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Tuesday 31 January 2012

goodenoughcaring.com - SOCIAL PEDAGOGY WEBSITE






The study was published online November 1 in the New England Journal of Medicine and funded by the Agency for Healthcare Research and Quality (AHRQ) and by the US Food and Drug Administration (FDA).Safety Confusion

According to the investigators, 2.7 million American children are prescribed ADHD medications each year.

They note that although previous research from the United States and Canada has linked cases of cardiovascular events with these medications, case reports "cannot reliably quantify risk."

Still, on the basis of concerns raised by these findings, in 2008 the American Heart Association recommended that "it is reasonable" to perform electrocardiography in pediatric patients before prescribing ADHD drugs.

"There's been a lot of confusion for families and for providers about the safety of these medicines. So we set out to do a study that was sufficiently large and sufficiently well-designed to address these issues as carefully as possible," said Dr. Cooper.

A recent, large observational study, published in May 2011 in Pediatrics and reported by Medscape Medical News at that time, also found no significant increase in cardiac events due to use of ADHD medications. However, it was funded by Shire — a manufacturer of ADHD drugs.

In the current study, computerized records dating from 1986 to 2005 were evaluated for 1,200,438 people between ages 2 and 24 years (mean age, 11.1 years; 71% male) from 4 large health plans: Tennessee Medicaid, Washington State Medicaid, Kaiser Permanente California, and OptumInsight Epidemiology. The mean duration of follow-up was 2.1 years.

This represented "2,579,104 person-years of follow-up, including 373,667 person-years of current use of ADHD drugs," the investigators note.

ADHD medications used included methylphenidate, dexmethylphenidate, dextroamphetamines, amphetamine salts, atomoxetine, and pemoline.

The primary outcome was a serious cardiovascular event by any of the participants (current ADHD medication users, past users, and nonusers). The types of events examined included sudden cardiac death, acute myocardial infarction, or stroke.

First of 3 Studies

Results showed that 81 serious cardiovascular events were experienced by the study population, including 33 sudden cardiac deaths, 39 strokes, and 9 acute myocardial infarctions.

The adjusted rate of serious cardiac events was not significantly increased for current users of ADHD medications compared with the nonusers (hazard ratio [HR], 0.75; 95% confidence interval [CI], 0.31 - 1.85) or for former users vs nonusers (HR, 1.03; 95% CI, 0.57 - 1.89).

In addition, there was no increased risk for cardiovascular events when current users were compared with former users (HR, 0.70; 95% CI, 0.29 - 1.72) and no increased risk for any of the individual events.

Finally, no increased risk was found for the specific use of methylphenidate (HR, 0.96; 95% CI, 0.31 - 2.97), "the most frequently used ADHD drug."

Still, Dr. Cooper said that the families of every child and young person being considered for these medications should work with their healthcare provider to carefully decide what the risks and benefits are, especially for those with serious chronic health conditions.

The FDA reports that this is the first of 3 "separate but related studies" that it is co-sponsoring with AHRQ to evaluate the potential risk for serious cardiovascular events after the use of ADHD medications. The remaining 2 studies will focus on adults only.

"I think a great next step would be for people that think about policies related to screenings of children who use these medications to hopefully use this study, along with others, to reach a decision on the best recommendations," said Dr. Cooper.

"In other words, we hope this study provides important information to guide some of those policy decisions."




Monday 30 January 2012


Labelling Unhappy Children As Depressed May Be Harmful

Main Category: Depression
Article Date: DECEMBER 2010

Unhappiness among children seems to be rising, but labelling it as depression and prescribing antidepressants is ineffective and possibly harmful, warns a child psychiatrist in this week's BMJ.

Increasing numbers of children are being treated for depression. At the end of 2003, over 50,000 children were prescribed antidepressants, however, the author argues that anti-depressants are ineffective and some may be dangerous in this age group.

So how did we get into this mess, asks the author? Undoubtedly, part of the problem is with pharmaceutical industry tactics, but changes in Western cultural beliefs have also resulted in more childhood behaviours being viewed as a medical problem.

With little clinical evidence to support the idea that childhood depression exists as a distinct clinical category, it is time to focus on the underlying reasons for increasing unhappiness in young people, she says. Childhood depression, as a label, may need to be abandoned and a multiperspective approach adopted to deal with children's unhappiness.

In two accompanying commentaries, experts agree that non-medical therapy is an important component of treatment, but they warn against abandoning the diagnosis of depression in children.

The danger of abandoning the diagnosis is that the evidence base for effective psychological and pharmacological treatments may also be disregarded, writes consultant psychiatrist Quentin Spender.

Research psychiatrist, Paul Wilkinson believes that though it is wrong to neglect psychosocial treatments, it is equally unacceptable to neglect evidence based drug treatments for those who may truly benefit and recover from a mental disorder that carries serious risks for recurrence into adult life.

(Rethinking childhood depression)


Paper: Sami Timimi, Consultant Child and Adolescent Psychiatrist, Lincolnshire Partnership NHS Trust, Lincolnshire, UK
Email: stimimi@talk21.com


Why labeling children is harmful: ODD, ADHD, Aspergias, Dyslexic etc.

By Leah Gray
Aug 15, 2007 in Health

No one is denying that there are variations of ability among children or that some struggle with particular subjects or situations more than others. That has always been the case with humans and always will be. We are 'different' to each other.
But in recent times it seems that different is now a 'mental health problem' and attracts a wide array of labels, which in themselves can be very harmful to children. They can become a self fulfilling prophecy as well as damaging the child's self esteem.
I am not anti using labels to diagnose a problem, as I understand that most labeling is necessary in order to identify a problem that needs specialist attention and can relieve the parent and child of wondering why they are not able to keep up with their peers. But I advise caution, as the side effect of this can be that we are too quick to find labels to suit what may otherwise be transient, fleeting problems.
It is bearing those short-term problems in mind that I am compelled to write this article.
Labels are all around us, but this article focuses on children particularly as children tend to adopt any labels given to them as 'their role in life'. We know that modern parenting books advise against telling children they are 'naughty' but rather we say the action was 'naughty' instead. I.e. 'Throwing that ball was naughty' rather than 'you are a naughty child for throwing that ball'. Children believe most of everything adults tell them, so if you tell them they are 'A' they will believe you and model their behavior accordingly.
Consider this:
If you were labeled ‘antisocial’ because you did not wish to participate in the street party that mostly everyone else in your street was enjoying, would you think that a fair and reasonable assessment of your character? Does the fact that you dislike crowds and hustle and bustle and noise and instead prefer quieter more select group activities mean that you are some how defective as a human being and deserving of a specialized label or worse labeled as having a mental health problem? Knowing that there are many like you does not reduce the likelihood of your being given this label. Are you abnormal as the label suggests and suffering from a mental health problem, or are you just different to those who enjoy the fayre?
Are we allowed to be different to the majority anymore without attracting a label?
According to what is happening in recent years with children the answer to that question is a resounding no. Children are not allowed to be different. Teaching standards fit a particular model of education and if that model does not suit your individual learning leads, you are diagnosed as having a 'mental health problem' and given a label that will follow you throughout your life. A simple adjustment to teaching style could eliminate your difficulty in certain areas but still the label remains.
Labeling creates an image you are defective which can lead to low self-esteem, hinder progress and worse become a self-fulfilling prophecy. Psychologists and Sociologists are aware of this problem so why is labeling the differences on the increase? Please view this very informative article, which discusses 'educational authorities' desire for labels and the harm they do.
This world is made up of a great many different people and necessarily so. As well as academics, we also need practical, creative, physical people to do those jobs that require, strength, passion, single mindedness, leadership, and courage. Yet if we try to create a ‘personality’ type that all children adhere to, the diversity of character required to fulfill those many different roles will disappear and we will be left with a group of people who can only perform a single function.
Diversity is a good thing, even if it does put pressure on educational services to accommodate the different learning styles! I am very wary of the popularity of labels being attached to what was previously a case of 'not having an aptitude' for a particular subject.
Different teaching methods in all subjects can show improvement as we all have different ways in which we process information. One of the reasons boys are no longer doing so well in schools is that the education method is now more geared towards a female style of learning than a males.
But if we are not careful rather than recognize the need for a different teaching method, we will start labeling boys (who are not effeminate) as having some educational deficit. What we need here is greater variety of teaching methods, rather than one size fits all and a bunch of unhelpful labels that convince the child they are 'abnormal' and cannot change.
Studies show that many children diagnosed as ADHD improve when on a proper diet with proper stimulation and guidance. The reason for this could be misdiagnosis of the behaviour, which was instead the result of poor diet etc and not neurological. Misdiagnosis is a common problem with this disorder. The results of misdiagnosis can be devastating for the child as it is has been shown that Ritalin can cause brain damage if prescribed incorrectly. Presumably they know this because it has been prescribed incorrectly and those are the results! I therefore advise caution before accepting a 'label' like this for your child and advise ruling out other possible causative factors first.
Labels once applied tend to focus our full attention on treating the symptoms. We forget about the possible cause. Meanwhile the child is stigmatised for life. A percentage will be unaffected by changes in diet and routine and support and possibly can benefit from medication but many are too easily labeled with disastrous results.
Supporting sources below:
"The harm labeling children as ‘depressed’ can reap. “So how did we get into this mess, asks the author? Undoubtedly, part of the problem is with pharmaceutical industry tactics, but changes in Western cultural beliefs have also resulted in more childhood behaviours being viewed as a medical problem"
"The writer argues that one of the worst existing problems occurs when children are mislabeled as 'special' education and just 'thrown' into some classification that is really unnecessary."
“From anxious, often upscale, parents of young students to teachers in troubled schools, Levine delivers the same message, that all people -- and especially students -- are wired differently. He preaches the virtues of helping kids understand their strengths and weaknesses as part of understanding the way learning works."
"I always tell people that from the moment a kid gets up in the morning until he goes to sleep at night, the central mission of the day is to avoid humiliation at all costs." - Dr. Mel Levine
David Boulton: Yes, but my sense is that you're not so much pushing a corpus of knowledge that you want people to behave in relationship to, as much as you're trying to help inspire and develop and inform a different kind of lens, a different orientation from which to participate.
Dr. Mel Levine: That's one hundred percent correct. So, it's a lens where you look for recurring themes. Where you don't label anybody. Where you’re humble about who is normal and who is abnormal. Where you’re willing to say that a kid is quirky and eccentric rather than that he has Asperger Syndrome, which is my least favourite designation."

