Attention deficit hyperactivity disorder
|Attention deficit hyperactivity disorder|
Children with ADHD find it more difficult to focus and to complete their schoolwork.
|Classification and external resources|
|Patient UK||Attention deficit hyperactivity disorder|
Attention deficit hyperactivity disorder (ADHD, similar to hyperkinetic disorder in the ICD-10) is a developmental neuropsychiatric disorder in which there are significant problems with executive functions (e.g., attentional control and inhibitory control) that cause attention deficits, hyperactivity, or impulsiveness which is not appropriate for a person's age. These symptoms must begin by age six to twelve and persist for more than six months for a diagnosis to be made. In school-aged individuals inattention symptoms often result in poor school performance.
Despite being the most commonly studied and diagnosed psychiatric disorder in children and adolescents, the cause in the majority of cases is unknown. It affects about 6–7% of children when diagnosed via the DSM-IV criteria and 1–2% when diagnosed via the ICD-10 criteria. Rates are similar between countries and depend mostly on how it is diagnosed. ADHD is diagnosed approximately three times more in boys than in girls. About 30–50% of people diagnosed in childhood continue to have symptoms into adulthood and between 2–5% of adults have the condition. The condition can be difficult to tell apart from other disorders as well as that of high normal activity.
ADHD management usually involves some combination of counseling, lifestyle changes, and medications. Medications are only recommended as a first-line treatment in children who have severe symptoms and may be considered for those with moderate symptoms who either refuse or fail to improve with counseling. Long-term effects of medications are not clear and they are not recommended in preschool-aged children. Adolescents and adults tend to develop coping skills which make up for some or all of their impairments.
ADHD, its diagnosis, and its treatment have been considered controversial since the 1970s. The controversies have involved clinicians, teachers, policymakers, parents, and the media. Topics include ADHD's causes and the use of stimulant medications in its treatment. Most healthcare providers accept ADHD as a genuine disorder, and the debate in the scientific community mainly centers on how it is diagnosed and treated.
- 1 Signs and symptoms
- 2 Cause
- 3 Pathophysiology
- 4 Diagnosis
- 5 Management
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 Society and culture
- 10 Special populations
- 11 References
- 12 External links
Signs and symptoms
Inattention, hyperactivity (restlessness in adults), disruptive behavior, and impulsivity are common in ADHD. Academic difficulties are frequent as are problems with relationships. The symptoms can be difficult to define as it is hard to draw a line at where normal levels of inattention, hyperactivity, and impulsivity end and significant levels requiring interventions begin.
To be diagnosed per the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), symptoms must be observed in multiple settings for six months or more and to a degree that is much greater than others of the same age. They must also cause problems in the person's social, academic, or work life.
An individual with inattention may have some or all of the following symptoms:
- Be easily distracted, miss details, forget things, and frequently switch from one activity to another
- Have difficulty maintaining focus on one task
- Become bored with a task after only a few minutes, unless doing something enjoyable
- Have difficulty focusing attention on organizing and completing a task or learning something new
- Have trouble completing or turning in homework assignments, often losing things (e.g., pencils, toys, assignments) needed to complete tasks or activities
- Not seem to listen when spoken to
- Daydream, become easily confused, and move slowly
- Have difficulty processing information as quickly and accurately as others
- Struggle to follow instructions
An individual with hyperactivity may have some or all of the following symptoms:
- Fidget and squirm in their seats
- Talk nonstop
- Dash around, touching or playing with anything and everything in sight
- Have trouble sitting still during dinner, school, doing homework, and story time
- Be constantly in motion
- Have difficulty doing quiet tasks or activities
These hyperactivity symptoms tend to go away with age and turn into "inner restlessness" in teens and adults with ADHD.
An individual with impulsivity may have some or all of the following symptoms:
- Be very impatient
- Blurt out inappropriate comments, show their emotions without restraint, and act without regard for consequences
- Have difficulty waiting for things they want or waiting their turns in games
- Often interrupt conversations or others' activities
People with ADHD more often have difficulties with social skills, such as social interaction and forming and maintaining friendships. This is true for all subtypes. About half of children and adolescents with ADHD experience social rejection by their peers compared to 10–15% of non-ADHD children and adolescents. People with ADHD have attention deficits which cause difficulty processing verbal and nonverbal language which can negatively affect social interaction. They also may drift off during conversations, and miss social cues.
Difficulties managing anger are more common in children with ADHD as are poor handwriting and delays in speech, language and motor development. Although it causes significant impairment, particularly in modern society, many children with ADHD have a good attention span for tasks they find interesting.
In children ADHD occurs with other disorders about ⅔ of the time. Some of the commonly associated conditions include:
- Learning disabilities have been found to occur in about 20–30% of children with ADHD. Learning disabilities can include developmental speech and language disorders and academic skills disorders. ADHD, however, is not considered a learning disability, but it very frequently causes academic difficulties.
- Oppositional defiant disorder (ODD) and conduct disorder (CD), which occur with ADHD in about 50% and 20% of cases respectively. They are characterized by antisocial behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, and stealing. About half of those with hyperactivity and ODD or CD develop antisocial personality disorder in adulthood. Brain imaging supports that conduct disorder and ADHD are separate conditions.
- Primary disorder of vigilance, which is characterized by poor attention and concentration, as well as difficulties staying awake. These children tend to fidget, yawn and stretch and appear to be hyperactive in order to remain alert and active.
- Hypokalemic sensory overstimulation is present in less than 50% of people with ADHD and may be the molecular mechanism for many people with ADHD.
- Mood disorders (especially bipolar disorder and major depressive disorder). Boys diagnosed with the combined ADHD subtype are more likely to have a mood disorder. Adults with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions.
- Anxiety disorders have been found to occur more commonly in the ADHD population.
- Obsessive-compulsive disorder (OCD) can co-occur with ADHD and shares many of its characteristics.
- Substance use disorders. Adolescents and adults with ADHD are at increased risk of developing a substance use problem. This is most commonly with alcohol or cannabis. The reason for this may be an altered reward pathway in the brains of ADHD individuals. This makes the evaluation and treatment of ADHD more difficult, with serious substance misuse problems usually treated first due to their greater risks.
- Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron deficiency anaemia. However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders.
- Sleep disorders and ADHD commonly co-exist. They can also occur as a side effect of medications used to treat ADHD. In children with ADHD, insomnia is the most common sleep disorder with behavioral therapy the preferred treatment. Problems with sleep initiation are common among individuals with ADHD but often they will be deep sleepers and have significant difficulty getting up in the morning. Melatonin is sometimes used in children who have sleep onset insomnia.
There is an association with persistent bed wetting, language delay, and developmental coordination disorder (DCD), with about half of people with DCD having ADHD. The language delay in people with ADHD can include problems with auditory processing disorders such as short-term auditory memory weakness, difficulty following instructions, slow speed of processing written and spoken language, difficulties listening in distracting environments e.g. the classroom, and weakness in reading comprehension.
The cause of most cases of ADHD is unknown; however, it is believed to involve interactions between genetic and environmental factors. Certain cases are related to previous infection of or trauma to the brain.
Twin studies indicate that the disorder is often inherited from one's parents with genetics determining about 75% of cases. Siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder. Genetic factors are also believed to be involved in determining whether or not ADHD persists into adulthood.
Typically a number of genes are involved, many of which directly affect dopamine neurotransmission. Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH. Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF. A common variant of a gene called LPHN3 is estimated to be responsible for about 9% of cases and when this gene is present, people are particularly responsive to stimulant medication.
As ADHD is common, natural selection likely favored the traits, at least individually, and they may have provided a survival advantage. For example, some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to ADHD in the gene pool. As it is more common in children of anxious or stressed mothers, some argue that ADHD is an adaptation that helps children face a stressful or dangerous environment with, for example, increased impulsivity and exploratory behavior.
Hyperactivity might have been beneficial, from an evolutionary perspective, in situations involving risk, competition, or unpredictable behavior (i.e. exploring new areas or finding new food sources). In these situations, ADHD could have been beneficial to society as a whole even while being harmful to the individual. Additionally, in certain environments it may have offered advantages to the individuals themselves, such as quicker response to predators or superior hunting skills.
Environmental factors are believed to play a lesser role. Alcohol intake during pregnancy can cause fetal alcohol spectrum disorder which can include symptoms similar to ADHD. Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD. Many children exposed to tobacco do not develop ADHD or only have mild symptoms which do not reach the threshold for a diagnosis. A combination of a genetic predisposition with tobacco exposure may explain why some children exposed during pregnancy may develop ADHD and others do not. Children exposed to lead, even low levels, or polychlorinated biphenyls may develop problems which resemble ADHD and fulfill the diagnosis. Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.
Very low birth weight, premature birth and early adversity also increase the risk as do infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella, rubella, enterovirus 71) and streptococcal bacterial infection. At least 30% of children with a traumatic brain injury later develop ADHD and about 5% of cases are due to brain damage.
