Despite being the most commonly studied and diagnosed mental disorder in children and adolescents, the exact cause is unknown in the majority of cases. It affects about 5-7% of children when diagnosed via the DSM-IV criteria and 1-2% when diagnosed via the ICD-10 criteria. As of 2015 it is estimated to affect about 51.1 million people globally. Rates are similar between countries and depend mostly on how it is diagnosed. ADHD is diagnosed approximately two times more often in boys than in girls, although the disorder is often overlooked in girls because their symptoms differ from those of boys. About 30-50% of people diagnosed in childhood continue to have symptoms into adulthood and between 2-5% of adults have the condition. In adults inner restlessness rather than hyperactivity may occur. The condition can be difficult to tell apart from other conditions, as well as to distinguish from high levels of activity that are still within the range of normative behaviors.
ADHD management recommendations vary by country and usually involve some combination of counseling, lifestyle changes, and medications. The British guideline only recommends medications as a first-line treatment in children who have severe symptoms and for medication to be considered in those with moderate symptoms who either refuse or fail to improve with counseling, though for adults medications are a first-line treatment. Canadian and American guidelines recommend that medications and behavioral therapy be used together as a first-line therapy, except in preschool-aged children. Stimulant medication therapy is not recommended as a first-line therapy in preschool-aged children in either guideline. Treatment with stimulants is effective for at least 14 months; however, their long term effectiveness is unclear. Adults often develop coping skills which make up for some or all of their impairments.
The medical literature has described symptoms similar to those of ADHD since the 18th century. 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 in children and adults, and the debate in the scientific community mainly centers on how it is diagnosed and treated. The condition was officially known as attention-deficit disorder (ADD) from 1980 to 1987, while before this it was known as hyperkinetic reaction of childhood.
has a short attention span and is easily distracted
makes careless mistakes - for example, in schoolwork
is unable to stick at tasks that are tedious or time-consuming
appears unable to listen to or carry out instructions
unable to sit still
fidgets, squirms in seat
leaves seat in inappropriate situations
takes risks with little thought for the dangers
"on the go" or "driven by a motor"
blurts out answers too early
has trouble waiting their turn
interrupts or intrudes on conversations
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.
According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), symptoms must be present for six months or more to a degree that is much greater than others of the same age and they must cause significant problems functioning in at least two settings (e.g., social, school/work, or home). The criteria must have been met prior to age twelve in order to receive a diagnosis of ADHD. This requires more than 5 symptoms of inattention or hyperactivity/impulsivity for those under 17 and more than 4 for those over 16 years old.
ADHD is divided into three subtypes: predominantly inattentive (ADHD-PI or ADHD-I), predominantly hyperactive-impulsive (ADHD-PH or ADHD-HI), and combined type (ADHD-C).
A person with ADHD inattentive type has most or all of following symptoms, excluding situations where these symptoms are better explained by another psychiatric or medical condition:
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 they find enjoyable
Have difficulty focusing attention on organizing or completing a task
Have trouble completing or turning in homework assignments, often losing things (e.g., pencils, toys, assignments) needed to complete tasks or activities
Appear not to be listening when spoken to
Daydream, become easily confused, and move slowly
Have difficulty processing information as quickly and accurately as others
Struggle to follow instructions
Have trouble understanding details; overlooks details
A person with ADHD hyperactive-impulsive type has most or all of the following symptoms, excluding situations where these symptoms are better explained by another psychiatric or medical condition:
Fidget or squirm a great deal
Dash around, touching or playing with anything and everything in sight
Have trouble sitting still during dinner, school, and while doing homework
Be constantly in motion
Have difficulty performing quiet tasks or activities
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 turn in games
Often interrupt conversations or others' activities
Girls with ADHD tend to display fewer hyperactivity and impulsivity symptoms but more symptoms pertaining to inattention and distractability. Symptoms of hyperactivity tend to go away with age and turn into "inner restlessness" in teens and adults with ADHD.