Read more: http://digitaljournal.com/article/217431#ixzz1kymLIk3H

Saturday 28 January 2012




The Medical Model of Mental Health and Psychiatric Labeling

Labeling and Drugging - An Inadequate Foundation for Mental Health Treatment

Also, Mental Health Disorders, Labeling and Stigma

Labeling, based on the medical model of psychiatry, is a method and a theory, although widespread and the standard approach in psychiatry, is not universally accepted in all professional communities.

John R. McHugh, M.D. is (2003)professor of psychiatry at John Hopkins University of Medicine and chief psychiatrist at John Hopkins hospital in Baltimore.

Espanaol - 19 prominent psychiatrists, psychologists and mental health professionals - (not an exhaustive list) - who disagree with the current medical model of mental health - Blog in Spnaish

The medical model is convenient, it gives therapist a clear-cut approach to handling individual situations, but most of all, it has been used by the psychiatric world in a way that leads to labeling and subsequent prescribing of psychiatric drugs. The typical procedure for the medical model of mental health involves, identifying symptoms, assigning an appropriate label, and administering what is deemed appropriate drugs.

Labeling and drugging is a convenient way of treating mental health disorders,
and is profitable for insurance and pharmaceutical companies.

This practice, along with the stigmatization of individuals who have mental health disorders, or who exhibit symptoms of such disorders, has come under the most scrutiny and criticism as lacking sound basis in professional circles in the field of mental health.

Pharmaceuticals are vigorously marketed to physicians, many times, with incentives.

Dr. Paul McHugh who chairs (2003), the department of psychiatry and behavioral sciences at Johs Hopkins University School of Medicine feels that the DSM label of Borderline Personality Disorder, has lost its usefulness. He is quoted in Time Magazine as stating that the DSM ("bible" of psychiatry labeling), has "permitted groups of 'experts' with a bias to propose the existence of conditions without anything more than a definition and a checklist of symptoms. This is just how witches used to be identified," cites multiple-personality disorder as an example of an "imagined diagnosis"; while much of the evidence supporting its existence has been debunked, multiple-personality disorder is still listed in the DSM, though today it's called "dissociative identity disorder." Diagnostics: How We Get Labeled, John Cloud. (Jan. 20, 2003). Time Magazine.

There are other mental health theories which provide a more practical, reasonable and accurate consideration of mental health issues such as the bioecological model of mental health, and positive psychology from Penn State University.

How Labeling and Stigma in Psychiatric Practice are Related

In a study by the American Sociological Association, of the theory of labeling in mental illness, the conclusion was reached that, "consistently support the prediction that the likelihood of social rejection increases after others gain knowledge of an individuals status as a mental patient."'

"When mental [health disorders] are used as labels, these labels hurt". SAMHSA

SAMHSA's, the US Government mental health association, gives this guideline, Before You Label People, Look At Their Contents. SAMHSA states, "When mental illnesses are used as labels - schizophrenic, manic, or hyperactive - these labels hurt."

The Brigadier General of the United States, and Director of the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury,
Loree Sutton, stated concerning many forms of mental illness, "Stigma is a toxic, deadly hazard, which must be eliminated," in a public service announcement.                                                                                           

"Psychiatric labels lead to stigma - Stigma leads to discrimination."Loree Sutton, Brigadier General of the United States

"Labels lead to stigma -- a word that means branding and shame. And stigma leads to discrimination. Everyone knows why it is wrong to discriminate against people because of their race, religion, culture, or appearance. They are less aware of how people with mental illnesses are discriminated against. Although such discrimination may not always be obvious, it exists-and it hurts."

Another thought to consider with persons who have or who have had mental illness is that labels stick. Even after a person may have recovered from bouts with serious mental illness, the label may have a long-lasting impact on other's perception of him or her.

"My son is bipolar."
Labels can be damaging and hurt the one being labeled,
affecting their view of themselves.

If a person recovers from cancer, do we refer to him or her as "being cancer," or he or her "is cancer". No, because we know that cancer is something that we can recover from and be cancer-free. With mental illness, labels are made, "he is OCD," "she is bipolar," as if to say, the word "bipolar" sums up one's whole existence, we don't need to take that person's actions good or bad too seriously, because it all comes down to the fact that he or she "is" this or that label.

In a study published in the American Journal of Psychiatry concerning the subject of stigma, the studies author Bernice A. Pescosolido notes that despite greater insights into mental health disorders in recent decades, one of the reasons for stigma surrounding mental illness lingers is that people tend to look at mental illness as something that never goes away. "When you attach a feeling of permanence to this, then it justifies, in some ways, a person's sense of 'otherness' or 'less-then-humanness'". Hitler took that idea of labeling and stigmatizing to the extreme, as we know, exterminating those with mental illness, but also labeling those who did not fit into his idealized schema as "untermenschen," meaning "sub-human" or "under-man".

That same type of stigmatizing can occur when considering those with mental health disorders as well. It should be noted that there are medical doctors who, before becoming doctors, started medical school after receiving a diagnosis of bipolar disorder. There are lawyers and collge professors with schizophrenia, who are active, productive members of the respective groups, no less than any other professional.

Full Recovery from Mental Illness is Possible

An Internet search on the key words, self help, provides numerous references for depression self help and ADHD self help, but comparatively few for bipolar disorder self help. Why? Because many who are labeled bipolar disorder are often taught to resign themselves to the label with a lifetime of taking psychiatric drugs in view. It is often thought of as an incurable disorder which must be managed with medication. Many who are labeled bipolar, then, may not take practical measures to help themselves. The label, in this case, can be a hindrance for many to take steps to help themselves.

Symptoms associated with bipolar disorder can be brought into remission
and full recovery is possible.

If you have the gout, as an example, you will no doubt be encouraged to change your diet. If you have diabetes, a diet free of excess sugar can be of much benefit. If you are diagnosed with bipolar disorder, then by all means, take positive self help steps to overcome the disorder.
Labeling can have profound effects on the level of will with which you exert yourself to try to ovecome mental health disorders. If you believe you can overcome a disorder, you are more likely to work very hard to do so. If you feel that the mountain cannot be climbed, then for sure, you will never try to climb it.

One encouraging account in relation to autism can be of help to persons with mental illness. In one well-known example of a boy, "Evan" who had suffered with autism, his mother utilized a tremendous amount of resources and therapy for her son's help, she didn't give up. Within a few years, the boy no longer qualified for the label, "autistic," he had sufficiently recovered from his symptoms.

Psychiatric Labels - Child From Dr. Scott Shannon, child psychiatrist.

The same has happened with many who have been labeled with ADHD, bipolar and other serious disorders. So, don't let yourself be put down by the label. Try to help yourself and fight your way out of the cocoon. If you do, you will gain a victory over stigma, and come out of it a more compassionate and understanding person, better able to take on the next set of challenges life presents.

Words of Stigma Can Be Poison

The stigma of mental illness is real, painful, and damaging to the lives of people with mental illness. Stigma prevents them from getting the treatment and support they need to lead healthy, normal lives. Many people don't want to be... labeled as "mentally ill" or "crazy."

Stigma keeps people from getting good jobs and advancing in the workplace. Some employers are reluctant to hire people who have mental illness. Thanks to the Americans with Disabilities Act (ADA), such discrimination is illegal. But it still happens!

Stigma leads to fear, mistrust, and violence. Even though the vast majority of people who have mental illness are no more violent than anyone else, the average television viewer sees three people with mental illness each week-and most of them are portrayed as violent. Even children's movies and cartoons can present a stereotypical version of mental illness, coloring children's view from an early age against those with mental health disorders. (Lawson, A., Calgary University). Such inaccurate portrayals lead people to fear those who have mental illnesses.

Stigma results in prejudice and discrimination. Many individuals try to prevent people who have mental illness from living in their neighborhoods.

Mayo Clinic similarly states,
"Stigma is a very real problem for people who have a mental [health disorer]. Based on stereotypes, stigma is a negative judgment based on a personal trait - in this case, having a mental health condition. It was once a common perception that having a mental illness was due to some kind of personal weakness. We still have a long way to go to overcome the many misconceptions, fears and biases people have about mental health, and the stigma these attitudes create.

Psychiatric stigma can be subtle, Mayo Clinic

Stigma may be obvious and direct, such someone making a negative remark about your mental health condition or your treatment. Or it can be subtle, such a someone assuming you could be violent or dangerous because you have a mental health condition. These and other forms of stigma can lead to feelings of anger, frustration, shame and low self-esteem - as well as discrimination at work, school and in other areas of your life. For someone with a mental illness, the consequences of stigma can be devastating."

