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Attention deficit hyperactivity disorder
Attention deficit hyperactivity disorder
Specialty	Psychiatry, child and adolescent psychiatry

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Attention-Deficit Hyperactivity Disorder (ADHD) is a neurobehavioral^[1] developmental disorder^[2]affecting about 3-5% of the world's population.^[3] It typically presents during childhood, and is characterized by a persistent pattern of impulsiveness and inattention, with or without a component of hyperactivity.^[4] ADHD occurs twice as commonly in boys as in girls.^[5] ADHD is generally a chronic^[6] disorder with 10 to 60% of individuals diagnosed in childhood continuing to meet diagnostic criteria in adulthood.^[7]^[8] As they mature, adolescents and adults with ADHD are likely to develop coping mechanisms to compensate for their impairment.^[9]

Though previously regarded as a childhood diagnosis, studies completed during the last few decades have shown that ADHD often continues throughout adulthood - though generally with a reduction in hyperactivity. ADHD has a strong genetic component.^[10] 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.^[11] Long term safety of stimulants however has not been determined^[7] and drug treatment of pre-school children is not recommended.^[12]

ADHD is one of the most controversial psychiatric disorders.^[13]^[14]^[15] The controversy involving clinicians, teachers, policymakers, parents, and the media with opinions regarding ADHD ranging from those who do not believe it exists to those who believe that there is genetic and physiological basis for the condition.^[16]

Classification

ADHD is best seen as the extreme of a continuous trait that is found throughout the population. ^[12] It 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^[17]. Using magnetic resonance imaging, this developmental lag has been estimated to range from 3 to 5 years in the prefrontal cortex.^[18]. These delays are considered to cause impairment. ADHD has also been classified as a behavior disorder and a neurological disorder. ^[19]

Symptoms

The most common symptoms of ADHD are^[20]^[21]:

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 some 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.^[21]
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.^[21]
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.^[21]
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.^[21]

Although the reasons are not clear, it has long been observed (and is not controversial) that many children seem to "outgrow" ADHD. These individuals include those with and without various combinations of medication and/or therapy, although both have proven generally effective and safe in easing symptoms and reducing impairment. It is also known that many adolescents and adults develop coping skills as they mature to offset impairments. An individual's development of helpful coping skills may be enhanced by therapy, but also may result with or without conscious effort of the individual.

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.^[22]

Genetic factors

Twin studies indicate that the disorder is highly heritable and that genetics cause about 75% of ADHD cases.^[17] Hyperactivity also seems to be primarily a genetic condition however other causes do have an effect.^[23]

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),^[24] the 10-repeat allele of the DAT1 gene,^[25] the 7-repeat allele of the DRD4 gene,^[25] and the dopamine beta hydroxylase gene (DBH TaqI).^[26]

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.^[27]

Environmental factors

Twin studies to date have suggested that approximately 9-20 percent of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be attributed to such nonshared environmental (nongenetic) factors.^[28]

Environmental factors implicated include alcohol and tobacco smoke exposure during pregnancy and lead exposure after birth.^[29] 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. ^[30]

Diet

A systematic review found that removing artificial food coloring had a small effect size on ADHD symptoms.^[31] Evidence however shows that sucrose (sugar) has no effect on behavior.^[32]^[33]

Preliminary evidence suggests that Omega-3/Omega-6 supplementation reduces ADHD symptoms.^[34]^[35]

Social factors

There is no compelling evidence that social factors alone can cause ADHD.^[17] 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,^[36] while other researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse.^[37] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

Alternative theories

Hunter vs. farmer theory of ADHD

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.^{[citation needed]}

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. ^[38]

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."^[12]

Neurobiological mechanisms

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 by Dr. Alan Zametkin that produced these images is still not definitive.^[39]^[40]^[41]

The pathophysiology of ADHD is unclear and there are a number of competing theories.^[42]

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.^[43]

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.^[44]

Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity),^[45] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. ^[46]^[47] 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.^[48]

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.

