Attention deficit hyperactivity disorder: Difference between revisions

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'''Attention-Deficit Hyperactivity Disorder (ADHD)''' is a chronic{{Fact|date=September 2008}} neurobehavioral developmental{{Fact|date=September 2008}} disorder{{Fact|date=September 2008}} affecting about 2-5% of the world's population depending on the diagnostic criteria used.<ref>{{cite journal |author=Katragadda S, Schubiner H |title=ADHD in children, adolescents, and adults |journal=Prim. Care |volume=34 |issue=2 |pages=317–41; abstract viii |year=2007 |month=June |pmid=17666230 |doi=10.1016/j.pop.2007.04.012 |url=}}</ref><ref name="Polanczyk"/><ref name=UTP2008/> It typically presents during childhood, and is characterized by a persistent pattern of [[impulsivity|impulsiveness]], [[hyperactivity]], and inattention.<ref name=DSM-IV-TR>{{cite web |url=http://www.behavenet.com/capsules/disorders/adhd.htm |title=Diagnostic and Statistical Manual of American Psychiatric Association, 2000. |accessdate=2008-09-11 |work= |publisher= |date=2000 }}</ref> ADHD occurs twice as commonly in boys as in girls.<ref>{{cite journal |author=Dulcan M |title=Practice parameters for the assessment and treatment of children, adolescents, and adults with attention-deficit/hyperactivity disorder. American Academy of Child and Adolescent Psychiatry |journal=J Am Acad Child Adolesc Psychiatry |volume=36 |issue=10 Suppl |pages=85S–121S |year=1997 |month=October |pmid=9334567 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0890-8567&volume=36&issue=10&spage=85S}}</ref>
'''Attention-Deficit Hyperactivity Disorder (ADHD)''' is a neurobehavioral developmental{{Fact|date=September 2008}} disorder{{Fact|date=September 2008}} affecting about 2-5% of the world's population depending on the diagnostic criteria used.<ref>{{cite journal |author=Katragadda S, Schubiner H |title=ADHD in children, adolescents, and adults |journal=Prim. Care |volume=34 |issue=2 |pages=317–41; abstract viii |year=2007 |month=June |pmid=17666230 |doi=10.1016/j.pop.2007.04.012 |url=}}</ref><ref name="Polanczyk"/><ref name=UTP2008/> It typically presents during childhood, and is characterized by a persistent pattern of [[impulsivity|impulsiveness]], [[hyperactivity]], and inattention.<ref name=DSM-IV-TR>{{cite web |url=http://www.behavenet.com/capsules/disorders/adhd.htm |title=Diagnostic and Statistical Manual of American Psychiatric Association, 2000. |accessdate=2008-09-11 |work= |publisher= |date=2000 }}</ref> ADHD occurs twice as commonly in boys as in girls.<ref>{{cite journal |author=Dulcan M |title=Practice parameters for the assessment and treatment of children, adolescents, and adults with attention-deficit/hyperactivity disorder. American Academy of Child and Adolescent Psychiatry |journal=J Am Acad Child Adolesc Psychiatry |volume=36 |issue=10 Suppl |pages=85S–121S |year=1997 |month=October |pmid=9334567 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0890-8567&volume=36&issue=10&spage=85S}}</ref>
ADHD is generally a chronic disorder with 10 to 60% of individuals diagnosed in childhood continuing to meet diagnostic criteria in adulthood.<ref name=TI2008/><ref>{{cite journal |author=Elia J, Ambrosini PJ, Rapoport JL |title=Treatment of attention-deficit-hyperactivity disorder |journal=N. Engl. J. Med. |volume=340 |issue=10 |pages=780–8 |year=1999 |month=March |pmid=10072414 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=10072414&promo=ONFLNS19}}</ref> Those affected are likely to develop [[coping skills|coping mechanisms]] as they mature thus compensating for their previous ADHD. <ref>{{cite journal |last=Gentile |first=Julie |authorlink= |coauthors= |year= |month= |title=Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management |journal=Psychiatry |volume=3 |issue=8 |pages=24-30 |id= |url=http://www.psychiatrymmc.com/displayArticle.cfm?articleID=article218 |accessdate=2008-09-11 |quote= }}</ref>
ADHD is generally a chronic disorder with 10 to 60% of individuals diagnosed in childhood continuing to meet diagnostic criteria in adulthood.<ref name=TI2008/><ref>{{cite journal |author=Elia J, Ambrosini PJ, Rapoport JL |title=Treatment of attention-deficit-hyperactivity disorder |journal=N. Engl. J. Med. |volume=340 |issue=10 |pages=780–8 |year=1999 |month=March |pmid=10072414 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=10072414&promo=ONFLNS19}}</ref> Those affected are likely to develop [[coping skills|coping mechanisms]] as they mature thus compensating for their previous ADHD. <ref>{{cite journal |last=Gentile |first=Julie |authorlink= |coauthors= |year= |month= |title=Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management |journal=Psychiatry |volume=3 |issue=8 |pages=24-30 |id= |url=http://www.psychiatrymmc.com/displayArticle.cfm?articleID=article218 |accessdate=2008-09-11 |quote= }}</ref>