People with ADHD of all ages are more likely to have problems 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 attention deficits are prone to having difficulty processing verbal and nonverbal language which can negatively affect social interaction. They also may drift off during conversations, miss social cues, and have trouble learning social skills.
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 difficulty, many children with ADHD have an attention span equal to or better than that of other children for tasks and subjects they find interesting.
In children, ADHD occurs with other disorders about two-thirds of the time. Some 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.
Substance use disorders. Adolescents and adults with ADHD are at increased risk of substance abuse. This is most commonly seen 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.
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.
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.
Sluggish cognitive tempo (SCT) is a cluster of symptoms that potentially comprises another attention disorder. It may occur in 30-50% of ADHD cases, regardless of the subtype.
A 2016 systematic review found a well established association between ADHD and obesity, asthma and sleep disorders, and tentative evidence for association with celiac disease and migraine, while another 2016 systematic review did not support a clear link between celiac disease and ADHD, and stated that routine screening for celiac disease in people with ADHD is discouraged.
Overall, studies have shown that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests. The significance of this is controversial due to the differences between people with ADHD and the difficulty determining the influence of symptoms, such as distractibility, on lower scores rather than intellectual capacity. In studies of ADHD, higher IQs may be over represented because many studies exclude individuals who have lower IQs despite those with ADHD scoring on average nine points lower on standardized intelligence measures.
Studies of adults suggest that differences in intelligence are not meaningful and may be explained by associated health problems.
Most ADHD cases are of unknown causes. It is believed to involve interactions between genetics, the environment, and social 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 ADHD persists into adulthood.
Evolution may have played a role in the high rates of ADHD, particularly hyperactive and impulsive traits in males. Some have hypothesized that some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to hyperactivity and impulsivity in the gene pool. Others have claimed that these traits may be an adaptation that help males face stressful or dangerous environments with, for example, increased impulsivity and exploratory behavior. In certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual. The high rates and heterogeneity of ADHD may have increased reproductive fitness and benefited society by adding diversity to the gene pool despite being detrimental to the individual. In certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.
In addition to genetics, some environmental factors might play a role in causing ADHD. Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it. Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD. Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive. Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.
Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people.
In some cases, the diagnosis of ADHD may reflect a dysfunctional family or a poor educational system, rather than problems with the individuals themselves. In other cases, it 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. Typical behaviors of ADHD occur more commonly in children who have experienced violence and emotional abuse.
The social construct theory of ADHD suggests that because the boundaries between "normal" and "abnormal" behavior are socially constructed, (i.e. jointly created and validated by all members of society, and in particular by physicians, parents, teachers, and others) it then follows that subjective valuations and judgements determine which diagnostic criteria are used and, thus, the number of people affected. This could lead to the 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 then given a name".
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. This effect has been seen across a number of countries. They also appear to use ADHD medications at nearly twice the rate as their peers.
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.
The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls. Inter-hemispheric asymmetries in white matter tracts have also been noted in ADHD youths, suggesting that disruptions in temporal integration may be related to the behavioral characteristics of ADHD.
The symptoms of ADHD arise from a deficiency in certain executive functions (e.g., attentional control, inhibitory control, and working memory). Executive functions are a set of cognitive processes that are required to successfully select and monitor behaviors that facilitate the attainment of one's chosen goals. The executive function impairments that occur in ADHD individuals result in problems with staying organized, time keeping, excessive procrastination, maintaining concentration, paying attention, ignoring distractions, regulating emotions, and remembering details. People with ADHD appear to have unimpaired long-term memory, and deficits in long-term recall appear to be attributed to impairments in working 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 often find it difficult to focus on long-term over short-term rewards, and exhibit impulsive behavior for short-term rewards.
ADHD is diagnosed by an assessment of a child's 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.
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.
As with many other psychiatric disorders, formal diagnosis should be 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 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.
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 first two 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). The symptoms must be inappropriate for a child of that age and there must be clear evidence that they are causing social, school or work related problems.
