ADHD!  ~Lorie

ADHD Symptom Chart from Child to Adult-great reference tool!

In ADHD on Saturday, 8 September 2012 at 13:49

ADHD Symptom Evolution From Childhood to Adulthood

  Childhood Adulthood
Inattention Difficulty sustaining attention Difficulty sustaining attention
(meetings, reading, paperwork)
  Failure to pay attention to details Makes careless errors
  Appears not to listen Easily distracted/forgetful
  Lacks follow-through Poor concentration
  Cannot organize Difficulty finishing tasks
  Loses important items Disorganized/misplaces items
     
Hyperactivity Squirming/fidgeting Inefficiencies at work
  Cannot stay seated Internal restlessness
  Cannot wait his/her turn Difficulty sitting through meetings
  Runs/climbs excessively Works more than 1 job
  Cannot play/work quietly Works long hours
  “On the go”/seems “driven by a motor” Self-selects very active jobs
  Talks excessively Overwhelmed
    Talks excessively
     
Impulsivity Blurts out answers Impulsive job changes
  Cannot wait in line Drives too fast
  Intrudes/interrupts others Interrupts others
    Easily frustrated

Goodman DW, Surman CB, Scherer P, Salinas G, Brown JJ. Assessment of physician practices in adult attention-deficit/hyperactivity disorder. Primary Care Companion. In press.

Saw this today and found it positively fascinating!

In ADHD on Thursday, 6 September 2012 at 20:55

Adult ADHD: New Findings in Neurobiology and Genetics 

Scott H. Kollins, PhD

http://www.medscape.org/viewarticle/765528

Introduction

Attention-deficit/hyperactivity disorder (ADHD) is one of the most common psychiatric disorders, affecting approximately 8% to 9% of school-aged children and 2.5% to 4.4% of adults in the United States.[1-4] Variants of the disorder have been recognized in pediatric populations for more than 100 years (and according to some sources, more than 200 years).[5] Recognition of ADHD as a persistent condition that affects a substantial minority of adult patients has increased substantially in the past 20 years. For example, the search term “adult ADHD” identified a total of 39 articles in the National Library of Medicine database in 1991, compared with 558 articles in 2011.

In recent years, much work on adult ADHD has focused on characterizing the neurobiology of the adult condition. This overview of the current state of knowledge of adult ADHD includes findings from genetics and pharmacogenetics studies, and from neuroimaging studies, and describes the potential clinical implications of these neurobiological discoveries for ADHD diagnosis and treatment in adults.

Adult ADHD is the form of ADHD that results in symptomatic and functional impairment in individuals above the age of 18. Wide variation exists in estimates of the prevalence and persistence of ADHD from childhood through adolescence; this is related to how such persistence is defined (eg, by strict diagnostic criteria vs high levels of symptoms).[6,7] A meta-analysis of long-term follow-up studies reported that approximately 65% of individuals experiencing ADHD as children continued to exhibit impairment into adulthood.[7] This article focuses on understanding the genetic, neurobiological, and treatment outcome studies for this group of individuals.

Genetics of Adult ADHD

ADHD has consistently been shown to be among the most heritable of all psychiatric conditions. A range of methodological approaches exists for assessing the genetic contributions to ADHD, including family studies, adoption studies, twin studies, and molecular genetic studies. We will consider evidence from each of these approaches with respect to the genetics of adult ADHD.

Family, Adoption, and Twin Studies

Family studies evaluate the extent to which disorders “run” in families across and within generations. If the risk of having a disorder is higher in relatives of an identified “case” than in the general population, the likelihood of genetic influences contributing to the development of the disorder is higher. ADHD tends to cluster in families; risk for the disorder is higher in siblings and parents of diagnosed children and in children of diagnosed parents.[8,9] Moreover, siblings of adults diagnosed with variants of ADHD also have been shown to be at significantly greater risk.[10] Familial risk of ADHD is increased in relatives of individuals whose ADHD persists from childhood into adolescence and adulthood, suggesting that adult ADHD may be a particularly heritable variant of the disorder.[11,12]

Family studies cannot fully evaluate the relative genetic contributions to the development of ADHD since members of the same family are also likely to share environments that can give rise to the condition. Adoption and twin studies can help to control for such shared environmental influences. In general, the risk for ADHD and related difficulties is higher among the biological relatives of identified cases compared with adoptive relatives, suggesting a stronger role for genetic factors in the expression of the condition.[13,14]