Controversy and Resolution in Labeling Theory

Labeling theory was first applied to the term "mentally ill" in 1966 when Thomas Scheff, Professor, Emeritus, Dept of Sociology, University of California, Santa Barbara, and former Chair of the section on the Sociology of Emotions, American Sociological Association, and President of the Pacific Sociological Association, published the book, Being Mentally Ill. Scheff challenged common perceptions of mental illness by claiming that mental illness is manifested solely as a result of societal influence. See George Albee, Ph.D. webpage.

He argued that society views certain actions as deviant and, in order to come to terms with and understand these actions, often places the label of mental illness on those who exhibit them. Certain expectations are then placed on these individuals and, over time, they unconsciously change their behavior to fulfill them.

The term "mentally ill" is considered by some to be a part of labeling,
Thomas Scheff, PhD.

Criteria for different mental illnesses are not consistently filled by those who are diagnosed with them because all of these people suffer from the same disorder, they are simply fulfilled because the "mentally ill" believe they are supposed to act a certain way so, over time, come to do so.

Scheff's theory had many critics, most notably Walter Gove. Gove consistently argued an almost opposite theory; he believed that society has no influence at all on "mental illness". Instead, any societal perceptions of the "mentally ill" come about as a direct result of these people's behaviors. In Gove's view, the mentally ill behave unnaturally a lot of the time because of their disorders, so we treat them differently.

Most sociologists' views of labeling and mental illness have fallen somewhere between those of Gove and Scheff.

On the other hand, it is almost impossible to deny, given both common sense and research findings, that society's negative perceptions of "crazy" people has had some effect on their perception of those with mental health disorders. Disney movies are one commonly known example, of labeling person's as "crazy," and "lunatic," many of their most popular movies have scenes of "crazy" people or humanized animals running amuck.

Words Can Heal - Ending Stigma and Mental Health Disorders

Here are six steps you can follow to help end the stigma which surrounds mental health disorders

1. Learn more. Many organizations sponsor nationwide programs about mental health and mental illness. Several are listed at the end of this article.

2. Insist on accountable media. Sometimes the media portray people who have mental illnesses inaccurately, and this makes stereotypes harder to change.

3. Obey the laws in the Americans with Disabilities Act (ADA). The ADA prohibits discrimination against people with disabilities in all areas of public life, including housing, employment, and public transportation. Mental illnesses are considered a disability covered under the ADA.

4. Recognize and appreciate the contributions to society made by people who have mental illnesses. (See Elyn Saks, schizophrenia, on this site). People who have mental illnesses are major contributors to American life-from the arts to the sciences, from medicine to entertainment to professional sports.

5. Treat people with the dignity and respect we all deserve. People who have mental illnesses may include your friends, your neighbors, and your family.

6. Think about the person - the contents behind the label.
Avoid labeling people by their diagnosis. Instead of saying, "She's a schizophrenic," say, "She has a mental illness." Actually, never use the term "mentally ill."

Programs to End Psychiatric Stigma

Many National and State groups have begun projects and campaigns to reverse stigma. These groups offer a range of programs and materials, from speakers bureaus to training programs for mental health professionals. To get involved, call.
To learn more about mental health, call SAMHSA's National Mental Health Information Center at 800-789-CMHS (2647).

SAMHSA's National Mental Health Information Center
P.O. Box 42557
Washington, DC 20015
800-789-CMHS (2647)


Labelling Theory

Labeling theory is closely related to interactionist and social construction theories. Labeling theory was developed by sociologists during the 1960's. Howard Saul Becker's book entitled Outsiders was extremely influential in the development of this theory and its rise to popularity. Labeling theory holds that deviance is not inherent to an act, but instead focuses on the tendency of majorities to negatively label minorities or those seen as deviant from standard cultural norms. The theory is concerned with how the self-identity and behavior of individuals may be determined or influenced by the terms used to describe or classify them, and is associated with the concept of a self-fulfilling prophecy and stereotyping. The theory was prominent during the 1960s and 1970s, and some modified versions of the theory have developed and are still currently popular. Unwanted descriptors or categorizations - including terms related to deviance, disability or a diagnosis of mental illness - may be rejected on the basis that they are merely "labels", often with attempts to adopt a more constructive language in its place.

Modified Labeling theory

Bruce Link and colleagues have conducted several studies which point to the influence that labeling can have on mental patients. Through these studies, which took place in 1987, 1989, and 1997, Link advanced a "modified labeling theory" indicating that expectations of labeling can have a large negative effect, that these expectations often cause patients to withdraw from society, and that those labeled as having a mental disorder are constantly being rejected from society in seemingly minor ways but that, when taken as a whole, all of these small slights can drastically alter their self concepts. They come to both anticipate and perceive negative societal reactions to them, and this potentially damages their quality of life.[67]

Modified Labeling theory has been described as a "sophisticated social-psychological model of 'why labels matter' ". In 2000 results from a prospective two-year study of patients discharged from a mental hospital (in the context of deinstitutionalization) showed that stigma was a powerful and persistent force in their lives, and that experiences of social rejection were a persistent source of social stress. Efforts to cope with labels, such as not telling anyone, educating people about mental distress/disorder, withdrawing from stigmatizing situations, could result in further social isolation and reinforce negative self-concepts. Sometimes an identity as a low self-esteem minority in society would be accepted. The stigma was associated with diminished motivation and ability to "make it in mainstream society" and with "a state of social and psychological vulnerability to prolonged and recurrent problems". There was an up and down pattern in self-esteem, however, and it was suggested that, rather than simply gradual erosion of self-worth and increasing self-deprecating tendencies, people were sometimes managing, but struggling, to maintain consistent feelings of self-worth. Ultimately, "a cadre of patients had developed an entrenched, negative view of themselves, and their experiences of rejection appear to be a key element in the construction of these self-related feelings" and "hostile neighbourhoods may not only affect their self-concept but may also ultimately impact the patient's mental health status and how successful they are".[68] 

Hard and soft labeling

    Hard labeling – People who believe in hard labeling believe that mental illness does not exist. It is merely deviance from the norms of society that cause people to believe in mental illness. Thus, mental illnesses are socially constructed illnesses and psychotic disorders do not exist.[69]
    Soft labeling – People who believe in soft labeling believe that mental illnesses do, in fact, exist. Unlike the supporters of hard labeling, soft labeling supporters believe that mental illnesses are not socially constructed.[69]

One of the most important approaches to the understanding of criminality.

Labeling Kids with Bogus 'Mental Disorders' is WRONG ! COURTESY OF CCHR






Labeling normal kids with ADHD as "mentally ill" is WRONG!! - COURTESY OF CCHR WEBSITE




Friday 27 January 2012







Weighing Benefits and Risks in Managing ADHD
Jay M. Pomerantz, MD

Posted: 09/15/2005;


In addition to the well-publicized safety issues involving antidepressants, physicians who prescribe behavioral health products may have a new worry. Adderall, a psychostimulant for the treatment of persons with attention deficit hyperactivity disorder (ADHD), has been pulled from the Canadian market. On February 9, 2005, Health Canada (Canada's equivalent of the FDA) suspended market authorization for Adderall XR.[1] This means that no version of Adderall can be marketed in Canada, including the immediate-release form of Ad derall that was never available there. Health Canada is concerned about the sudden deaths, heart-related deaths, and strokes in children and adults taking usual recommended doses of Adderall and Adderall XR.

Health Canada cited results from a review of safety information provided by Shire US, the manufacturer, which indicated that there were 20 reports of sudden death in patients taking either Adderall or Adderall XR worldwide. None of the deaths occurred in Canada, nor were any deaths associated with overdose, misuse, or abuse of the medication. Fourteen of those who died were children. There were 12 reports of stroke, 2 of which occurred in children. The Canadian warning went on to say that a preliminary review of safety data for other stimulants used in the management of ADHD did not show as many serious adverse reactions leading to death as did Adderall and Adderall XR.[1]

On the same day that Health Canada suspended market authorization for Adderall XR, the FDA chose to deliver a different message. Rather than suspending distribution of Adderall preparations, the FDA issued a warning that the products not be used in children or adults who have structural cardiac abnormalities. The FDA substantiated its position by reviewing all 12 cases of sudden death in pediatric patients who were being treated for ADHD with either form of Adderall. All cases reviewed were from the FDA's Adverse Reporting System database for the years 1999 to 2003. During this period, approximately 30 million prescriptions for Adderall products were written. The 12 deaths were all of boys between the ages of 7 and 16, who had been treated from 1 day to 8 years with total daily doses ranging from 10 to 50 mg.

Significantly, autopsies in 5 of the 12 pediatric sudden death cases revealed underlying cardiac risk factors, including previously undiagnosed cardiac abnormalities (eg, aberrant origin of coronary artery, bicuspid aortic valve, and idiopathic hypertrophic subaortic stenosis). In one case, there was a family history of ventricular arrhythmia. Seven of the cases were complicated by other illnesses (eg, type 1 diabetes mellitus, fatty liver, and myocardial infarction) or heat exhaustion and rigorous exercise. Unusual and unexplained accumulation of drug, resulting in toxic levels during usual therapeutic dosing, also appears to have played a role in several deaths.[2] The FDA commented that the number of cases of sudden death reported for Adderall is only slightly higher, per million prescriptions, than the number reported for methylphenidate products, which are also commonly used to treat children with ADHD.[2]

Because it appeared that patients with underlying heart defects might be at increased risk for sudden death, the labeling was changed in August 2004 to warn that such patients should ordinarily not be treated with Adderall or Adderall XR.[3] As amphetamines, both forms of Adderall already carried black-box warnings cautioning physicians against prescribing them for children or adults with cardiovascular disease or hypertension.

