Attention-deficit hyperactivity disorder

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Attention-deficit/hyperactivity disorder (USA)
Classification and external resources
ICD-10 F90.
ICD-9 314.00, 314.01
OMIM 143465
DiseasesDB 6158
MedlinePlus 001551
eMedicine med/3103  ped/177
MeSH D001289

Attention-deficit/hyperactivity disorder (AD/HD or ADHD) is a neurobehavioral[1] developmental disorder.[2] It affects about 3 to 5% of children with symptoms starting before seven years of age.[3] Global prevalence for children is approximately 5%, with wide variability dependent on research methodologies utilized in studies.[4] It is characterized by a persistent pattern of impulsiveness and inattention, with or without a component of hyperactivity.[5] ADHD is twice as common in boys as in girls[6], though studies suggest this discrepancy may be due to subjective bias.[7] ADHD is generally a chronic[8] disorder with 30 to 50% of individuals diagnosed in childhood continuing to have symptoms into adulthood.[9][10] As they mature, adolescents and adults with ADHD are likely to develop coping mechanisms to compensate for their impairment.[11]

Though previously regarded as a childhood diagnosis, ADHD can continue throughout adulthood.[12] ADHD has a strong genetic component.[13]

Methods of treatment usually involve some combination of medications, behavior modifications, life-style changes, and counseling. The American Academy of Pediatrics states that stimulant medications and/or behavior therapy are appropriate and generally safe treatments for ADHD.[14] However, a 2006 meta-analysis found a lack of data regarding ADHD drugs' potential adverse effects,[15] with very few studies assessing the safety or efficacy of treatments beyond 4 months,[16] and no randomized controlled trials assessing either for periods of usage longer than two years.[17][18][12] Treatment of pre-school children is not recommended.[19]

ADHD and its diagnosis and treatment have been considered controversial since the 1970s.[20][21][22][23] The controversies have involved clinicians, teachers, policymakers, parents, and the media, with opinions regarding ADHD that range from not believing it exists at all to believing there are genetic and physiological bases for the condition, and also include disagreement about the use of stimulant medications in treatment.[21]

Contents

[edit] Classification

ADHD may be seen as an extreme of one or more continuous traits found throughout the population.[19] ADHD is a developmental disorder in which certain traits such as impulse control lag in development when compared to the general population.[24] Using magnetic resonance imaging of the prefrontal cortex, this developmental lag has been estimated to range from 3 to 5 years.[25] These delays are considered to cause impairment. ADHD has also been classified as a behavior disorder.[26] A diagnosis of ADHD does not, however, imply a neurological disease.[19]

ADHD is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder, and antisocial disorder.[27]

[edit] Symptoms

The most common symptoms[28][29] of ADHD are:

  • Impulsiveness: acting before thinking of consequences, jumping from one activity to another, disorganization, tendency to interrupt other peoples' conversations.[28]
  • Hyperactivity: restlessness, often characterized by an inability to sit still, fidgeting, squirminess, climbing on things, restless sleep.[28]
  • Inattention: easily distracted, day-dreaming, not finishing work, difficulty listening.[28]

The DSM-IV categorizes the symptoms of ADHD into three clusters, referred to as subtypes: (1) Inattentive; (2) hyperactive/impulsive; and (3) combined.[30] Most people exhibit some of these behaviors but not to the point where they significantly interfere with a person's work, relationships, or studies. ADHD may accompany other disorders such as anxiety or depression.

Hyperactivity is common among children with ADHD but tends to disappear during adulthood. However, over half of children with ADHD continue to have some symptoms of inattention throughout their lives.

Inattention and "hyperactive" behavior are not the only problems in children with ADHD. ADHD exists alone in only about 1/3 of the children diagnosed with it. Many co-existing conditions require other courses of treatment and should be diagnosed separately instead of being grouped in the ADHD diagnosis. Some of the associated conditions are:

  • Oppositional defiant disorder (35%) and conduct disorder (26%) which both are characterized by anti-social behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, or stealing.[29]
  • Primary disorder of vigilance, which is characterized by poor attention and concentration, as well as difficulties staying awake. These children tend to fidget, yawn and stretch, and appear to be hyperactive in order to remain alert and active.[29]
  • Mood disorders. Boys diagnosed with the combined subtype have been shown more likely to suffer from a mood disorder.[31]
  • Bipolar disorder. As many as 25% of children with ADHD have bipolar disorder. Children with this combination may demonstrate more aggression and behavioral problems than those with ADHD alone.[29]
  • Anxiety disorder, which has been found to be more common in girls diagnosed with the inattentive subtype of ADHD.[32]
  • Obsessive-compulsive disorder. OCD is believed to share a genetic component with ADHD, and shares many of its characteristics.[29]

[edit] Causes

A specific cause of ADHD is not known.[33] There are, however, a number of factors that may contribute to ADHD including genetics, diet and social and physical environments.

[edit] Genetic factors

Twin studies indicate that the disorder is highly heritable and that genetics are a factor in about 75% of ADHD cases.[19] Hyperactivity also seems to be primarily a genetic condition; however, other causes do have an effect.[34]

Researchers believe that a large majority of ADHD cases arise from a combination of various genes, many of which affect dopamine transporters. Candidate genes include dopamine transporter, dopamine receptor D4, dopamine beta-hydroxylase, monoamine oxidase A, catecholamine-methyl transferase, serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), 5-hydroxytryptamine 1B receptor (5-HT1B),[35] the 10-repeat allele of the DAT1 gene,[36] the 7-repeat allele of the DRD4 gene,[36] and the dopamine beta hydroxylase gene (DBH TaqI).[37]

The broad selection of targets indicates that ADHD does not follow the traditional model of a "genetic disease" and should therefore be viewed as a complex interaction among genetic and environmental factors. Even though all these genes might play a role, to date no single gene has been shown to make a major contribution to ADHD.[38]

[edit] Environmental factors

Twin studies to date have also suggested that approximately 9% to 20% of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be attributed to nonshared environmental (nongenetic) factors.[39][40]

Environmental factors implicated include alcohol and tobacco smoke exposure during pregnancy and environmental exposure to lead in very early life.[41] The relation of smoking to ADHD could be due to nicotine causing hypoxia (lack of oxygen) to the fetus in utero.[42] It could also be that women with ADHD are more likely to smoke[43] and therefore, due to the strong genetic component of ADHD, are more likely to have children with ADHD.[44] Complications during pregnancy and birth—including premature birth—might also play a role.[45]

[edit] Diet

[edit] Additives

A meta-analysis has found that dietary elimination of artificial food coloring and preservatives provides a statistically significant benefit in children with ADHD.[46] Other more recent studies agree with these conclusions.[47][48]

The European Food Safety Authority (EFSA) reviewed the literature on the association between food additives and hyperactivity and concluded that there is only limited evidence of an association between the intake of additives and activity and attention, and then only in some children studied. They further indicated that the effects reported in the study were not consistent for the two age groups and for the two food additive mixtures used in the study.[49] Others have suggested a trial of removing additives from the diet for children with ADHD as it is harmless and might be helpful.[50]

The UK Food Standards Agency (FSA) has called for a ban on the use of six artificial food colorings[51] and the European Union (EU) has ruled that some food dyes must be labeled with the relevant E number as well as this warning: "may have an adverse effect on activity and attention in children."[52]

[edit] Sugar regulation

A number of studies have found that sucrose (sugar) has no effect on behavior and in particular it does not exacerbate the symptoms of children diagnosed with ADHD.[53][54][55] Corn syrup and high fructose corn syrup, the sugars found in most sweets, were not part of any of these studies.