Twin studies compare the concordance rates of ADHD in identical/monozygotic twins vs fraternal/dizygotic twin pairs. The extent to which concordance rates are higher among monozygotic twins reflects the relative genetic contributions to the disorder. Across several dozen studies of child twin pairs, ADHD is consistently one of the most highly heritable of all child psychiatric disorders, with most studies reporting heritability estimates of between 0.60 and 0.95, indicating that 60% to 95% of the variance in the presentation of the disorder can be accounted for by genetic factors.[15,16] In adult studies, however, heritability estimates are substantially lower: 30% to 41%.[17-19] The lower heritability estimates in adult studies of ADHD are likely associated with increased measurement error of the phenotype (eg, self-report ratings in adults may be less reliable and valid than parent/teacher ratings of symptoms in children). Nonetheless, the pattern of heritability findings in adult twin studies of ADHD are remarkably consistent with those observed in children, including no gender differences in heritability estimates, stability of heritability estimates across the age span, and similar correlations between the heritability of inattention vs hyperactivity-impulsivity symptoms.[20]

Molecular Genetic Studies

A number of techniques have been developed to isolate the specific gene(s) that confer risk for ADHD as shown by family, adoption, and twin studies. Two such methods include genome-wide association studies (GWAS) and candidate gene studies.

Genome-Wide Association Studies of ADHD

GWAS studies of ADHD and other psychiatric disorders have become increasingly common, due in part to the development of sophisticated analytical methods that are able to examine hundreds of thousands or even millions of single nucleotide polymorphisms (SNPs) across the entire genome. GWAS studies generally involve recruitment of hundreds or thousands of clinical case patients diagnosed with a well-characterized phenotype/disorder and a group of nondiagnosed comparison subjects. The statistical power for these so-called “case-control” designs to identify significant genetic markers for a particular disorder depends on a number of factors, including the total sample size, the relative genetic risk of the disorder, and the population frequency of the minor allele under study. An important component of GWAS studies is that they are atheoretical, with no a priori predictions about specific genes that may or may not be involved. Rather, the entire genome is probed to identify regions that are consistently associated with a disorder. As a result of this approach, however, rigorous statistical corrections are used to control for chance findings that might arise from a large number of tests. Studies therefore often refer to findings reaching “genome-wide” significance for a particular region being associated with a condition. Several good reviews of GWAS approaches in psychiatric genetics broadly[21] and ADHD specifically[22,23] have recently been published.

To date, only 2 studies have been published employing GWAS methods in samples of adults with ADHD, although a number of other GWAS studies have been reported with child samples. Lesch and colleagues[24] did not report any risk genes that met genome-wide significance for ADHD, but did report several candidates with considerable overlap with genes implicated in GWAS studies of substance use disorders, including genes coding for cell adhesion molecules and regulators of synaptic plasticity.[24] A more recent study reported that SNPs located in the diacylglycerol kinase eta (DGKH) gene were associated not only with adult ADHD but also bipolar disorder and unipolar major depression at levels that withstood stringent statistical corrections for multiple testing.[25] These data were interpreted to suggest that the mood dysregulation observed in all 3 of these conditions may be related to variation in the DGKH gene, which modulates the activity of protein kinase C, which has in turn been implicated in a range of psychiatric conditions, including ADHD, bipolar disorder, and substance use disorders.[26-28]

Although more limited in number, results from GWAS studies of adult ADHD have generally been more fruitful than similar approaches in studies of pediatric populations, which have failed to report findings reaching genome-wide significance.[29] If additional GWAS studies of adult samples demonstrate similar patterns of effects, it would suggest that relatively common genetic variants may exert stronger effects for persistent forms of ADHD (ie, the adult form of the disorder) than in child samples. In any case, it is increasingly recognized that GWAS studies for ADHD and other psychiatric conditions will require ever-growing, large, multi-institution, and multinational collaborations to assemble sample sizes large enough to detect relevant effects. It has been estimated that sample sizes exceeding 12,000 individuals (cases plus controls) will be required to detect genome-wide significant findings for ADHD.[20]

Candidate Gene Studies of Adult ADHD

In addition to GWAS studies, a second approach for identifying the genetic substrates of ADHD (or any complex disorder) is to identify specific genes that are hypothesized to be involved with the disorder and then examine whether variations in these genes are associated with aspects of the disorder. The genes are usually selected on the basis of a priori hypotheses about the causes of the disorder. Also, results from GWAS studies can suggest specific chromosomal regions or genes or both that may confer risk for ADHD. To date, hundreds of studies reporting on associations of dozens of candidate genes have emerged, though the majority of these studies have been conducted in pediatric populations. Meta-analyses of candidate gene studies of pediatric ADHD have reported replicable evidence for associations between variants of several candidate genes and risk for the disorder, including the dopamine transporter gene (DAT1) and the dopamine D4 receptor gene (DRD4), although even in meta-analytic studies, these results are not always consistent.[15,30-32]