If the FDA were to follow Canada in banning Adderall, where would that leave us in terms of options for managing ADHD? According to the FDA, methylphenidate preparations may carry a similar risk of sudden death in users. What are the alternatives? We know that double-blind placebo-controlled studies of the effectiveness of bupropion[4] and desipramine[5] show that these antidepressants are more effective than placebo for treatment of ADHD, although possibly less effective than stimulants.

Atomoxetine (Strattera), a selective norepinephrine reuptake inhibitor, and thus similar to some antidepressants, is approved by the FDA for managing ADHD in children and adults. Results of several studies show good efficacy compared with placebo.[6] However, we are still in the middle of the controversy about antidepressants and suicide risk.

In addition, on December 17, 2004, the FDA put out a new warning for Strattera.[7] The labeling for that medication is being updated with a bold-type warning about the potential for severe liver injury after 2 reports. One case occurred in a teenager and the other in an adult, after they were treated with Strattera for several months. Both patients recovered, but the new labeling warns that severe liver injury may progress to liver failure resulting in death or the need for a liver transplant in a small percentage of persons. There were no signs of hepatotoxicity in the original clinical trials of atomoxetine. Since marketing began in 2002, some 2 million children and adults have been treated with the medication.

I think that the FDA is being prudent in not rushing to join Health Canada in banning Adderall and Adderall XR. There may be risks associated with all medications used in the treatment of ADHD, as well as great benefit. As usual, a careful clinical assessment is needed before these medications are prescribed, and patients should be carefully monitored thereafter. That is the position of the American Academy of Child and Adolescent Psychiatry, which has advised its members that it is safe to continue prescribing psychostimulants for patients with ADHD (including Adderall and Adderall XR) by using clinical practices that were already in place before the FDA's latest warning.[8]

It is interesting that the Adderall controversy does not involve a new medication, but one that has been on the market for years. Adderall, a mixture of 4 different amphetamine salts (dextroamphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate, and amphetamine sulfate) was first developed for weight control 20 years ago by Rexar and marketed under the name Obetrol. Adderall was approved by the FDA for the treatment of ADHD in 1996.

Just as with the more substantiated and clear concerns about hormone replacement therapy in postmenopausal women, the increased risk of myocardial infarction for persons taking cyclooxygenase-2 inhibitors, and the increased risk of suicide associated with antidepressants that are prescribed for children and adolescents, it is not enough to determine safety and efficacy in short-term studies with a select population. Larger, ongoing studies with diverse populations may be required for both new and old medications to ensure that we really understand the safety/efficacy equation for each one.



Oseltamivir's adverse reactions
Fifty sudden deaths may be related to central suppression
BMJ 2007; 335 doi: 10.1136/bmj.39262.448877.BE (Published 12 July 2007)
Cite this as: BMJ 2007;335:59.1



The QT interval and psychotropic medications in children
Recommendations for clinicians

Paul McNally, Fiona McNicholas and Paul Oslizlok

Oseltamivir's adverse reactions
Fifty sudden deaths may be related to central suppression
BMJ 2007; 335 doi: 10.1136/bmj.39262.448877.BE (Published 12 July 2007)
Cite this as: BMJ 2007;335:59.1



European Child & Adolescent Psychiatry

Volume 16, Number 1, 33-47, DOI: 10.1007/s00787-006-0573-0

The QT interval and psychotropic medications in children
Recommendations for clinicians

Paul McNally, Fiona McNicholas and Paul Oslizlok

The use of psychotropic medications in children has increased significantly in the last few years. There have been several case reports of sudden death in children taking specific psychotropic medications. Fears that these deaths might have been caused by ventricular arrhythmias have been enhanced by reports of electrocardiographic abnormalities, including prolongation of the QTc interval, in patients taking these medications. Several factors including genetic susceptibility, pre-existing cardiac disease, abnormalities of drug clearance and concomitant use of other medications known to affect the QTc interval can increase the susceptibility of the heart to conduction abnormalities. This article discusses the potential of particular psychotropic drugs to prolong the QTc interval in children, and examines other factors that may contribute to conduction abnormalities. We aim to provide clear clinical recommendations for the prescription of these drugs and the monitoring of children taking them. 

Thursday 26 January 2012


Attention deficit hyperactivity disorder - Medications and their Dangerous Side-Effects.

An in-depth report on the causes, diagnosis, treatment, and prevention of ADHD.

Several types of medication are available to treat ADHD.
Psychostimulants: Methylphenidate (Ritalin) and Similar Drugs

Psychostimulants are the primary drugs used to treat ADHD. Although these drugs stimulate the central nervous system, they have a calming effect on people with ADHD.

These drugs include:

    Methylphenidate (Ritalin, Concerta, Metadate, Daytrana)
    Dexmethylphenidate (Focalin)
    Amphetamine-Dextroamphetamine (Adderall)
    Dextroamphetamine (Dexedrine, Dextrostat)
    Lisdexamfetamine (Vyvanse)

Pemoline (Cylert), another stimulant drug, was withdrawn from the U.S. market in 2005 after several reports of liver failure.

Methylphenidate and Dexmethylphenidate. Methylphenidate drugs (Ritalin, Metadate, Concerta, Daytrana) are the most commonly used psychostimulants for treating ADHD in both children and adults. Dexmethylphenidate (Focalin) is a similar drug. These drugs increase dopamine, a neurotransmitter important for cognitive functions such as attention and focus.

With the exception of Daytrana, all of these drugs are pills taken by mouth. Daytrana, approved in 2006, is the first skin patch drug for ADHD. A patch is applied to the hip each day and delivers a 9-hour dose of methylphenidate.

These drugs are available in short-acting and long-acting dosage forms. The short-acting forms need to be taken several times a day, including during school hours. As the drug wears off, a rebound effect can occur, and ADHD symptoms can intensify. For this reason, the long-acting dosage forms have become popular.

Amphetamine, Dextroamphetamine, and Lisdexamfetamine. Amphetamine-dextroamphetamine (Adderall), dextroamphetamine (Dexedrine, Dextrostat), and lisdexamfetamine (Vyvanse) work by blocking the reabsorption of the brain chemicals dopamine and norepinephrine. Side effects can include stomach problems and mood changes, including sadness, anxiety, and irritability.

Risks of Stimulants:

Psychostimulant medications are associated with some significant risks. All ADHD stimulant drugs carry warnings that they should not be used by patients with structural heart problems or pre-existing heart conditions (high blood pressure, heart failure, heart rhythm disturbances, or congenital heart disease). These drugs have been associated with sudden death in children with heart problems. They have also been associated with sudden death, stroke, and heart attack in adults with a history of heart disease.

The American Heart Association (AHA) currently recommends cardiac testing prior to prescribing stimulant drugs for children. The AHA recommends that doctors:

    Get a complete patient and family history
    Conduct a physical exam to check for heart problems, including heart murmurs and high blood pressure
    Arrange a consultation with a pediatric cardiologist if necessary
    Consider ordering an electrocardiogram (ECG) to check for heart abnormalities (in contrast, the American Academy of Pediatrics does not recommend routine use of ECGs before starting stimulant therapy)
    Monitor patients on stimulant drugs for emergence of cardiac symptoms

The AHA notes that stimulant drugs remain a reasonable option for children with stable heart disease or those who are currently receiving care from a pediatric cardiologist.

Stimulant drugs may also:

    Worsen behavior and thought disturbance in patients with a pre-existing psychotic disorder. These drugs may also slightly increase the risk for auditory hallucinations, paranoia, and manic behavior even in patients who do not have a history of psychiatric problems.
    Cause a mixed or manic episode in patients who have both ADHD and bipolar disorder.
    Increase aggressive behavior or hostility. Patients beginning stimulant drug treatment should be monitored for worsening of these behaviors.
    Slow growth and weight gain in children. Children who take stimulant drugs should have their growth monitored. If they do not gain height or weight at a normal rate, they may need to stop taking the drug.

The FDA has directed manufacturers of ADHD medications to warn all patients taking these medicines of their potential cardiovascular and psychiatric risks.

Side Effects. All stimulants have a number of side effects:

    The most common side effects of any stimulant are nervousness and sleeplessness, although some parents have reported improved sleep patterns in their children after taking stimulants.
    Tics or jerky, disordered movements occur in about 9% of children.
    Other side effects include irritability, stomach pain, headache, depression, hair loss, and lack of spontaneity.

Symptoms of Overdose:

Symptoms of overdose include changes in heart rhythm and rate, hypertension, confusion, breathing difficulties, sweating, vomiting, and muscle twitches. If they occur, parents should call the doctor immediately. Even among young people who abuse Ritalin, however, less than 1% experience severe side effects (rapid heart rate, hypertension), and outcomes are generally good. Side effects may be very severe, however, if Ritalin is overused and taken with other drugs.

Concerns for Abuse:

Studies on both animals and humans suggest that Ritalin lacks the properties that create addiction, particularly in doses used for treating ADHD. Although methylphenidates have properties similar to amphetamines, their drug levels rise very slowly in the brain at the oral doses given for ADHD. This slow rise prevents a so-called "high" and subsequent addiction to the drug. Some stimulant drugs, such as lisdexamfetamine, may pose a lower risk for abuse than others.

The primary danger for drug abuse from stimulants appears to occur in young people without ADHD who purchase these drugs illegally. In one study, 16% of children with ADHD reported pressure from their fellow students to sell or give them their medication. While people ages 18 - 25 are more likely to use ADHD drugs for non-medical uses, children ages 12 - 17 are more likely to suffer adverse effects from medication misuse and to require treatment at an emergency room. If a child abuses another drug (alcohol, prescription medication) along with the ADHD medication, the chance for serious side effects is even greater.