In the implementation version of ICD-11, the disorder is classified under 6A05 (Attention deficit hyperactivity disorder) and hyperkinetic disorder no longer exists.
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.
It is estimated that between 2-5% of adults have ADHD. Around 25-50% of children with ADHD continue to experience ADHD symptoms into adulthood, while the rest experiences fewer or no symptoms. Currently, most adults remain untreated. Many adults with ADHD without diagnosis and treatment have a disorganized life and some use non-prescribed drugs or 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 they 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-V criteria do specifically deal with adults, unlike those in DSM-IV, which were criticized for not being appropriate for adults; those who presented differently may lead to the claim that they outgrew the diagnosis.
ADHD symptoms which are related to other disorders
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 hyperactivity and inattentiveness.Obstructive sleep apnea can also cause ADHD type symptoms.
Reviews of ADHD biomarkers have noted that platelet monoamine oxidase expression, urinary norepinephrine, urinary MHPG, and urinary phenethylamine levels consistently differ between ADHD individuals and healthy control. These measurements could potentially serve as diagnostic biomarkers for ADHD, but more research is needed to establish their diagnostic utility. Urinary and blood plasma phenethylamine concentrations are lower in ADHD individuals relative to controls and the two most commonly prescribed drugs for ADHD, amphetamine and methylphenidate, increase phenethylamine biosynthesis in treatment-responsive individuals with ADHD. Lower urinary phenethylamine concentrations are also associated with symptoms of inattentiveness in ADHD individuals.Electroencephalography (EEG) is not accurate enough to make the diagnosis.
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. In those who have trouble focusing on long-term rewards, a large amount of positive reinforcement improves task performance. ADHD stimulants also improve persistence and task performance in children with ADHD.
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.ADHD-specific support groups can provide information 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.
Regular physical exercise, particularly aerobic exercise, is an effective add-on treatment for ADHD in children and adults, particularly when combined with stimulant medication, although the best intensity and type of aerobic exercise for improving symptoms are not currently known. In particular, the long-term effects of regular aerobic exercise in ADHD individuals include better behavior and motor abilities, improved executive functions (including attention, inhibitory control, and planning, among other cognitive domains), faster information processing speed, and better memory. Parent-teacher ratings of behavioral and socio-emotional outcomes in response to regular aerobic exercise include: better overall function, reduced ADHD symptoms, better self-esteem, reduced levels of anxiety and depression, fewer somatic complaints, better academic and classroom behavior, and improved social behavior. Exercising while on stimulant medication augments the effect of stimulant medication on executive function. It is believed that these short-term effects of exercise are mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.
There are a number of non-stimulant medications, such as atomoxetine, bupropion, guanfacine, and clonidine that may be used as alternatives, or added to stimulant therapy. 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. Atomoxetine, due to its lack of addiction liability, may be preferred in those who are at risk of recreational or compulsive stimulant use. There is little evidence on the effects of medication on social behaviors. As of June 2015[update], the long-term effects of ADHD medication have yet to be fully determined.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. A 2018 review found the greatest short term benefit with methylphenidate in children and amphetamines in adults.
Guidelines on when to use medications vary by country, with the United Kingdom's National Institute for Health and Care Excellence (NICE) recommending use for children only in severe cases, though for adults medication is a first-line treatment. While most United States guidelines recommend medications in most age groups. Medications are not recommended for preschool children. Underdosing of stimulants can occur and result in a lack of response or later loss of effectiveness. This is particularly common in adolescents and adults as approved dosing is based on school-aged children, causing some practitioners to use weight based or benefit based off-label dosing instead. School-age boys are twice as likely as their female counterparts to take medication, while among adults, women are far more likely to take medication than men.[medical ]
While stimulants and atomoxetine are usually safe, there are side-effects and contraindications to their use. There is low quality evidence of an association between methylphenidate and both serious and non-serious harmful side effects when taken by children and adolescents. Careful monitoring of children while taking this medication is recommended. A large overdose on ADHD stimulants is commonly associated with symptoms such as stimulant psychosis and mania. Although very rare, at therapeutic doses these events appear to occur in approximately 0.1% of individuals within the first several weeks after starting amphetamine therapy. Administration of an antipsychotic medication has been found to effectively resolve the symptoms of acute amphetamine psychosis. Regular monitoring has been recommended in those on long-term treatment. Stimulant therapy should be stopped periodically to assess continuing need for medication, decrease possible growth delay, and reduce tolerance. Long-term misuse of stimulant medications at doses above the therapeutic range for ADHD treatment is associated with addiction and dependence. Untreated ADHD, however, is also associated with elevated risk of substance use disorders 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.