Gene variants consistently found to confer risk for ADHD in pediatric populations have been the most widely studied candidates in genetic studies of adult ADHD. A recent review summarized studies of adult ADHD that examined the effects of variants in DAT1 and DRD4.[20] In general this review found that studies with adult samples did not follow the same pattern of findings as studies with pediatric samples with respect to these specific risk genes, suggesting that the relationship between DAT1 and DRD4 risk variants are different in pediatric ADHD compared with persistent adult ADHD. Other genes involved in dopamine neurotransmission have also been examined in samples of adults with ADHD. Several studies of adult ADHD and variants of the dopamine D5 (DRD5) receptor have reported similar results as pediatric ADHD studies, whereas studies of catecholamine-O-methyltransferase (COMT) have reported results in adult studies that conflict with results in children.[20]

Studies examining genes associated with serotonergic neurotransmission, noradrenergic neurotransmission, and neurotrophic factors have generally been inconsistent or negative, although some nominal associations have been reported. For example, 1 large study of adult ADHD with more than 3500 cases and controls reported some evidence of an association between a variant of the tryptophan hydroxylase 1 gene (TPH1) and risk for the disorder.[33] A handful of additional candidate genes have been identified but are in need of replication. Variants of the latrophilin 3 (LPHN3) gene,[34,35] the brain-specific angiogenesis inhibitor-1 associated protein (BAIAP2) gene,[36] and the nitric oxide synthase 1 (NOS1) gene[37] have all been found to be associated with adult ADHD in single studies and make theoretical sense in terms of how they may confer risk for the disorder. As such, independent replication of these findings will be critical in future studies.

Pharmacogenetic Studies of Adult ADHD

The use of molecular genetic approaches to predict drug treatment response in individuals with ADHD has considerable clinical implications.[38] A number of studies have examined both efficacy and adverse events with stimulant and nonstimulant treatment in children with ADHD. For example, variants of all of the following genes have been reported to be associated with differential treatment response in pediatric samples: adrenergic α 2-A receptor (ADRA2), DRD4, SNAP-25, DAT1, COMT, and the serotonin transporter genes.[39-44]

However, very few studies have examined the pharmacogenetics of adult ADHD. Three studies have examined variants of the DAT1 gene in relation to treatment response in adults with ADHD. One study reported a positive association between the DAT1 genotype and positive treatment response in 42 adults with ADHD.[45] However, 2 other studies failed to report an association between DAT1 and methylphenidate treatment response in considerably larger samples (N=106 and 142, respectively).[46,47] One additional study of the ADRA2 gene and treatment response to methylphenidate in adults with ADHD failed to report significant findings.[48]

Overall, research on the pharmacogenetics of adult ADHD is in its infancy. Given that a larger proportion of adults vs children with the disorder respond optimally to medication, and because a wide range of compounds affecting multiple brain systems has been evaluated or is currently being evaluated, pharmacogenetic studies of adult ADHD hold promise for truly individualizing treatment.

Neuroimaging in Adult ADHD

The field of neuroimaging has dramatically advanced our understanding of the neuroscience of all psychiatric disorders, including ADHD. As with studies in the genetics of ADHD, there are generally fewer neuroimaging studies in adults than in children. Nevertheless, the number of imaging studies in adults with ADHD has steadily increased in each of the last 5 years.

A wide range of imaging modalities can be used to probe different aspects of brain structure and function. Structural brain imaging techniques can examine brain volume and composition, whereas functional brain imaging studies can elucidate activity of the brain during certain tasks. In the following sections, we examine the evidence for altered brain structure and function in adults with ADHD, including a discussion of how these findings are similar to or different from neuroimaging studies in children.

Structural Neuroimaging Studies of Adult ADHD

Structural or morphometric magnetic resonance imaging (MRI) studies allow for the comparison of size, volume, or organization of the whole brain or specific brain regions in individuals with and without ADHD. Inferences can therefore be made about the functional significance of any differences that are identified. A number of studies in children with ADHD have reported reduced volume across a number of brain regions, including the basal ganglia, frontal lobes, and cerebellum.[49] Moreover, several longitudinal studies have shown that brain volume and cortical thickness and structure are maturationally delayed in children with ADHD.[50-53]

Structural imaging studies in adults have generally replicated findings reported in pediatric populations. Compared with studies of nondiagnosed peers, structural MRI studies in adults with ADHD have found overall reductions in cortical gray matter, and reductions in volume and cortical thickness in the superior frontal and orbitofrontal cortex, anterior cingulate cortex, inferior frontal cortex, dorsolateral prefrontal cortex, and temporoparietal, cerebellar, and occipital regions.[54-58] Moreover, volumetric reductions in subcortical areas — including the amygdala, caudate, and nucleus accumbens — have been reported in adults with ADHD compared with nondiagnosed controls.[58-60]