[edit] Omega-3 supplement

Preliminary research suggests that Omega-3 supplementation might be effective in the treatment of ADHD; however, some of the studies give conflicting results. [56]

[edit] Social factors

There is no compelling evidence that social factors alone can cause ADHD.[24] Many researchers believe that relationships with caregivers have a profound effect on attentional and self-regulatory abilities. A study of foster children found that a high number of them had symptoms closely resembling ADHD,[57] while other researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse.[58][19] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD.[citation needed] ADHD is considered a contributing factor to Sensory Integration Disorders.[59]

[edit] Alternative theories

[edit] Hunter vs. farmer theory of ADHD

Main article: Hunter vs. farmer theory

The hunter vs. farmer theory is a hypothesis proposed by author Thom Hartmann about the origins of ADHD. He believes that these conditions may be a result of adaptive behavior of the human species. His theory states that those with ADHD retain some of the older "hunter" characteristics associated with early pre-agricultural human society.[60]

[edit] Neurodiversity

Main article: Neurodiversity

Proponents of this theory assert that atypical (neurodivergent) neurological development is a normal human difference that is to be tolerated and respected just like any other human difference. Social critics argue that while biological factors may play a large role in difficulties with sitting still in class and/or concentrating on schoolwork in some children, these children could have failed to integrate others' social expectations of their behavior for a variety of other reasons.[61]

[edit] Social construct theory of ADHD

Main article: Social construct theory of ADHD

Some social critics question whether or not ADHD is wholly or even predominantly a biological illness. A minority of these critics maintain that ADHD was "invented and not discovered." They believe that no such disorder exists and that the behavior observed is not abnormal and can better be explained by environmental causes or simply the personality of the "patient."[19]

[edit] Low arousal theory

Main article: Low arousal theory

The low arousal theory explains that people with ADHD seek self-stimulation or excessive activity in order to ascend their state of abnormally low arousal.[62][63] The theory states that those with ADHD cannot self-moderate, and their attention can only be gained by means of environmental stimuli.[62]

One with ADHD creates a great deal of theta brainwaves, which are slow and create a haze through which high levels of physical activity or stimulation can pass. The theory explains, that among many other tendencies and preferences for high-stimulation activities in ADHD subjects, why an activity of high stimulation, such as playing a video game, attracts more attention from an ADHD child than reading a novel, which is a low-stimulation activity.

Without enough stimulation coming from the environment, an ADHD child will create it him or herself by walking around, fidgeting, talking, etc. This theory also explains why stimulant medications have high success rates and can induce a calming effect at therapeutic dosages among children with ADHD. It establishes a strong link with scientific data that ADHD is connected to abnormalities with the neurochemical dopamine and a powerful link with low-stimulation PET scan results in ADHD subjects. [62]

[edit] Head injury

ADHD patients have been observed to have higher than average rates of head injuries;[64] however, current evidence does not indicate that head injuries are the cause of ADHD in the patients observed.[65]

[edit] Pathophysiology

PET scans measure the activity of various parts of the brain. The image on the right illustrates glucose metabolism in the brain of a person diagnosed with ADHD while doing an assigned task. The image on the left illustrates glucose metabolism in the brain of a normal subject when given that same task. The significance of the research was that the harder a person with ADHD concentrated the less activity was measured. This was the exact opposite for the non ADHD group. However, that was remedied when the ADHD subjects took stimulant medication. These findings are still not definitive.[66][67]

The pathophysiology of ADHD is unclear and there are a number of competing theories.[68] Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are only used for research purposes.[69]

In one study a delay in development of certain brain structures by an average of three years occurred in ADHD elementary school aged patients. The delay was most prominent in the frontal cortex and temporal lobe, which are believed to be responsible for the ability to control and focus thinking. In contrast, the motor cortex in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the fidgetiness that characterizes ADHD.[70]

The same laboratory had previously found involvement of the "7-repeat" variant of the dopamine D4 receptor gene, which accounts for about 30 percent of the genetic risk for ADHD, in unusual thinness of the cortex of the right side of the brain; however, in contrast to other variants of the gene found in ADHD patients, the region normalized in thickness during the teen years in these children, coinciding with clinical improvement.[71]

Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity),[72] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. [73][74] Medications focused on treating ADHD (such as methylphenidate) work by reducing dopamine reuptake in certain areas of the brain, such as those that control and regulate concentration. As dopamine is a stimulant, this increases neural activity and thus blood flow in these areas (blood flow is a marker for neural activity). A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain's ability to produce dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to "childhood learning problems" in healthy subjects as well.[75]

Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are the molecular abnormality of ADHD or a secondary consequence of a problem elsewhere. Researchers have described a form of ADHD in which the abnormality appears to be sensory overstimulation resulting from a disorder of ion channels in the peripheral nervous system.

A 1990 PET scan study by Alan J. Zametkin et al found that global cerebral glucose metabolism was 8% lower in medication-naive adults who had been hyperactive since childhood.[76] The image on the left illustrates glucose metabolism in the brain of a 'normal' adult while doing an assigned auditory attention task; the image on the right illustrates the areas of activity in the brain of an adult who had been hyperactive since childhood when given that same task. The regions with the greatest deficit of activity included the premotor cortex and the superior prefrontal cortex.[76] Further studies found that chronic stimulant treatment had little effect on global glucose metabolism,[77] a study in girls failed to find a decreased global glucose metabolism,[78] and in teenagers PET scans were unable to differentiate normal children from those with ADHD.[79] The significance of the research by Zametkin has not been determined and neither his group nor any other has been able to replicate the 1990 results.[80][81][82] It may represent a biological phenomenon, ( a physical difference in their brain) or it may simply mean that the ADHD subjects were not using the parts of the brain ordinarily associated with focusing on a task, exactly what would be expected from some one with ADHD from whatever cause.

[edit] Diagnosis

No objective test exists to make a diagnosis of ADHD. It thus remains a clinical diagnosis.[83]

In North America, the DSM-IV criteria are often the basis for a diagnosis, while European countries usually use the ICD-10.[84]

Many of the symptoms of ADHD occur from time to time in everyone; in patients with ADHD, the frequency of these symptoms is greater and significantly impairs their life. This impairment must occur in multiple settings to be classified as ADHD. As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these criteria are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

  1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
  2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
  3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

The previously used term ADD expired with the most recent revision of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

[edit] DSM-IV criteria

I. Either A or B:[30]

A. Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:
  1. Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
  2. Often has trouble keeping attention on tasks or play activities.
  3. Often does not seem to listen when spoken to directly.
  4. Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).
  5. Often has trouble organizing activities.
  6. Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
  7. Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
  8. Is often easily distracted.
  9. Often forgetful in daily activities.
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:
  • Hyperactivity:
  1. Often fidgets with hands or feet or squirms in seat.
  2. Often gets up from seat when remaining in seat is expected.
  3. Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless).
  4. Often has trouble playing or enjoying leisure activities quietly.
  5. Is often "on the go" or often acts as if "driven by a motor".
  6. Often talks excessively.
  • Impulsiveness:
  1. Often blurts out answers before questions have been finished.
  2. Often has trouble waiting one's turn.
  3. Often interrupts or intrudes on others (e.g., butts into conversations or games).

II. Some symptoms that cause impairment were present before age 7 years.

III. Some impairment from the symptoms is present in two or more settings (e.g. at school/work and at home).

IV. There must be clear evidence of significant impairment in social, school, or work functioning.

V. The symptoms do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The symptoms are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).

[edit] ICD-10

In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADHD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10[85]) is present, the condition is referred to as "Hyperkinetic conduct disorder". Otherwise the disorder is classified as "Disturbance of Activity and Attention", "Other Hyperkinetic Disorders" or "Hyperkinetic Disorders, Unspecified". The latter is sometimes referred to as, "Hyperkinetic Syndrome".[85]

[edit] Other diagnostic guidelines

The American Academy of Pediatrics Clinical Practice Guideline for children with ADHD emphasizes that a reliable diagnosis is dependent upon the fulfillment of three criteria:[14]

  • The use of explicit criteria for the diagnosis using the DSM-IV-TR.
  • The importance of obtaining information about the child’s symptoms in more than one setting.
  • The search for coexisting conditions that may make the diagnosis more difficult or complicate treatment planning.

All three criteria are determined using the patient's history given by the parents, teachers and/or the patient.

Adults often continue to be impaired by ADHD. Adults with ADHD are diagnosed under the same criteria, including the stipulation that their symptoms must have been present prior to the age of seven.[86] Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning, usually having more symptoms of inattention and fewer of hyperactivity or impulsiveness than children do.[87]

[edit] Comorbid conditions

Common comorbid conditions include oppositional defiant disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder.[88] Learning disorders are more common when there are inattention symptoms.[89]

Comorbid disorders or substance abuse can make the diagnosis and treatment of ADHD more difficult. Psychosocial therapy is useful in treating some comorbid conditions.[90]

[edit] Differential diagnoses

To make the diagnosis of ADHD, a number of other possible medical and psychological conditions must be excluded.