Revision as of 03:35, 20 September 2008

Attention deficit hyperactivity disorder
SpecialtyPsychiatry, child and adolescent psychiatry Edit this on Wikidata

Attention-Deficit Hyperactivity Disorder (ADHD) is a neurobehavioral developmental[citation needed] disorder[citation needed] affecting about 2-5% of the world's population depending on the diagnostic criteria used.[1][2][3] It typically presents during childhood, and is characterized by a persistent pattern of impulsiveness, hyperactivity, and inattention.[4] ADHD occurs twice as commonly in boys as in girls.[5] ADHD is generally a chronic disorder with 10 to 60% of individuals diagnosed in childhood continuing to meet diagnostic criteria in adulthood.[6][7] Those affected are likely to develop coping mechanisms as they mature thus compensating for their previous ADHD. [8]

Though typically regarded as a diagnosis in children Adult ADHD has been increasingly recognized in the last few decades. ADHD has a strong genetic component.[9] 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.[10] Long term safety of stimulants however has not been determined.[6]

ADHD is one of the most controversial pediatric disorders.[11][12]

Classification

ADHD is usually classified by the Diagnostic and Statistical Manual of Mental Disorders (DSM IV). The DSM IV identifies three subtypes:

  • Primarily Inattentive (ADHD-I): previously known as ADD-H or Attention Deficit Disorder without Hyperactivity
  • Primarily Hyperactive/Impulsive (ADHD-HI): previously known as ADHD
  • Combined type (ADHD-C): previously known as ADD+H or Attention Deficit Disorder with Hyperactivity

ADHD has been classified as a developmental disorder, a behavior disorder and a neurological disorder.

ADHD is a developmental disorder where certain traits such as impulse control lag in development when compared to the general population[13]. Using magnetic resonance imaging, this developmental lag has been estimated to range from 3 to 5 years in the prefrontal cortex.[14]. These delays are considered to cause impairment. ADHD has also been classified as a behavior disorder and a neurological disorder. [15]

Symptoms

The most common symptoms of ADHD are[16][3]:

  • Impulsiveness: a person who acts quickly without thinking things through.
  • Hyperactivity: a person who is unable to sit still.
  • Inattention: a person who daydreams or seems to be in another world.

The DSM IV categorises the symptoms of ADHD into two clusters: inattention symptoms and hyperactivity/impulsivity symptoms. Most ordinary people exhibit some of these behaviors but not to the point where they significantly interfere with the person's work, relationships, or studies or cause 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 symptoms of inattention throughout their lives.

Inattention and "hyperactive" behavior are not the only problems with children with ADHD. ADHD exists alone in only about 1/3 of the children diagnosed with it. Many of these 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%). These are both characterized by anti-social behaviors such as aggression, frequent temper tantrums, deceitfulness, lying, or stealing.[3]
  • Primary disorder of vigilance. 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.[3]
  • 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.[3]
  • Anxiety Disorders. Commonly accompany ADHD, particularly Obsessive-Compulsive Disorder. OCD is believed to share a genetic component with ADHD, and shares many of its characteristics.[3]

Causes

ADHD is generally inherited, but it can also be caused by various problems, including difficulties with pregnancy, birth, early childhood severe illness, and environmental toxins.[17]

Genetic factors

Twin studies indicate that the disorder is highly heritable and that genetics cause about 75% of ADHD cases.[13] Hyperactivity also seems to be primarily a genetic condition however other causes do have an effect.[18]

Researchers believe that a large majority of ADHD arises 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),[19] the 10-repeat allele of the DAT1 gene,[20] the 7-repeat allele of the DRD4 gene,[20] and the dopamine beta hydroxylase gene (DBH TaqI).[21]

The broad selection of targets indicates that ADHD does not follow the traditional model of a "genetic disease" and should 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.[22]

Environmental factors

The estimated contribution of non-genetic factors to all cases of ADHD is 20 percent.[citation needed]