A relatively new approach for characterizing brain structure in individuals with ADHD is diffusion tensor imaging (DTI), which allows for examination of white matter integrity across brain regions. At least 3 studies have used DTI to examine white matter abnormalities in samples of individuals with ADHD. An early study using this approach reported that white matter fiber tracts in adults with ADHD were smaller in size in an area connecting the anterior cingulate cortex to the dorsolateral prefrontal cortex. This region is also reported to be critically involved in executive functioning and attention.[61] In another study of adults with ADHD and healthy control subjects, Konrad and colleagues found significant differences in white matter integrity in frontostriatal regions, and the abnormalities were significantly correlated with measures of both attention and impulsivity.[62] Finally, a recent DTI study of adults with ADHD and a matched group of controls found that white matter integrity was compromised in frontostriatal and left temporal regions in the ADHD group, and that the degree of white matter deficits was negatively correlated with attentional performance on a neuropsychological task.[63]

Although some findings from structural MRI studies in adults with ADHD have conflicted with findings in children and adolescents,[64] the relatively few published reports have shown patterns of deficits similar to those observed in children. A wide range of gray and white matter abnormalities has been found, and the degree of structural abnormalities has often been associated with behavioral or cognitive/neuropsychological outcomes. Continued work to determine the causal factors of structural (eg, genetic) differences as well as the functional and clinical implications is needed.

Functional Neuroimaging Studies of Adult ADHD

Critical companions to methods that precisely characterize brain structure are those techniques that capture brain activation both during task performance and at rest. A range of techniques allows for observing brain activity, including traditional task-based functional MRI (fMRI), positron emission tomography (PET), and, more recently, functional connectivity analyses, which have examined circuit-based connectivity both during tasks and at rest.

fMRI and Adult ADHD. Although fMRI studies of adult ADHD are still fewer in number than studies in children, considerable progress has been made in this area. Two recent review papers summarized the findings from adult ADHD imaging studies.[65,66] A number of different cognitive processes known to be disrupted in adult ADHD have been examined with brain imaging studies. Table 1 lists 5 of these processes, summarizes the imaging findings, and notes whether the results are consistent with studies in pediatric samples.

Table 1. Summary of fMRI Studies in Adults with ADHD

Task/Process Imaging findings Consistent with Child Studies? Comments
Motor inhibition (eg, stop-signal task; go/no-go task) Reduced frontostriatal activation; increased activation in medial frontal and parietal regions (but not observed in medication-naïve adults)[67,68] Yes Overactivation of certain regions during task completion may be associated with effects of medication
Interference inhibition (eg, the Stroop effect) Underactivation of anterior cingulate and inferior prefrontal cortex[69-71] Yes Some differences across studies with respect to laterality of underactivation
Attention (eg, vigilance task; attentional switch task) Underactivation of left inferior and dorsolateral prefrontal cortex[67,71] Yes Findings more lateralized in adults vs children
Working memory (eg, paced serial addition task) Underactivation in inferior ventrolateral, prefrontal, parietal, temporo-occipital, and cerebellar regions[67,71] Insufficient child studies to determine One study with large number of women found that activation deficits are only present in men and not women[72]
Reward processing and motivation (eg, gambling tasks) Consistent evidence for differential functioning in a range of regions, including the limbic/paralimbic, ventral striatum, amygdala, and ventromedial and orbital prefrontal cortex[67,71] Yes Some variation across studies with respect to over- vs underactivation of certain regions; likely related to characteristics of task and sample[73,74]

Adapted from Cubillo A, et al. Expert Rev Neurother. 2010;10:603-620.[65]

Several conclusions can be drawn from the fMRI literature in adults with ADHD. First, there is consistent evidence for disrupted brain function in several regions known to be involved in specific neuropsychological processes implicated in ADHD.Although not consistently reported across studies, some evidence also exists for so-called “compensatory activation,” in which adults with ADHD exhibit increases in brain activation in regions not typically associated with task performance. This finding may be associated with a general level of inefficient neural processing in adults with ADHD.[75] Moreover, the patterns of functional abnormalities are remarkably consistent across pediatric and adult studies. This further validates the conceptualization of ADHD as a disorder with a clinical presentation that is strongly mediated by neurobiological processes. Finally, the collective literature on fMRI in adults with ADHD suggests that additional work needs to be done, especially with respect to samples that are representative of true clinical populations, such as those with a high proportion of women and individuals with comorbid conditions.