Non-Stimulant: Atomoxetine:

Atomoxetine (Strattera) was the first non-stimulant approved for ADHD in children and the first treatment approved for adult ADHD. The drug works by increasing levels of both norepinephrine and dopamine, which are generally lower than normal in ADHD. The most common side effect is decreased appetite. A few cases of atomoxetine-associated liver injury have been reported, and the FDA has warned doctors that the drug should be discontinued at the first signs of jaundice (yellowing of skin and eyes) and liver problems. Long-term effects, such as any impact on growth, are still unknown. Atomoxetine may cause suicidal thinking in children and adolescents, especially during the first few months of treatment. Parents should monitor children taking atomoxetine for any changes in mood or behavior, and immediately contact their doctor if changes occur.


Antidepressants are not FDA-approved for ADHD treatment, but may be helpful in certain circumstances. Because antidepressants appear to work about as well as behavioral therapy, doctors recommend that patients first try psychotherapy before using antidepressants.

Bupropion (Wellbutrin) and tricyclics are the types of antidepressants used for ADHD. Bupropion affects the reuptake of the serotonin, norepinephrine, and dopamine neurotransmitters. Side effects include restlessness, agitation, sleeplessness, headache, and stomach problems. Bupropion should not be used by patients who have a seizure disorder.

Tricyclics are an older type of antidepressant that can be beneficial but have many side effects. Imipramine (Tofranil) and nortriptyline (Pamelor, Aventil) are the tricyclics most commonly prescribed for ADHD. A third tricyclic, desipramine (Norpramin) should only be used if patients are not helped by other tricyclics. (Desipramine has caused sudden death in some children and adolescents.)
Tricyclic antidepressants can cause disturbances in heart rhythm. Children should have an electrocardiogram when they first begin to take this drug, and after any dose increase.

Alpha-2 Agonists (Clonidine)

Alpha-2 agonists stimulate the neurotransmitter norepinephrine, which appears to be important for concentration. They include clonidine (Catapres) and guanfacine (Tenex). They are used for Tourette syndrome and may be beneficial when other drugs have failed for ADHD children with tics or those whose primary symptoms are severe impulsivity and aggression. These drugs are mainly prescribed in combination with a stimulant.

These drugs have a number of side effects. Sedation is the most common. A clonidine skin patch, which gradually releases the medication, helps reduce the sedative effect. Because clonidine slows the heart down, it can have adverse effects in some children. Going off too quickly or missing doses can cause rapid heartbeats and other symptoms that may lead to severe problems. Doctors strongly recommend that no child be given this medication without a preliminary examination for heart problems, and no child with existing heart, kidney, or circulatory problems should take it.

Read more: http://www.umm.edu/patiented/articles/what_medications_attention-deficit_hyperactivity_disorder_000030_8.htm#ixzz1kayPgVS5



People's sensitivity and response to drugs varies enormously. One person may be able to tolerate standard doses with no significant side effects, while someone else may find the same dose has intolerable results.

Neuromuscular effects

Antipsychotics, as a group, have a large number of side effects in common. Because they interfere with dopamine, which is important in controlling movement, many of the side effects are to do with the neuromuscular system. These neuromuscular effects include: Parkinsonism, loss of movement, restlessness and muscle spasms.


Some side effects resemble Parkinson's disease, which is caused by the loss of dopamine:

    Muscles become stiff and weak, so that your face may lose its animation, and you find fine movement difficult.
    You may develop a slow tremor (shaking), especially in your hands.
    Your fingers may move as if you were rolling a pill.
    When walking, you may lean forward, take small steps, and find it difficult to start and stop.
    Your mouth may hang open and produce excessive saliva.

Loss of movement (akinesia)

You may find it difficult to move, and your muscles may feel very weak. This may be mistaken for a symptom of depression.

Restlessness (akathisia)

You may feel intensely restless and unable to sit still. This is more than just a physical restlessness and can make you feel emotionally tense and uneasy, as well. The compulsion to move may be overwhelming. You may rock from foot to foot, shuffle your legs, cross or swing your legs repeatedly, or continuously pace up and down. Nursing staff sometimes misread this as a sign of agitation or anxiety, and may wish to treat it by increasing your dose of antipsychotics. If you are very troubled by akathisia, your doctor may be able to prescribe something to reduce it.

Muscle spasms/dystonia (dysphonia and oculogyric crisis)
These are acute muscle contractions that are uncontrolled and may be painful. They particularly affect young men. Sometimes the problem affects the muscles of the larynx (voice box), which makes it difficult to speak normally (dysphonia). It can be socially disabling, but is treatable.

Another form of muscle spasm affects the muscles that control eye movements. Called 'oculogyric crisis', it makes the eyes turn suddenly, so that you can't control where you look. This is very unpleasant and can make it dangerous crossing the road, or pouring hot water, for instance. It's also very disconcerting for people around you.

Such neuromuscular symptoms can be reduced with the sorts of drugs that are prescribed to treat Parkinson's disease (see below for more information on these drugs). These symptoms die down while you are asleep, so if you take the antipsychotics as a single daily dose in the evening, you could avoid the worst of them (as well as avoiding daytime sedation). You may want to discuss this with your doctor to find out whether it would be an option for you.

Sexual side effects

Many antipsychotic drugs cause levels of the hormone prolactin to rise, which is related to some very common sexual side effects for both women and men, who may feel embarrassed to talk about them:

    Breast development and the production of breast milk can affect men as well as women.
    A drop in sexual desire can make men and women less easily aroused, and cause impotence and sterility in men. Some drugs can interfere with erection and affect ejaculation.
    Priapism, a persistent erection of the penis without sexual arousal, sometimes results. This is rare, but if it occurs you should treat it as an emergency and seek medical advice, because it may cause serious harm to the penis.
    Spontaneous ejaculation is sometimes a problem.
    Loss of periods, vaginal dryness, unwanted hair and acne may occur in women.
    Osteoporosis (loss of bone density) as a consequence of hormone changes is a serious risk for men and women, and increases the risk of fractures.

Some of the atypical antipsychotics have less effect on prolactin and produce fewer of these problems. Note: women who change from an older antipsychotic to an atypical should bear in mind that this may cause prolactin levels to drop back down.  This may cause their periods to return and they may need to think about contraception.

Antimuscarinic or anticholinergic effects

The drugs affect acetylcholine (another chemical messenger) and this may cause drowsiness, dry mouth, blurred vision, dizziness, constipation, feeling sick, difficulty passing water and rapid heartbeat. Constipation may be severe, and should be taken seriously. Low blood pressure can be a problem, especially in older and frail people, and it may contribute to falls; hot baths increase the risk.

Heart rhythm

Several antipsychotics have been implicated in sudden deaths. Although these have been investigated, with no clear conclusion, sudden deaths have been linked to high doses of antipsychotics (above the BNF maximum) and to polypharmacy, when people are on several different antipsychotics at the same time. Many of these drugs affect the heart rhythm. The Royal College of Psychiatrists' guidelines suggest that people on high doses of antipsychotics should be given an ECG before treatment starts and every one to three months, while the dose remains high. Whatever your dose, if you have unexplained blackouts, you should have your heart rhythm monitored. Be cautious with grapefruit and grapefruit juice, because it's thought this might increase the impact on heart rhythm.


Sleepiness is a common side effect with antipsychotics, but some, such as chlorpromazine, are more sedating than others.

Eye problems

Various antipsychotics may be responsible for different eye disorders. These include blurred vision and difficulty reading, a build up of granular deposits in the cornea and lens (which doesn't usually affect sight), degeneration of the retina (the light-sensitive part of the eye) that restricts vision and may be serious, an oculogyric crisis (see above), and glaucoma (increased pressure inside the eye). Any antipsychotic can cause narrow-angle glaucoma, which is a medical emergency. You should not take the low-potency antipsychotics if you have had glaucoma.

Weight gain

Weight gain is a very common side effect with a number of antipsychotics, including some of the atypical drugs, and causes a lot of distress. It is linked to increased appetite and decreased activity, but is mainly caused by changes in metabolism - the way your body uses food and converts it to energy or stores it as fat. This means that dieting may be of limited use. You may put on a lot of weight, and this may increase your risk of developing diabetes, and other physical health problems.

Metabolic syndrome, including diabetes

Some side effects, associated especially, but not exclusively, with atypical antipsychotics, are linked, and have begun to be referred to as 'metabolic syndrome'. This group of symptoms: weight gain and obesity; high blood sugar; high blood pressure, and high cholesterol, puts people at risk of heart disease, stroke and diabetes. The risk is increased by dietary factors, such as drinking sugary carbonated drinks and eating a lot of fatty, sugary foods. Everyone, especially those with a family history of diabetes, should have their blood glucose monitored while they are taking these drugs. You should also tell your doctor if you have a family history of cardiovascular disease such as high blood pressure or heart attack. Metabolic syndrome is thought to cause a two- to three-fold increase in the risk of death from cardiovascular disease.


A number of blood disorders are linked to antipsychotics. The most serious is agranulocytosis, a serious blood disorder, which involves the loss of one type of white blood cell. It reduces resistance to infection and has led to deaths in the past. It's very rare with the older antipsychotics, and is a particular risk of clozapine.

Other physical effects

Some people develop blood clots in the veins (thromboembolism), linked to low-potency drugs as well as clozapine.

Liver disorders and jaundice are sometimes linked to using these drugs.

There are various skin problems that may occur. If you get a rash, you should go to the doctor straight away. Any allergic rashes usually occur within the first two months of starting treatment and disappear when the drug is stopped. Some types of skin may develop a blue-grey discoloration. Your skin may become more sensitive to sunlight, especially at high doses, so you should protect your skin from the sun.

You may have problems with regulating body temperature. It may be too high or too low, both of which may make you feel a little unwell.

