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Attention deficit hyperactivity disorder

From EverybodyWiki Bios & Wiki

Attention deficit hyperactivity disorder
Other namesAttention-deficit disorder, hyperkinetic disorder (ICD-10)
An image of children
Children with ADHD may find it more difficult than others to focus and to complete their schoolwork.
SpecialtyLua error in Module:WikidataIB at line 665: attempt to index field 'wikibase' (a nil value).
SymptomsProblems paying attention, excessive activity, difficulty controlling behavior[1][2]
Usual onsetBefore age 6–12[3]
Duration>6 months[3]
CausesUnknown[4]
Diagnostic methodBased on symptoms after other possible causes ruled out[1]
Differential diagnosisNormally active young child, conduct disorder, oppositional defiant disorder, learning disorder, bipolar disorder[5]
TreatmentCounseling, lifestyle changes, medications[1]
MedicationStimulants, atomoxetine, guanfacine[6][7]
Frequency51.1 million (2015)[8]

Attention deficit hyperactivity disorder (ADHD) is a mental disorder of the neurodevelopmental type.[9][10] It is characterized by problems paying attention, excessive activity, or difficulty controlling behavior which is not appropriate for a person's age.[1][2] The symptoms appear before a person is twelve years old, are present for more than six months, and cause problems in at least two settings (such as school, home, or recreational activities).[3][11] In children, problems paying attention may result in poor school performance.[1] Although it causes impairment, particularly in modern society, many children with ADHD have a good attention span for tasks they find interesting.[12]

Despite being the most commonly studied and diagnosed mental disorder in children and adolescents, the exact cause is unknown in the majority of cases.[4] It affects about 5–7% of children when diagnosed via the DSM-IV criteria[2][13] and 1–2% when diagnosed via the ICD-10 criteria.[14] As of 2015 it is estimated to affect about 51.1 million people globally.[8] Rates are similar between countries and depend mostly on how it is diagnosed.[15] ADHD is diagnosed approximately three times more often in boys than in girls, although the disorder is often overlooked in girls because their symptoms differ from those of boys.[16][17][18] About 30–50% of people diagnosed in childhood continue to have symptoms into adulthood and between 2–5% of adults have the condition.[19][20][21] 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.[11]

ADHD management recommendations vary by country and usually involve some combination of counseling, lifestyle changes, and medications.[1] 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.[22] Canadian and American guidelines recommend that medications and behavioral therapy be used together as a first-line therapy, except in preschool-aged children.[23][24] Stimulant medication therapy is not recommended as a first-line therapy in preschool-aged children in either guideline.[22][24] Treatment with stimulants is effective for up to 14 months; however, its long term effectiveness is unclear.[25][26][27][28] Adolescents and adults tend to develop coping skills which make up for some or all of their impairments.[29]

The medical literature has described symptoms similar to those of ADHD since the 19th century.[30] ADHD, its diagnosis, and its treatment have been considered controversial since the 1970s.[31] 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.[32] 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.[33][34][35] 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.[36][37]

Signs and symptoms[edit]

ADHD symptoms[38]
Inattention Hyperactivity-impulsivity
  • gives no close attention to details
  • has trouble holding attention on tasks
  • has trouble organizing tasks and activities
  • loses things necessary for tasks
  • appears forgetful in daily activities
  • 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"
  • talks excessively
  • 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.[39][40] Academic difficulties are frequent as are problems with relationships.[39] 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.[41]

According to the fifth version 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[2] and they must cause significant problems functioning in at least two settings (e.g., social, school/work, or home).[2] The full criteria must have been met prior to age twelve in order to receive a diagnosis of ADHD.[2]

Subtypes[edit]

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).[2][41]

A child 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:[2][42]

  • 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 child 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:[2][42]

  • Fidget or squirm a great deal
  • 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 performing quiet tasks or activities
  • Be 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 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.[43] Symptoms of hyperactivity tend to go away with age and turn into "inner restlessness" in teens and adults with ADHD.[19]

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.[44]

Difficulties managing anger are more common in children with ADHD[45] as are poor handwriting[46] and delays in speech, language and motor development.[47][48] 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.[12]

Associated disorders[edit]

In children, ADHD occurs with other disorders about two-thirds of the time.[12] Some commonly associated conditions include:

  • Epilepsy[49]
  • Tourette's syndrome[49]
  • Autistic spectrum disorder (ASD): this disorder affects social skills, ability to communicate, behaviour, and interests.[49]
  • Anxiety disorders have been found to occur more commonly in the ADHD population.[50]
  • 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.[51] ADHD, however, is not considered a learning disability, but it very frequently causes academic difficulties.[51]
  • Obsessive–compulsive disorder (OCD) can co-occur with ADHD and shares many of its characteristics.[52]
  • Substance use disorders. Adolescents and adults with ADHD are at increased risk of substance abuse.[19] This is most commonly seen with alcohol or cannabis.[19] The reason for this may be an altered reward pathway in the brains of ADHD individuals.[19] This makes the evaluation and treatment of ADHD more difficult, with serious substance misuse problems usually treated first due to their greater risks.[53][54]
  • 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.[55][56] 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.[57] Melatonin is sometimes used in children who have sleep onset insomnia.[58]
  • Oppositional defiant disorder (ODD) and conduct disorder (CD), which occur with ADHD in about 50% and 20% of cases respectively.[59] They are characterized by antisocial behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, and stealing.[52] About half of those with hyperactivity and ODD or CD develop antisocial personality disorder in adulthood.[60] Brain imaging supports that conduct disorder and ADHD are separate conditions.[61]
  • 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.[62]
  • 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.[63]
  • Mood disorders (especially bipolar disorder and major depressive disorder). Boys diagnosed with the combined ADHD subtype are more likely to have a mood disorder.[50] Adults with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions.[64]
  • Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron deficiency anemia.[65][66] However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders.[67]
  • People with ADHD have an increased risk of persistent bed wetting.[68]
  • 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,[69] 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.[70]

Intelligence[edit]

Overall, studies have shown that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests.[71] 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.[71] 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.[72]

Causes[edit]

Most ADHD cases are of unknown causes.[73][74] It is believed to involve interactions between genetics, the environment, and social factors.[73][74] Certain cases are related to previous infection of or trauma to the brain.[73]

Genetics[edit]

Twin studies indicate that the disorder is often inherited from one's parents with genetics determining about 75% of cases.[25][75][76] Siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.[77] Genetic factors are also believed to be involved in determining whether ADHD persists into adulthood.[78]

Typically, a number of genes are involved, many of which directly affect dopamine neurotransmission.[79][80] Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.[80][81][82] Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.[79][80] A common variant of a gene called Latrophilin 3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication.[83] The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioral phenotypes, including ADHD symptoms reflecting split attention.[84]

Evolution may have played a role in the high rates of ADHD, particularly hyperactive and impulsive traits in males.[85] 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.[86] 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.[85][86] In certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual.[85][86][87] 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.[87] In certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.[88]

People with Down syndrome are more likely to have ADHD.[89]

Environment[edit]

See also: Diet and attention deficit hyperactivity disorder

In addition to genetics, some environmental factors might play a role in causing ADHD.[90] Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it.[91] Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD.[4][92] Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.[93] Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.[4][94]

Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk[4][95] as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71).[96] There is an association between long term but not short term use of acetaminophen during pregnancy and ADHD.[97][98] At least 30% of children with a traumatic brain injury later develop ADHD[99] and about 5% of cases are due to brain damage.[100]

Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms,[4][101] but the evidence is weak and may only apply to children with food sensitivities.[101][102][103] The United Kingdom and the European Union have put in place regulatory measures based on these concerns.[104] In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.[105]

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.[40]

Society[edit]

In some cases, the diagnosis of ADHD may reflect a dysfunctional family or a poor educational system, rather than problems with the individuals themselves.[106] 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.[100] Typical behaviors of ADHD occur more commonly in children who have experienced violence and emotional abuse.[25]

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.[107] 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.[18] Thomas Szasz, a supporter of this theory, has argued that ADHD was " ... invented and then given a name".[108]

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.[109][110][111] This effect has been seen across a number of countries.[111] They also appear to use ADHD medications at nearly twice the rate as their peers.[112]

Pathophysiology[edit]

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.[113][114] 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.[113][115] The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behavior), motivation, reward perception, and motor function;[113][114][115] these pathways are known to play a central role in the pathophysiology of ADHD.[113][115][116][117] Larger models of ADHD with additional pathways have been proposed.[114][116][117]

Brain structure[edit]

Left prefrontal cortex is often affected in ADHD.

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.[114][118] The posterior parietal cortex also shows thinning in ADHD individuals compared to controls.[114] 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.[114][116][117]

The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls.[119] 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.[120]

Neurotransmitter pathways[edit]

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.[121] Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system.[113][114][115] ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems.[114][115][122] There may additionally be abnormalities in serotoninergic, glutamatergic, or cholinergic pathways.[122][123][124]

Executive function and motivation[edit]

The symptoms of ADHD arise from a deficiency in certain executive functions (e.g., attentional control, inhibitory control, and working memory).[57][114][115][125] 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.[57][115][125] 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.[57][114][115] 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.[57][126] The criteria for an executive function deficit are met in 30–50% of children and adolescents with ADHD.[127] 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.[128] 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.[57]

ADHD has also been associated with motivational deficits in children.[129] Children with ADHD often find it difficult to focus on long-term over short-term rewards, and exhibit impulsive behavior for short-term rewards.[129]

Diagnosis[edit]

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.[53] It often takes into account feedback from parents and teachers[11] with most diagnoses begun after a teacher raises concerns.[100] It may be viewed as the extreme end of one or more continuous human traits found in all people.[130] 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.[131]

In North America, DSM-5 criteria are 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.[18] It is classified as neurodevelopmental psychiatric disorder.[10][19] Additionally, it is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder, and antisocial personality disorder.[132] A diagnosis does not imply a neurological disorder.[25]

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.[133]