PET Studies of Adult ADHD. PET studies have been used for a number of years to measure brain activity in real time. PET imaging methods involve the injection or inhalation of radioactive materials that are distributed in the brain and can then be measured using specialized equipment. PET studies of patients with ADHD conducted in the United States have almost exclusively involved adult populations because of concerns over radiation exposure in pediatric populations. Some of the earliest studies were conducted more than 20 years ago,[76] and most studies since that time have focused on characterizing the activity of the dopamine system. There have been discrepancies across studies, though. For example, some studies have reported higher levels of dopamine transporters in adults with ADHD compared with control participants, whereas others have reported lower levels of dopamine transporters.[77] Despite these differences, PET studies have generally reported that individuals with ADHD differ from non-ADHD comparison subjects with respect to frontostriatal functioning, that the disorder can also be characterized by deficits in dopamine release in the caudate and limbic regions, and that these differences provide a rationale for the therapeutic action of commonly used stimulant drugs.[78,79]

One of the largest and arguably most definitive PET studies of ADHD to date compared 53 medication-naïve adults with ADHD with 44 matched controls. The adults with ADHD exhibited significantly diminished dopamine activity in areas of the brain that are known to be involved in reward processing and motivation, including the nucleus accumbens and the caudate nucleus. Moreover, ratings of attention were associated with dopamine activity in a number of regions, indicating that the degree of dopamine hypoactivity was correlated with the degree of problems with attention. This study also found evidence for decreased dopamine activity in the hypothalamic regions, which was interpreted to be a potential underpinning of comorbidities seen commonly with ADHD, such as sleep problems, obesity, and abnormal reactions to stress.[80]

Several follow-up studies of this same sample have also been published.[81,82] In the first follow-up analysis, deficits in motivation were significantly correlated with dopamine activity in the reward pathway in the cohort with ADHD, but not in controls.[81] More recently, a subset (n=20) of the original 53 adults with ADHD were examined after 12 months of carefully controlled treatment with methylphenidate. Findings showed that subjects experienced significant improvement in self- and clinician ratings of ADHD symptoms and that the magnitude of clinical response was associated with the level of methylphenidate-induced increases in dopamine in ventral striatum. Combined with previous studies of this sample, results were interpreted to suggest that one possible mechanism of long-term stimulant treatment in ADHD is to augment dopamine neurotransmission, which is deficient prior to treatment.[82]

Another potentially significant recent advance using PET imaging has been the characterization of the norepinephrine transporter (NET) in human subjects. A recent study measured the extent to which oral methylphenidate occupied NET in healthy participants without ADHD and reported that clinically relevant doses of the drug significantly occupied this receptor to a degree that was comparable with or greater than the dopamine transporter.[83] This study has implications for better understanding the therapeutic effects of methylphenidate and other drugs used to treat ADHD, such as the selective norepinephrine reuptake inhibitor atomoxetine. Further PET studies of the NET will be important to conduct in patients with ADHD.

Functional Connectivity Studies in Adult ADHD. While traditional functional imaging approaches have focused on brain activation (or lack thereof) in specific regions, functional connectivity approaches focus on “the temporal correlation or coherence of spatially remote neurophysiological events.”[84] As such, functional connectivity analyses allow for examination of much broader systems of neural functioning and how these systems relate to different psychopathological conditions. In general, functional connectivity analyses have examined brain circuits both at rest (ie, not engaged in a specific task) or during some set of demands designed to engage some kind of process (ie, working memory, inhibitory control). Although this is a relatively recent area of research, the number of functional connectivity studies has increased rapidly, including studies in adults. Some of the earliest work on functional connectivity in ADHD focused on a specific set of interrelated brain regions known as the “default mode network” (DMN). This network, comprising nodes in the precuneus/posterior cingulate cortex, the medial prefrontal cortex, and the medial, lateral, and inferior parietal cortex, is associated with task-irrelevant mental processes and exhibits strongest connectivity during rest.[85] Connectivity in the DMN is also reduced during task performance and the degree of deactivation is associated with more complex task demands.[86] Conversely, unsuccessful suppression of DMN connectivity during task demands is associated with greater lapses in attention.[87] These cognitive neuroscientific findings have led to the hypothesis that individuals with ADHD have dysfunctional deactivation of DMN during task demands, which leads to poorer performance.[88] One of the earliest studies to evaluate the integrity of the DMN was conducted in adults with ADHD and found that, compared with nondiagnosed controls, those with ADHD demonstrated less connectivity of the DMN. [89]

Several studies have also examined task-related functional connectivity in adults with ADHD. In 1 study, adults with and without ADHD performed a working memory task; connectivity among several different brain regions was examined. Similar to traditional fMRI findings, this study reported that, compared with adults without ADHD, adults with ADHD demonstrated lower functional connectivity of a network involving the inferior prefrontal cortex, left anterior cingulate cortex, superior medial frontal cortex, superior parietal regions, and cerebellum. However, adults with ADHD also showed increased connectivity in a different network involving the left dorsal anterior cingulate, right superior frontal gyrus, and left occipital lobe.[90] Using a task of motor inhibitory control, another study reported that adults with ADHD demonstrated less functional connectivity in a network known to subserve this process, including the right inferior prefrontal cortex, caudate/thalamus, anterior and posterior cingulate, and bilateral temporoparietal regions.[67]

Overall, functional connectivity studies of adults with ADHD are consistent with studies conducted in children and also complement research using other modalities of brain imaging. Increasingly, neuroimaging studies have been able to isolate the brain regions and networks associated with ADHD in both children and adults.