Dietary modifications may be of benefit to a small proportion of children with ADHD. A 2013 meta-analysis found less than a third of children with ADHD see some improvement in symptoms with free fatty acid supplementation or decreased eating of artificial food coloring. These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications. This review also found that evidence does not support removing other foods from the diet to treat ADHD. A 2014 review found that an elimination diet results in a small overall benefit. A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is discouraged. Chronic deficiencies of iron, magnesium and iodine may have a negative impact on ADHD symptoms. There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD. In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD. However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD. There is evidence of a modest benefit of omega 3 fatty acid supplementation, but it is not recommended in place of traditional medication.
ADHD persists into adulthood in about 30-50% of cases. Those affected are likely to develop coping mechanisms as they mature, thus compensating to some extent for their previous symptoms. Children with ADHD have a higher risk of unintentional injuries. Effects of medication on functional impairment and quality of life (e.g. reduced risk of accidents) have been found across multiple domains. But learning disorders and executive function deficits do not seem to respond to ADHD medications.
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-5 will increase the percentage of people diagnosed with ADHD, especially among adults.
Timeline of ADHD diagnostic criteria, prevalence, and treatment
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.[page needed] The first clear description of ADHD is credited to George Still in 1902 during a series of lectures he gave to the Royal College of Physicians of London. He noted both nature and nurture could be influencing this disorder.
Tredgold proposed an association between brain damage and behavioral or learning problems which was able to be validated by the encephalitis lethargica epidemic from 1917 through 1928.
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," and 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-5 in 2013. Other terms have included "minimal brain damage" used in the 1930s.
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. The use of stimulants to treat ADHD was first described in 1937. Charles Bradley gave the children with behavioral disorders benzedrine and found it improved academic performance and behavior.
Until the 1990s, many studies "implicated the prefrontal-striatal network as being smaller in children with ADHD". During this same period, a genetic component was identified and ADHD was acknowledged to be a persistent, long-term disorder which lasted from childhood into adulthood. ADHD was split into the current three subtypes beecause of a field trial completed by Lahey and colleagues.
ADHD, its diagnosis, and its treatment have been controversial since the 1970s. The controversies involve clinicians, teachers, policymakers, parents, and the media. Positions range from the view that ADHD is within the normal range of behavior to the hypothesis that ADHD is a genetic condition. Other areas of controversy include the use of stimulant medications in children, the method of diagnosis, and the possibility of overdiagnosis. In 2009, 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 in a The New York Times article. In contrast, a 2014 peer-reviewed medical literature review indicated that ADHD is underdiagnosed in adults.
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, that is, the turning of the previously 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 greater number of people with mild symptoms.
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^Bridgett DJ, Walker ME (March 2006). "Intellectual functioning in adults with ADHD: a meta-analytic examination of full scale IQ differences between adults with and without ADHD". Psychological Assessment. 18 (1): 1-14. doi:10.1037/1040-3518.104.22.168. PMID16594807.
^Burt SA (July 2009). "Rethinking environmental contributions to child and adolescent psychopathology: a meta-analysis of shared environmental influences". Psychological Bulletin. 135 (4): 608-37. doi:10.1037/a0015702. PMID19586164.