An early PET scan study found that global cerebral glucose metabolism was 8% 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. The regions with the greatest deficit of activity included the premotor cortex and the superior prefrontal cortex.^[49] The significance of the research by Dr. Alan Zametkin that produced these images is still not definative.^[50]^[51]^[52]

Diagnosis

No objective test exists to make a diagnosis of ADHD. It thus remains a clinical diagnosis.^[53]

In North America, the DSM-IV criteria are often the basis for a diagnosis while European countries usually use the ICD-10.^[54]

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:

ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
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:

Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
Often has trouble keeping attention on tasks or play activities.
Often does not seem to listen when spoken to directly.
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).
Often has trouble organizing activities.
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).
Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
Is often easily distracted.
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:

Often fidgets with hands or feet or squirms in seat.
Often gets up from seat when remaining in seat is expected.
Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless).
Often has trouble playing or enjoying leisure activities quietly.
Is often "on the go" or often acts as if "driven by a motor".
Often talks excessively.

Impulsiveness:

Often blurts out answers before questions have been finished.
Often has trouble waiting one's turn.
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).

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^[55]) 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".^[55]

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:^[56]

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 patients history given by the parents, teachers and/or the patient.

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.^{[citation needed]} 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.^{[citation needed]}

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.^[57] 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.^[58]

Common comorbid conditions are Oppositional Defiance Disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder.^[59] Learning disorders are more common when there are inattention symptoms.^[60]

Management

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

Behavioral interventions

Many believe that concepts such as, self-regulatin, self-monitoring, and effortful control are at the center of the functional impairments regarding ADHD. There are Cognitive-Behavioral interventions designed to improve these areas and boost self-efficacy, social competence, and emotional control, which can affect attention and self-regulation. One such program is the Challenge Software Program. This program uses media in the form of interactive videos and games to grab and hold an inattentive child's attention and engage them in the process quickly. The program also offers measurable Pre and Post outcomes to illustrate improvement.

Family therapy has shown little benefit in the treatment of ADHD.^[61] Education to help parents understand ADHD have shown short term benefits.^[62]

Pharmacological treatment

Stimulant medications are the most clinically and cost effective method of treating ADHD. ^[62]^[63] No significant differences between the various drugs in terms of efficacy or side effects has been found.^[64]^[65] About 70% of children improve after being treated with stimulants.^[66] Medications, however, are not recommended for pre-school children with ADHD.^[67]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.^[68]

Long term safety, however, has not been determined. There are no randomized controlled trials assessing the harms or benefits of treatment beyond two years.^[7] 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.^[69] The FDA has added black box warning to some ADHD medications.^[70] Amphetamines ( Adderall ) has warnings about potential for abuse, drug dependence, and sudden death.^[71]

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.^[72]

Support groups

In the UK, the Hyperactive Children's Support Group (HACSG) ^[73] is a registered charity which aims to help ADHD/Hyperactive children and their families. The HACSG is a proponent of a dietary approach to the problem of hyperactivity.

Prognosis

ADHD diagnosed in childhood resolves in 40 to 90% of individuals by the time they reach adulthood.^[7]^[74] Those affected are likely to develop coping mechanisms as they mature thus compensating for their previous ADHD. ^[75]

37% of those with ADHD do not get a high school diploma even though many of them will receive special education services.^[17] The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish high school.^[76] In the United States, less than 5% of individuals with ADHD get a college degree^[77] compared to 28% of the general population.^[78]

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 children in North America appearing to have a higher rate of ADHD than children in Africa and the Middle East.^[3] 10% of males and 4% of females have been diagnosed in the United States^[79] This difference between genders may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.^[80]^[81]

History

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/behavioural disabilities" and "hyperactivity". Some of these labels became problematic as knowledge expanded. For example, as they became aware that many children with no indication of brain damage also displayed the syndrome, the label which included the words "brain damage" didn't seem appropriate.

The DSM-II in 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 basically unchanged).^[82]

Under the DSM-IV, within the ADHD syndrome, there are three sub-types, including one which lacks the hyperactivity component.^[83] 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.