Neurobiological Next Steps: Combining Brain Imaging and Molecular Genetics

The pace of discovery is rapid in both molecular genetics and the neuroimaging of ADHD, with several hundred papers published each year. One emerging field that holds promise for integrating these areas in the service of more fully elucidating the etiology and pathophysiology of ADHD is imaging genetics.[91] In this approach, brain markers (either structural or functional) can be used as endophenotypes for ADHD and linked to genetic variance. Several recent studies highlight the potential of this area for advancing our understanding of the genetics and neurobiology of ADHD. For example, variants of the ADRA2 gene have been shown to be associated with differences in blood flow in relevant brain regions (eg, the orbitofrontal cortex) in children with and without ADHD.[92] Functional connectivity in brain regions associated with cognitive control has been found to be related to familial risk for ADHD, indicating the potential heritability of brain functioning.[93]

Imaging genetics studies have also been conducted in adults with ADHD. For example, in a relatively large sample of 91 adult individuals (n=53 with ADHD, n=38 non-ADHD controls), variants of the DAT1 gene were associated with the presence of adult ADHD, as well as task-related suppression of portions of the DMN. Moreover, a small statistical interaction between genotype and diagnosis was observed for activity in the anterior cingulate cortex, suggesting that DAT1 genotype effects on brain function were particularly pronounced among individuals with ADHD.[94]

Clinical Implications of Neurobiological Findings in Adult ADHD

This review has summarized 2 active and key areas relevant to the neurobiology of adult ADHD: genetics/molecular genetics and neuroimaging. In addition, the emerging field of imaging genetics, which combines these areas, was also discussed. Methodological advances in these areas provide for an array of complex findings. But the relevant clinical questions of how these advances will influence and improve the prevention, identification, and treatment of persistent adult ADHD remain unanswered. The myriad findings from genetic and neuroimaging studies likely vary with respect to how close they are to influencing clinical practice. What are the possible clinical implications of the main findings?

ADHD Is Highly Heritable and Runs in Families

Long before the advent of molecular genetic techniques, it was well established that ADHD tended to run in families and was more common in identical vs fraternal twins. This pattern of heritability likely provides more clinical utility than findings from molecular studies of specific genes or genome scans. Since it is well established that the risk for ADHD is significantly higher in biological parents of children diagnosed with ADHD and vice versa, careful history gathering during an assessment can help a clinician determine whether family members of a patient have been affected and use this information to inform decision making about a diagnosis. If the child of an adult patient has been diagnosed with ADHD, it is not a foregone conclusion that the parent will have the disorder, but it does help the clinician weigh the rest of the clinical evidence in drawing diagnostic conclusions.

Limited GWAS Findings in Adults Have Been Somewhat More Promising Than Findings in Pediatric Samples

Across a number of GWAS studies in children, no consistently replicated regions have been identified that are associated with the disorder and withstand rigorous statistical correction. In adults, 2 GWAS studies have been conducted, with 1 reporting significant findings for association between ADHD and a gene that has also been implicated in mood disorders and substance abuse. This suggests that common genetic variants identified in such studies may be more strongly associated with persistent (ie, adult) forms of the disorder and associated with features of the disorder (ie, mood problems, risk for drug use) that are not part of the core diagnostic criteria. Such findings underscore the common clinical observation that mood dysregulation and other impairments are common in adults with ADHD, but otherwise GWAS studies are not yet advanced enough to directly inform clinical practice.

A Number of Relatively Common Candidate Gene Variants Have Been Associated With Adult ADHD

Findings from candidate gene studies in adults with ADHD have varied somewhat from studies in pediatric populations. This suggests that the molecular genetic basis for persistent ADHD may be somewhat different than the basis for pediatric ADHD. In any case, a number of gene variants have been shown to confer risk for the disorder. Moreover, the functions of identified genes make theoretical sense in terms of how they might affect neural processes to give rise to the clinical condition. Nevertheless, the effect sizes for any individual candidate gene are quite small. Stated differently, even for the risk genes with the largest effects, the majority of patients with a true diagnosis of ADHD will not carry the risk variant, and a considerable minority of the population without a true diagnosis may also carry the risk gene. As such, the immediate clinical utility of such findings is, at present, limited.