Another problem that might occur is difficulty urinating.
Emotional effects

Antipsychotics can sometimes make people more excited, agitated and aggressive. They can also cause emotional changes, such as depression. Others may have an antidepressant effect, although the available information about this is contradictory. Some drugs cause an emotional unease, making people restless, giving them bizarre dreams and disturbing their sleep. They can make people feel out of touch with reality or strange in familiar surroundings (depersonalised and derealised). It may also cause them to become more withdrawn, socially.

What is neuroleptic malignant syndrome (NMS)?

This neurological complication is thought to occur in about one per cent of hospital patients taking antipsychotic drugs. It can be very dangerous if it's not detected and treated, but the symptoms can be mistaken for an infection.

The symptoms are: sweating or fever, with a high temperature; tremor, rigidity or loss of movement; difficulty speaking and swallowing; changes in consciousness, from lethargy and confusion to stupor or coma; rapid heartbeat, very rapid breathing and changes in blood pressure. Blood tests show abnormal results. NMS develops rapidly over 24 to 72 hours, and rigidity and a high temperature are usually the first symptoms to appear.

The condition mostly affects people under forty, and is twice as common in men. It can occur if you are taking standard doses of antipsychotics, and if you have been taking the drugs for many years. The main trigger seems to be a change of dose within the last 4 to 11 days. High-potency antipsychotics may produce greater risk, but it can happen with all of these drugs, including the atypical group.

Treatment varies and can include reducing the fever, giving drugs to relax the muscles, and drugs to counter the chemical imbalance that is thought to cause NMS. Electroconvulsive therapy has also been used effectively.

The symptoms may last for days, or even weeks, after stopping the drugs. Although the criteria for making the diagnosis are not clear, it seems that only about one per cent of people on antipsychotics are likely to get NMS. Out of these, 11 per cent may be fatal. Many people who have had NMS once go on to get it again, so you should only take antipsychotics afterwards if they are absolutely essential, and then only the low-potency drugs at the lowest doses.

What is tardive dyskinesia (TD)?

TD is a disorder of the central nervous system, which causes abnormal, uncontrollable, disfiguring, and embarrassing movements. These usually start in the face and mouth, as involuntary tongue movements and slight grimacing. The problem can spread to the rest of the body, with writhing movements in the limbs, muscle spasms, tremors and tics.

Most psychiatrists agree that TD is caused by antipsychotics, mainly affecting people who have been taking moderate to high doses for long periods of time, and who have had quite severe Parkinson's symptoms. It's rare in someone who has been taking antipsychotics for less than six months, if the doses have been small. It seems that people are more likely to get TD if they get bad Parkinson's effects. Women, children and older people may be more vulnerable, and possibly those with a mood disorder such as manic depression (bipolar disorder).

The problem may not be discovered until after you stop taking the antipsychotics, because they mask the symptoms of TD. Unfortunately, stopping and starting the drugs may make TD more persistent, once it has developed.

Some people remain on the drugs as a way of dealing with the symptoms, although this may result in further damage. Sometimes when drugs are withdrawn, withdrawal dyskinesias may occur, but this is not necessarily the same as TD.

There's disagreement about how common TD is, and about the number of people who are permanently affected. Estimates of the risks of developing TD, after long-term use, range from 5 to 56 per cent, but 20 per cent is a widely accepted estimate for those treated for four years, or longer. The risk is higher for people on depot preparations. There is believed to be much less risk of TD with the atypical drugs.


Sudden Death and Use of Stimulant Medications in Youths
Madelyn S. Gould; B. Timothy Walsh; Jimmie Lou Munfakh; Marjorie Kleinman; Naihua Duan; Mark Olfson; Laurence Greenhill; Thomas Cooper

Am J Psychiatry 2009;166:992-1001.
The authors sought to determine whether a significant association exists between the use of stimulants and the rare event of sudden unexplained death in children and adolescents. Method: A matched case-control design was performed. Mortality data from 1985—1996 state vital statistics were used to identify 564 cases of sudden death occurring at ages 7 through 19 years across the United States along with a matched group of 564 young people who died as passengers in motor vehicle traffic accidents. The primary exposure measure was the presence of amphetamine, dextroamphetamine, methamphetamine, or methylphenidate according to informant reports or as noted in medical examiner records, toxicology results, or death certificates. Results: In 10 (1.8%) of the sudden unexplained deaths it was determined that the youths were taking stimulants, specifically methylphenidate; in contrast, use of stimulants was found in only two subjects in the motor vehicle accident comparison group (0.4%), with only one involving methylphenidate use. A significant association of stimulant use with sudden unexplained death emerged from the primary analysis, which was based on exact conditional logistic regression (odds ratio=7.4, 95% CI=1.4 to 74.9). A comprehensive series of sensitivity analyses yielded qualitatively similar findings. Conclusions: This case-control study provides support for an association between the use of stimulants and sudden unexplained death among children and adolescents. Although sudden unexplained death is a rare event, this finding should be considered in the context of other data about the risk and benefit of stimulants in medical treatment.

Figures in this Article

Reports of sudden death among children and adolescents receiving stimulant medications for treatment of attention deficit hyperactivity disorder (ADHD) have raised concerns about the safety of these agents. There have been reports of pediatric stroke after long-term use of methylphenidate within therapeutic ranges (1). Acute myocardial infarction has been reported in one adolescent taking methylphenidate for an unknown period of time (2) and in another adolescent 1 week after restarting a daily 20-mg prescription of mixed amphetamine salts (3). Cardiac arrest occurred in another adolescent who was taking methylphenidate for ADHD and who had previously had a normal baseline echocardiogram (4). The Food and Drug Administration (FDA), using the Adverse Event Reporting System, reported 11 sudden deaths in pediatric patients taking methylphenidate from January 1992 to February 2005 (5). While the FDA’s reporting rate of sudden death in stimulant-treated children was the same as the base rate in the general population, spontaneous reports of sudden deaths may underestimate their true incidence, and limited available information on total number of prescriptions precludes reliable estimates of stimulant exposure (5). Less serious cardiovascular effects have also been reported in association with stimulant medications. An average increase in diastolic blood pressure of 4 mm Hg has been found among stimulant-treated youths in placebo-controlled trials (5, 6). A 10-year analysis of Florida Medicaid claims data revealed that stimulant use among youths diagnosed with ADHD was associated with increases of 20% and 21% in risk of emergency department visits and physician office visits for cardiac symptoms, respectively (7). No cardiac sudden deaths occurred during the 42,612 person-years of current stimulant use; however, as the authors noted, the rarity of sudden death and cardiac mortality in this age group would have necessitated a sample size 16 times larger, i.e., approximately 2,000,000 person-years, to detect a significant difference between the stimulant use and nonuse groups.
There continues to be controversy surrounding whether there exists an association between stimulant use for the treatment of ADHD and serious cardiovascular events, including sudden death, with accompanying debate over clinical recommendations for physicians and families (8, 9). The FDA’s Pediatric Advisory Committee in March of 2006 voted unanimously against a black box warning, which had been proposed by an earlier FDA advisory committee, but recommended a warning targeted to specific high-risk children, such as those with structural heart defects, cardiomyopathy, or heart-rhythm disturbances (10). In 2008, the American Heart Association recommended considering routine ECGs prior to starting children with ADHD on stimulant and other psychotropic therapy regimens (11) but underscored the need for future studies to assess the risk of sudden death associated with stimulant medication use in children and adolescents. The American Academy of Pediatrics (12) has also highlighted the "absence of scientific data to establish an increased risk of sudden death in individuals receiving stimulant medications."
The present article provides empirical data on the risk of sudden death and stimulant drug use in children and adolescents. In light of the rarity of sudden death in this age group (estimated at 0.8 to 8.5 cases per 100,000 patient-years) (13, 14), a matched case-control design was employed. The analysis seeks to estimate the strength of association between use of stimulant medications and sudden unexplained death.

Abstract  |  Method  |  Results  |  Discussion  |  References 
This study was initiated in 1996, with support from the National Institute of Mental Health (NIMH), to examine the association between sudden death in children and adolescents and the use of tricyclic antidepressants or concomitant methylphenidate and clonidine therapy (15, 16). During the course of the study, there was a marked decrease in the use of tricyclic antidepressants in youths (17) and an associated significant increase in the use of selective serotonin reuptake inhibitors (SSRIs), which led to an attenuation of the clinical relevance of our examination of the association of tricyclic antidepressants and sudden death. Thus, these analyses were not pursued further. In light of concerns over the safety of stimulant medications, the FDA in 2006 requested an expansion of the inquiry of stimulants to include amphetamine, dextroamphetamine, and methamphetamine. The current report focuses on stimulant use among children and adolescents.