Environmental factors implicated include alcohol and tobacco smoke exposure during pregnancy and lead exposure after birth.[23] Smoking relation to ADHD could be due nicotine causing hypoxia (lack of oxygen) in utero, however it could also be that women with ADHD are more likely to smoke and therefore due to the strong genetic component of ADHD more likely to have children with ADHD.[citation needed] Complications during pregnancy and birth—including premature birth—might also play a role.[citation needed]

Current evidence does not support an association between head injuries and ADHD. [24]

Diet

A systematic review found that removing artificial food coloring from the diet improved ADHD symptoms.[25] Evidence however shows that sucrose (sugar) has no effect on behavior.[26][27]

Preliminary evidence suggests that Omega-3/Omega-6 supplementation reduces ADHD symptoms.[28][29]

Social factors

There is no compelling evidence that social factors alone can cause ADHD.[13] Many researchers believe that relationships with caregivers have a profound effects on attentional and self-regulatory abilities. A study of foster children found that a high number of them had symptoms closely resembling ADHD.[30] Well other researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse.[31] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

Neurobiological mechanisms

The pathophysiology of ADHD is unclear and there are a number of competing theories.[32]

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 characterize an ADHD diagnosis.[33]

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.[34]

Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity),[35] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. [36][37] 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.[38]

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.

PET scans of glucose metabolism in the brains of a normal adult (left) compared to an adult diagnosed with ADHD (right).[39] "This PET scan was taken from Zametkin's landmark 1990 study, which found lower glucose metabolism, in the brains of patients with ADHD who had never taken medication. Scans were taken while patients were engaging in tasks requiring focused attention. The greatest deficits were found in the premotor cortex and superior prefrontal cortex."

An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children. 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 diagnosed with ADHD as a child when given that same task; these are not pictures of individual brains, which would contain substantial overlap, these are images constructed to illustrate group-level differences. Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex.[39] A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADHD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADHD patients (relative to the controls). Most notably, lower metabolic activity in one specific region of the left anterior frontal lobe was significantly inversely correlated with symptom severity.[40] These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.[citation needed]

Diagnosis

No objective test exists to confirm a diagnosis of ADHD. It thus remains a clinical diagnosis.[41] Many of the symptoms of ADHD occur from time to time in everyone. In patients with ADHD, however, the frequency of these symptoms is greater and significantly impair their life. This impairment must occur in multiple setting. 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 critera 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 terminology of ADD expired with the revision of the most current version 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).

DSM-IV criteria

I. Either A or B:

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).

Other diagnostic criteria

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[42]) 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".[42]

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:[43]

  • 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 five criteria are proven using specifically designed test or using the patients history given by the parents, teachers or the patient's memory.

The Centers for Disease Control and Prevention (CDC) state that a diagnosis of ADD should only be made by trained health care providers, as many of the symptoms may also be part of other conditions, such as bodily illness or other physiological disorders, such as hypothyroidism. It is not uncommon that physically and mentally nonpathological individuals exhibit at least some of the symptoms from time to time. Severity and pervasiveness of the symptoms leading to prominent functional impairment across different settings (school, work, social relationships) are major factors in a positive diagnosis.

Adults often continue to be impaired by ADD. Adults with ADD are diagnosed under the same criteria, including the stipulation that their symptoms must have been present prior to the age of seven.[44] 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.[45]

Common comorbid conditions are Oppositional Defiance Disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder.[46] Learning disorders are more common when there are inattention symptoms.[47]

Management

Main article: Attention-deficit hyperactivity disorder treatments

Methods of treatment often involve some combination of medications, behavior modifications, life style changes, and counseling.

Behavioral interventions

Family therapy has shown little benefit in the treatment of ADHD.[48] Education to help parents understand ADHD have shown short term benefits.[49]

Pharmacological treatment

Stimulant medications are the most clinically and cost effective method of treating ADHD. [49][50] No significant differences between the various drugs in terms of efficacy or side effects has been found.[51][52] About 70% of children improve with treatment with stimulents.[53]

Stimulants, in the short term, have been found to be safe in the appropriately selected patient however long term safety has not been determined. There are no randomized controlled trials assessing the harms or benefits of treatment beyond two years.[6] On February 9, 2006, the FDA voted to recommend a "black-box" warning describing the cardiovascular risks of stimulant drugs used to treat attention deficit–hyperactivity disorder (ADHD).[54] 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.[55]

Comorbid disorders or substance abuse can make the diagnosis and the treatment of ADHD more difficult. Psychosocial therapy is useful in treating some comorbid conditions.[56]