Genetic Variation Has Been Associated With Response to Treatment, Although the Effects Are Not Consistent Across Studies of Adults With ADHD

The possibility of stratifying patients with respect to their likely response (or nonresponse) to various pharmacological treatments is a promising application of molecular genetics. Although some consistency has been seen in pediatric pharmacogenetic studies, far fewer studies have been conducted with adult samples and the findings are more mixed. Several aspects of the current state of pharmacotherapy of adults with ADHD suggest that continued pharmacogenetic studies could yield considerable clinical utility. First, as awareness of adult ADHD has increased, use of pharmacotherapy in this population has also increased. Second, a number of drugs are available or in development for use in adults that target a range of neurotransmitter systems in the brain. To the extent that the functioning of these different systems is partially regulated by genetic factors, a large number of genetic targets may be explored with respect to predicting treatment response. For example, using genetic data to determine whether an individual is more likely to respond to a stimulant (eg, methylphenidate or amphetamine), a norepinephrine reuptake inhibitor (eg, atomoxetine), some other agent (eg, α-2 adrenergic agonists), or a combination of these could be useful from a clinical perspective. Such studies have not yet been conducted, but their potential benefits are sizeable.

Size and Structure of the Brains of Adults With ADHD Differ From Adults Without ADHD

This finding, which is similar to findings reported in pediatric populations, does not provide much in the way of direct clinical implications on its own. It is not much use to clinicians to know that, on average, an adult with ADHD might have a brain volume or cortical thickness that is 8% to 10% less than that of an average adult without ADHD. Still, these consistent findings do provide information about the etiology of ADHD, which could eventually lead to better diagnostic tools. At present, however, these findings have not been translated into clinical utility.

Brain Activation Tends to Be Different in Adults With ADHD

This finding is consistent with studies conducted in pediatric populations. Differential activation across a range of brain regions has been demonstrated with tasks measuring inhibitory control, interference, and working memory, among others. Importantly, many of these studies have also shown that adults with ADHD (like children with the disorder) may also exhibit increased or compensatory activity in other brain regions. This finding has led to speculation about inefficiencies of neural processing as a core feature of ADHD. Although, on average, adults with ADHD exhibit altered patterns of brain activation, the effect sizes across these studies are not enough to discriminate a priori individuals with the disorder from normal individuals. Similar to genetic risk variants, many adults with ADHD will exhibit normal brain activation in relevant regions, and many adults without ADHD will exhibit altered activation patterns. Enhancing the signal of differential brain activation via task refinements or more sophisticated approaches to measuring activation may increase the potential diagnostic utility of brain imaging techniques for identifying ADHD.

Dopamine Activity Is Disrupted in Adults With ADHD

It has long been speculated that ADHD is related to altered dopamine function. The mechanism of action of stimulant drugs known to be effective to treat ADHD, early findings of genetic risk variants in dopamine-related genes, and findings from fMRI studies provide convergent evidence for the involvement of the dopamine system. More recently, studies of real-time dopamine activity have more strongly supported the role of the dopamine system, particularly in motivation and reward pathways. These findings are not ready for direct clinical application but have important implications for the development of new pharmacological compounds to treat the disorder, the measurement of how treatment (pharmacological or other modalities) influences dopamine activity, and the understanding of common conditions that are comorbid with ADHD.

Interconnectivity of Different Brain Regions Is Altered in Adults With ADHD

Technological and analytical advances in recent years have allowed for the measurement of correlated activity across spatially distinct brain regions. These techniques have demonstrated that adults with ADHD differ not only in activation patterns in specific brain regions but also in the activity across brain regions. These differences have been demonstrated for both task-related activity as well as activity at rest. Although not currently of clinical use, functional connectivity analyses, similar to studies of brain activation, hold some promise as objective diagnostic tools if patterns of connectivity can be identified that reliably discriminate individuals with ADHD from those without the disorder.

Conclusion

At present, the direct clinical implications of genetic and neuroimaging findings are limited. However, the volume of information generated from these studies and the pace at which data are generated hold promise for continuing to better understand the genetic and neurobiological basis of this common and highly impairing disorder.

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A comprehensive list of symptoms associated with ADHD-R. Barkley

In ADHD on Thursday, 6 September 2012 at 10:16

I wanted to attach a comprehensive list of symptoms associated with ADHD.  I find in my work that people always have a list in their heads of what ADHD IS and IS NOT and will attribute or misattribute certain symptoms to “prove” their point that their child does or does not have ADHD.  I hear parents tell me all the time things such as, “My kid CAN’T have ADHD.  He can sit and play on his computer ALL day.”  At any rate, I have found Barkley’s list (below) a great resource to elucidate parents and teachers.