Definition of Sudden Unexplained Death
A case of sudden unexplained death was defined as any cause of death listed as ICD-9 codes E798 (sudden death, cause unknown), E799.9 (other unknown and unspecified causes), or E427 (cardiac dysrhythmia). These codes reflected causes of death in case reports of sudden death in children using tricyclic medications (15), consistent with the original goal of the study. We targeted cases 7 through 19 years of age, identified from mortality data from 1985 —1996 state vital statistics across the United States.
Exclusion criteria were 1) deaths with known causes—such as accidental deaths, suicides, overdoses, homicides, and natural causes (e.g., asthma)—initially misclassified on death certificate as unknown and subsequently amended; 2) deaths in which there were medical intervention complications or among individuals hospitalized for more than 48 hours at the time of death; or 3) coexisting physical disorders known or suspected to be associated with sudden death but not listed as the cause of death on the death certificate or autopsy report, such as Marfan’s syndrome (14), Wolff-Parkinson-White syndrome (18), severe cerebral palsy (19), profound developmental delays (20), seizure disorders (21), sickle cell anemia (22), morbid obesity (23), asthma (24), anorexia nervosa (25), prolonged QT interval in the deceased or in any first-degree relative, history of sudden death among first-degree relatives, conduction disorders in the deceased, and evidence of cardiac disease or abnormal anatomical finding on autopsy, such as cardiomegaly, cardiac hypertrophy, and cardiomyopathy (14).
Comparison Group
Individuals who died as passengers in motor vehicle traffic accidents with another motor vehicle (ICD-9 code E812.1) were also examined. A comparison group of deceased youngsters was necessary to avoid differential recall biases. Parents of both sudden unexplained death and motor vehicle accident victims had experienced a sudden, traumatic loss of their children. Unlike other victims of injuries (28), motor vehicle passenger victims were selected because they have been found not to be at greater risk for hyperactivity and other deficits in vigilance, attention, and impulse control. Thus, we avoided inappropriately increasing the likelihood of stimulant use among the comparison group. In this way, subjects were likely to be representative of the general population of youths 7 through 19 years of age. The same exclusion criteria noted for sudden unexplained death subjects were applied to the motor vehicle accident victims.
Comparison subjects were individually matched to sudden unexplained death cases by year of death (within 3 years), age (within 3 years), gender, and data source available. Each matched pair was unique; an individual motor vehicle accident victim was matched to one and only one case of sudden unexplained death. Limitations in the pool of comparison subjects precluded matching on race and census geographic region of death, factors that may affect rate of stimulant medication use (7, 26).

Definition of Exposure
The primary exposure variable was evidence of stimulant use immediately prior to death, indicated by presence of amphetamine, dextroamphetamine, methamphetamine, methylphenidate, or their derivatives, as noted by informants or in medical examiner records, toxicology findings, or death certificates. Information was also obtained about use of clonidine, tricyclic antidepressants, and SSRI antidepressants.
Sources of Data
Mortality data and death certificates were obtained from state vital statistics offices across the United States (including New York City and the District of Columbia) for 1985 through 1996. Indiana, Kansas, Maryland, Wisconsin, and Wyoming were excluded because their state statutes did not allow direct interviewing of families of deceased individuals or had restrictive contact requirements.
For informant reports, the names of the deceased child and his or her parents and the address at time of death were identified from the death certificate, on public record, from the state vital statistics offices. Parents were approached by letter describing the purpose of the study and were asked to complete a survey. The survey included items assessing medical history, medications taken at time of death, a list of medical problems, and the use of over-the-counter and prescription medications. A history of sudden death among relatives was also assessed. To locate informants, various Internet search engine white pages, a credit bureau database (without access to credit information), ChoicePoint (CDB Infotek), and PrivateEye were used.
Medical examiner records and toxicology findings were used to identify medication use and assist in the identification of exclusion criteria. Medical examiner reports could include informant- or toxicology-based findings, as well as autopsy reports. The applied postmortem detection threshold for a blood or urine stimulant level to be deemed positive varied considerably across jurisdictions. Thus, our reports of a positive finding reflect a value above the stated threshold for each individual laboratory.
Data collection, from March 1997 to January 2008, involved the following phases. Cases of sudden unexplained death were identified through state mortality data, and death certificates were obtained from state vital statistics offices. Death certificates were reviewed for eligibility by the research team. Parents were approached for surveys and consent for records, if required by state law. Autopsy and toxicology records obtained from medical examiners were reviewed and abstracted. The same procedures were applied to motor vehicle accident victims matched to sudden unexplained death cases with surveys or toxicology results.
A two-stage determination of eligibility for all subjects was conducted by the two principal investigators (M.S.G. and B.T.W.) and research staff, blind to medication status. The first stage involved the examination of death certificates, and the second involved review of informant reports and medical examiner, autopsy, toxicology, and medical records.
The Institutional Review Board of the New York State Psychiatric Institute/Columbia University Department of Psychiatry approved study procedures, and a Certificate of Confidentiality was issued by NIMH.

Analytic Strategy
The basic unit of analysis is the matched dyad, rather than the individual subject. We estimated the association between sudden unexplained death and stimulant exposure using a logistic regression model that predicted sudden unexplained death from stimulant exposure. Race and region of death were included as covariates in all logistic regression models. In light of matching on sources of information (e.g., medical examiner records, toxicology, and informant reports), only sources available for both members of the matched pair were used to define exposure status. In the primary analysis, using the total sample, exposure was defined as any stimulant indication. A series of sensitivity analyses varied the exposure definition, including the presence of any stimulant as noted by informants; any stimulant reported in medical examiner records or toxicology reports; methylphenidate reported by any source; methylphenidate noted by informants; and methylphenidate disclosed in medical examiner records or toxicology reports. Each sensitivity analysis used the subsample of dyads with observed data for the specific information source.
In light of the original study’s intent to examine the association of sudden death with tricyclic antidepressants and with concomitant methylphenidate and clonidine use, we conducted another series of analyses to assess whether these associations might be significant in our sample in order to determine whether the concomitant use of these medications needed to be taken into account in our current sensitivity analyses of stimulant exposure.
Pairing of subjects (27) was incorporated into the conditional logistic regression model through exact conditional logistic regression using the EXACT statement in the LOGISTIC procedure in SAS statistical software, release 8.1.

Abstract  |  Method  |  Results  |  Discussion  |  References 
Eligible individuals (N=926) were identified from a pool of 3,211 youths with deaths listed as ICD-9 codes E798, E799.9, or E427 (Figure 1). Table 1 provides the reasons for ineligibility. The overall study inclusion rate was 60.9% (N=564 of 926). Study exclusion was due largely to our inability to locate informants listed on the death certificates and obtain medical examiner or toxicology records. There were no significant differences in gender or race between the sudden unexplained death cases included and excluded from the study. However, there were significant differences in age, region of death, and year of death (Table 2).
The group of 564 comparison subjects was obtained from a potential pool of 1,014 motor vehicle passenger fatalities, identified from jurisdictions that conducted informative toxicology screens. Thus, 55.6% of the total pool of motor vehicle passenger fatalities were matched to a sudden unexplained death case. Table 2 displays the demographic characteristics of the sudden unexplained death cases included in the study and the motor vehicle accident comparison group; race and region of death significantly differed between the two groups. The distribution of the information sources available for the 564 matched pairs was as follows: informant reports only (29.6%); medical examiner records or toxicology reports only (55.5%); informant reports and medical examiner records but no toxicology report (5.3%); and all three sources (9.6%).
Matched Pair Analyses
Ten of the 564 sudden unexplained death cases (1.8%) were identified as having used stimulants at the time of their deaths (Table 3). In each of these cases, the stimulant detected was methylphenidate. Stimulants were identified in two of the 564 motor vehicle accident comparison subjects (0.4%). Detailed information on the dose or duration of stimulant use was not available. Rates of stimulant use among subjects fell within the range reported for the years of study (26, 28, 29). Results of the primary analysis and sensitivity analyses are presented in Table 4, and the rates of exposure in the groups for each of these analyses are presented in Figure 2. The odds ratio derived from the primary exact logistic regression was 7.4 (95% CI=1.4—74.9; p=0.02). Sensitivity analyses using alternative measures of stimulant exposure revealed qualitatively similar findings, indicating that qualitatively our finding is insensitive to the stimulant exposure algorithm. In particular, all odds ratios observed were clinically significant (30), with the smallest one being 4.2 for the scenario "any stimulant, limited to medical examiner/toxicology reports."
Preliminary analysis of the association of tricyclic antidepressants with sudden death indicated that they might be associated in our sample (six exposures among our sudden death cases and none among our motor vehicle accident comparison subjects). Thus, another series of sensitivity analyses, paralleling those described previously, was conducted deleting any individuals with concomitant tricyclic antidepressant and stimulant use (Table 4 and bottom half of Figure 2). The sensitivity analyses, excluding the stimulant-exposed sudden death case with concomitant tricyclic antidepressants, yielded essentially the same results, with the smallest odds ratio being 3.2, again for the scenario "any stimulant, limited to medical examiner/toxicology reports." The use of clonidine appeared not to be associated with sudden death, providing no justification to delete the case with concomitant clonidine and stimulants. In analyses with reduced numbers of total observations or exposures, some of the p values fell below statistical significance. However, the focus of sensitivity analysis is on the effect sizes (the odds ratios), which reflect the strength of the association, rather than the p values, which are a function of sample size (31).
Examination of Potential Biases

Threshold postmortem blood levels of detection of the targeted stimulant exposure varied by jurisdiction, raising the possibility that the thresholds for sudden unexplained death cases might be more sensitive than for the comparison group of motor vehicle accident victims. Mean threshold detection levels available for 83 cases of sudden unexplained death and 66 motor vehicle accident deaths indicated that their thresholds for methylphenidate were not significantly different (mean=127.7 ng/ml versus 108.8 ng/ml, respectively; t=1.2, df=147, p=0.23).
Since a matched comparison subject was only sought after the identification of a case with appropriate documents, the interval between date of death and informant survey was significantly longer for the comparison subjects (mean=12.8 years, SD=4.5) than the sudden unexplained death cases (mean=9.8 years, SD=5.2) (t=9.5, df=252, p<0.01), suggesting a possible recall bias. However, deleting all three motor vehicle accident victims whose death-to-survey interval was greater than two standard deviations above the mean of the sudden unexplained death cases did not change the results of the matched-pair analysis (odds ratio=7.3, 95% CI=1.4—74.0; p=0.02). Moreover, the death-to-survey interval was not significantly related to reports of stimulant exposure among sudden unexplained death cases (odds ratio=0.99, 95% CI=0.98—1.01; p=0.46). An informant survey was available for only one stimulant-exposed motor vehicle accident victim, precluding the inclusion of motor vehicle accident victims in a similar analysis. The distribution of informants did not significantly differ by group (χ2=8.1, df=6, p=0.23). A great majority of informants for sudden unexplained death cases (91.2%) and motor vehicle accident victims (93.2%) were parents/legal guardians, suggesting that differential recall bias is unlikely to be an important source of bias.