Hippocrates, Shakespeare

Researchers speculate that earlier references to the condition as mentioned in the examples below, have been made throughout history. ^{[citation needed]}

In 493 BCE, physician-scientist Hippocrates described a condition that seems to be compatible with what we now know as ADHD.^{[citation needed]} 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."^[84]

Russell Barkley ^[85] has argued that Shakespeare made reference to a "malady of attention" in King Henry VII, although the actual quote appears to come from King Henry IV, part II.

20th century

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.^{[citation needed]} Dr. 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.^[86] At the time it was commonly thought that inattention and lack of inhibitory control were the primary characteristics of the syndrome. ^[87]

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." ^[88]

Response to stimulant medication

The first reported evidence of stimulant medication used to treat children with concentration and hyperactivity problems came in 1937. ^[89] Dr. Charles Bradley in Providence, RI reported that a group of children with behavioral problems improved after being treated with the stimulant Benzedrine.^[90] 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]}

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]}

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]}

Adults

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. ^[91] 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. They often have such associated psychiatric comorbidities as depression, anxiety, bipolar disorder, substance abuse, or a learning disability. ^[92] 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. ^[93]

A diagnosis of ADHD may offer an adult insight into their behaviors and allow the patient to become more aware and seek help with coping and treatment strategies. ^[94] Studies show that adult ADHD is treated successfully with a combination of medication and behavior therapy.^[95]

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. 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.^[96] For adults, most treatments with medication and therapy are basically similar; a mature patient may more able to provide feedback and help self-direct the process.

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

^[97]

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.” ^[98] 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.^[99]

Controversies

Attention-deficit hyperactivity disorder (ADHD) "is a highly controversial pediatric disorder despite being a well validated clinical diagnosis".^[100]^[101] The controversy involving clinicians, teachers, policymakers, parents, and the media with opinions regarding ADHD ranging from those who do not believe it exists to those who believe that there is genetic and physiological basis for the condition.^[102] The controversy is discussed in depth in the Sept. 2008 UK publication of the NICE guidelines on ADHD.^[12]

Researchers from McMaster identified six 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.^[103]

The British Psychological Society states that: “The idea that children who don’t attend or who don’t sit still in school have a mental disorder is not entertained by most British clinicians.”^[104]

In the Harvard Review of Psychiatry, three authors from Departments of Political Science and Psychology at the University of California campuses in Richmond and Berkeley stated "ADHD is one of the most controversial psychiatric disorders, in part because it is also the most commonly diagnosed mental disorder among minors."^[105] There is concern about the effects of an ADHD diagnosis on the mental state and self-esteem of patients.^[106]^[107] There is disagreement over the cause of ADHD and there are questions about research methodologies ^[108], and skepticism toward its classification as a mental disorder. ^[106] 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.^[109]

Concern exists that "elevated but still developmentally normal levels of motor activity, impulsiveness, or inattention" traits of childhood could be inappropriately interpreted as ADHD.^[110] The National Institute of Mental Health states that, "stimulant drugs, when used with medical supervision, are usually considered quite safe."^[111] Some parents and professionals have raised questions about the side effects of drugs and their long term use.^[112] 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.

References

^ NINDS Attention Deficit-Hyperactivity Disorder Information Page. National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.
^ Dr. Russell A. Barkley Official Site, Authority ADHD, Attention Deficit Hyperactivity Disorder
^ ^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)
^ "Diagnostic and Statistical Manual of American Psychiatric Association, 2000". 2000. Retrieved 2008-09-11.
^ 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)
^ Van Cleave J, Leslie LK (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. {{cite journal}}: Unknown parameter |month= ignored (help)
^ ^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)
^ 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)
^ 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)
^ 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)
^ "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)
^ ^a ^b ^c ^d "CG72 Attention deficit hyperactivity disorder (ADHD): full guideline" (PDF). NHS. 24 September 2008. Retrieved 2008-10-08.
^ "Treatment of Attention-Deficit/Hyperactivity Disorder". US department of health and human services. 1999. Retrieved 2008-10-02. {{cite web}}: Unknown parameter |month= ignored (help)
^ 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)
^ Cohen, Donald J.; Cicchetti, Dante (2006). Developmental psychopathology. Chichester: John Wiley & Sons. ISBN 0-471-23737-X.{{cite book}}: CS1 maint: multiple names: authors list (link)
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^ ^a ^b ^c ^d "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Barkley, Russell. Retrieved 2008-09-19.
^ Brain Matures A Few Years Late In ADHD, But Follows Normal Pattern
^ "LONI: Laboratory of Neuro Imaging". Retrieved 2008-09-19.
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^ Caron, Samuel R., Ph.D. A Short Introduction to ADHD. adhd1.net. Retrieved on 2008-07-01.
^ Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26.
^ 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
^ ^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
^ 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
^ 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)
^ {Levy et al., 1997; Nigg, 2006; Sherman, Iacono et al., 1997; Silberg et al., 1996}
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^ 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)
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^ 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)
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^ 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)
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^ 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)
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^ "CG72 Attention deficit hyperactivity disorder (ADHD): NICE guideline" (PDF). NHS. 24 September 2008. Retrieved 2008-10-08.
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^ "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)
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External links