A small number of children may react negatively to food dyes or preservatives. It is possible that certain food coloring may act as a trigger in those who are genetically predisposed but the evidence is weak.:452 The United Kingdom and European Union have put in place regulatory measures based on these concerns; the FDA has not.
The diagnosis of ADHD can represent family dysfunction or a poor educational system rather than an individual problem. Some cases may be explained by increasing academic expectations, with a diagnosis being a method for parents in some countries to get extra financial and educational support for their child. The youngest children in a class have been found to be more likely to be diagnosed as having ADHD possibly due to their being developmentally behind their older classmates. Behavior typical of ADHD occurs more commonly in children who have experienced violence and emotional abuse.
Per social construction theory it is societies that determine the boundary between normal and abnormal behavior. Members of society, including physicians, parents, and teachers, determine which diagnostic criteria are used and, thus, the number of people affected. This leads to the current situation where the DSM-IV arrives at levels of ADHD three to four times higher than those obtained with the ICD 10. Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and not discovered."
Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine. The dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes. The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum (particularly, the nucleus accumbens) are directly responsible for modulating executive function (cognitive control of behavior), motivation, and reward perception; these pathways are known to play a central role in the pathophysiology of ADHD. Larger models of ADHD with additional pathways have been proposed.
In children with ADHD there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex. The posterior parietal cortex also shows thinning in ADHD individuals compared to controls. Other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without ADHD.
Previously it was thought that the elevated number of dopamine transporters in people with ADHD was part of the pathophysiology but it appears that the elevated numbers are due to adaptation to exposure to stimulants. Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system. ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems. There may additionally be abnormalities in serotoninergic and cholinergic pathways. Neurotransmission of glutamate, a cotransmitter with dopamine in the mesolimbic pathway, seems to be also involved.
Executive function and motivation
ADHD symptoms involve a difficulty with executive functions. Executive function refers to a number of mental processes that are required to regulate, control, and manage daily life tasks. Some of these impairments include problems with organization, time keeping, excessive procrastination, concentration, processing speed, regulating emotions, and utilizing working memory. People usually have decent long-term memory. The criteria for an executive function deficit are met in 30–50% of children and adolescents with ADHD. One study found that 80% of individuals with ADHD were impaired in at least one executive function task, compared to 50% for individuals without ADHD. Due to the rates of brain maturation and the increasing demands for executive control as a person gets older, ADHD impairments may not fully manifest themselves until adolescence or even early adulthood.
ADHD has also been associated with motivational deficits in children. Children with ADHD find it difficult to focus on long-term over short-term rewards, and exhibit impulsive behavior for short-term rewards. In these individuals, a large amount of positive reinforcement effectively improves task performance. ADHD stimulants may improve persistence in ADHD children as well.
ADHD is diagnosed by an assessment of a person's childhood behavioral and mental development, including ruling out the effects of drugs, medications and other medical or psychiatric problems as explanations for the symptoms. It often takes into account feedback from parents and teachers with most diagnoses begun after a teacher raises concerns. It may be viewed as the extreme end of one or more continuous human traits found in all people. Whether someone responds to medications does not confirm or rule out the diagnosis. As imaging studies of the brain do not give consistent results between individuals, they are only used for research purposes and not diagnosis.
In North America, the DSM-IV or DSM-V criteria are often used for diagnosis, while European countries usually use the ICD-10. With the DSM-IV criteria a diagnosis of ADHD is 3–4 times more likely than with the ICD-10 criteria. It is classified as a psychiatric disorder of the neurodevelopmental disorder type. Additionally it is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder and antisocial personality disorder. A diagnosis does not imply a neurological disorder.
Associated conditions that should be screened for include anxiety, depression, oppositional defiant disorder, conduct disorder, and learning and language disorders. Other conditions that should be considered are other neurodevelopmental disorders, tics, and sleep apnea.
Diagnosis of ADHD using quantitative EEG is an ongoing area of investigation, although the value of EEG in ADHD is currently unclear. In the United States the Food and Drug Administration has approved the use of EEG to evaluate the morbidity of ADHD.
Diagnostic and Statistical Manual
As with many other psychiatric disorders, formal diagnosis is made by a qualified professional based on a set number of criteria. In the United States these criteria are defined by the American Psychiatric Association in the Diagnostic and Statistical Manual of Mental Disorders (DSM). Based on the DSM-criteria, there are three sub types of ADHD:
- ADHD predominantly inattentive type (ADHD-PI) presents with symptoms including being easily distracted, forgetful, daydreaming, disorganization, poor concentration, and difficulty completing tasks. Often people refer to ADHD-PI as "attention deficit disorder" (ADD), however, the latter has not been officially accepted since the 1994 revision of the DSM.
- ADHD, predominantly hyperactive-impulsive type presents with excessive fidgetiness and restlessness, hyperactivity, difficulty waiting and remaining seated, immature behavior; destructive behaviors may also be present.
- ADHD, combined type is a combination of the two other subtypes.
This subdivision is based on presence of at least six out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both. To be considered, the symptoms must have appeared by the age of six to twelve and occur in more than one environment (e.g. at home and at school or work).[medical citation needed] The symptoms must be not appropriate for a child of that age and there must be evidence that it is causing social, school or work related problems.
Most children with ADHD have the combined type. Children with the inattention subtype are less likely to act out or have difficulties getting along with other children. They may sit quietly, but without paying attention resulting in the child difficulties being overlooked.[medical citation needed]
International Classification of Diseases
In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the signs of ADHD are given the name "hyperkinetic disorders". When a conduct disorder (as defined by ICD-10) 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.
Adults with ADHD are diagnosed under the same criteria, including that their signs must have been present by the age of six to twelve. Questioning parents or guardians as to how the person behaved and developed as a child may form part of the assessment; a family history of ADHD also adds weight to a diagnosis. While the core symptoms of ADHD are similar in children and adults they often present differently in adults than in children, for example excessive physical activity seen in children may present as feelings of restlessness and constant mental activity in adults.
|ADHD symptoms which may be related to other disorders|
Symptoms of ADHD such as low mood and poor self-image, mood swings, and irritability can be confused with dysthymia, cyclothymia or bipolar disorder as well as with borderline personality disorder. Some of the symptoms that are due to anxiety disorders, antisocial personality disorder, developmental disabilities or mental retardation or the effects of substance abuse such as intoxication and withdrawal can overlap with some ADHD. These disorders can also sometimes occur along with ADHD. Medical conditions which can cause ADHD type symptoms include: hyperthyroidism, seizure disorder, lead toxicity, hearing deficits, hepatic disease, sleep apnea, drug interactions, and head injury.
Primary sleep disorders may affect attention and behavior and the symptoms of ADHD may affect sleep. It is thus recommended that children with ADHD be regularly assessed for sleep problems. Sleepiness in children may result in symptoms ranging from the classic ones of yawning and rubbing the eyes, to impulsivity, hyperactivity, aggressiveness, mood swing and inattentiveness.[medical citation needed] Obstructive sleep apnea, can also cause ADHD type symptoms.
The management of ADHD typically involves counseling or medications either alone or in combination. While treatment may improve long-term outcomes it does not get rid of negative outcomes entirely.
Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants. They have at least some effect in about 80% of people. Dietary modifications may also be of benefit with evidence supporting free fatty acids and reduced exposure to food coloring. Removing other foods from the diet is not currently supported by the evidence.
There is good evidence for the use of behavioral therapies in ADHD and they are the recommended first line treatment in those who have mild symptoms or are preschool-aged. Psychological therapies used include: psychoeducational input, behavior therapy, cognitive behavioral therapy (CBT), interpersonal psychotherapy, family therapy, school-based interventions, social skills training, parent management training, and neurofeedback. Parent training and education have been found to have short-term benefits. There is little high quality research on the effectiveness of family therapy for ADHD, but the evidence that exists shows that it is similar to community care and better than a placebo. Several ADHD specific support groups exist as informational sources and may help families cope with ADHD.
Training in social skills, behavioral modification and medication may have some limited beneficial effects. The most important factor in reducing later psychological problems, such as major depression, criminality, school failure, and substance use disorders is formation of friendships with people who are not involved in delinquent activities.
Stimulant medications are the pharmaceutical treatment of choice and improve symptoms, at least in the short term. There are a number of non-stimulant medications, such as atomoxetine, bupropion, guanfacine, and clonidine that may be used as alternatives. There are no good studies comparing the various medications; however, they appear more or less equal with respect to side effects. Stimulants appear to improve academic performance while atomoxetine does not. There is little evidence on their effects on social behaviors. Medications are not recommended for preschool children, as the long-term effects in this age group are not known. The long-term effects of stimulants generally are unclear with one study finding benefit, another finding no benefit and a third finding evidence of harm. Magnetic resonance imaging studies suggest that long-term treatment with amphetamine or methylphenidate decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function of the right caudate nucleus. Atomoxetine, due to its lack of abuse potential, may be preferred in those who are at risk of abusing stimulant medication. Guidelines on when to use medications vary by country, with the United Kingdom's National Institute for Health and Care Excellence recommending use only in severe cases, while most United States guidelines recommend medications in nearly all cases.