Medical conditions

Medical conditions that must be excluded include: hypothyroidism, anemia, lead poisoning, chronic illness, hearing or vision impairment, substance abuse, medication side effects, sleep impairment, and child abuse, among others.[91]

Sleep conditions

Among other psychological and neurological issues, the relationship between ADHD and sleep is complex. In addition to clinical observations, there is substantial empirical evidence from a neuroanatomic standpoint to suggest that there is considerable overlap in the central nervous system centers that regulate sleep and those that regulate attention/arousal.[92] Primary sleep disorders play a role in the clinical presentation of symptoms of inattention and behavioral dysregulation. There are multilevel and bidirectional relationships among sleep, neurobehavioral functioning, and the clinical syndrome of ADHD.[93]

Behavioral manifestations of sleepiness in children range from classic manifestations (yawning, rubbing eyes), to externalizing behaviors (impulsivity, hyperactivity, aggressiveness), to mood lability and inattentiveness.[92]

From a clinical standpoint, mechanisms that account for the phenomenon of excessive daytime sleepiness include:

All of these are important causes of symptoms which may overlap with the cardinal symptoms of ADHD, and children with ADHD should be regularly and systematically assessed for sleep problems.[92][94]

[edit] Management

Main article: Attention-deficit hyperactivity disorder management

Methods of treatment often involve some combination of behavior modifications, life-style changes, counseling, and medication. Several ADHD specific support groups exist as informational sources and to help families cope with challenges associated with dealing with ADHD.

[edit] Behavioral interventions

Psychological therapies use to treat ADHD include psychoeducational input, behavior therapy, cognitive behavioral therapy (CBT), interpersonal psychotherapy (IPT), family therapy, school-based interventions, social skills training and parent management training.[19]

Parent training and education have been found to have short term benefits.[95] Family therapy has shown to be of little use in the treatment of ADHD,[96] though it may be worth noting that parents of children with ADHD are more likely to divorce than parents of children without ADHD, particularly when their children are under the age of 8 years.[97]

[edit] Pharmacological treatment

Stimulant medications are the most clinically and cost effective method of treating ADHD.[98] A 2008 review found that the use of stimulants improved teachers' and parents' ratings of disruptive behavior; however, it did not improve academic achievement.[17] Stimulants neither increased nor decreased rates of delinquency or substance abuse at 3 years.[17] No significant differences between the various drugs in terms of efficacy or side effects have been found.[15][99] About 70% of children improve after being treated with stimulants.[100] Medications, however, are not recommended for pre-school children with ADHD.[19] Stimulants, in the short term, have been found to be safe in the appropriately selected patient and appear well tolerated over 5 years of treatment.[101] A 2007 drug class review found that there are no good studies of comparative effectiveness between various drugs for ADHD, and that there is a lack of quality evidence on their effects on overall academic performance and social behaviors.[102]

Long term safety, however, has not been determined. There are no randomized controlled trials assessing the harms or benefits of treatment beyond two years.[17] The American Heart Association and the American Academy of Pediatrics feels that it is prudent to carefully assess children for heart conditions before treating them with stimulant medications.[103] The FDA has added black-box warnings to some ADHD medications.[104] Amphetamines such as Adderall have warnings about potential for abuse, drug dependence, and sudden death.[105]

A recent review states that ADHD studies "have major methodological deficiencies which are compounded by their restriction to school-age children, relatively short follow-up, and few data on adverse effects."[106]

[edit] Lifestyle

Aerobic fitness may improve cognitive functioning and neural organization related to executive control during pre-adolescent development, though more studies are needed in this area[107]. One study suggests that athletic performance in boys with ADHD may increase peer acceptance when accompanied by fewer negative behaviors[108].

[edit] Prognosis

The proportion of children meeting the diagnostic criteria for ADHD dropped by about 50% over three years after the diagnosis. This occurred regardless of the treatments used.[17][109] It persists into adulthood in about 30-50% of cases.[9] Those affected are likely to develop coping mechanisms as they mature thus compensating for their previous ADHD. [11]

In the United States, 37% of those with ADHD do not get a high school diploma even though many of them will receive special education services.[24] The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish high school.[110] Also in the US, less than 5% of individuals with ADHD get a college degree[111] compared to 28% of the general population.[112]

People with ADHD tend to work better in less structured environments with fewer rules[citation needed]. Self-employment or jobs with greater autonomy are generally well suited for them. Hyperactive types are likely to change jobs often due to their constant need for new interests and stimulations to keep motivated. Recent studies suggest that many expatriates[citation needed] have the 7-repeat allele of DRD4 associated with the ADHD diagnosis.

[edit] Epidemiology

ADHD's global prevalence is estimated at 3-5% in people under the age of 19. There is, however, both geographical and local variability among studies. Geographically, children in North America appear to have a higher rate of ADHD than children in Africa and the Middle East,[113] well published studies have found rates of ADHD as low as 2% and as high as 14% among school aged children.[114] The rates of diagnosis and treatment of ADHD are also much higher on the east coast of the USA than on the west coast.[115] The frequency of the diagnosis differs between male children (10%) and female children (4%) in the United States.[116] This difference between genders may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[117]

Rates of ADHD diagnosis and treatment have increased in both the UK and the USA since the 1970s. In the UK an estimated 0.5 per 1,000 children had ADHD in the 1970s, while 3 per 1,000 received ADHD medications in the late 1990s. In the USA in the 1970s 12 per 1,000 children had the diagnosis, while in the late 1990s 34 per 1,000 had the diagnosis and the numbers continue to increase.[19]

[edit] History

[edit] Terminology

It may be helpful to understand that "ADD" and "ADHD" are the same thing, and constitute a single syndrome, with several important and distinctive variations. The clinical definition of "ADHD" dates to the mid-20th century, but was known by other names. Physicians developed a diagnosis for a set of conditions variously referred to as "minimal brain damage", "minimal brain dysfunction", "learning/behavioral disabilities" and "hyperactivity". Some of these labels became problematic as knowledge expanded. For example, as awareness grew that many children with no indication of brain damage also displayed the syndrome, the label which included the words "brain damage" did not seem appropriate.

The DSM-II (1968) began to call it "Hyperkinetic Reaction of Childhood" even though the professionals were aware that many of the children so diagnosed exhibited attention deficits without any signs of hyperactivity. In 1980, the DSM-III introduced "ADD (Attention-Deficit Disorder) with or without hyperactivity." That terminology (ADD) technically expired with the revision in 1987 to ADHD in the DSM-III-R. In the DSM-IV, published in 1994, ADHD with sub-types was presented. The current version (as of 2008), the DSM-IV-TR was released in 2000, primarily to correct factual errors and make changes to reflect recent research; ADHD was largely unchanged.[118]

Under the DSM-IV, within the ADHD syndrome, there are three sub-types, including one which lacks the hyperactivity component.[119] Approximately one-third of people with ADHD have the predominantly inattentive type (ADHD-I), meaning that they do not have the hyperactive or overactive behavior components of the other ADHD subtypes.

Even today, the ADHD terminology is objectionable to many. There is some preference for using the ADHD-I, ADD, and AADD terminology when describing individuals lacking the hyperactivity component, especially among older adolescents and adults who find the term "hyperactive" inaccurate, inappropriate and even derogatory.

[edit] 18th century

In 1798, a Scottish-born physician and author, Sir Alexander Crichton (1763–1856), described what seems to be a mental state much like the inattentive subtype of ADHD, in his book An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects. In the chapter "Attention", Crichton described a "mental restlessness".[120][121]

"The incapacity of attending with a necessary degree of constancy to any one object, almost always arises from an unnatural or morbid sensibility of the nerves, by which means this faculty is incessantly withdrawn from one impression to another. It may be either born with a person, or it may be the effect of accidental diseases.