Prognosis

ADHD diagnosed in childhood resolves in 40 to 90% of individuals by the time they reach adulthood.[6][57] Those affected are likely to develop coping mechanisms as they mature thus compensating for their previous ADHD. [58]

37% of those with ADHD do not get a high school diploma even though many of them will receive special education services.[13] The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish high school.[59] In the United States, less than 5% of individuals with ADHD get a college degree[60] compared to 28% of the general population.[61]

Epidemiology

ADHD's global prevalence is estimated at 5% in people under the age of 19. There is however wide variability in theses estimates with North America children appearing to have a higher rate of ADHD than Africa and the Middle East children.[2] There is also a gender difference in children diagnosed with ADHD. 10% of males and 4% of females have been diagnosed in the United States[62] This sex difference may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[63][64]

History

The clinical definition of "ADHD" dates to the mid-20th century, when physicians developed a diagnosis for a set of conditions variously referred to as "minimal brain damage", "minimal brain dysfunction", "learning/behavioural disabilities" and "hyperactivity". Researchers speculate that earlier references to the condition as mentioned in the examples below, have been made throughout history.

In 493 BCE, physician-scientist Hippocrates described a condition that seems to be compatible with what we now know as ADHD. He described patients who had "quickened responses to sensory experience, but also less tenaciousness because the soul moves on quickly to the next impression". Hippocrates attributed this condition to an "overbalance of fire over water”. His remedy for this "overbalance" was "barley rather than wheat bread, fish rather than meat, water drinks, and many natural and diverse physical activities."[65] Shakespeare made reference to a "malady of attention", in King Henry VIII.

In 1902, the English pediatrician George Still gave a series of lectures to the Royal College of Physicians in England, and described a condition which some have claimed is analogous to ADHD. Still described a group of children with significant behavioral problems, caused, he believed, by an innate hereditary dysfunction and not by poor child rearing or environment.[66]

In 1937, Dr. Charles Bradley in Providence, RI reported that a group of children with behavioral problems improved after being treated with the stimulant Benzedrine.[67] In 1957, the stimulant methylphenidate (Ritalin, which was first produced in 1950) became available under various names (including Focalin, Concerta, Metadate, and Methylin); it remains one of the most widely prescribed medications for ADHD. Initially the drug was used to treat narcolepsy, chronic fatigue, depression, and to counter the sedating effects of other medications. The drug began to be used for ADHD in the 1960s and steadily rose in use.[citation needed]

Psychiatry officially codified a condition called “hyperkinetic reaction of childhood” in 1968, displaying the psychoanalytical influences of that time. The name Attention Deficit Disorder (ADD) was first introduced in DSM-III, the 1980 edition. By 1987 – The DSM-IIIR was released changing the diagnosis to "Undifferentiated Attention Deficit Disorder." Further revisions to the DSM were made in 1994 – DSM-IV described three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination.[citation needed]

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. Current research indicates that up to 60% of children with ADHD carry their symptoms into adulthood. [68]

In 1975, pemoline (Cylert) was approved by the FDA for use in the treatment of ADHD. While an effective agent for managing the symptoms, the development of liver failure in 14 cases over the next 27 years would result in the manufacturer withdrawing this medication from the market. New delivery systems for medications were invented in 1999 that eliminated the need for multiple doses across the day or taking medication at school. These new systems include pellets of medication coated with various time-release substances to permit medications to dissolve hourly across an 8–12 hour period (Metadate CD, Adderall XR, Focalin XR) and an osmotic pump that extrudes a liquid methylphenidate sludge across an 8–12 hour period after ingestion (Concerta).[citation needed]

It has also been suggested that the disparities in diagnosis levels per capita between countries are affected by differences in knowledge and understanding of the condition. For example, more widespread knowledge and greater acceptance of the condition amongst both doctors and teaching professionals within a region will increase the likelihood of identification and subsequent diagnosis of the condition.[citation needed]

During 1996, ADHD accounted for at least 40% of child psychiatry references.[69]

In 2003, atomoxetine (Strattera) received the first FDA approval for a nonstimulant drug to be used specifically for ADHD. In 2007, lisdexamfetamine (Vyvanse) becomes the first prodrug to receive FDA approval for ADHD. The landmark study of 1999 – The largest study of treatment for ADHD in history – is published in the American Journal of Psychiatry. Known as the Multimodal Treatment Study of ADHD (MTA Study), it involved more than 570 children with ADHD at 6 sites in the United States and Canada randomly assigned to 4 treatment groups. Results generally showed that medication alone was more effective than psychosocial treatments alone, but that their combination was beneficial for some subsets of ADHD children beyond the improvement achieved only by medication. More than 40 studies have subsequently been published from this massive dataset.[citation needed]