While stimulants and atomoxetine are usually safe, there are side-effects and contraindications to their use. Stimulants may result in psychosis or mania; however, this is relatively uncommon. Regular monitoring has been recommended in those on long-term treatment. Stimulant therapy should be stopped from time to time to assess for continuing need for medication. Stimulant medications have the potential for abuse and dependence; several studies indicate that untreated ADHD is associated with elevated risk of substance abuse and conduct disorders. The use of stimulants appears to either reduce this risk or have no effect on it. The safety of these medications in pregnancy is unclear.
Zinc deficiency has been associated with inattentive symptoms and there is evidence that zinc supplementation can benefit children with ADHD who have low zinc levels. Iron, magnesium and iodine may also have an effect on ADHD symptoms. There is evidence of a modest benefit of omega 3 fatty acid supplementation, but it is not recommended in place of traditional medication.
An 8-year follow up of children diagnosed with ADHD (combined type) found that they often have difficulties in adolescence, regardless of treatment or lack thereof. In the US, less than 5% of individuals with ADHD get a college degree, compared to 28% of the general population aged 25 years and older. The proportion of children meeting criteria for ADHD drops by about half in the three years following the diagnosis and this occurs regardless of treatments used. ADHD persists into adulthood in about 30–50% of cases. Those affected are likely to develop coping mechanisms as they mature, thus compensating for their previous symptoms.
ADHD is estimated to affect about 6–7% of people aged 18 and under when diagnosed via the DSM-IV criteria. When diagnosed via the ICD-10 criteria rates in this age group are estimated at 1–2%. Children in North America appear to have a higher rate of ADHD than children in Africa and the Middle East; this is believed to be due to differing methods of diagnosis rather than a difference in underlying frequency. If the same diagnostic methods are used, the rates are more or less the same between countries. It is diagnosed approximately three times more often in boys than in girls. This difference between sexes may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.
Rates of diagnosis and treatment have increased in both the United Kingdom and the United States since the 1970s. This is believed to be primarily due to changes in how the condition is diagnosed and how readily people are willing to treat it with medications rather than a true change in how common the condition is. It is believed that changes to the diagnostic criteria in 2013 with the release of the DSM V will increase the percentage of people diagnosed with ADHD especially among adults.
Hyperactivity has long been part of the human condition. Sir Alexander Crichton describes "mental restlessness" in his book An inquiry into the nature and origin of mental derangement written in 1798. ADHD was first clearly described by George Still in 1902. The terminology used to describe the condition has changed over time and has included: in the DSM-I (1952) "minimal brain dysfunction", in the DSM-II (1968) "hyperkinetic reaction of childhood", in the DSM-III (1980) "attention-deficit disorder (ADD) with or without hyperactivity". In 1987 this was changed to ADHD in the DSM-III-R and the DSM-IV in 1994 split the diagnosis into three subtypes, ADHD inattentive type, ADHD hyperactive-impulsive type and ADHD combined type. These terms were kept in the DSM-V in 2013. Other terms have included "minimal brain damage" used in the 1930s.
The use of stimulants to treat ADHD was first described in 1937. In 1934, Benzedrine became the first amphetamine medication approved for use in the United States. Methylphenidate was introduced in the 1950s, and enantiopure dextroamphetamine in the 1970s.
Society and culture
ADHD and its diagnosis and treatment have been considered controversial since the 1970s. The controversies have involved clinicians, teachers, policymakers, parents and the media. Positions regarding ADHD range from believing it is simply the far end of a normal range of behavior to considering that it is the result of an underlying genetic condition. Other areas of controversy include the use of stimulant medications and specifically their use in children, as well as the method of diagnosis and the possibility of overdiagnosis. In 2012, the National Institute for Health and Care Excellence, while acknowledging the controversy, states that the current treatments and methods of diagnosis are based on the dominant view of the academic literature. In 2014, Keith Conners, one of the early advocates for recognition of the disorder, spoke out against overdiagnosis.
With widely differing rates of diagnosis across countries, states within countries, races, and ethnicities, some suspect factors other than the presence of the symptoms of ADHD are playing a role in diagnosis. Some sociologists consider ADHD to be an example of the medicalization of deviant behavior, or in other words, the turning of the previously non-medical issue of school performance into a medical one. Most healthcare providers accept ADHD as a genuine disorder, at least in the small number of people with severe symptoms. Among healthcare providers the debate mainly centers on diagnosis and treatment in the much larger number of people with less severe symptoms.
As of 2009[update], 8% of all United States Major League Baseball players had been diagnosed with ADHD, making the disorder common among this population. The increase coincided with the League's 2006 ban on stimulants, which has raised concern that some players are mimicking or falsifying the symptoms or history of ADHD to get around the ban on the use of stimulants in sport.
A number of notable individuals have given controversial statements regarding ADHD. Tom Cruise has referred to the medications Ritalin and Adderall as "street drugs". Ushma S. Neill criticized this view, stating that the doses of stimulants used in the treatment of ADHD do not cause addiction and that there is some evidence of a reduced risk of later substance addiction in children treated with stimulants. In England, Susan Greenfield spoke out publicly in 2007 in the House of Lords about the need for a wide-ranging inquiry into the dramatic increase in the diagnosis of ADHD in the UK and possible causes. Her comments followed a BBC Panorama program that highlighted research that suggested medications are no better than other forms of therapy in the long term. In 2010, the BBC Trust criticized the 2007 BBC Panorama program for summarizing the research as showing "no demonstrable improvement in children's behavior after staying on ADHD medication for three years" when in actuality "the study found that medication did offer a significant improvement over time" although the long-term benefits of medication were found to be "no better than children who were treated with behavior therapy."
It is estimated that between 2–5% of adults have ADHD. Around half of children with ADHD continue to have ADHD as adults. Of those who continue to have symptoms approximately 25% have the full disorder and 75% partially 'grow out' of it. Most adults remain untreated. Many have a disorganized life and use non-prescribed drugs and alcohol as a coping mechanism. Other problems may include relationship and job difficulties, and an increased risk of criminal activities. Associated mental health problems include: depression, anxiety disorder, and learning disabilities.
Some ADHD symptoms in adults differ from those seen in children. While children with ADHD may climb and run about excessively, adults may experience an inability to relax or talk excessively in social situations. Adults with ADHD may start relationships impulsively, display sensation-seeking behavior, and be short-tempered. Addictive behavior such as substance abuse and gambling are common. The DSM-IV criteria have been criticized for not being appropriate for adults; those who present differently may lead to the claim that they outgrew the diagnosis.
Children with high IQ scores
The diagnosis of ADHD and the significance of its impact on children with a high intelligence quotient (IQ) is controversial. Most studies have found similar impairments regardless of IQ, with higher rates of repeating grades and having social difficulties. Additionally, more than half of people with high IQ and ADHD experience major depressive disorder or oppositional defiant disorder at some point in their lives. Generalised anxiety disorder, separation anxiety disorder and social phobia are also more common. There is some evidence that individuals with high IQ and ADHD have a lowered risk of substance abuse and anti-social behavior compared to children with low and average IQ and ADHD. Children and adolescents with high IQ can have their level of intelligence mismeasured during a standard evaluation and may require more comprehensive testing.
- Kooij SJ, Bejerot S, Blackwell A, Caci H, Casas-Brugué M, Carpentier PJ, Edvinsson D, Fayyad J, Foeken K, Fitzgerald M, Gaillac V, Ginsberg Y, Henry C, Krause J, Lensing MB, Manor I, Niederhofer H, Nunes-Filipe C, Ohlmeier MD, Oswald P, Pallanti S, Pehlivanidis A, Ramos-Quiroga JA, Rastam M, Ryffel-Rawak D, Stes S, Asherson P (2010). "European consensus statement on diagnosis and treatment of adult ADHD: The European Network Adult ADHD". BMC Psychiatry 10: 67. doi:10.1186/1471-244X-10-67. PMC 2942810. PMID 20815868.
- Lange KW, Reichl S, Lange KM, Tucha L, Tucha O (December 2010). "The history of attention deficit hyperactivity disorder". Atten Defic Hyperact Disord 2 (4): 241–255. doi:10.1007/s12402-010-0045-8. PMC 3000907. PMID 21258430.
- Sroubek A, Kelly M, Li X (February 2013). "Inattentiveness in attention-deficit/hyperactivity disorder". Neurosci Bull 29 (1): 103–110. doi:10.1007/s12264-012-1295-6. PMID 23299717.
- Caroline SC, ed. (2010). Encyclopedia of Cross-Cultural School Psychology. Springer Science & Business Media. p. 133. ISBN 9780387717982. Retrieved 17 January 2014.
- Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–321. ISBN 9780071481274.
• Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans.