"When born with a person it becomes evident at a very early period of life, and has a very bad effect, inasmuch as it renders him incapable of attending with constancy to any one object of education. But it seldom is in so great a degree as totally to impede all instruction; and what is very fortunate, it is generally diminished with age."[122]

Dr. Crichton further observed: "In this disease of attention, if it can with propriety be called so, every impression seems to agitate the person, and gives him or her an unnatural degree of mental restlessness. People walking up and down the room, a slight noise in the same, the moving of a table, the shutting a door suddenly, a slight excess of heat or of cold, too much light, or too little light, all destroy constant attention in such patients, inasmuch as it is easily excited by every impression."[123]

Crichton has noted that "they have a particular name for the state of their nerves, which is expressive enough of their feelings. They say they have the fidgets".[124] Dr. Crichton suggested that these children needed special educational intervention and noted that it was obvious that they had a problem attending even how hard they did try. "Every public teacher must have observed that there are many to whom the dryness and difficulties of the Latin and Greek grammars are so disgusting that neither the terrors of the rod, nor the indulgence of kind intreaty can cause them to give their attention to them."[125]

Alexander Crichton was almost two centuries ahead of his time in his observations of what is now known as the Inattention subtype of ADHD. He wrote about the salient features of this disorder, including attentional problems, restlessness, early onset, and how it can affect schooling, without any of the moralism introduced by George Still and later authors.[126][127]

[edit] 20th century

On 4th, 6th and 11th March 1902, the father of British paediatrics Sir George Frederick Still (1868–1941) gave a series of lectures to the Royal College of Physicians in London under the name “Goulstonian lectures” on ‘some abnormal psychical conditions in children’, which were published later the same year in the Lancet.[128]

He described 43 children who had serious problems with sustained attention and self-regulation, who were often aggressive, defiant, resistant to discipline, excessively emotional or passionate, which showed little inhibitory volition, had serious problems with sustained attention and could not learn from the consequences of their actions; though their intellect was normal. He wrote “I would point out that a notable feature in many of these cases of moral defect without general impairment of intellect is a quite abnormal incapacity for sustained attention.[129]

Dr. Still wrote: “there is a defect of moral consciousness which cannot be accounted for by any fault of environment” When Still was talking about Moral Control, he was referring to it as William James had done before him, but to Still, the moral control of behavior meant “the control of action in conformity with the idea of the good of all” [130]

"Another boy, aged 6 years, with marked moral defect was unable to keep his attention even to a game for more than a very short time, and as might be expected, the failure of attention was very noticeable at school, with the result that in some cases the child was backward in school attainments, although in manner and ordinary conversation he appeared as bright and intelligent as any child could be."[131] He proposed a biological predisposition to this behavioral condition that was probably hereditary in some children and the result of pre- or postnatal injury in others. [132] [133]

George Still certainly did not use the current terminology for this disorder, but many historians of ADHD have inferred that the children he described in his series of three published lectures to the Royal College of Physicians would likely have qualified for the current disorder of ADHD combined type, among other disorders. [134][135] [136]

[edit] Encephalitis epidemic 1917–1918

The treatment of children with similar behavioral problems who had survived the epidemic of encephalitis lethargica from 1917 to 1918 and the pandemic of influenza from 1919 to 1920 led to terminology which referred to "brain damage." [137]

[edit] Adult ADHD

Main article: Adult attention-deficit disorder

In the 1970s researchers began to realize that the condition now known as ADHD did not always disappear in adolescence, as was once thought. At about the same time, some of the symptoms were also noted in many parents of the children under treatment. The condition was formally recognized as afflicting adults in 1978, often informally called adult ADD, since symptoms associated with hyperactivity are generally less pronounced.

It has been estimated that about eight million adults have ADHD in the United States.[138] Untreated adults with ADHD often have chaotic life-styles, may appear to be disorganized, and may rely on non-prescribed drugs and alcohol to get by.[139] They often have such associated psychiatric comorbidities as depression, anxiety, bipolar disorder, substance abuse, or a learning disability.[139] In 2004, noted researchers estimated the yearly income loss for adults with ADHD in the United States as $77 billion. This may be partially because it is also estimated that only 15% of adults in the U.S. with ADHD are aware that they have the disorder, although many adults struggle with it.[140]

A diagnosis of ADHD may offer adults insight into their behaviors and allow patients to become more aware and seek help with coping and treatment strategies.[138] Studies show that adult ADHD is treated successfully with a combination of medication and behavior therapy.[141] A mature patient, moreso than a child, may be able to provide feedback and help self-direct the process.

Many professionals have speculated that in the next DSM (tentatively DSM-V), ADHD in adults may be differentiated from the syndrome as it occurs in children.[142] Only recognized as occurring in adults in 1978, it is currently not addressed separately. Obstacles that clinicians face when assessing adults who may have ADHD include developmentally inappropriate diagnostic criteria, age-related changes, comorbidities, and the possibility that high intelligence or situational factors can mask ADHD symptoms.[143]

[edit] Society and culture

ADHD has been found across the world when DSM-IV criteria are used in diagnosis.[144] The DSM-IV estimates that 3%-7% of children suffer from ADHD. Some studies have estimated higher rates in community samples, and ADHD is diagnosed 2 - 4 times more often in boys than in girls.[145][146] The core impairments are expressed in different cultural contexts[147] although there is disagreement about this observation.[148] ADHD is considered differently based on how those who have an interest in the topic approach the subject. They can use descriptors used in the DSM4. They can frame the issue on a biological basis verse character flaws. Others see relief and hope in identifying and labeling a real problem.[149]

The media has reported on many issues related to ADHD. In 2001 PBS's Frontline aired a one-hour program about the effects of the diagnosing and treating of ADHD in minors, entitled "Medicating Kids."[150] The program included a selection of interviews with representatives of various points of view. In one segment, entitled backlash, retired neurologist Fred Baughman and Peter Breggin who PBS described as "outspoken critics who insist [ADHD is] a fraud perpetrated by the psychiatric and pharmaceutical industries on families anxious to understand their children's behavior,"[151] were interviewed on the legitimacy of the disorder. Russell Barkley and Xavier Castellanos, then head of ADHD research at the National Institute of Mental Health (NIMH), defended the viability of the disorder. In Castellanos's interview he stated how little is scientifically understood.[152] Lawrence Diller was interviewed on the business of ADHD along with a representative from Shire Plc.[citation needed]

A number of notable individuals have given controversial opinions on ADHD. Scientologist Tom Cruise's interview with Matt Lauer was widely watched by the public. In this interview he spoke about postpartum depression and also referred to Ritalin and Adderall as being "street drugs" rather than as ADHD medication.[153] In England Baroness Susan Greenfield, a leading neuroscientist,[154] spoke out publicly about the need for a wide-ranging inquiry in the House of Lords into the dramatic increase in the diagnosis of ADHD in the UK and possible causes[155] following a 2007 BBC Panorama programme which highlighted US research (The Multimodal Treatment Study of Children with ADHD by the University of Buffalo showing treatment results of 600) suggesting drugs are no better than therapy for ADHD in the long-term.[citation needed]

[edit] Major League Baseball

As of 2009, eight percent of all Major League Baseball players have been diagnosed with ADHD, making the disease epidemic among this population. The increase coincided with the League's 2006 ban on stimulants (q.v. Major League Baseball drug policy).[156]

[edit] Controversies

Main article: Attention-deficit hyperactivity disorder controversies

Attention-deficit hyperactivity disorder (ADHD) is a highly controversial psychiatric disorder.[157][158] The controversies have involved clinicians, teachers, policymakers, parents, and the media, with opinions regarding ADHD ranging from those who do not believe it exists at all to those who believe that there are genetic and physiological bases for the condition.[159]

Researchers from the McMaster University Evidence-based Practice Center identified five features of ADHD that contribute to its controversial nature: 1) it is a clinical diagnosis for which there are no laboratory or radiological confirmatory tests or specific physical features; 2) diagnostic criteria have changed frequently; 3) there is no curative treatment, so long-term therapies are required; 4) therapy often includes stimulant drugs that are thought to have abuse potential; and 5) the rates of diagnosis and of treatment substantially differ across countries.[160]

There are questions about the long term effectiveness and side effects of the medication used to treat ADHD.[161]