Attention-Deficit / Hyperactivity Disorder (ADHD) at the Center for Disease Control
The Challenge Software Program - Interactive Web-based Intervention for Children
Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder at NIH
National Institute of Mental Health on ADHD
Today Show segment on adult ADHD, June 5, 2008
Patient Voices: A.D.H.D , NYTimes.com

[autogenerated1-1] 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] Dr. Russell A. Barkley Official Site, Authority ADHD, Attention Deficit Hyperactivity Disorder

[Polanczyk-3] 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)

[DSM-IV-TR-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] Van Cleave J, Leslie LK (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. {{cite journal}}: Unknown parameter |month= ignored (help)

[TI2008-7] "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)

[8] 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)

[9] 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)

[10] 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)

[AAP2001-11] "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)

[NICE2008-12] "CG72 Attention deficit hyperactivity disorder (ADHD): full guideline" (PDF). NHS. 24 September 2008. Retrieved 2008-10-08.

[13] "Treatment of Attention-Deficit/Hyperactivity Disorder". US department of health and human services. 1999. Retrieved 2008-10-02. {{cite web}}: Unknown parameter |month= ignored (help)

[14] 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)

[15] Cohen, Donald J.; Cicchetti, Dante (2006). Developmental psychopathology. Chichester: John Wiley & Sons. ISBN 0-471-23737-X.{{cite book}}: CS1 maint: multiple names: authors list (link)

[16] "Treatment of Attention-Deficit/Hyperactivity Disorder". US department of health and human services. 1999. Retrieved 2008-10-02. {{cite web}}: Unknown parameter |month= ignored (help)

[BarkleyContEd-17] "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Barkley, Russell. Retrieved 2008-09-19.

[18] Brain Matures A Few Years Late In ADHD, But Follows Normal Pattern

[autogenerated4-19] "LONI: Laboratory of Neuro Imaging". Retrieved 2008-09-19.

[20] "Attention Deficit Hyperactivity Disorder (ADHD)". National Institute of Mental Health. April 3, 2008. Retrieved 2008-09-12.

[UTP2008-21] "Evaluation and diagnosis of attention deficit hyperactivity disorder in children". Uptodate. December 5, 2007. Retrieved 2008-09-12.

[22] Caron, Samuel R., Ph.D. A Short Introduction to ADHD. adhd1.net. Retrieved on 2008-07-01.

[23] Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26.

[dopamine-24] 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

[gene-25] Swanson JM, Flodman P, Kennedy J, et al. "Dopamine Genes and ADHD." Neurosci Biobehav Rev. 2000 Jan;24(1):21–5. PMID 10654656

[26] 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

[autogenerated2-27] 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)

[28] {Levy et al., 1997; Nigg, 2006; Sherman, Iacono et al., 1997; Silberg et al., 1996}

[pmid17185283-29] 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)

[30] "Mental Health: A report of the surgeon general". 1999. Retrieved 2008-09-15.

[31] 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)

[32] 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)

[33] "Attention Deficit Hyperactivity Disorder". April 3, 2008. Retrieved 2008-09-19.

[34] 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)

[Johnson08-35] 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)

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