^ abBerry 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. CiteSeerX10.1.1.329.563. doi:10.2174/157488707779318107. PMID18473983. Archived from the original on 1 February 2017. Although there is little direct evidence, changes in trace amines, in particular PE, have been identified as a possible factor for the onset of attention deficit/hyperactivity disorder (ADHD). ... Further, amphetamines, which have clinical utility in ADHD, are good ligands at trace amine receptors. Of possible relevance in this aspect is modafanil, which has shown beneficial effects in ADHD patients and has been reported to enhance the activity of PE at TAAR1. Conversely, methylphenidate, ...showed poor efficacy at the TAAR1 receptor. In this respect it is worth noting that the enhancement of functioning at TAAR1 seen with modafanil was not a result of a direct interaction with TAAR1.
^ abcGlover V (April 2011). "Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 52 (4): 356-67. doi:10.1111/j.1469-7610.2011.02371.x. PMID21250994.
^ abCardo E, Nevot A, Redondo M, Melero A, de Azua B, García-De la Banda G, Servera M (March 2010). "[Attention deficit disorder and hyperactivity: a pattern of evolution?]" [Attention deficit disorder and hyperactivity: a pattern of evolution?]. Revista de Neurologia (in Spanish). 50 Suppl 3: S143-7. PMID20200842.
^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]". Fortschritte der Neurologie-Psychiatrie (Review) (in German). 79 (9): 500-6. doi:10.1055/s-0031-1273360. PMID21739408.
^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 Paediatrica (Review. Research Support, Non-U.S. Gov't). 101 (8): 811-8. doi:10.1111/j.1651-2227.2012.02693.x. PMID22458970.
^Abbott LC, Winzer-Serhan UH (April 2012). "Smoking during pregnancy: lessons learned from epidemiological studies and experimental studies using animal models". Critical Reviews in Toxicology (Review). 42 (4): 279-303. doi:10.3109/10408444.2012.658506. PMID22394313.
^ abcdSonuga-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". The American Journal of Psychiatry. 170 (3): 275-89. doi:10.1176/appi.ajp.2012.12070991. PMID23360949. Free fatty acid supplementation and artificial food color exclusions appear to have beneficial effects on ADHD symptoms, although the effect of the former are small and those of the latter may be limited to ADHD patients with food sensitivities...
^Tomaska LD, Brooke-Taylor S (2014). "Food Additives - General". In Motarjemi Y, Moy GG, Todd EC. Encyclopedia of Food Safety. 3 (1st ed.). Amsterdam: Elsevier/Academic Press. pp. 449-54. ISBN978-0-12-378613-5. OCLC865335120.
^ abcdefghijkMalenka 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, 315, 318-323. ISBN978-0-07-148127-4. 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.
^ abcdefghMalenka 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. ISBN978-0-07-148127-4. 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. NOTE: DA: dopamine, LC: locus coeruleus, VTA: ventral tegmental area, 5HT: serotonin (5-hydroxytryptamine)
^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". The American Journal of Psychiatry. 169 (3): 264-72. doi:10.1176/appi.ajp.2011.11060940. PMID22294258.
^Cortese S (September 2012). "The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD): what every clinician should know". European Journal of Paediatric Neurology. 16 (5): 422-33. doi:10.1016/j.ejpn.2012.01.009. PMID22306277.
^Lesch KP, Merker S, Reif A, Novak M (June 2013). "Dances with black widow spiders: dysregulation of glutamate signalling enters centre stage in ADHD". European Neuropsychopharmacology. 23 (6): 479-91. doi:10.1016/j.euroneuro.2012.07.013. PMID22939004.
^ abDiamond A (2013). "Executive functions". Annual Review of Psychology. 64: 135-68. doi:10.1146/annurev-psych-113011-143750. PMC4084861. PMID23020641. 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.
^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?". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 51 (8): 895-904. doi:10.1111/j.1469-7610.2010.02248.x. PMID20406332.
^Nigg JT, Willcutt EG, Doyle AE, Sonuga-Barke EJ (June 2005). "Causal heterogeneity in attention-deficit/hyperactivity disorder: do we need neuropsychologically impaired subtypes?". Biological Psychiatry. 57 (11): 1224-30. doi:10.1016/j.biopsych.2004.08.025. PMID15949992.