[edit] See also

General

Related disorders

Controversy

[edit] References

  1. ^ NINDS Attention Deficit-Hyperactivity Disorder Information Page. National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.
  2. ^ Zwi M, Ramchandani P, Joughin C (October 2000). "Evidence and belief in ADHD". BMJ (Clinical research ed.) 321 (7267): 975–6. doi:10.1136/bmj.321.7267.975. PMID 11039942. PMC: 1118810. http://bmj.com/cgi/pmidlookup?view=long&pmid=11039942. 
  3. ^ "NIMH · ADHD · Complete Publication". http://www.nimh.nih.gov/health/publications/adhd/complete-publication.shtml. 
  4. ^ Polanczyk G, de Lima MS, Horta BL, Biederman J, Rohde LA (2007). "The worldwide prevalence of ADHD: a systematic review and metaregression analysis". Am J Psychiatry 164 (6): 942–8. doi:10.1176/appi.ajp.164.6.942. PMID 17541055. 
  5. ^ "Diagnostic and Statistical Manual of American Psychiatric Association, 2000.". 2000. http://www.behavenet.com/capsules/disorders/adhd.htm. Retrieved on 2008-09-11. 
  6. ^ Dulcan M (October 1997). "Practice parameters for the assessment and treatment of children, adolescents, and adults with attention-deficit/hyperactivity disorder. American Academy of Child and Adolescent Psychiatry". J Am Acad Child Adolesc Psychiatry 36 (10 Suppl): 85S–121S. PMID 9334567. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0890-8567&volume=36&issue=10&spage=85S. 
  7. ^ Sciutto, M.J., Nolfi, C.J., & Bluhm, C. (2004). Effects of Child Gender and Symptom Type on Referrals for ADHD by Elementary School Teachers. Journal of Emotional and Behavioral Disorders, 12(4), 247-253.
  8. ^ Van Cleave J, Leslie LK (August 2008). "Approaching ADHD as a chronic condition: implications for long-term adherence". Journal of psychosocial nursing and mental health services 46 (8): 28–37. PMID 18777966. 
  9. ^ a b Bálint S, Czobor P, Mészáros A, Simon V, Bitter I (2008). "[Neuropsychological impairments in adult attention deficit hyperactivity disorder: a literature review]" (in Hungarian). Psychiatr Hung 23 (5): 324–35. PMID 19129549. 
  10. ^ Elia J, Ambrosini PJ, Rapoport JL (March 1999). "Treatment of attention-deficit-hyperactivity disorder". N. Engl. J. Med. 340 (10): 780–8. doi:10.1056/NEJM199903113401007. PMID 10072414. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=10072414&promo=ONFLNS19. 
  11. ^ a b Gentile, Julie (2004). "Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management". Psychiatry 3 (8): 24–30. doi:10.1383/psyt.3.8.24.43396. http://www.psychiatrymmc.com/displayArticle.cfm?articleID=article218. Retrieved on 2008-09-11. 
  12. ^ a b Stern HP, Stern TP (September 2002). "When children with attention-deficit/hyperactivity disorder become adults". South. Med. J. 95 (9): 985–91. PMID 12356139. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0038-4348&volume=95&issue=9&spage=985. 
  13. ^ Hechtman L (August 1996). "Families of children with attention deficit hyperactivity disorder: a review". Can J Psychiatry 41 (6): 350–60. PMID 8862854. 
  14. ^ a b "Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder". Pediatrics 108 (4): 1033–44. October 2001. doi:10.1542/peds.108.4.1033. PMID 11581465. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11581465. 
  15. ^ a b King S, Griffin S, Hodges Z, et al (July 2006). "A systematic review and economic model of the effectiveness and cost-effectiveness of methylphenidate, dexamfetamine and atomoxetine for the treatment of attention deficit hyperactivity disorder in children and adolescents". Health Technol Assess 10 (23): iii–iv, xiii–146. PMID 16796929. http://www.hta.ac.uk/execsumm/summ1023.htm. 
  16. ^ Murphy, Kevin R.; Barkley, Russell A. (2005). Attention-Deficit Hyperactivity Disorder, Third Edition : A Clinical Workbook. New York: The Guilford Press. ISBN 1-59385-227-4. http://books.google.ca/books?id=EkyTTvjNRZAC&pg=PA626&lpg=PA626&dq=long+term+safety+of+stimulants&source=web&ots=AFB-MtfAvw&sig=J5rqYBXyT3bjYKtFmFmEJ33s5Zk&hl=en&sa=X&oi=book_result&resnum=5&ct=result#PPA626,M1. 
  17. ^ a b c d e "What is the evidence for using CNS stimulants to treat ADHD in children? | Therapeutics Initiative". http://www.ti.ubc.ca/letter69. 
  18. ^ Lerner M, Wigal T (January 2008). "Long-term safety of stimulant medications used to treat children with ADHD". Pediatric annals 37 (1): 37–45. doi:10.3928/00904481-20080101-11. PMID 18240852. 
  19. ^ a b c d e f g h i "CG72 Attention deficit hyperactivity disorder (ADHD): full guideline" (PDF). NHS. 24 September 2008. http://www.nice.org.uk/nicemedia/pdf/CG72FullGuideline.pdf. Retrieved on 2008-10-08. 
  20. ^ Parrillo, Vincent (2008). Encyclopedia of Social Problems. SAGE. pp. 63. ISBN 9781412941655. http://books.google.ca/books?id=mRGr_B4Y1CEC&pg=PA63&dq=percent+who+consider+ADHD+controversial&ei=kIEJScO6CY_-sQPYp62HAg. 
  21. ^ a b "Treatment of Attention-Deficit/Hyperactivity Disorder". US department of health and human services. December 1999. http://www.ahrq.gov/clinic/epcsums/adhdsum.htm. Retrieved on 2008-10-02. 
  22. ^ Mayes R, Bagwell C, Erkulwater J (2008). "ADHD and the rise in stimulant use among children". Harv Rev Psychiatry 16 (3): 151–66. doi:10.1080/10673220802167782. PMID 18569037. 
  23. ^ Cohen, Donald J.; Cicchetti, Dante (2006). Developmental psychopathology. Chichester: John Wiley & Sons. ISBN 0-471-23737-X. 
  24. ^ a b c "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity.". Barkley, Russell. http://www.continuingedcourses.net/active/courses/course003.php. Retrieved on 2008-09-19. 
  25. ^ Brain Matures A Few Years Late In ADHD, But Follows Normal Pattern
  26. ^ "LONI: Laboratory of Neuro Imaging". http://www.loni.ucla.edu/Research/Projects/ADHD.shtml#CurrentResearch. Retrieved on 2008-09-19. 
  27. ^ Jerry M., M. D. Wiener; Wiener, Jerry M.; Dulcan, Mina K. (2003). The American Psychiatric Publishing Textbook Of Child And Adolescent Psychiatry. Washington, DC: American Psychiatric Association. doi:http://books.google.ca/books?id=EIgGKcp0SpkC&pg=RA2-PA485&lpg=RA2-PA485&dq=%22psychiatrists+find+ADHD+controversial%22&source=web&ots=JYD7o1_uzS&sig=eOQtiaj_1_a2MfmJv2chRGamFK0&hl=en&sa=X&oi=book_result&resnum=8&ct=result#PRA2-PA487,M1. ISBN 1-58562-057-2. 
  28. ^ a b c d "Attention Deficit Hyperactivity Disorder (ADHD)". National Institute of Mental Health. April 3, 2008. http://www.nimh.nih.gov/healthinformation/adhdmenu.cfm. Retrieved on 2008-09-12. 
  29. ^ a b c d e "Evaluation and diagnosis of attention deficit hyperactivity disorder in children" (Subscription required). Uptodate. December 5, 2007. http://www.uptodate.com/online/content/topic.do?topicKey=behavior/8293#5. Retrieved on 2008-09-12. 
  30. ^ a b "ADHD - Symtoms of ADHD". Center for Decease Control and Prevention, department of Health and Human Services. September 20,2005. http://www.cdc.gov/ncbddd/adhd/symptom.htm. Retrieved on 2008-11-17. 
  31. ^ Bauermeister, J., Shrout, P., Chávez, L., Rubio-Stipec, M., Ramírez, R., Padilla, L., et al. (2007, August). ADHD and gender: are risks and sequela of ADHD the same for boys and girls?. Journal of Child Psychology & Psychiatry, 48(8), 831-839. Retrieved February 17, 2009, doi:10.1111/j.1469-7610.2007.01750.x
  32. ^ Bauermeister, J., Shrout, P., Chávez, L., Rubio-Stipec, M., Ramírez, R., Padilla, L., et al. (2007, August). ADHD and gender: are risks and sequela of ADHD the same for boys and girls?. Journal of Child Psychology & Psychiatry, 48(8), 831-839.
  33. ^ "Stimulant medication for the treatment of attention-deficit hyperactivity disorder: evidence-b(i)ased practice? -- Bailly 29 (8): 284 -- Psychiatric Bulletin". http://pb.rcpsych.org/cgi/content/full/29/8/284. 