Cultural aspects

People talk about ADHD in 5 different ways:

  • appropriating the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) descriptors;
  • schools as identity-construction sites
  • resistance: biology versus moral culpability
  • alternative solutions to a real problem
  • relief and hope in naming experience

[70]

Another study looked at Colombian and Castillejos, Zambales schoolchildren to examine whether ADHD is merely a cultural phenomenon, or a cultural phenomenon with a biological basis. The authors conclude: “If ADHD were explicable as a culturally formulated psychiatric phenomenon, then it would be predicted that the same hyperactive and inattentive behaviors displayed in different cultural contexts would be associated with differing degrees of harmful dysfunction. In this study we found that children's hyperactive and inattentive behavior were similarly expressed in diverse populations and systematically related to children's social and academic wellbeing across those varied cultural contexts.” [71] This study was later criticized for assuming a homogenous culture for the United States population, failing to mention the socioeconomic backgrounds of the populations, and using two study populations that share European cultural origins.[72]

Concerns and alternative theories

Main article: Attention-deficit hyperactivity disorder controversies

Attention-deficit hyperactivity disorder (ADHD) hold the distinction of being one of the most controversial pediatric disorders.[73]Despite being well-validated Attention deficit–hyperactivity disorder (ADHD) is a controversial diagnosis. [74] Many professionals have concerns about the effects of an ADHD diagnosis on the mental state of patients and its effects on self-esteem.[75][76] There is disagreement over the cause of ADHD and there are questions about research methodologies [77], and skepticism toward its classification as a mental disorder. [78] Social critics point to changing standards of diagnosis [citation needed], such as the American Academy of Pediatrics (AAP) issuing a more careful set of standards in 2000 to aid clinicians than merely using DSM-IV.[79]

Concern exists that "elevated but still developmentally normal levels of motor activity, impulsiveness, or inattention" traits of childhood could be inappropriately interpreted as ADHD.[80] The National Institute of Mental Health states that, "stimulant drugs, when used with medical supervision, are usually considered quite safe."[81] Some parents and professionals have raised questions about the side effects of drugs and their long term use.[82] Calls for greater scrutiny are made by some news sources, social critics, religions, and medical professionals. Ethical and legal issues with regard to treatment have been key areas of concern for these critics. "Alternative theory" critics contend that the symptoms of ADHD can be better explained by the Hunter vs. farmer theory or Neurodiversity. Fringe critics question if ADHD exists at all as a disorder social construct theory of ADHD. Fringe critics question if ADHD exists at all as a disorder. Scientologists and certain factions of the Antipsychiatry movement are against almost all aspects of psychiatric practice, and are highly skeptical that the diagnosis denotes a genuine impairment. (Conversely, those critical of Scientology believe that much of the controversy generated about ADHD is manufactured).

Concerns about the impact of labeling

Parents could be concerned that telling children they have a brain disorder could possibly harm their self-esteem. Dr. Russell Barkley believes labeling is a double-edged sword; there are many pitfalls to labeling but that by using a precise label, services can be accessed. He also believes that labeling can help the individual understand and make an informed decision how best to deal with the disorder using evidence based knowledge.[83] Furthermore studies also show that the education of the siblings and parents has at least a short term impact on the outcome of treatment. [49] Dr. Russell Barkley states this about ADHD rights: "..because of various legislation that has been passed to protect them. There are special education laws with the Americans with Disabilities Act, for example, mentioning ADHD as an eligible condition. If you change the label, and again refer to it as just some variation in normal temperament, these people will lose access to these services, and will lose these hard-won protections that keep them from being discriminated against. . . ."[83] Psychiatrist Harvey Parker, who founded CHAAD, states, "we should be celebrating the fact that school districts across the country are beginning to understand and recognize kids with ADHD, and are finding ways of treating them. We should celebrate the fact that the general public doesn't look at ADHD kids as "b-a-d" kids, as brats, but as kids who have a problem that they can overcome".[84]

Social critics believe that this knowledge can effectively become a self-fulfilling prophecy mainly through self-doubt. Dr. Thomas Armstrong states that the ADHD label is a "tragic decoy" which severely erodes the potential to see the best in a child [85]. Armstrong is a proponent of the idea that there are many types of "smarts" and has adopted the term neurodiversity (first used by autistic rights activists) as an alternative, less damaging, label [86]. Thom Hartmann has said that the brain disorder label is "a pretty wretched label for any child to have to bear."[87]

Hunter vs. farmer theory of ADHD

Main article: Hunter vs. farmer theory

The hunter vs. farmer theory is a hypothesis proposed by Thom Hartmann, a radio host, about the origins of attention-deficit hyperactivity disorder (ADHD). He believes that these conditions may be a result of adaptive behavior of the species. His theory believes that those with ADHD retained some of the older hunter characteristics.