^ abcdModesto-Lowe V, Chaplin M, Soovajian V, Meyer A (July 2013). "Are motivation deficits underestimated in patients with ADHD? A review of the literature". Postgraduate Medicine. 125 (4): 47-52. doi:10.3810/pgm.2013.07.2677. PMID23933893. 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.
^Ogrim G, Kropotov J, Hestad K (August 2012). "The quantitative EEG theta/beta ratio in attention deficit/hyperactivity disorder and normal controls: sensitivity, specificity, and behavioral correlates". Psychiatry Research. 198 (3): 482-8. doi:10.1016/j.psychres.2011.12.041. PMID22425468.
^Smith BJ, Barkley RA, Shapiro CJ (2007). "Attention-Deficit/Hyperactivity Disorder". In Mash EJ, Barkley RA. Assessment of Childhood Disorders (4th ed.). New York, NY: Guilford Press. pp. 53-131. ISBN978-1-59385-493-5.
^ abcdScassellati C, Bonvicini C, Faraone SV, Gennarelli M (October 2012). "Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses". Journal of the American Academy of Child and Adolescent Psychiatry. 51 (10): 1003-1019.e20. doi:10.1016/j.jaac.2012.08.015. PMID23021477.
^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". Clinical Psychology Review. 29 (2): 129-40. doi:10.1016/j.cpr.2008.11.001. PMID19131150.
^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". The Psychiatric Clinics of North America. 32 (1): 39-56. doi:10.1016/j.psc.2008.10.001. PMID19248915.
^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". Clinical EEG and Neuroscience. 40 (3): 180-9. doi:10.1177/155005940904000311. PMID19715181.
^Cortese S, Ferrin M, Brandeis D, Holtmann M, Aggensteiner P, Daley D, Santosh P, Simonoff E, Stevenson J, Stringaris A, Sonuga-Barke EJ (June 2016). "Neurofeedback for Attention-Deficit/Hyperactivity Disorder: Meta-Analysis of Clinical and Neuropsychological Outcomes From Randomized Controlled Trials". Journal of the American Academy of Child and Adolescent Psychiatry. 55 (6): 444-55. doi:10.1016/j.jaac.2016.03.007. hdl:1854/LU-8123796. PMID27238063.
^Bjornstad G, Montgomery P (April 2005). Bjornstad GJ, ed. "Family therapy for attention-deficit disorder or attention-deficit/hyperactivity disorder in children and adolescents". The Cochrane Database of Systematic Reviews (2): CD005042. doi:10.1002/14651858.CD005042.pub2. PMID15846741.
^ abKamp CF, Sperlich B, Holmberg HC (July 2014). "Exercise reduces the symptoms of attention-deficit/hyperactivity disorder and improves social behaviour, motor skills, strength and neuropsychological parameters". Acta Paediatrica. 103 (7): 709-14. doi:10.1111/apa.12628. PMID24612421. We may conclude that all different types of exercise ... attenuate the characteristic symptoms of ADHD and improve social behaviour, motor skills, strength and neuropsychological parameters without any undesirable side effects. Available reports do not reveal which type, intensity, duration and frequency of exercise is most effective
^ abCastells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M (June 2011). Castells X, ed. "Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults". The Cochrane Database of Systematic Reviews (6): CD007813. doi:10.1002/14651858.CD007813.pub2. PMID21678370.
^Storebø OJ, Ramstad E, Krogh HB, Nilausen TD, Skoog M, Holmskov M, et al. (November 2015). "Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD)". The Cochrane Database of Systematic Reviews. 11 (11): CD009885. doi:10.1002/14651858.CD009885.pub2. PMID26599576.
^ abRuiz-Goikoetxea M, Cortese S, Aznarez-Sanado M, Magallón S, Alvarez Zallo N, Luis EO, de Castro-Manglano P, Soutullo C, Arrondo G (January 2018). "Risk of unintentional injuries in children and adolescents with ADHD and the impact of ADHD medications: A systematic review and meta-analysis". Neuroscience and Biobehavioral Reviews. 84: 63-71. doi:10.1016/j.neubiorev.2017.11.007. PMID29162520.