  34. ^ Barkley, Russel A.. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". http://www.continuingedcourses.net/active/courses/course003.php. Retrieved on 2006-06-26. 
  35. ^ Roman T, Rohde LA, Hutz MH. (2004). "Polymorphisms of the dopamine transporter gene: influence on response to methylphenidate in attention deficit-hyperactivity disorder." American Journal of Pharmacogenomics 4(2):83–92 PMID 15059031
  36. ^ a b Swanson JM, Flodman P, Kennedy J, et al. "Dopamine Genes and ADHD." Neurosci Biobehav Rev. 2000 Jan;24(1):21–5. PMID 10654656
  37. ^ Smith KM, Daly M, Fischer M, et al. "Association of the dopamine beta hydroxylase gene with attention deficit hyperactivity disorder: genetic analysis of the Milwaukee longitudinal study." Am J Med Genet B Neuropsychiatr Genet. 2003 May 15;119(1):77–85. PMID 12707943
  38. ^ M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine 6 (1): 1–15. doi:10.1097/01.GIM.0000110413.07490.0B. 
  39. ^ {Levy et al., 1997; Nigg, 2006; Sherman, Silberg et al., 1996}
  40. ^ Sherman DK, Iacono WG, McGue MK (June 1997). "Attention-deficit hyperactivity disorder dimensions: A twin study of inattention and impulsivity-hyperactivity". J Am Acad Child Adolesc Psychiatry 36 (6): 745-753. PMID 9183128. 
  41. ^ Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP (2006). "Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children". Environ. Health Perspect. 114 (12): 1904–9. doi:10.1289/ehp.10274. PMID 17185283. 
  42. ^ "Bad behaviour 'linked to smoking'". BBC. 31 July 2005. http://news.bbc.co.uk/1/hi/health/4727197.stm. Retrieved on 30-12-2008. 
  43. ^ "Ability To Quit Smoking May Depend On ADHD Symptoms, Researchers Find". Science Daily. 24 November 2008. http://www.sciencedaily.com/releases/2008/11/081121125602.htm. Retrieved on 30-12-2008. 
  44. ^ "Prenatal Smoking Increases ADHD Risk In Some Children". Science Daily. 11 April 2007. http://www.sciencedaily.com/releases/2007/04/070410190421.htm. Retrieved on 30-12-2008. 
  45. ^ "ADHD 'linked to premature birth'". BBC. 4 June 2006. http://news.bbc.co.uk/1/hi/health/5042308.stm. Retrieved on 30-12-2008. 
  46. ^ Schab DW, Trinh NH (2004). "Do artificial food colors promote hyperactivity in children with hyperactive syndromes? A meta-analysis of double-blind placebo-controlled trials". Journal of developmental and behavioral pediatrics : JDBP 25 (6): 423–34. doi:10.1097/00004703-200412000-00007. PMID 15613992. 
  47. ^ Bateman B, Warner JO, Hutchinson E, Dean T, Rowlandson P, Gant C, Grundy J, Fitzgerald C, Stevenson J. (2004). "The effects of a double blind, placebo controlled, artificial food colourings and benzoate preservative challenge on hyperactivity in a general population sample of preschool children.". Archives of Disease in Childhood 89 (6): 506–11. doi:10.1136/adc.2003.031435. PMID 15155391. 
  48. ^ Donna McCann et al (2007). "Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial". The Lancet in press. 
  49. ^ "www.efsa.europa.eu". http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178694645855.htm. 
  50. ^ Kemp A (May 2008). "Food additives and hyperactivity". BMJ 336 (7654): 1144. doi:10.1136/bmj.39582.375336.BE. PMID 18497374. 
  51. ^ "Europe-wide call for food colour ban | Manufacturing | ICM Commercial & Business News". http://news.icm.ac.uk/business/retail/europe-wide-call-for-food-colour-ban/419/. 
  52. ^ "Modernising the Rules on Food Additives and Labelling of Azo Dyes - Food Industry News". http://www.flex-news-food.com/console/PageViewer.aspx?page=17642. 
  53. ^ Benton D (May 2008). "Sucrose and behavioral problems". Crit Rev Food Sci Nutr 48 (5): 385–401. doi:10.1080/10408390701407316. PMID 18464029. 
  54. ^ "Attention Deficit Hyperactivity Disorder". April 3, 2008. http://www.nimh.nih.gov/health/publications/adhd/complete-publication.shtml#pub4. Retrieved on 2008-09-19. 
  55. ^ Herman Staudenmayer (1999). Environmental Illness: Myth and Reality. CRC Press. pp. 58–62. ISBN 1566703050. 
  56. ^ Frölich J, Döpfner M (March 2008). "[The treatment of Attention-Deficit/Hyperactivity Disorders with polyunsaturated fatty acids - an effective treatment alternative?]" (in German). Z Kinder Jugendpsychiatr Psychother 36 (2): 109–16. doi:10.1024/1422-4917.36.2.109. PMID 18622940. 
  57. ^ What Keeps Children in Foster Care from Succeeding in School.PDF (661 KB)
  58. ^ Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
  59. ^ "Sensory integration disorder". healthatoz.com. 14-08-2006. http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?requestURI=/healthatoz/Atoz/ency/sensory_integration_disorder.jsp. Retrieved on 30-12-2008. 
  60. ^ Hartmann, Thom (2003). The Edison gene: ADHD and the gift of the hunter child. Rochester, Vt: Park Street Press. doi:http://books.google.ca/books?id=L0l5EaHppyoC&dq=hunter+vs+farmer+The+Edison+Gene:+ADHD+and+the+Gift+of+the+Hunter+Child&lr=&source=gbs_summary_s&cad=0. ISBN 0-89281-128-5. 
  61. ^ Rethinking ADHD >> Palgrave.com : Title Page
  62. ^ a b c http://www.incrediblehorizons.com/Understanding%20Add.htm
  63. ^ http://www.sci.csuhayward.edu/~dsandberg/CHLDPATHLECTS/ChldPathLect05ADHD.htm
  64. ^ Keenan HT, Hall GC, Marshall SW (2008). "Early head injury and attention deficit hyperactivity disorder: retrospective cohort study;". BMJ 337: a1984. doi:10.1136/bmj.a1984. PMID 18988644. PMC: 2590885. http://bmj.com/cgi/pmidlookup?view=long&pmid=18988644. 
  65. ^ "Mental Health: A report of the surgeon general". 1999. http://www.surgeongeneral.gov/library/mentalhealth/chapter3/sec4.html. Retrieved on 2008-09-15. 
  66. ^ Ernst M, Liebenauer LL, King AC, Fitzgerald GA, Cohen RM, Zametkin AJ (1994). "Reduced brain metabolism in hyperactive girls". J Am Acad Child Adolesc Psychiatry 33 (6): 858–68. doi:10.1097/00004583-199407000-00012. PMID 8083143. 
  67. ^ http://www.ncbi.nlm.nih.gov/pubmed/16555214?dopt=Abstract
  68. ^ "Evaluation and diagnosis of attention deficit hyperactivity disorder in children". December 5, 2007. http://www.uptodate.com/online/content/topic.do?topicKey=behavior/8293&selectedTitle=4~150&source=search_result. Retrieved on 2008-09-15. 
  69. ^ "MerckMedicus Modules: ADHD - Pathophysiology". http://www.merckmedicus.com/pp/us/hcp/diseasemodules/adhd/pathophysiology.jsp. 
  70. ^ Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern NIMH Press Release, November 12, 2007
  71. ^ Gene Predicts Better Outcome as Cortex Normalizes in Teens with ADHD NIMH Press Release, August 6, 2007
  72. ^ Lou HC, Andresen J, Steinberg B, McLaughlin T, Friberg L. "The striatum in a putative cerebral network activated by verbal awareness in normals and in ADHD children." Eur J Neurol. 1998 Jan;5(1):67–74. PMID 10210814
  73. ^ Dougherty DD, Bonab AA, Spencer TJ, Rauch SL, Madras BK, Fischman AJ (1999). "Dopamine transporter density in patients with attention deficit hyperactivity disorder". Lancet 354 (9196): 2132–-33. doi:10.1016/S0140-6736(99)04030-1. PMID 10609822. 
  74. ^ Dresel SH, Kung MP, Plössl K, Meegalla SK, Kung HF (1998). "Pharmacological effects of dopaminergic drugs on in vivo binding of [99mTc]TRODAT-1 to the central dopamine transporters in rats". European journal of nuclear medicine 25 (1): 31–9. PMID 9396872. 
  75. ^ Coccaro EF, Hirsch SL, Stein MA (2007). "Plasma homovanillic acid correlates inversely with history of learning problems in healthy volunteer and personality disordered subjects". Psychiatry research 149 (1–3): 297–302. doi:10.1016/j.psychres.2006.05.009. PMID 17113158. 