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 as any other human difference. Social critics argue that while biological factors may obviously play a large role in difficulties sitting still and/or concentrating on schoolwork in some children, for a variety of reasons they have failed to integrate into the social expectations that others have of them. [88]

Social construct theory of ADHD

Main article: Social construct theory of ADHD

Social critics question whether 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 disorder exists and that the behaviour observed is not abnormal and can be better explained by environmental causes or just the personality of the "patient."

See also

General

Related disorders

Controversy

References

  1. ^ Katragadda S, Schubiner H (2007). "ADHD in children, adolescents, and adults". Prim. Care. 34 (2): 317–41, abstract viii. doi:10.1016/j.pop.2007.04.012. PMID 17666230. {{cite journal}}: Unknown parameter |month= ignored (help)
  2. ^ a b 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ a b c d e f "Evaluation and diagnosis of attention deficit hyperactivity disorder in children". Uptodate. December 5, 2007. Retrieved 2008-09-12.
  4. ^ "Diagnostic and Statistical Manual of American Psychiatric Association, 2000". 2000. Retrieved 2008-09-11.
  5. ^ Dulcan M (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. {{cite journal}}: Unknown parameter |month= ignored (help)
  6. ^ a b c d "What is the evidence for using CNS stimulants to treat ADHD in children?". March - May 2008. Retrieved 2008-09-10. {{cite web}}: Check date values in: |date= (help)
  7. ^ Elia J, Ambrosini PJ, Rapoport JL (1999). "Treatment of attention-deficit-hyperactivity disorder". N. Engl. J. Med. 340 (10): 780–8. PMID 10072414. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Gentile, Julie. "Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management". Psychiatry. 3 (8): 24–30. Retrieved 2008-09-11. {{cite journal}}: Cite has empty unknown parameters: |month= and |coauthors= (help)
  9. ^ Hechtman L (1996). "Families of children with attention deficit hyperactivity disorder: a review". Can J Psychiatry. 41 (6): 350–60. PMID 8862854. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ "Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder". Pediatrics. 108 (4): 1033–44. 2001. PMID 11581465. {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Foreman DM (2006). "Attention deficit hyperactivity disorder: legal and ethical aspects". Arch. Dis. Child. 91 (2): 192–4. doi:10.1136/adc.2004.064576. PMID 16428370. {{cite journal}}: Unknown parameter |month= ignored (help)
  13. ^ a b c d "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Barkley, Russell. Retrieved 2008-09-19.
  14. ^ Brain Matures A Few Years Late In ADHD, But Follows Normal Pattern
  15. ^ "LONI: Laboratory of Neuro Imaging". Retrieved 2008-09-19.
  16. ^ "Attention Deficit Hyperactivity Disorder (ADHD)". National Institute of Mental Health. April 3, 2008. Retrieved 2008-09-12.
  17. ^ Caron, Samuel R., Ph.D. A Short Introduction to ADHD. adhd1.net. Retrieved on 2008-07-01.
  18. ^ Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26.
  19. ^ 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
  20. ^ 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
  21. ^ 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
  22. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ "Mental Health: A report of the surgeon general". 1999. Retrieved 2008-09-15.
  25. ^ 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". J Dev Behav Pediatr. 25 (6): 423–34. PMID 15613992. {{cite journal}}: Unknown parameter |month= ignored (help)
  26. ^ Benton D (2008). "Sucrose and behavioral problems". Crit Rev Food Sci Nutr. 48 (5): 385–401. doi:10.1080/10408390701407316. PMID 18464029. {{cite journal}}: Unknown parameter |month= ignored (help)
  27. ^ "Attention Deficit Hyperactivity Disorder". April 3, 2008. Retrieved 2008-09-19.
  28. ^ Frölich J, Döpfner M (2008). "[The treatment of Attention-Deficit/Hyperactivity Disorders with polyunsaturated fatty acids - an effective treatment alternative?]". Z Kinder Jugendpsychiatr Psychother (in German). 36 (2): 109–16. doi:10.1024/1422-4917.36.2.109. PMID 18622940. {{cite journal}}: Unknown parameter |month= ignored (help)