^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". European Child & Adolescent Psychiatry. 22 (4): 203-16. doi:10.1007/s00787-012-0346-x. PMID23179416.
^ abKiely B, Adesman A (June 2015). "What we do not know about ADHD... yet". Current Opinion in Pediatrics. 27 (3): 395-404. doi:10.1097/MOP.0000000000000229. PMID25888152. In addition, a consensus has not been reached on the optimal diagnostic criteria for ADHD. Moreover, the benefits and long-term effects of medical and complementary therapies for this disorder continue to be debated. These gaps in knowledge hinder the ability of clinicians to effectively recognize and treat ADHD.
^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): 286-90. doi:10.1097/YCO.0b013e32834742db. PMID21519262.
^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): 185-98. doi:10.1001/jamapsychiatry.2013.277. PMID23247506.
^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 Scandinavica. 125 (2): 114-26. doi:10.1111/j.1600-0447.2011.01786.x. PMID22118249. 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.
^Cortese, Samuele; Adamo, Nicoletta; Del Giovane, Cinzia; Mohr-Jensen, Christina; Hayes, Adrian J; Carucci, Sara; Atkinson, Lauren Z; Tessari, Luca; Banaschewski, Tobias; Coghill, David; Hollis, Chris; Simonoff, Emily; Zuddas, Alessandro; Barbui, Corrado; Purgato, Marianna; Steinhausen, Hans-Christoph; Shokraneh, Farhad; Xia, Jun; Cipriani, Andrea (September 2018). "Comparative efficacy and tolerability of medications for attention-deficit hyperactivity disorder in children, adolescents, and adults: a systematic review and network meta-analysis". The Lancet Psychiatry. 5 (9): 727-738. doi:10.1016/S2215-0366(18)30269-4.
^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): 347-66, ix. doi:10.1016/j.chc.2007.11.004. PMID18295150.
^Biederman, Joseph (2003). "New-Generation Long-Acting Stimulants for the Treatment of Attention-Deficit/Hyperactivity Disorder". Medscape. Archived from the original on 7 December 2003. Retrieved 2016. As most treatment guidelines and prescribing information for stimulant medications relate to experience in school-aged children, prescribed doses for older patients are lacking. Emerging evidence for both methylphenidate and Adderall indicate that when weight-corrected daily doses, equipotent with those used in the treatment of younger patients, are used to treat adults with ADHD, these patients show a very robust clinical response consistent with that observed in pediatric studies. These data suggest that older patients may require a more aggressive approach in terms of dosing, based on the same target dosage ranges that have already been established - for methylphenidate, 1-1.5-2 mg/kg/day, and for D,L-amphetamine, 0.5-0.75-1 mg/kg/day.... In particular, adolescents and adults are vulnerable to underdosing, and are thus at potential risk of failing to receive adequate dosage levels. As with all therapeutic agents, the efficacy and safety of stimulant medications should always guide prescribing behavior: careful dosage titration of the selected stimulant product should help to ensure that each patient with ADHD receives an adequate dose, so that the clinical benefits of therapy can be fully attained.
^ abStorebø OJ, Pedersen N, Ramstad E, Kielsholm ML, Nielsen SS, Krogh HB, Moreira-Maia CR, Magnusson FL, Holmskov M, Gerner T, Skoog M, Rosendal S, Groth C, Gillies D, Buch Rasmussen K, Gauci D, Zwi M, Kirubakaran R, Håkonsen SJ, Aagaard L, Simonsen E, Gluud C (May 2018). "Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents - assessment of adverse events in non-randomised studies". The Cochrane Database of Systematic Reviews. 5: CD012069. doi:10.1002/14651858.CD012069.pub2. PMID29744873.