  76. ^ a b Zametkin AJ, Nordahl TE, Gross M, et al (November 1990). "Cerebral glucose metabolism in adults with hyperactivity of childhood onset". N. Engl. J. Med. 323 (20): 1361–6. PMID 2233902. 
  77. ^ Matochik JA, Liebenauer LL, King AC, Szymanski HV, Cohen RM, Zametkin AJ (May 1994). "Cerebral glucose metabolism in adults with attention deficit hyperactivity disorder after chronic stimulant treatment". Am J Psychiatry 151 (5): 658–64. PMID 8166305. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=8166305. 
  78. ^ Ernst M, Cohen RM, Liebenauer LL, Jons PH, Zametkin AJ (October 1997). "Cerebral glucose metabolism in adolescent girls with attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry 36 (10): 1399–406. doi:10.1097/00004583-199710000-00022. PMID 9334553. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0890-8567&volume=36&issue=10&spage=1399. 
  79. ^ Zametkin AJ, Liebenauer LL, Fitzgerald GA, et al (May 1993). "Brain metabolism in teenagers with attention-deficit hyperactivity disorder". Arch. Gen. Psychiatry 50 (5): 333–40. PMID 8489322. 
  80. ^ Armstrong, Thomas (1999). MAVM2K6SdAfcSf0nGYQ&hl=en&sa=X&oi=book_result&resnum=1&ct=result#PPA3,M1 Add/Adhd Alternatives in the Classroom. ASCD. pp. 3–5. ISBN 9780871203595. http://books.google.ca/books?id=EzXt100I4A8C&pg=PA3&lpg=PA3&dq=National+Institute+of+Mental+Health+ADHD+PET+scan&source=web&ots=GlP-TIeiqN&sig=JADzxFyez- MAVM2K6SdAfcSf0nGYQ&hl=en&sa=X&oi=book_result&resnum=1&ct=result#PPA3,M1. 
  81. ^ Ernst M, Liebenauer LL, King AC, Fitzgerald GA, Cohen RM, Zametkin AJ (1994). "Reduced brain metabolism in hyperactive girls". J Am Acad Child Adolesc Psychiatry 33 (6): 858–68. doi:10.1097/00004583-199407000-00012. PMID 8083143. 
  82. ^ Díaz-Heijtz R, Mulas F, Forssberg H (February 2006). "[Alterations in the pattern of dopaminergic markers in attention-deficit/hyperactivity disorder]" (in Spanish; Castilian). Rev Neurol 42 Suppl 2: S19–23. PMID 16555214. http://www.revneurol.com/LinkOut/formMedLine.asp?Refer=2005798&Revista=RevNeurol. 
  83. ^ Joughin C, Ramchandani P, Zwi M (May 2003). "Attention-deficit/hyperactivity disorder". Am Fam Physician 67 (9): 1969–70. PMID 12751659. http://www.aafp.org/afp/20030501/british.html. 
  84. ^ Moffitt TE, Melchior M (June 2007). "Why does the worldwide prevalence of childhood attention deficit hyperactivity disorder matter?". The American journal of psychiatry 164 (6): 856–8. doi:10.1176/appi.ajp.164.6.856. PMID 17541041. 
  85. ^ a b ICD Version 2006: F91. World Health Organization. Retrieved on December 11, 2006.
  86. ^ "PsychiatryOnline". http://www.psychiatryonline.com/content.aspx?aID=7721. 
  87. ^ "Medscape.com Log In". http://medoffice.medscape.com/viewarticle/530193_2. 
  88. ^ Pliszka S (2000). "Patterns of psychiatric comorbidity with attention-deficit/hyperactivity disorder". Child Adolesc Psychiatr Clin N Am 9 (3): 525–40, vii. PMID 10944655. 
  89. ^ Lamminmäky T et al (1995). "Attention deficit hyperactivity disorder subtypes: Are there differences in academic problems?". Dev neuropsychology (11): 297–310. 
  90. ^ Foster, et al (2007). "Treatment of ADHD: Is More Complex Treatment Cost-Effective for More Complex Cases?". HSR: Health Services Research 42 (1): 165–182 (Page:177). doi:10.1111/j.1475-6773.2006.00599.x. PMID 17355587. 
  91. ^ Smucker WD, Hedayat M (September 2001). "Evaluation and treatment of ADHD". Am Fam Physician 64 (5): 817–29. PMID 11563573. 
  92. ^ a b c Owens, Judith A. (August 2005). "The ADHD and Sleep Conundrum: A Review". Journal of Developmental & Behavioral Pediatrics (Lippincott Williams & Wilkins, Inc.) 26 (4): 312–322. doi:10.1097/00004703-200508000-00011. ISSN 0196-206X. PMID 16100507. 
  93. ^ Owens, J. A. (October 2008). "Sleep disorders and attention-deficit/hyperactivity disorder" (Abstract). Curr Psychiatry Rep. 10 (5): 439–44. doi:10.1007/s11920-008-0070-x. PMID 18803919. http://www.ncbi.nlm.nih.gov/pubmed/18803919?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed. Retrieved on 2008-12-08. 
  94. ^ Walters, A. S.; Silvestri, R.; Zucconi, M.; Chandrashekariah, R.; Konofal, E. (2008). "Review of the possible relationship and hypothetical links between attention deficit hyperactivity disorder (ADHD) and the simple sleep related movement disorders, parasomnias, hypersomnias, and circadian rhythm disorders" (Review, abstract). J Clin Sleep Med 4 (6): 591–600. 20083790. http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=20083790. Retrieved on 2009-01-22. 
  95. ^ Pliszka S (July 2007). "Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry 46 (7): 894–921. doi:10.1097/chi.0b013e318054e724. PMID 17581453. 
  96. ^ "Family therapy for attention-deficit disorder or attention-deficit/hyperactivity disorder in children and adolescents". The Cochrane Collaboration. April 20, 2005. http://www.cochrane.org/reviews/en/ab005042.html. Retrieved on 2008-09-19. 
  97. ^ Wymbs, B.T., Pelham Jr,W.E., MoIina, B.S.G., Gnagy, E.M., Wilson, T.K., & Greenhouse, J.L. (2008). Rate and Predictors of Divorce Among Parents of Youths With ADHD. Journal of Consulting and Clinical Psychology, 76(5), 735.
  98. ^ Jensen, et al (2005). "Cost-Effectiveness of ADHD Treatments: Findings from the Multimodal Treatment Study of Children With ADHD". American Journal of Psychiatry 162: 1628–1636 (Page:1633). doi:10.1176/appi.ajp.162.9.1628. PMID 16135621. 
  99. ^ Brown RT, Amler RW, Freeman WS, et al (June 2005). "Treatment of attention-deficit/hyperactivity disorder: overview of the evidence". Pediatrics 115 (6): e749–57. doi:10.1542/peds.2004-2560. PMID 15930203. 
  100. ^ Schachter HM, Pham B, King J, Langford S, Moher D (November 2001). "How efficacious and safe is short-acting methylphenidate for the treatment of attention-deficit disorder in children and adolescents? A meta-analysis". CMAJ 165 (11): 1475–88. PMID 11762571. PMC: 81663. http://www.cmaj.ca/cgi/pmidlookup?view=long&pmid=11762571. 
  101. ^ Barkley, Russell (2006). Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. New York: The Guildford Press. pp. 608–645. ISBN 2005016986. 
  102. ^ McDonagh MS, Peterson K, Dana T, Thakurta S. (2007). Drug Class Review on Pharmacologic Treatments for ADHD. Results.
  103. ^ &Na;, (August 2008). "American Academy of Pediatrics/American Heart Association clarification of statement on cardiovascular evaluation and monitoring of children and adolescents with heart disease receiving medications for ADHD: May 16, 2008". J Dev Behav Pediatr 29 (4): 335. doi:10.1097/DBP.0b013e31318185dc14. PMID 18698199. http://circ.ahajournals.org/cgi/content/full/117/18/2407. 
  104. ^ "FDA News". FDA. February 21, 2007. http://www.fda.gov/bbs/topics/NEWS/2007/NEW01568.html. Retrieved on 2008-10-01. 
  105. ^ "ADDERALL (CII)" (PDF). FDA. MARCH 2007. http://www.fda.gov/cder/foi/label/2007/011522s040lbl.pdf. Retrieved on 2008-10-01. 
  106. ^ Lerner M, Wigal T (January 2008). "Long-term safety of stimulant medications used to treat children with ADHD". Pediatric annals 37 (1): 37–45. doi:10.3928/00904481-20080101-11. PMID 18240852. 
  107. ^ Hillman, C., Buck, S.M., Themanson, J.R., Pontifex, M.B, & Castelli, D.M. (2009). Aerobic fitness and cognitive development: Event-related brain potential and task performance indices of executive control in preadolescent children. Developmental Psychology 45(1), 114-125.
  108. ^ Andy Lopez-Williams, Anil Chacko, Brian T Wymbs, Gregory A Fabiano, et al. (2005). Athletic Performance and Social Behavior as Predictors of Peer Acceptance in Children Diagnosed With Attention-Deficit/Hyperactivity Disorder. Journal of Emotional and Behavioral Disorders, 13(3), 173-180.