• Working memory is a short-term, capacity-limited cognitive buffer that stores information and permits its manipulation to guide decision-making and behavior. ...
These diverse inputs and back projections to both cortical and subcortical structures put the prefrontal cortex in a position to exert what is often called “top-down” control or cognitive control of behavior. ... The prefrontal cortex receives inputs not only from other cortical regions, including association cortex, but also, via the thalamus, inputs from subcortical structures subserving emotion and motivation, such as the amygdala (Chapter 14) and ventral striatum (or nucleus accumbens; Chapter 15). ...
In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 15), or in attention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result. ... ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. Compared with healthy individuals, those with ADHD have diminished ability to suppress inappropriate prepotent responses to stimuli (impaired response inhibition) and diminished ability to inhibit responses to irrelevant stimuli (impaired interference suppression). ... Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior. ... Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention.
- Diamond A (2013). "Executive functions". Annu Rev Psychol 64: 135–168. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641.
Core EFs are inhibition [response inhibition (self-control—resisting temptations and resisting acting impulsively) and interference control (selective attention and cognitive inhibition)], working memory, and cognitive flexibility (including creatively thinking “outside the box,” seeing anything from different perspectives, and quickly and flexibly adapting to changed circumstances). ... EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not. You can see the deleterious effects of stress, sadness, loneliness, and lack of physical health or fitness at the physiological and neuroanatomical level in prefrontal cortex and at the behavioral level in worse EFs (poorer reasoning and problem solving, forgetting things, and impaired ability to exercise discipline and self-control). ...
EFs can be improved (Diamond & Lee 2011, Klingberg 2010). ... At any age across the life cycle EFs can be improved, including in the elderly and in infants. There has been much work with excellent results on improving EFs in the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al. 2011) ... Inhibitory control (one of the core EFs) involves being able to control one’s attention, behavior, thoughts, and/or emotions to override a strong internal predisposition or external lure, and instead do what’s more appropriate or needed. Without inhibitory control we would be at the mercy of impulses, old habits of thought or action (conditioned responses), and/or stimuli in the environment that pull us this way or that. Thus, inhibitory control makes it possible for us to change and for us to choose how we react and how we behave rather than being unthinking creatures of habit. It doesn’t make it easy. Indeed, we usually are creatures of habit and our behavior is under the control of environmental stimuli far more than we usually realize, but having the ability to exercise inhibitory control creates the possibility of change and choice.
- Childress AC, Berry SA (February 2012). "Pharmacotherapy of attention-deficit hyperactivity disorder in adolescents". Drugs 72 (3): 309–325. doi:10.2165/11599580-000000000-00000. PMID 22316347.
- "Attention-Deficit / Hyperactivity Disorder (ADHD)". Centers for Disease Control and Prevention. National Center on Birth Defects and Developmental Disabilities. 19 September 2014. Retrieved 3 November 2014.
- Dulcan MK, Lake MB (2011). Concise Guide to Child and Adolescent Psychiatry (4th ed.). American Psychiatric Publishing. p. 34. ISBN 9781585624164. Retrieved 17 January 2014.
- Willcutt EG (July 2012). "The prevalence of DSM-IV attention-deficit/hyperactivity disorder: a meta-analytic review". Neurotherapeutics 9 (3): 490–499. doi:10.1007/s13311-012-0135-8. PMC 3441936. PMID 22976615.
- Cowen P, Harrison P, Burns T (12 October 2012). Shorter Oxford Textbook of Psychiatry (6th ed.). Oxford University Press. p. 546. ISBN 9780199605613.
- Tsuang MT, Tohen M, Jones P, ed. (25 March 2011). "Chapter 25". Textbook of Psychiatric Epidemiology (3rd ed.). John Wiley & Sons. p. 450. ISBN 9780470977408.
- Emond V, Joyal C, Poissant H (April 2009). "Structural and functional neuroanatomy of attention-deficit hyperactivity disorder (ADHD)". Encephale (in French) 35 (2): 107–114. doi:10.1016/j.encep.2008.01.005. PMID 19393378.
- Singh I (December 2008). "Beyond polemics: science and ethics of ADHD". Nat. Rev. Neurosci. 9 (12): 957–964. doi:10.1038/nrn2514. PMID 19020513.
- Bálint S, Czobor P, Mészáros A, Simon V, Bitter I (2008). "[Neuropsychological impairments in adult attention deficit hyperactivity disorder: a literature review]". Psychiatr Hung (in Hungarian) 23 (5): 324–335. PMID 19129549.
- National Collaborating Centre for Mental Health (2009). Attention Deficit Hyperactivity Disorder: Diagnosis and Management of ADHD in Children, Young People and Adults. British Psychological Society. pp. 19–27, 23, 38, 130, 133, 317. ISBN 9781854334718.
- Gentile JP, Atiq R, Gillig PM (August 2006). "Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management". Psychiatry (Edgmont) 3 (8): 25–30. PMC 2957278. PMID 20963192.
- Parrillo VN (2008). Encyclopedia of Social Problems. SAGE. p. 63. ISBN 9781412941655. Retrieved 2 May 2009.
- Mayes R, Bagwell C, Erkulwater J (2008). "ADHD and the rise in stimulant use among children". Harv Rev Psychiatry 16 (3): 151–166. doi:10.1080/10673220802167782. PMID 18569037.
- Cohen DJ (7 March 2006). Cicchetti D, ed. Developmental Psychopathology, Developmental Neuroscience (2nd, illustrated ed.). John Wiley & Sons. ISBN 9780471237372.
- Sim MG, Hulse G, Khong E (August 2004). "When the child with ADHD grows up" (PDF). Aust Fam Physician 33 (8): 615–618. PMID 15373378. Retrieved 8 November 2014.
- Silver LB (2004). Attention-deficit/hyperactivity disorder (3rd ed.). American Psychiatric Publishing. pp. 4–7. ISBN 9781585621316.
- Schonwald A, Lechner E (April 2006). "Attention deficit/hyperactivity disorder: complexities and controversies". Curr. Opin. Pediatr. 18 (2): 189–195. doi:10.1097/01.mop.0000193302.70882.70. PMID 16601502.
- Dobie C (2012). "Diagnosis and management of attention deficit hyperactivity disorder in primary care for school-age children and adolescents". Institute for Clinical Systems Improvement. p. 79.
- "Facts About ADHD". Centers for Disease Control and Prevention. National Center on Birth Defects and Developmental Disabilities. Retrieved 13 November 2012.
- Ramsay JR (2007). Cognitive behavioral therapy for adult ADHD. Routledge. pp. 4, 25–26. ISBN 0415955017.
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington: American Psychiatric Publishing. pp. 59–65. ISBN 0890425558.
- National Institute of Mental Health (2008). "Attention Deficit Hyperactivity Disorder (ADHD)". National Institutes of Health.
- Coleman WL (August 2008). "Social competence and friendship formation in adolescents with attention-deficit/hyperactivity disorder". Adolesc Med State Art Rev 19 (2): 278–99, x. PMID 18822833.
- "ADHD Anger Management Directory". Webmd.com. Retrieved 17 January 2014.
- Racine MB, Majnemer A, Shevell M, Snider L (April 2008). "Handwriting performance in children with attention deficit hyperactivity disorder (ADHD)". J. Child Neurol. 23 (4): 399–406. doi:10.1177/0883073807309244. PMID 18401033.
- "ICD-10 Version:2010". World Health Organisation. 2010. Retrieved 2 November 2014.
- Bellani M, Moretti A, Perlini C, Brambilla P (December 2011). "Language disturbances in ADHD". Epidemiol Psychiatr Sci 20 (4): 311–315. doi:10.1017/S2045796011000527. PMID 22201208.
- Walitza S, Drechsler R, Ball J (August 2012). "[The school child with ADHD]". Ther Umsch (in German) 69 (8): 467–473. doi:10.1024/0040-5930/a000316. PMID 22851461.
- Bailey, Eileen. "ADHD and Learning Disabilities: How can you help your child cope with ADHD and subsequent Learning Difficulties? There is a way.". Remedy Health Media, LLC. Retrieved 15 November 2013.
- "Attention Deficit Hyperactivity Disorder (ADHD)". The National Institute of Mental Health (NIMH). Retrieved 15 November 2013.
- McBurnett K, Pfiffner LJ (November 2009). "Treatment of aggressive ADHD in children and adolescents: conceptualization and treatment of comorbid behavior disorders". Postgrad Med 121 (6): 158–165. doi:10.3810/pgm.2009.11.2084. PMID 19940426.
- Krull KR (5 December 2007). "Evaluation and diagnosis of attention deficit hyperactivity disorder in children" (Subscription required). Uptodate. Wolters Kluwer Health. Retrieved 12 September 2008.
- Hofvander B, Ossowski D, Lundström S, Anckarsäter H (2009). "Continuity of aggressive antisocial behavior from childhood to adulthood: The question of phenotype definition". Int J Law Psychiatry 32 (4): 224–234. doi:10.1016/j.ijlp.2009.04.004. PMID 19428109.