  29. ^ Johnson M, Ostlund S, Fransson G, Kadesjö B, Gillberg C. (2008 Apr 30). "Omega-3/Omega-6 Fatty Acids for Attention Deficit Hyperactivity Disorder: A Randomized Placebo-Controlled Trial in Children and Adolescents". J Atten Disord. PMID 18448859. {{cite journal}}: Check date values in: |year= (help)CS1 maint: multiple names: authors list (link)
  30. ^ Template:PDFlink
  31. ^ Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
  32. ^ "Evaluation and diagnosis of attention deficit hyperactivity disorder in children". December 5, 2007. Retrieved 2008-09-15.
  33. ^ Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern NIMH Press Release, November 12, 2007
  34. ^ Gene Predicts Better Outcome as Cortex Normalizes in Teens with ADHD NIMH Press Release, August 6, 2007
  35. ^ 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
  36. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ a b Zametkin AJ, Nordahl TE, Gross M, et al. "Cerebral glucose metabolism in adults with hyperactivity of childhood onset." N Engl J Med. 1990 November 15;323(20):1361–6. PMID 2233902
  40. ^ Zametkin AJ, Liebenauer LL, Fitzgerald GA,, et al. "Brain metabolism in teenagers with attention-deficit hyperactivity disorder." Arch Gen Psychiatry.. 1993 May 50;333(5). PMID 2233902
  41. ^ Joughin C, Ramchandani P, Zwi M (2003). "Attention-deficit/hyperactivity disorder". Am Fam Physician. 67 (9): 1969–70. PMID 12751659. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  42. ^ a b ICD Version 2006: F91. World Health Organization. Retrieved on December 11, 2006.
  43. ^ Perrin JM, Stein MT, Amler RW, Blondius TA. 2001. "Clinical practice guideline: treatment of school-aged children with Attention Deficit/Hyperactivity Disorder". Pediatrics 108 (4):1033-1044. PMID 11581465
  44. ^ Attention-Deficit/Hyperactivity Disorder. Psychiatry Online. Retrieved on 2007-08-13.
  45. ^ Jensen, PS. Exploring the Neurocircuitry of the Brain and Its Impact on Treatment Selections in ADD. Medscape. Retrieved on 2007-08-13.
  46. ^ 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.
  47. ^ Lamminmäky T ; et al. (1995). "Attention deficit hyperactivity disorder subtypes: Are there differences in academic problems?". Dev neuropsychology (11): 297–310. {{cite journal}}: Explicit use of et al. in: |author= (help)
  48. ^ "Family therapy for attention-deficit disorder or attention-deficit/hyperactivity disorder in children and adolescents". The Cochrane Collaboration. April 20. 2005. Retrieved 2008-09-19. {{cite web}}: Check date values in: |date= (help)
  49. ^ a b c Practice Parameter for the Assessment and Treatment of Children and Adolescents With Attention-Deficit/Hyperactivity Disorder http://www.aacap.org/galleries/PracticeParameters/JAACAP_ADHD_2007.pdf
  50. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)
  51. ^ King S, Griffin S, Hodges Z; et al. (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. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  52. ^ Brown RT, Amler RW, Freeman WS; et al. (2005). "Treatment of attention-deficit/hyperactivity disorder: overview of the evidence". Pediatrics. 115 (6): e749–57. doi:10.1542/peds.2004-2560. PMID 15930203. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  53. ^ Schachter HM, Pham B, King J, Langford S, Moher D (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. PMC 81663. PMID 11762571. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  54. ^ Nissen SE (2006). "ADHD drugs and cardiovascular risk". N. Engl. J. Med. 354 (14): 1445–8. doi:10.1056/NEJMp068049. PMID 16549404. {{cite journal}}: Unknown parameter |month= ignored (help)
  55. ^ "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. 2008. doi:10.1097/DBP.0b013e31318185dc14. PMID 18698199. {{cite journal}}: Unknown parameter |month= ignored (help)
  56. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)
  57. ^ Elia J, Ambrosini PJ, Rapoport JL (1999). "Treatment of attention-deficit-hyperactivity disorder". N. Engl. J. Med. 340 (10): 780–8. PMID 10072414. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  58. ^ Gentile, Julie. "Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management". Psychiatry. 3 (8): 24–30. Retrieved 2008-09-11. {{cite journal}}: Cite has empty unknown parameters: |month= and |coauthors= (help)
  59. ^ Template:PDFlink