^ abcShoptaw SJ, Kao U, Ling W (January 2009). Shoptaw SJ, Ali R, ed. "Treatment for amphetamine psychosis". The Cochrane Database of Systematic Reviews (1): CD003026. doi:10.1002/14651858.CD003026.pub3. PMID19160215. A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. More common (about 18%) is for frequent amphetamine users to report psychotic symptoms that are sub-clinical and that do not require high-intensity intervention ... About 5-15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) ... Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.
^"Adderall XR Prescribing Information"(PDF). United States Food and Drug Administration. Shire US Inc. December 2013. Archived(PDF) from the original on 30 December 2013. Retrieved 2013. Treatment-emergent psychotic or manic symptoms, e.g., hallucinations, delusional thinking, or mania in children and adolescents without prior history of psychotic illness or mania can be caused by stimulants at usual doses. ... In a pooled analysis of multiple short-term, placebo controlled studies, such symptoms occurred in about 0.1% (4 patients with events out of 3482 exposed to methylphenidate or amphetamine for several weeks at usual doses) of stimulant-treated patients compared to 0 in placebo-treated patients.
^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): 611-6. doi:10.1542/peds.2008-0185. PMID19171629.
^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". Clinical Neuropharmacology. 33 (4): 204-6. doi:10.1097/WNF.0b013e3181e29174. PMID20571380.
^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?". European Neuropsychopharmacology. 21 (8): 584-99. doi:10.1016/j.euroneuro.2011.03.008. PMID21530185.
^ abcMalenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY, eds. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 323, 368. ISBN978-0-07-148127-4. supervised use of stimulants at therapeutic doses may decrease risk of experimentation with drugs to self-medicate symptoms. Second, untreated ADHD may lead to school failure, peer rejection, and subsequent association with deviant peer groups that encourage drug misuse. ... amphetamines and methylphenidate are used in low doses to treat attention deficit hyperactivity disorder and in higher doses to treat narcolepsy (Chapter 12). Despite their clinical uses, these drugs are strongly reinforcing, and their long-term use at high doses is linked with potential addiction
^Krause J (April 2008). "SPECT and PET of the dopamine transporter in attention-deficit/hyperactivity disorder". Expert Review of Neurotherapeutics. 8 (4): 611-25. doi:10.1586/1473722.214.171.1241. PMID18416663. Zinc binds at ... extracellular sites of the DAT , serving as a DAT inhibitor. In this context, controlled double-blind studies in children are of interest, which showed positive effects of zinc [supplementation] on symptoms of ADHD [105,106]. It should be stated that at this time [supplementation] with zinc is not integrated in any ADHD treatment algorithm.
^Rasmussen N (July 2006). "Making the first anti-depressant: amphetamine in American medicine, 1929-1950". Journal of the History of Medicine and Allied Sciences. 61 (3): 288-323. doi:10.1093/jhmas/jrj039. PMID16492800. (Subscription required (help)).
^Gross, M. (1995). "Origin of Stimulant Use for Treatment of Attention Deficit Disorder". American Journal of Psychiatry: 298-299.
^Brown, W. (1998). "Charles Bradley, M.D.". American Journal of Psychiatry: 968.
^Barkley, R. (2006). Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. New York: Guilford.
^Biederman, J.; Faraone, S.; Keenan, K.; Knee, D.; Tsuang, M. (1990). "Family-Genetic and Psychosocial Risk Factors in DSM-III Attention Deficit Disorder". Journal of the American Academy of Child and Adolescent Psychiatry: 526-533.
^Lahey, B.; Applegate, B.; McBurnett, K.; Biederman, J.; Greenhill, L.; Hynd, G; Barkley, R.; Newcorn, J.; Jensen, P. (1994). "DSM-IV Field Trials for Attention Deficit Hyperactivity Disorder in Children and Adolescents". The American Journal of Psychiatry: 1673-1685.
^Faraone SV (February 2005). "The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder". European Child & Adolescent Psychiatry. 14 (1): 1-10. doi:10.1007/s00787-005-0429-z. PMID15756510. (Subscription required (help)).