- Rubia K (June 2011). ""Cool" inferior frontostriatal dysfunction in attention-deficit/hyperactivity disorder versus "hot" ventromedial orbitofrontal-limbic dysfunction in conduct disorder: a review". Biol. Psychiatry 69 (12): e69–87. doi:10.1016/j.biopsych.2010.09.023. PMID 21094938.
- Segal MM (July 2014). "We cannot say whether attention deficit hyperactivity disorder exists, but we can find its molecular mechanisms". Pediatr. Neurol. 51 (1): 15–16. doi:10.1016/j.pediatrneurol.2014.04.014. PMID 24938135.
- Wilens TE, Spencer TJ (September 2010). "Understanding attention-deficit/hyperactivity disorder from childhood to adulthood". Postgrad Med 122 (5): 97–109. doi:10.3810/pgm.2010.09.2206. PMC 3724232. PMID 20861593.
- Baud P, Perroud N, Aubry JM (June 2011). "[Bipolar disorder and attention deficit/hyperactivity disorder in adults: differential diagnosis or comorbidity]". Rev Med Suisse (in French) 7 (297): 1219–1222. PMID 21717696.
- Wilens TE, Morrison NR (July 2011). "The intersection of attention-deficit/hyperactivity disorder and substance abuse". Curr Opin Psychiatry 24 (4): 280–285. doi:10.1097/YCO.0b013e328345c956. PMC 3435098. PMID 21483267.
- Merino-Andreu M (March 2011). "Trastorno por déficit de atención/hiperactividad y síndrome de piernas inquietas en niños" [Attention deficit hyperactivity disorder and restless legs syndrome in children]. Rev Neurol (in Spanish). 52 Suppl 1: S85–95. PMID 21365608.
- Picchietti MA, Picchietti DL (August 2010). "Advances in pediatric restless legs syndrome: Iron, genetics, diagnosis and treatment". Sleep Med. 11 (7): 643–651. doi:10.1016/j.sleep.2009.11.014. PMID 20620105.
- Karroum E, Konofal E, Arnulf I (2008). "[Restless-legs syndrome]". Rev. Neurol. (Paris) (in French) 164 (8–9): 701–721. doi:10.1016/j.neurol.2008.06.006. PMID 18656214.
- Corkum P, Davidson F, Macpherson M (June 2011). "A framework for the assessment and treatment of sleep problems in children with attention-deficit/hyperactivity disorder". Pediatr. Clin. North Am. 58 (3): 667–683. doi:10.1016/j.pcl.2011.03.004. PMID 21600348.
- Tsai MH, Huang YS (May 2010). "Attention-deficit/hyperactivity disorder and sleep disorders in children". Med. Clin. North Am. 94 (3): 615–632. doi:10.1016/j.mcna.2010.03.008. PMID 20451036.
- Brown TE (October 2008). "ADD/ADHD and Impaired Executive Function in Clinical Practice". Curr Psychiatry Rep 10 (5): 407–411. doi:10.1007/s11920-008-0065-7. PMID 18803914.
- Bendz LM, Scates AC (January 2010). "Melatonin treatment for insomnia in pediatric patients with attention-deficit/hyperactivity disorder". Annals of Pharmacotherapy 44 (1): 185–191. doi:10.1345/aph.1M365. PMID 20028959.
- Shreeram S, He JP, Kalaydjian A, Brothers S, Merikangas KR (January 2009). "Prevalence of enuresis and its association with attention-deficit/hyperactivity disorder among United States children: results from a nationally representative study". J Am Acad Child Adolesc Psychiatry 48 (1): 35–41. doi:10.1097/CHI.0b013e318190045c. PMC 2794242. PMID 19096296.
- Hagberg BS, Miniscalco C, Gillberg C (2010). "Clinic attenders with autism or attention-deficit/hyperactivity disorder: cognitive profile at school age and its relationship to preschool indicators of language delay". Res Dev Disabil 31 (1): 1–8. doi:10.1016/j.ridd.2009.07.012. PMID 19713073.
- Fliers EA, Franke B, Buitelaar JK (2011). "[Motor problems in children with ADHD receive too little attention in clinical practice]". Ned Tijdschr Geneeskd (in Dutch; Flemish) 155 (50): A3559. PMID 22186361.
- Greathead, Philippa. "Language Disorders and Attention Deficit Hyperactivity Disorder ." ADDIS Information Centre. ADDIS, 6 November 2013. Web. 6 November 2013. <http://www.addiss.co.uk/languagedisorders.htm>.
- Millichap, J. Gordon (2010). Attention Deficit Hyperactivity Disorder Handbook a Physician's Guide to ADHD (2nd ed.). New York, NY: Springer Science. p. 26. ISBN 9781441913975. Retrieved 17 January 2014.
- Thapar A, Cooper M, Eyre O, Langley K (January 2013). "What have we learnt about the causes of ADHD?". J Child Psychol Psychiatry 54 (1): 3–16. doi:10.1111/j.1469-7610.2012.02611.x. PMC 3572580. PMID 22963644.
- Neale BM, Medland SE, Ripke S, Asherson P, Franke B, Lesch KP, Faraone SV, Nguyen TT, Schäfer H, Holmans P, Daly M, Steinhausen HC, Freitag C, Reif A, Renner TJ, Romanos M, Romanos J, Walitza S, Warnke A, Meyer J, Palmason H, Buitelaar J, Vasquez AA, Lambregts-Rommelse N, Gill M, Anney RJ, Langely K, O'Donovan M, Williams N, Owen M, Thapar A, Kent L, Sergeant J, Roeyers H, Mick E, Biederman J, Doyle A, Smalley S, Loo S, Hakonarson H, Elia J, Todorov A, Miranda A, Mulas F, Ebstein RP, Rothenberger A, Banaschewski T, Oades RD, Sonuga-Barke E, McGough J, Nisenbaum L, Middleton F, Hu X, Nelson S (September 2010). "Meta-analysis of genome-wide association studies of attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry 49 (9): 884–897. doi:10.1016/j.jaac.2010.06.008. PMC 2928252. PMID 20732625.
- Burt SA (July 2009). "Rethinking environmental contributions to child and adolescent psychopathology: a meta-analysis of shared environmental influences". Psychol Bull 135 (4): 608–637. doi:10.1037/a0015702. PMID 19586164.
- Nolen-Hoeksema S (2013). Abnormal Psychology (Sixth ed.). p. 267. ISBN 9780078035388.
- Franke B, Faraone SV, Asherson P, Buitelaar J, Bau CH, Ramos-Quiroga JA, Mick E, Grevet EH, Johansson S, Haavik J, Lesch KP, Cormand B, Reif A (October 2012). "The genetics of attention deficit/hyperactivity disorder in adults, a review". Mol. Psychiatry 17 (10): 960–987. doi:10.1038/mp.2011.138. PMC 3449233. PMID 22105624.
- Gizer IR, Ficks C, Waldman ID (July 2009). "Candidate gene studies of ADHD: a meta-analytic review". Hum. Genet. 126 (1): 51–90. doi:10.1007/s00439-009-0694-x. PMID 19506906.
- Kebir O, Tabbane K, Sengupta S, Joober R (March 2009). "Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies". J Psychiatry Neurosci 34 (2): 88–101. PMC 2647566. PMID 19270759.
- Berry, MD (January 2007). "The potential of trace amines and their receptors for treating neurological and psychiatric diseases". Reviews on recent clinical trials 2 (1): 3–19. doi:10.2174/157488707779318107. PMID 18473983.
- Sotnikova TD, Caron MG, Gainetdinov RR (August 2009). "Trace amine-associated receptors as emerging therapeutic targets". Mol. Pharmacol. 76 (2): 229–235. doi:10.1124/mol.109.055970. PMC 2713119. PMID 19389919.
- Arcos-Burgos M, Muenke M (November 2010). "Toward a better understanding of ADHD: LPHN3 gene variants and the susceptibility to develop ADHD". Atten Defic Hyperact Disord 2 (3): 139–147. doi:10.1007/s12402-010-0030-2. PMC 3280610. PMID 21432600.
- Cardo E, Nevot A, Redondo M, et al. (March 2010). "Trastorno por déficit de atención/hiperactividad: ¿un patrón evolutivo?" [Attention deficit disorder and hyperactivity: a pattern of evolution?]. Rev Neurol (in Spanish). 50 Suppl 3: S143–7. PMID 20200842.
- Williams J, Taylor E (June 2006). "The evolution of hyperactivity, impulsivity and cognitive diversity". J R Soc Interface 3 (8): 399–413. doi:10.1098/rsif.2005.0102. PMC 1578754. PMID 16849269.
- Glover V (April 2011). "Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective". J Child Psychol Psychiatry 52 (4): 356–67. doi:10.1111/j.1469-7610.2011.02371.x. PMID 21250994.
- Behavioral neuroscience of attention deficit hyperactivity disorder and its treatment. New York: Springer. 13 January 2012. pp. 132–134. ISBN 978-3-642-24611-1.