  60. ^ Cimera, Robert (2002). Making ADHD a gift: teaching Superman how to fly. Lanham, Maryland: Scarecrow Press, Inc. pp. pg. 116. ISBN 0810843188. {{cite book}}: |pages= has extra text (help)
  61. ^ [http://www.census.gov/Press-Release/www/releases/archives/education/004214.html College Degree Nearly Doubles Annual Earnings, Census Bureau Reports] U.S. Census Bureau March 28, 2005. Retrieved on 2008-08-02.
  62. ^ Template:PDFlink. Centers for Disease Control (March, 2004). Retrieved on December 11, 2006.
  63. ^ Staller J, Faraone SV. (2006) "Attention-deficit hyperactivity disorder in girls: epidemiology and management." CNS Drugs. 2006;20(2):107–23. PMID 16478287
  64. ^ Biederman J, Faraone SV. (2004) "The Massachusetts General Hospital studies of gender influences on attention-deficit/hyperactivity disorder in youth and relatives." Psychiatr Clin North Am. Jun;27(2):225–32. PMID 15063995
  65. ^ What is ADHD? ADHD.org.nz. Retrieved on 2007-08-13.
  66. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008-1012
  67. ^ Charles Bradley, M.D., 1902–1979, retrieved September 15, 2008. American Journal of Psychiatry, 155:968
  68. ^ What is Adult ADD?
  69. ^ Castellanos FX, Giedd JN, Marsh WL, et al. (1996). "Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder". Archives of General Psychiatry, 53, 607–616. PMID 14765004
  70. ^ Danforth, Scot (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. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  71. ^ Brewis, Alexandra (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. {{cite journal}}: |access-date= requires |url= (help); Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  72. ^ Caldararo, Niccolo (2002-03). "Comment on Brewis et al". American Anthropologist. 104 (1): 282–283. doi:10.1525/aa.2002.104.1.282. {{cite journal}}: |access-date= requires |url= (help); Check date values in: |date= (help); Cite has empty unknown parameter: |coauthors= (help)
  73. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  74. ^ Foreman DM (2006). "Attention deficit hyperactivity disorder: legal and ethical aspects". Arch. Dis. Child. 91 (2): 192–4. doi:10.1136/adc.2004.064576. PMID 16428370. {{cite journal}}: Unknown parameter |month= ignored (help)
  75. ^ name="Tim&Rad"
  76. ^ Article for Ethical Human Sciences and Services
  77. ^ http://www.psychminded.co.uk/news/news2006/feb06/Disordered%20thinking.htm Comment by James, Adam, “Disordered thinking?” Psychminded 14 Feb. 2006.
  78. ^ name="Tim&Rad">Timimi, Sami & Radcliffe, Nick. “The Rise and Rise of ADHD.” Making and Breaking Children's Lives. Ed. Craig Newnes. Ross-on-Wye: PCCS Books, 2005. 63-70.
  79. ^ PBS - frontline: medicating kids: adhd: american academy of pediatrics' guidelines
  80. ^ Lakhan SE, Hagger-Johnson GE (2007). "The impact of prescribed psychotropics on youth". Clin Pract Epidemol Ment Health. 3: 21. doi:10.1186/1745-0179-3-21. PMC 2100041. PMID 17949504.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  81. ^ NIMH · ADHD · The Treatment of ADHD
  82. ^ 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).
  83. ^ a b PBS - frontline: medicating kids: interviews: russell barkley
  84. ^ PBS - frontline: medicating kids: interviews: harvey parker
  85. ^ Myth of ADD
  86. ^ Special Education and the Concept of Neurodiversity
  87. ^ Hartmann Interview
  88. ^ Rethinking ADHD >> Palgrave.com : Title Page

Further reading

  • Barkley, Russell A. Take Charge of ADHD: The Complete Authoritative Guide for Parents (2005) New York: Guilford Publications.
  • Conrad, Peter Identifying Hyperactive Children (Ashgate, 2006).
  • Crawford, Teresa I'm Not Stupid! I'm ADHD!
  • Green, Christopher, Kit Chee, Understanding ADD; Doubleday 1994; ISBN 0-86824-587-9
  • Hanna, Mohab. (2006) Making the Connection: A Parent's Guide to Medication in AD/HD, Washington D.C.: Ladner-Drysdale.
  • Kelly, Kate, Peggy Ramundo. (1993) You Mean I'm Not Lazy, Stupid or Crazy?! A Self-Help Book for Adults with Attention deficit Disorder. ISBN 0-684-81531-1
  • Matlen, Terry. (2005) "Survival Tips for Women with AD/HD". ISBN 1886941599
  • Ninivaggi, F.J. "Attention-Deficit/Hyperactivity Disorder in Children and Adolescents: Rethinking Diagnosis and Treatment Implications for Complicated Cases", Connecticut Medicine. September 1999; Vol. 63, No. 9, 515-521. PMID 10531701

External links

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