  109. ^ Jensen PS, Arnold LE, Swanson JM, et al (August 2007). "3-year follow-up of the NIMH MTA study". J Am Acad Child Adolesc Psychiatry 46 (8): 989–1002. doi:10.1097/CHI.0b013e3180686d48. PMID 17667478. 
  110. ^ http://eric.ed.gov/ERICDocs/data/ericdocs2/content_storage_01/0000000b/80/22/94/d6.pdfPDF
  111. ^ Cimera, Robert (2002). Making ADHD a gift: teaching Superman how to fly. Lanham, Maryland: Scarecrow Press, Inc.. pp. 116. ISBN 0810843188. http://www.rowmaneducation.com/Catalog/SingleBook.shtml?command=Search&db=^DB/CATALOG.db&eqSKUdata=0810843196. 
  112. ^ College Degree Nearly Doubles Annual Earnings, Census Bureau Reports U.S. Census Bureau March 28, 2005. Retrieved on 2008-08-02.
  113. ^ Polanczyk G, de Lima MS, Horta BL, Biederman J, Rohde LA (2007). "The worldwide prevalence of ADHD: a systematic review and metaregression analysis". Am J Psychiatry 164 (6): 942–48. doi:10.1176/appi.ajp.164.6.942. PMID 17541055. 
  114. ^ Jerry M., M. D. Wiener; Wiener, Jerry M.; Dulcan, Mina K. (2003). The American Psychiatric Publishing Textbook Of Child And Adolescent Psychiatry. Washington, DC: American Psychiatric Association. doi:http://books.google.ca/books?id=EIgGKcp0SpkC&pg=RA2-PA485&lpg=RA2-PA485&dq=%22psychiatrists+find+ADHD+controversial%22&source=web&ots=JYD7o1_uzS&sig=eOQtiaj_1_a2MfmJv2chRGamFK0&hl=en&sa=X&oi=book_result&resnum=8&ct=result#PRA2-PA487,M1. ISBN 1-58562-057-2. 
  115. ^ "ADHD Home". http://www.cdc.gov/ncbddd/ADHD/. 
  116. ^ "www.cdc.gov" (PDF). http://www.cdc.gov/nchs/data/series/sr_10/sr10_221.pdf. 
  117. ^ Staller J, Faraone SV (2006). "Attention-deficit hyperactivity disorder in girls: epidemiology and management". CNS Drugs 20 (2): 107–23. doi:10.2165/00023210-200620020-00003. PMID 16478287. 
  118. ^ http://kadi.myweb.uga.edu/The_Development_of_the_DSM.html
  119. ^ What is Adult ADD?
  120. ^ [1] An Early Description of ADHD (Inattentive Subtype): Dr Alexander Crichton and `Mental Restlessness' (1798) Child and Adolescent Mental Health, Volume 6, Number 2, May 2001 , pp. 66–73(8)
  121. ^ p 271, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.[2]Complete history with pictures of the original citation sources
  122. ^ p 271, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.[3] Complete history with pictures of the original citation sources
  123. ^ p 272, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.[4]Complete history with pictures of the original citation sources
  124. ^ p 272, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.[5]Complete history with pictures of the original citation sources
  125. ^ p 278, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.[6]Complete history with pictures of the original citation sources
  126. ^ Palmer, E. D., and Finger, S. 2001. An early description of ADHD(Inattention Subtype): Dr. Alexander Crichton and the "MentalRestlessness" (1798). Child Psychology and Psychiatry Reviews, 6, 66-73.
  127. ^ An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.[7]Complete history with pictures of the original citation sources
  128. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008–1012[8]The complete history with some original pictures
  129. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008–1012[9]The complete history with some original pictures
  130. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008–1012[10]The complete history with some original pictures
  131. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008–1012[11]The complete history with some original pictures
  132. ^ Russell A. Barkley: The Relevance of the Still Lectures to Attention Deficit Hyperactivity Disorder A Commentary. 2006; 10; 137 J Atten Disord.
  133. ^ Palmer, E. D., and Finger, S. 2001. An early description of ADHD(Inattention Subtype): Dr. Alexander Crichton and the "MentalRestlessness" (1798). Child Psychology and Psychiatry Reviews, 6, 66-73.
  134. ^ Russell A. Barkley: The Relevance of the Still Lectures to Attention Deficit Hyperactivity Disorder A Commentary. 2006; 10; 137 J Atten Disord.
  135. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008–1012[12]With som original pictures
  136. ^ Palmer, E. D., and Finger, S. 2001. An early description of ADHD(Inattention Subtype): Dr. Alexander Crichton and the "MentalRestlessness" (1798). Child Psychology and Psychiatry Reviews, 6, 66-73.
  137. ^ http://www.healthcentral.com/adhd/c/7930/23979/adhds-history-effects
  138. ^ a b http://www.uspharmacist.com/index.asp?page=ce/10135/default.htm
  139. ^ a b http://www.psychiatrymmc.com/displayArticle.cfm?articleID=article218
  140. ^ http://news.healingwell.com/index.php?p=news1&id=521145
  141. ^ You've Got Adult ADD… Now What?, ADDitude magazine, 2007
  142. ^ http://www.adhd-information-exchange.com/DSM-V.html
  143. ^ http://www.neuropsychiatryreviews.com/feb00/npr_feb00_ADHD.html
  144. ^ http://www.continuingedcourses.net/active/courses/course003.php
  145. ^ "What is Attention-Deficit/Hyperactivity Disorder (ADHD)?". http://www.cdc.gov/ncbddd/adhd/what.htm. 
  146. ^ "UpToDate Inc.". http://www.uptodate.com/online/content/topic.do?topicKey=behavior/8293&linkTitle=EPIDEMIOLOGY&source=preview&selectedTitle=4~150&anchor=2#2. 
  147. ^ Brewis, Alexandra; Karen L. Schmidt, Mary Meyer (2000-12). "ADHD-Type Behavior and Harmful Dysfunction in Childhood: A Cross-Cultural Model". American Anthropologist 102 (4): 826. doi:10.1525/aa.2000.102.4.823. 
  148. ^ Caldararo, Niccolo (2002-03). "Comment on Brewis et al". American Anthropologist 104 (1): 282–283. doi:10.1525/aa.2002.104.1.282. 
  149. ^ Danforth, Scot; Joy Yogawin (2001). "Hyper Talk: Sampling the Social Construction of ADHD in Everyday Language". Anthropology & Education Quarterly 32 (2): 167–190. doi:10.1525/aeq.2001.32.2.167. 
  150. ^ http://www.pbs.org/wgbh/pages/frontline/shows/medicating/adhd/ Medicating Kids
  151. ^ PBS - frontline: medicating kids: opponents and backlash
  152. ^ PBS - frontline: medicating kids: interviews: xavier castellanos, m.d
  153. ^ "'I'm passionate about life'". msnbc.msn.com. http://www.msnbc.msn.com/id/8343367/page/2/. Retrieved on 30-12-2008. 
  154. ^ Baroness Susan Greenfield
  155. ^ BBC NEWS | Health | Peer calls for ADHD care review
  156. ^ Saletan, William (2009-01-12). "Doping Deficit Disorder. Need performance-enhancing drugs? Claim ADHD". Slate. http://www.slate.com/id/2208429/. 
  157. ^ Mayes R, Bagwell C, Erkulwater J (2008). "ADHD and the rise in stimulant use among children". Harv Rev Psychiatry 16 (3): 151–66. doi:10.1080/10673220802167782. PMID 18569037. 
  158. ^ Foreman DM (February 2006). "Attention deficit hyperactivity disorder: legal and ethical aspects". Arch. Dis. Child. 91 (2): 192–4. doi:10.1136/adc.2004.064576. PMID 16428370. 
  159. ^ "Treatment of Attention-Deficit/Hyperactivity Disorder". US department of health and human services. December 1999. http://www.ahrq.gov/clinic/epcsums/adhdsum.htm. Retrieved on 2008-10-02. 
  160. ^ Jadad AR, Booker L, Gauld M, et al (December 1999). "The treatment of attention-deficit hyperactivity disorder: an annotated bibliography and critical appraisal of published systematic reviews and metaanalyses". Canadian journal of psychiatry. Revue canadienne de psychiatrie 44 (10): 1025–35. PMID 10637682. https://ww1.cpa-apc.org/French_Site/Publications/Archives/CJP/1999/Dec/jadad.htm. 
  161. ^ Lakhan SE; Hagger-Johnson G. http://www.cpementalhealth.com/content/3/1/21 The impact of prescribed psychotropics on youth. Clinical Practice and Epidemiology in Mental Health 2007;3(21).

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