- Burger PH, Goecke TW, Fasching PA, Moll G, Heinrich H, Beckmann MW, Kornhuber J (September 2011). "[How does maternal alcohol consumption during pregnancy affect the development of attention deficit/hyperactivity syndrome in the child]". Fortschr Neurol Psychiatr (in German) 79 (9): 500–506. doi:10.1055/s-0031-1273360. PMID 21739408.
- Abbott LC, Winzer-Serhan UH (April 2012). "Smoking during pregnancy: lessons learned from epidemiological studies and experimental studies using animal models". Crit. Rev. Toxicol. 42 (4): 279–303. doi:10.3109/10408444.2012.658506. PMID 22394313.
- Neuman RJ, Lobos E, Reich W, Henderson CA, Sun LW, Todd RD (15 June 2007). "Prenatal smoking exposure and dopaminergic genotypes interact to cause a severe ADHD subtype". Biol Psychiatry 61 (12): 1320–1328. doi:10.1016/j.biopsych.2006.08.049. PMID 17157268. Lay summary.
- Eubig PA, Aguiar A, Schantz SL (December 2010). "Lead and PCBs as risk factors for attention deficit/hyperactivity disorder". Environ. Health Perspect. 118 (12): 1654–1667. doi:10.1289/ehp.0901852. PMC 3002184. PMID 20829149.
- de Cock M, Maas YG, van de Bor M (August 2012). "Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review". Acta Paediatr. 101 (8): 811–818. doi:10.1111/j.1651-2227.2012.02693.x. PMID 22458970.
- Thapar, A.; Cooper, M.; Jefferies, R.; Stergiakouli, E. (March 2012). "What causes attention deficit hyperactivity disorder?". Arch Dis Child 97 (3): 260–5. doi:10.1136/archdischild-2011-300482. PMID 21903599.
- Millichap JG (February 2008). "Etiologic classification of attention-deficit/hyperactivity disorder". Pediatrics 121 (2): e358–65. doi:10.1542/peds.2007-1332. PMID 18245408.
- Eme, R (April 2012). "ADHD: an integration with pediatric traumatic brain injury". Expert Rev Neurother 12 (4): 475–83. doi:10.1586/ern.12.15. PMID 22449218.
- Mayes R, Bagwell C, Erkulwater JL (2009). Medicating Children: ADHD and Pediatric Mental Health (illustrated ed.). Harvard University Press. pp. 4–24. ISBN 9780674031630.
- Millichap JG, Yee MM (February 2012). "The diet factor in attention-deficit/hyperactivity disorder". Pediatrics 129 (2): 330–337. doi:10.1542/peds.2011-2199. PMID 22232312.
- Tomaska LD and Brooke-Taylor, S. Food Additives - General pp 449-454 in Encyclopedia of Food Safety, Vol 2: Hazards and Diseases. Eds, Motarjemi Y et al. Academic Press, 2013. ISBN 9780123786135
- FDA. Background Document for the Food Advisory Committee: Certified Color Additives in Food and Possible Association with Attention Deficit Hyperactivity Disorder in Children: March 30-31, 2011
- "Mental health of children and adolescents" (PDF). 15 January 2005. Archived from the original on 24 October 2009. Retrieved 13 October 2011.
- Elder TE (September 2010). "The importance of relative standards in ADHD diagnoses: evidence based on exact birth dates". J Health Econ 29 (5): 641–656. doi:10.1016/j.jhealeco.2010.06.003. PMC 2933294. PMID 20638739.
- Parritz R (2013). Disorders of Childhood: Development and Psychopathology. Cengage Learning. p. 151. ISBN 9781285096063. Retrieved 17 January 2014.
- Parens E, Johnston J (2009). "Facts, values, and Attention-Deficit Hyperactivity Disorder (ADHD): an update on the controversies". Child Adolesc Psychiatry Ment Health 3 (1): 1. doi:10.1186/1753-2000-3-1. PMC 2637252. PMID 19152690.
- Chriss, James J. (2007). Social control: an introduction. Cambridge, UK: Polity. p. 230. ISBN 0-7456-3858-9.
- Szasz, Thomas Stephen (2001). Pharmacracy: medicine and politics in America. New York: Praeger. p. 212. ISBN 0-275-97196-1.
- Malenka RC, Nestler EJ, Hyman SE (2009). "Chapters 10 and 13". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 266, 318–323. ISBN 9780071481274.
New, palatable foods cause dopamine release from VTA neurons of the midbrain that project to the nucleus accumbens, prefrontal cortex, and other limbic structures that regulate emotion. Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. ... It acts in the orbital prefrontal cortex to set a value on rewards ...
Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. Positron emission tomography (PET) demonstrates that methylphenidate decreases regional cerebral blood flow in the dorsolateral prefrontal cortex and posterior parietal cortex while improving performance of a spacial working memory task. This suggests that cortical networks that normally process spatial working memory become more efficient in response to the drug. ... [It] is now believed that dopamine and norepinephrine, but not serotonin, produce the beneficial effects of stimulants on working memory. At abused (relatively high) doses, stimulants can interfere with working memory and cognitive control ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors.
- Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 148, 154–157. ISBN 9780071481274.
DA has multiple actions in the prefrontal cortex. It promotes the "cognitive control" of behavior: the selection and successful monitoring of behavior to facilitate attainment of chosen goals. Aspects of cognitive control in which DA plays a role include working memory, the ability to hold information "on line" in order to guide actions, suppression of prepotent behaviors that compete with goal-directed actions, and control of attention and thus the ability to overcome distractions. Cognitive control is impaired in several disorders, including attention deficit hyperactivity disorder. ... Noradrenergic projections from the LC thus interact with dopaminergic projections from the VTA to regulate cognitive control. ... it has not been shown that 5HT makes a therapeutic contribution to treatment of ADHD.
- Castellanos FX, Proal E (January 2012). "Large-scale brain systems in ADHD: beyond the prefrontal-striatal model". Trends Cogn. Sci. (Regul. Ed.) 16 (1): 17–26. doi:10.1016/j.tics.2011.11.007. PMC 3272832. PMID 22169776.
Recent conceptualizations of ADHD have taken seriously the distributed nature of neuronal processing [10,11,35,36]. Most of the candidate networks have focused on prefrontal-striatal-cerebellar circuits, although other posterior regions are also being proposed .
- Cortese S, Kelly C, Chabernaud C, Proal E, Di Martino A, Milham MP, Castellanos FX (October 2012). "Toward systems neuroscience of ADHD: a meta-analysis of 55 fMRI studies". Am J Psychiatry 169 (10): 1038–1055. doi:10.1176/appi.ajp.2012.11101521. PMC 3879048. PMID 22983386.
- Krain AL, Castellanos FX (August 2006). "Brain development and ADHD". Clin Psychol Rev 26 (4): 433–444. doi:10.1016/j.cpr.2006.01.005. PMID 16480802.
- Fusar-Poli P, Rubia K, Rossi G, Sartori G, Balottin U (March 2012). "Striatal dopamine transporter alterations in ADHD: pathophysiology or adaptation to psychostimulants? A meta-analysis". Am J Psychiatry 169 (3): 264–72. doi:10.1176/appi.ajp.2011.11060940. PMID 22294258.
- Bidwell LC, McClernon FJ, Kollins SH (August 2011). "Cognitive enhancers for the treatment of ADHD". Pharmacol. Biochem. Behav. 99 (2): 262–274. doi:10.1016/j.pbb.2011.05.002. PMC 3353150. PMID 21596055.
- Cortese S (September 2012). "The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD): what every clinician should know". Eur. J. Paediatr. Neurol. 16 (5): 422–433. doi:10.1016/j.ejpn.2012.01.009. PMID 22306277.
- Gu XL (October 2010). "Deciphering the corelease of glutamate from dopaminergic terminals derived from the ventral tegmental area". J. Neurosci. 30 (41): 13549–13551. doi:10.1523/JNEUROSCI.3802-10.2010. PMC 2974325. PMID 20943895.
- Lesch KP, Merker S, Reif A, Novak M (June 2013). "Dances with black widow spiders: dysregulation of glutamate signalling enters centre stage in ADHD". Eur Neuropsychopharmacol 23 (6): 479–491. doi:10.1016/j.euroneuro.2012.07.013. PMID 22939004.
- Lambek R, Tannock R, Dalsgaard S, Trillingsgaard A, Damm D, Thomsen PH (August 2010). "Validating neuropsychological subtypes of ADHD: how do children with and without an executive function deficit differ?". J Child Psychol Psychiatry 51 (8): 895–904. doi:10.1111/j.1469-7610.2010.02248.x. PMID 20406332.
- Nigg JT, Willcutt EG, Doyle AE, Sonuga-Barke EJ (June 2005). "Causal heterogeneity in attention-deficit/hyperactivity disorder: do we need neuropsychologically impaired subtypes?". Biol. Psychiatry 57 (11): 1224–1230. doi:10.1016/j.biopsych.2004.08.025. PMID 15949992.