Comprehensive List of Symptoms and Difficulties Noted in Adults Diagnosed with ADHD

1. Find it difficult to tolerate waiting; impatient

2. Make decisions impulsively

3. Unable to inhibit my reactions or responses to events or others

4. Have difficulty stopping my activities or behavior when I should do so

5. Have difficulty changing my behavior when I am given feedback about my mistakes

6. Easily distracted by irrelevant thoughts when I must concentrate on something

7. Prone to daydreaming when I should be concentrating on something

8. Procrastinate or put off doing things until the last minute

9. Make impulsive comments to others

10. Likely to take short cuts in my work and not do all that I am supposed to do

11. Likely to skip out on work early if its boring or hard to do

12. Can’t seem to defer gratification or to put off doing things that are rewarding now so as to work for a later goal

13. Likely to do things without considering the consequences for doing them

14. Change my plans at the last minute on a whim or last-minute impulse

15. Start a project or task without reading or listening to directions carefully

16. Poor sense of time

17. Waste or mismanage my time

18. Fail to consider past relevant events or past personal experiences before responding to situations

19. Do not think about the future as much as others of my age seem to do

20. Not prepared for work or assigned tasks

21. Fail to meet deadlines for assignments

22. Have trouble planning ahead or preparing for upcoming events

23. Forget to do things I am supposed to do

24. Have difficulties with mental arithmetic

25. Not able to comprehend what I read as well as I should be able to do; have to reread material to get its meaning

26. Can’t seem to remember what I previously heard or read about

27. Can’t seem to accomplish the goals I set for myself

28. Late for work or scheduled appointments

29. Trouble organizing my thoughts or thinking clearly

30. Not aware of things I say or do

31. Can’t seem to hold in mind things I need to remember to do

32. Have difficulty being objective about things that affect me

33. Find it hard to take other people’s perspectives about a problem or situation

34. Have difficulty keeping in mind the purpose or goal of my activities

35. Forget the point I was trying to make when talking to others

36. When shown something complicated to do, cannot keep the information in mind so as to imitate or do it correctly

37. Give poor attention to details in my work

38. Find it difficult to keep track of several activities at once

39. Can’t seem to get things done unless there is an immediate deadline

40. Dislike work or school activities where I must think more than usual

41. Have difficulty judging how much time it will take to do something or get somewhere 42. Have trouble motivating myself to start work

43. Quick to get angry or become upset

44. Easily frustrated

45. Overreact emotionally

46. Have difficulty motivating myself to stick with my work and get it done

47. Can’t seem to persist at things I do not find interesting

48. Do not put as much effort into my work as I should or as others are able to do

49. Have trouble staying alert or awake in boring situations

50. Easily excited by activities going on around me

51. Not motivated to prepare in advance for things I know I am supposed to do

52. Can’t seem to sustain my concentration on reading, paperwork, lectures, or work

53. Easily bored

54. Others tell me I am lazy or unmotivated

55. Have to depend on others to help me get my work done

56. Things must have an immediate payoff for me or I do not seem to get them done

57. Have trouble completing one activity before starting a new one

58. Have difficulty resisting the urge to do something fun or more interesting when I am supposed to be working

59. Can’t seem to sustain friendships or close relationships as long as other people

60. Inconsistent in the quality or quantity of my work performance

61. Don’t seem to worry about future events as much as others

62. Don’t think about or talk things over with myself before doing something

63. Unable to work as well as others without supervision or frequent instruction

64. Have trouble doing what I tell myself to do

65. Poor follow-through on promises or commitments I may make to others

66. Lack self-discipline

67. Have difficulty using sound judgment in problem situations or when under stress

68. Trouble following the rules in a situation

69. Not very flexible in my behavior or approach to a situation; overly rigid in how I like things done

70. Have trouble organizing my thoughts

71. Have difficulties saying what I want to say

72. Unable to come up with or invent as many solutions to problems as others seem to do 73. Often at a loss for words when I want to explain something to others

74. Have trouble putting my thoughts down in writing as well or as quickly as others

75. Feel I am not as creative or inventive as others of my level of intelligence

76. In trying to accomplish goals or assignments, find I am not able to think of as many ways of doing things as others

77. Have trouble learning new or complex activities as well as others

78. Have difficulty explaining things in their proper order or sequence

79. Can’t seem to get to the point of my explanations as quickly as others

80. Have trouble doing things in their proper order or sequence

81. Unable to “think on my feet” or respond as effectively as others to unexpected events 82. Clumsy; not as coordinated in my movements as others

83. Poor or sloppy handwriting

84. Have difficulty arranging or doing my work by its priority or importance; can’t “prioritize” well

85. Slower to react to unexpected events

86. Get silly, clown around, or act foolishly when I should be serious

87. Can’t seem to remember things I have done or places I have been as well as others seem to do

88. Accident prone

89. More likely to drive a motor vehicle much faster than others (excessive speeding)

90. Have difficulties managing my money or credit cards

91. I am less able to recall events from my childhood compared to others

 

Reference

Barkley, Russell A. (2011-04-04). Taking Charge of Adult ADHD (Kindle Locations 5356-5369). Guilford Press. Kindle   Edition.

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