Abstract  |  Method  |  Results  |  Discussion  |  References 
In recent years, concerns have arisen that stimulants may be associated with an increased risk of death. Results of the current study are consistent with these concerns. The odds of using stimulant medications were approximately six to seven times greater for the cases of sudden unexplained death than for the matched motor vehicle accident victims. Such an association is biologically plausible given the central and peripheral catecholaminergic effects of stimulants and significant increases in heart rate and blood pressure that accompany their use (32).

The present study has several strengths. 
First, it employed a matched case-control design, which yielded substantial power to detect rare outcomes. Second, multiple sources of information were used to increase the sensitivity of detecting stimulant use. Third, the availability of parent reports lessened the possibility that the findings reflect illicit stimulant use, since it is unlikely that parents would have known of or reported illicit stimulant use. The single youth who appeared likely to have used stimulants illicitly was a motor vehicle accident victim, whose "positive" exposure was detected by toxicology alone. Fourth, several potential confounding factors, such as asthma, that are associated with both ADHD (33) and sudden death (24), were excluded. Furthermore, because ADHD (34) and impaired attention (35) are common among youths with some congenital structural cardiac diseases, we excluded individuals with evidence of cardiomegaly, cardiac hypertrophy, and cardiomyopathy. Three individuals receiving stimulants were excluded from our group of sudden unexplained death cases because of notations of cardiac hypertrophy in their autopsies, even though the cardiac abnormalities were not cited as the cause of death. Moreover, we deleted a sudden death case with concomitant use of stimulants and tricyclic antidepressants, another possible confounding factor, in a second series of sensitivity analyses, and this had little effect on the results. Fifth, the study’s dates of inquiry (1985—1996) predated the use of Adderall, first approved by the FDA in 1996, which has been the stimulant medication most strongly implicated in sudden death (36).

The study also has important limitations. 
First, while case-control studies are a powerful method of detecting association, they cannot establish causality. It is conceivable that, despite our rigorous efforts to exclude or adjust for potential confounding factors, some unmeasured factors other than stimulant use were responsible for the observed association. For example, although gross structural cardiac disease was presumably excluded by autopsy, autopsy data were not available for two sudden unexplained death cases with stimulant exposure, and forensic pathology varies substantially in its ability to identify physiological as opposed to anatomic cardiovascular disease. Physiological abnormalities that confer risk (e.g., cardiac depolarization and repolarization abnormalities such as Brugada syndrome and long QT syndrome) could not be reliably excluded from the analysis. We attempted to exclude subjects with known prolonged QT interval, other conduction disorders, or a family history of long QT or sudden cardiac death, but clinically significant cardiac abnormalities may have passed undetected. However, a sensitivity analysis revealed that even if 40% of sudden unexplained death cases were excluded due to undetected cardiac disease, the primary analysis would still yield a significant association.

Second, we were unable to systematically obtain information on the psychiatric status of the decedents, including their clinical diagnoses. While this information was occasionally noted in a medical record or by an informant, it was not available for all subjects. Therefore, we are unable to estimate accurately the rates of ADHD in our sample, nor can we determine whether untreated ADHD was associated with sudden unexplained death. Although we excluded the known presence of structural cardiac diseases (24), as well as asthma (24, 33), there may be other unidentified mechanisms that were not controlled.

Third, we attempted to avoid differential recall biases, an important potential limitation of retrospective case-control studies, by employing a comparison group of deceased youths whose parents/legal guardians had also experienced a sudden, traumatic loss of their children. However, we cannot exclude the possibility that relative to a motor vehicle passenger fatality, an "unexplained" death may have prompted medical personnel to ask more questions about medications at the time of death. Yet the primary analysis remains significant (odds ratio=7.3, 95% CI=1.4—74.8, p=0.015) following exclusion of the one sudden unexplained death case whose methylphenidate exposure was detected solely from the medical examiner’s report. Although conceivable, we consider it unlikely that parents of sudden unexplained death cases remembered stimulant medications more vividly than parents of children who died in accidents. It is reassuring that medical records available for two sudden unexplained death cases whose "positive" exposures were based solely on the parental survey corroborated these informant reports. Because we were unable to obtain medical records on a majority of our subjects, we did not use them to identify "positive" exposures.

Fourth, toxicological assays were not conducted consistently across jurisdictions and may not have been sufficiently sensitive to detect therapeutic levels of methylphenidate, yielding an unreliable measure of exposure. The average detection threshold in toxicological assays (approximately 100 ng/ml) appeared to be higher than blood levels achieved during routine therapeutic use of immediate-release methylphenidate preparations (24 ng/ml) (37), or the even lower peak plasma levels of 8—10 ng/ml achieved by the more recently marketed single daily dose, long-duration methylphenidate preparations, such as OROS methylphenidate (38). The short half-life of methylphenidate (37, 39) and the interval between the last ingestion of medication and the acquisition of the blood samples is another potential source of insensitivity of the toxicology screens. Because sustained-release stimulants had not yet been widely marketed during the years of study (1985—1996), a therapeutic dose may not have remained in the blood for sufficient time to be detected by postmortem toxicology screens. This may explain why stimulants were not detected in the toxicology reports of five sudden unexplained death cases whose stimulant use was reported by the informant or noted in the medical examiner’s record (as reported by an informant at the time of death). Thus, while we are confident that the toxicology screens accurately ruled out overdoses, they may have been insensitive in some cases to therapeutic levels of methylphenidate. Nevertheless, since only sources of information available for both sudden unexplained death cases and matched motor vehicle fatality victims were used in the analyses, limitations in a particular source of exposure, whether toxicology records or informant reports, were comparable across groups. Moreover, sensitivity analyses suggest that qualitatively our results were not sensitive to method of stimulant measurement.

Fifth, we were able to include in our analyses only 61% of the eligible cases of sudden unexplained death. Although there were no significant differences in gender or race between included and excluded subjects, these groups did significantly differ in age, region, and year of death. Sudden unexplained death cases included in the study were significantly older, less likely to have died in the South, more likely to have died in the West, and more likely to have died in the later years of the study. Nationally representative studies indicate that stimulant use rates vary by age, region, and year (26, 28). Differences in age would likely have yielded lower rates of stimulant use among those included because age is inversely related to stimulant use (26, 28). Similarly, since the South has the highest rate of stimulant use and the West has the second lowest rate (26), rates of stimulant use among sudden unexplained death cases included in the study would likely have been lower than in those excluded. Conversely, the steep increase in the utilization of stimulants over time (26, 28, 29) would bias toward more stimulant use among the included than the excluded subjects. Although included subjects are not representative of all sudden unexplained death cases, pairs were either matched (age, gender, and date of death) or adjusted (race and region of death) for these sociodemographic and vital characteristics. Nevertheless, there may be unknown selection biases related to our inability to obtain information from all potential cases.
Last, because the project was originally funded to examine the association of sudden death and the use of tricyclic antidepressant medication, we did not include pediatric stroke and acute myocardial infarction, other causes of death linked to methylphenidate in case reports (1—3, 40). This may have yielded an underestimation of the association between sudden death and stimulant use.
This study reports a significant association or "signal" between sudden unexplained death and the use of stimulant medication, specifically methylphenidate. While the data have limitations that preclude a definitive conclusion, our findings draw attention to the potential risks of stimulant medications for children and adolescents, which warrant clinical attention and further study.

Presented in part at the 55th annual meeting of the American Academy of Child and Adolescent Psychiatry, Chicago, Oct. 28—Nov. 2, 2008. Received April 4, 2009; revisions received April 13, April 27, and May 11, 2009; accepted May 12, 2009 (doi: 10.1176/appi.ajp.2009.09040472). From the Division of Child and Adolescent Psychiatry, Division of Clinical Therapeutics, Division of Biostatistics and Data Coordination, and Division of Clinical and Genetic Epidemiology, New York State Psychiatric Institute, New York; the Department of Psychiatry and Division of Child and Adolescent Psychiatry, Columbia University College of Physicians & Surgeons, New York; the Department of Epidemiology and Department of Biostatistics, Columbia University School of Public Health, New York; and the Analytical Psychopharmacology Laboratory, Nathan Kline Institute, Orangeburg, N.Y. Address correspondence and reprint requests to Dr. Gould, Division of Child and Adolescent Psychiatry, New York State Psychiatric Institute, 1051 Riverside Dr., New York, NY 10032; gouldm@childpsych.columbia.edu (e-mail).

Dr. Walsh has received research support from AstraZeneca. Dr. Duan has received research support from Pfizer. Dr. Olfson has received research funding from Eli Lilly and AstraZeneca and has worked as a consultant for AstraZeneca and Pfizer and as a speaker for Janssen. Dr. Greenhill has received research support from Johnson & Johnson, Otsuka, and Forest. The remaining authors report no competing interests.
Supported in part by a contract from the Food and Drug Administration and a grant from NIMH (R01-MH56250).
The authors thank Judi Forman for her role in the initial implementation of the project and Elizabeth Altschuler and Francesca Osuna for their assistance in the preparation of the manuscript.

Abstract  |  Method  |  Results  |  Discussion  |  References 
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