- Modesto-Lowe V, Chaplin M, Soovajian V, Meyer A (2013). "Are motivation deficits underestimated in patients with ADHD? A review of the literature". Postgrad Med 125 (4): 47–52. doi:10.3810/pgm.2013.07.2677. PMID 23933893.
Behavioral studies show altered processing of reinforcement and incentives in children with ADHD. These children respond more impulsively to rewards and choose small, immediate rewards over larger, delayed incentives. Interestingly, a high intensity of reinforcement is effective in improving task performance in children with ADHD. Pharmacotherapy may also improve task persistence in these children. ... Previous studies suggest that a clinical approach using interventions to improve motivational processes in patients with ADHD may improve outcomes as children with ADHD transition into adolescence and adulthood.
- "MerckMedicus Modules: ADHD –Pathophysiology". August 2002. Archived from the original on 1 May 2010.
- Wiener JM, Dulcan MK (2004). Textbook Of Child and Adolescent Psychiatry (illustrated ed.). American Psychiatric Publishing. ISBN 9781585620579. Retrieved 2 November 2014.
- Wolraich M, Brown L, Brown RT, DuPaul G, Earls M, Feldman HM, Ganiats TG, Kaplanek B, Meyer B, Perrin J, Pierce K, Reiff M, Stein MT, Visser S (November 2011). "ADHD: clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents". Pediatrics 128 (5): 1007–1022. doi:10.1542/peds.2011-2654. PMID 22003063.
- Sand T, Breivik N, Herigstad A (February 2013). "[Assessment of ADHD with EEG]". Tidsskr. Nor. Laegeforen. (in Norwegian) 133 (3): 312–316. doi:10.4045/tidsskr.12.0224. PMID 23381169.
- Millichap JG, Millichap JJ, Stack CV (July 2011). "Utility of the electroencephalogram in attention deficit hyperactivity disorder". Clin EEG Neurosci 42 (3): 180–184. PMID 21870470.
- "FDA permits marketing of first brain wave test to help assess children and teens for ADHD". United States Food and Drug Administration. 15 July 2013.
- Steinau S (2013). "Diagnostic Criteria in Attention Deficit Hyperactivity Disorder – Changes in DSM 5". Front Psychiatry 4: 49. doi:10.3389/fpsyt.2013.00049. PMC 3667245. PMID 23755024.
- Berger I (September 2011). "Diagnosis of attention deficit hyperactivity disorder: much ado about something" (PDF). Isr. Med. Assoc. J. 13 (9): 571–574. PMID 21991721.
- Consumer Reports (March 2012). "Evaluating Prescription Drugs Used to Treat: Attention Deficit Hyperactivity Disorder (ADHD) Comparing Effectiveness, Safety, and Price" (pdf). Consumer Reports. p. 2. Retrieved 12 April 2013.
- Gentile JP, Atiq R, Gillig PM (August 2006). "Adult ADHD: Diagnosis, Differential Diagnosis, and Medication Management". Psychiatry (Edgmont) 3 (8): 25–30. PMC 2957278. PMID 20963192.
- Owens JA (October 2008). "Sleep disorders and attention-deficit/hyperactivity disorder". Curr Psychiatry Rep 10 (5): 439–444. PMID 18803919.
- Walters AS, Silvestri R, Zucconi M, Chandrashekariah R, Konofal E (December 2008). "Review of the possible relationship and hypothetical links between attention deficit hyperactivity disorder (ADHD) and the simple sleep related movement disorders, parasomnias, hypersomnias, and circadian rhythm disorders". J Clin Sleep Med 4 (6): 591–600. PMC 2603539. PMID 19110891.
- Lal C, Strange C, Bachman D (June 2012). "Neurocognitive impairment in obstructive sleep apnea". Chest 141 (6): 1601–1610. doi:10.1378/chest.11-2214. PMID 22670023.
- Shaw M, Hodgkins P, Caci H, Young S, Kahle J, Woods AG, Arnold LE (4 September 2012). "A systematic review and analysis of long-term outcomes in attention deficit hyperactivity disorder: effects of treatment and non-treatment". BMC Med 10: 99. doi:10.1186/1741-7015-10-99. PMC 3520745. PMID 22947230.
- "Chapter 7: Pharmacological Treatment of ADHD" (pdf). Canadian ADHD Resource Alliance. March 2014. Retrieved 2 November 2014.
- Nigg JT, Lewis K, Edinger T, Falk M (January 2012). "Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives". J Am Acad Child Adolesc Psychiatry 51 (1): 86–97. doi:10.1016/j.jaac.2011.10.015. PMID 22176942.
- Sonuga-Barke EJ, Brandeis D, Cortese S, Daley D, Ferrin M, Holtmann M, Stevenson J, Danckaerts M, van der Oord S, Döpfner M, Dittmann RW, Simonoff E, Zuddas A, Banaschewski T, Buitelaar J, Coghill D, Hollis C, Konofal E, Lecendreux M, Wong IC, Sergeant J (March 2013). "Nonpharmacological interventions for ADHD: systematic review and meta-analyses of randomized controlled trials of dietary and psychological treatments". Am J Psychiatry 170 (3): 275–289. doi:10.1176/appi.ajp.2012.12070991. PMID 23360949.
- Fabiano GA, Pelham WE, Coles EK, Gnagy EM, Chronis-Tuscano A, O'Connor BC (March 2009). "A meta-analysis of behavioral treatments for attention-deficit/hyperactivity disorder". Clin Psychol Rev 29 (2): 129–140. doi:10.1016/j.cpr.2008.11.001. PMID 19131150.
- Kratochvil CJ, Vaughan BS, Barker A, Corr L, Wheeler A, Madaan V (March 2009). "Review of pediatric attention deficit/hyperactivity disorder for the general psychiatrist". Psychiatr. Clin. North Am. 32 (1): 39–56. doi:10.1016/j.psc.2008.10.001. PMID 19248915.
- Arns M, de Ridder S, Strehl U, Breteler M, Coenen A (July 2009). "Efficacy of neurofeedback treatment in ADHD: the effects on inattention, impulsivity and hyperactivity: a meta-analysis". Clin EEG Neurosci 40 (3): 180–189. PMID 19715181.
- Pliszka S (July 2007). "Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry 46 (7): 894–921. doi:10.1097/chi.0b013e318054e724. PMID 17581453.
- Bjornstad G, Montgomery P (2005). Bjornstad GJ, ed. "Family therapy for attention-deficit disorder or attention-deficit/hyperactivity disorder in children and adolescents". Cochrane Database Syst Rev (2): CD005042. doi:10.1002/14651858.CD005042.pub2. PMID 15846741.
- Turkington C, Harris J (2009). The Encyclopedia of the Brain and Brain Disorders. Infobase Publishing. p. 47. ISBN 9781438127033. Retrieved 17 January 2014.
- Mikami AY (June 2010). "The importance of friendship for youth with attention-deficit/hyperactivity disorder". Clin Child Fam Psychol Rev 13 (2): 181–98. doi:10.1007/s10567-010-0067-y. PMC 2921569. PMID 20490677.
- Wigal SB (2009). "Efficacy and safety limitations of attention-deficit hyperactivity disorder pharmacotherapy in children and adults". CNS Drugs. 23 Suppl 1: 21–31. doi:10.2165/00023210-200923000-00004. PMID 19621975.
- Castells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M (2011). Castells X, ed. "Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults". Cochrane Database Syst. Rev. (6): CD007813. doi:10.1002/14651858.CD007813.pub2. PMID 21678370.
- McDonagh MS, Peterson K, Thakurta S, Low A (December 2011). "Drug Class Review: Pharmacologic Treatments for Attention Deficit Hyperactivity Disorder". United States Library of Medicine. PMID 22420008.
- Prasad V, Brogan E, Mulvaney C, Grainge M, Stanton W, Sayal K (April 2013). "How effective are drug treatments for children with ADHD at improving on-task behaviour and academic achievement in the school classroom? A systematic review and meta-analysis". Eur Child Adolesc Psychiatry 22 (4): 203–216. doi:10.1007/s00787-012-0346-x. PMID 23179416.
- Greenhill LL, Posner K, Vaughan BS, Kratochvil CJ (April 2008). "Attention deficit hyperactivity disorder in preschool children". Child and Adolescent Psychiatric Clinics of North America 17 (2): 347–366, ix. doi:10.1016/j.chc.2007.11.004. PMID 18295150.
- Hazell P (July 2011). "The challenges to demonstrating long-term effects of psychostimulant treatment for attention-deficit/hyperactivity disorder". Current Opinion in Psychiatry 24 (4): 286–290. doi:10.1097/YCO.0b013e32834742db. PMID 21519262.
- Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K (February 2013). "Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects". JAMA Psychiatry 70 (2): 185–198. doi:10.1001/jamapsychiatry.2013.277. PMID 23247506.
- Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A, Faraone SV, Biederman J (September 2013). "Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies". J. Clin. Psychiatry 74 (9): 902–917. doi:10.4088/JCP.12r08287. PMC 3801446. PMID 24107764.
- Frodl T, Skokauskas N (February 2012). "Meta-analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects.". Acta psychiatrica Scand. 125 (2): 114–126. doi:10.1111/j.1600-0447.2011.01786.x. PMID 22118249.
Basal ganglia regions like the right globus pallidus, the right putamen, and the nucleus caudatus are structurally affected in children with ADHD. These changes and alterations in limbic regions like ACC and amygdala are more pronounced in non-treated populations and seem to diminish over time from child to adulthood. Treatment seems to have positive effects on brain structure.
- "Canadian ADHD Practice Guidelines". Canadian ADHD Alliance. Retrieved 4 February 2011.
- Mosholder AD, Gelperin K, Hammad TA, Phelan K, Johann-Liang R (February 2009). "Hallucinations and other psychotic symptoms associated with the use of attention-deficit/hyperactivity disorder drugs in children". Pediatrics 123 (2): 611–616. doi:10.1542/peds.2008-0185. PMID 19171629.
- Kraemer M, Uekermann J, Wiltfang J, Kis B (July 2010). "Methylphenidate-induced psychosis in adult attention-deficit/hyperactivity disorder: report of 3 new cases and review of the literature". Clin Neuropharmacol 33 (4): 204–6. doi:10.1097/WNF.0b013e3181e29174. PMID 20571380.
- van de Loo-Neus GH, Rommelse N, Buitelaar JK (August 2011). "To stop or not to stop? How long should medication treatment of attention-deficit hyperactivity disorder be extended?". Eur Neuropsychopharmacol 21 (8): 584–599. doi:10.1016/j.euroneuro.2011.03.008. PMID 21530185.
- Oregon Health & Science University, Portland, Oregon (2009). "Black box warnings of ADHD drugs approved by the US Food and Drug Administration". United States National Library of Medicine. Retrieved 17 January 2014.
- Ashton H, Gallagher P, Moore B (September 2006). "The adult psychiatrist's dilemma: psychostimulant use in attention deficit/hyperactivity disorder". J. Psychopharmacol. (Oxford) 20 (5): 602–610. doi:10.1177/0269881106061710. PMID 16478756.
- Millichap JG, Yee MM (February 2012). "The diet factor in attention-deficit/hyperactivity disorder". Pediatrics 129 (2): 330–7. doi:10.1542/peds.2011-2199. PMID 22232312.
- Konikowska K, Regulska-Ilow B, Rózańska D (2012). "The influence of components of diet on the symptoms of ADHD in children". Rocz Panstw Zakl Hig 63 (2): 127–134. PMID 22928358.
- Bloch MH, Qawasmi A (October 2011). "Omega-3 fatty acid supplementation for the treatment of children with attention-deficit/hyperactivity disorder symptomatology: systematic review and meta-analysis". J Am Acad Child Adolesc Psychiatry 50 (10): 991–1000. doi:10.1016/j.jaac.2011.06.008. PMC 3625948. PMID 21961774.
- Molina BS, Hinshaw SP, Swanson JM, et al (May 2009). "The MTA at 8 years: prospective follow-up of children treated for combined-type ADHD in a multisite study". Journal of the American Academy of Child and Adolescent Psychiatry 48 (5): 484–500. doi:10.1097/CHI.0b013e31819c23d0. PMC 3063150. PMID 19318991.
- Cimera, Robert E. (2002). Making ADHD a gift : teaching Superman how to fly. Lanham, Md.: Scarecrow Press. p. 116. ISBN 978-0-8108-4318-9. Retrieved 17 January 2014.
- "College Degree Nearly Doubles Annual Earnings, Census Bureau Reports". Archived from the original on 30 March 2005. Retrieved 2 October 2008.
- Jensen PS, Arnold LE, Swanson JM (August 2007). "3-year follow-up of the NIMH MTA study". Journal of the American Academy of Child and Adolescent Psychiatry 46 (8): 989–1002. doi:10.1097/CHI.0b013e3180686d48. PMID 17667478.
- "What is the evidence for using CNS stimulants to treat ADHD in children? | Therapeutics Initiative". Archived from the original on 6 September 2010.
- Polanczyk G, de Lima MS, Horta BL, Biederman J, Rohde LA (June 2007). "The worldwide prevalence of ADHD: a systematic review and metaregression analysis". The American Journal of Psychiatry 164 (6): 942–8. doi:10.1176/appi.ajp.164.6.942. PMID 17541055.
- Staller J, Faraone SV (2006). "Attention-deficit hyperactivity disorder in girls: epidemiology and management". CNS Drugs 20 (2): 107–23. doi:10.2165/00023210-200620020-00003. PMID 16478287.
- "ADHD Throughout the Years". Center For Disease Control and Prevention. Retrieved 2 August 2013.
- Dalsgaard, S (February 2013). "Attention-deficit/hyperactivity disorder (ADHD)". European child & adolescent psychiatry. 22 Suppl 1: S43–8. doi:10.1007/s00787-012-0360-z. PMID 23202886.
- Palmer ED, Finger S (May 2001). "An early description of ADHD (inattentive subtype): Dr Alexander Crichton and 'Mental restlessness' (1798)". Child and Adolescent Mental Health 6 (2): 66–73. doi:10.1111/1475-3588.00324.
- Crichton A (1798). An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects. United Kingdom: AMS Press. p. 271. ISBN 9780404082123. Retrieved 17 January 2014.
- Millichap GJ (April 2010). "Chapter 1: Definition and History of ADHD". Attention Deficit Hyperactivity Disorder Handbook. Springer Verlag Gmbh. pp. 2–3. ISBN 9781441914095.
- Weiss M (2010). ADHD in Adulthood: A Guide to Current Theory, Diagnosis, and Treatment. JHU Press. ISBN 9781421401317. Retrieved 17 January 2014.
- Patrick KS, Straughn AB, Perkins JS, González MA (January 2009). "Evolution of stimulants to treat ADHD: transdermal methylphenidate". Human Psychopharmacology 24 (1): 1–17. doi:10.1002/hup.992. PMC 2629554. PMID 19051222.
- Rasmussen N (July 2006). "Making the first anti-depressant: amphetamine in American medicine, 1929–1950". J . Hist. Med. Allied Sci. 61 (3): 288–323. doi:10.1093/jhmas/jrj039. PMID 16492800.
- Foreman DM (February 2006). "Attention deficit hyperactivity disorder: legal and ethical aspects". Archives of Disease in Childhood 91 (2): 192–194. doi:10.1136/adc.2004.064576. PMC 2082674. PMID 16428370.
- Faraone, Stephen V (2005). "The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder". Eur Child Adolesc Psychiatry 14 (1): 1–10. doi:10.1007/s00787-005-0429-z. PMID 15756510.
- Cormier E (October 2008). "Attention deficit/hyperactivity disorder: a review and update". J Pediatr Nurs 23 (5): 345–357. doi:10.1016/j.pedn.2008.01.003. PMID 18804015.
- Schwarz, Alan (December 14, 2013). "The Selling of Attention Deficit Disorder" (December 14, 2013). The New York Times. Retrieved 26 February 2015.
- Saletan, William (12 January 2009). "Doping Deficit Disorder. Need performance-enhancing drugs? Claim ADHD". Slate. Archived from the original on 21 May 2009. Retrieved 2 May 2009.
- Neill US (August 2005). "Tom Cruise is dangerous and irresponsible". J. Clin. Invest. 115 (8): 1964–5. doi:10.1172/JCI26200. PMC 1180571. PMID 16075033.
- "Peer calls for ADHD care review". BBC News. 14 November 2007. Retrieved 29 January 2012.
- Singh A (25 February 2010). "BBC must broadcast apology over inaccurate Panorama programme". The Telegraph. Retrieved 29 January 2012.
- Culpepper, L, Mattingly G (2010). "Challenges in identifying and managing attention-deficit/hyperactivity disorder in adults in the primary care setting: a review of the literature". Prim Care Companion J Clin Psychiatry 12 (6): PCC.10r00951. doi:10.4088/PCC.10r00951pur. PMC 3067998. PMID 21494335.
- Antshel, KM (2008). "Attention-Deficit Hyperactivity Disorder in the context of a high intellectual quotient/giftedness". Dev Disabil Res Rev 14 (4): 293–299. doi:10.1002/ddrr.34. PMID 19072757.
|Look up ADHD, ADHD-PI, ADHD-C, or ADHD-PH/I in Wiktionary, the free dictionary.|
|Wikimedia Commons has media related to Attention Deficit Hyperactivity Disorder.|
- Attention deficit hyperactivity disorder at DMOZ
- National Institute of Mental Health on ADHD
- New Zealand MOH Guidelines for the Assessment and Treatment of Attention-Deficit/Hyperactivity Disorder