Diagnosis of ADHD using quantitative electroencephalography (QEEG) is an ongoing area of investigation, although the value of QEEG in ADHD is currently unclear.[134][135] In the United States, the Food and Drug Administration has approved the use of QEEG to evaluate ADHD.[136] The approved test uses the ratio of EEG theta to beta activity to guide diagnosis; however, at least five studies have failed to replicate the finding.[137][138]

Self-rating scales, such as the ADHD rating scale and the Vanderbilt ADHD diagnostic rating scale are used in the screening and evaluation of ADHD.[139]

Diagnostic and Statistical Manual[edit]

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:[2][38]

  1. ADHD predominantly inattentive type (ADHD-PI) presents with symptoms including being easily distracted, forgetful, daydreaming, disorganization, poor concentration, and difficulty completing tasks.[3][2]
  2. 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.[3][2]
  3. ADHD, combined type is a combination of the first two subtypes.[3][2]

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.[140] 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).[3] The symptoms must be inappropriate for a child of that age[3][141] and there must be clear evidence that they are causing social, school or work related problems.[140]

International Classification of Diseases[edit]

In the tenth revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) by the World Health Organization, the symptoms of "hyperkinetic disorder" are analogous to ADHD in the DSM-5. When a conduct disorder (as defined by ICD-10)[47] 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.[47]

In the implementation version of ICD-11, the disorder is classified under 6A05 (Attention deficit hyperactivity disorder) and hyperkinetic disorder no longer exists.[142]

Adults[edit]

Main article: Adult attention deficit hyperactivity disorder

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.[19] 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.[19]

It is estimated that between 2–5% of adults have ADHD.[19] Around 25–50% of children with ADHD continue to experience ADHD symptoms into adulthood, while the rest experiences fewer or no symptoms.[2][19] Currently, most adults remain untreated.[143] Many adults with ADHD without diagnosis and treatment have a disorganized life and some use non-prescribed drugs or alcohol as a coping mechanism.[29] Other problems may include relationship and job difficulties, and an increased risk of criminal activities.[19] Associated mental health problems include: depression, anxiety disorder, and learning disabilities.[29]

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.[19]

Differential diagnosis[edit]

ADHD symptoms which are related to other disorders[144]
Depression Anxiety disorder Bipolar disorder
  • persistent feeling of anxiety
  • irritability
  • occasional feelings of panic or fear
  • being hyperalert
  • inability to pay attention
  • tire easily
  • low tolerance for stress
  • difficulty maintaining attention
in manic state
in depressive state
  • same symptoms as in depression section

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.[19] Some 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, untreated celiac disease, and head injury.[29][70]

Primary sleep disorders may affect attention and behavior and the symptoms of ADHD may affect sleep.[145] It is thus recommended that children with ADHD be regularly assessed for sleep problems.[146] Sleepiness in children may result in symptoms ranging from the classic ones of yawning and rubbing the eyes, to hyperactivity and inattentiveness.[147] Obstructive sleep apnea can also cause ADHD type symptoms.[147]

Biomarker research[edit]

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.[148][149] These measurements could potentially serve as diagnostic biomarkers for ADHD, but more research is needed to establish their diagnostic utility.[149] 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.[81][148][149] Lower urinary phenethylamine concentrations are also associated with symptoms of inattentiveness in ADHD individuals.[149] Electroencephalography (EEG) is not accurate enough to make the diagnosis.[150]

Management[edit]

Main article: Attention deficit hyperactivity disorder management

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.[151] Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants.[50][122] In those who have trouble focusing on long-term rewards, a large amount of positive reinforcement improves task performance.[129] ADHD stimulants also improve persistence and task performance in children with ADHD.[114][129]

Behavioral therapies[edit]

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.[152][153] Psychological therapies used include: psychoeducational input, behavior therapy, cognitive behavioral therapy (CBT), interpersonal psychotherapy, family therapy, school-based interventions, social skills training, behavioral peer intervention, organization training,[154] parent management training,[25] and neurofeedback.[155] Parent training may improve a number of behavioral problems including oppositional and noncompliant behaviors.[156] It is unclear if neurofeedback is useful.[157]

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.[158] ADHD-specific support groups can provide information and may help families cope with ADHD.[159]

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.[160]

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.[161][162][163] 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.[161][162][163] 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.[161] Exercising while on stimulant medication augments the effect of stimulant medication on executive function.[161] It is believed that these short-term effects of exercise are mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.[161]

Medication[edit]

Stimulant medications are the pharmaceutical treatment of choice.[164][165] They have at least some effect on symptoms, in the short term, in about 80% of people.[28][166] Methylphenidate appears to improve symptoms as reported by teachers and parents.[28][167] Stimulants may also reduce the risk of unintentional injuries in children with ADHD.[168]

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.[164][169] There are no good studies comparing the various medications; however, they appear more or less equal with respect to side effects.[170] Stimulants appear to improve academic performance while atomoxetine does not.[171] Atomoxetine, due to its lack of addiction liability, may be preferred in those who are at risk of recreational or compulsive stimulant use.[19] There is little evidence on the effects of medication on social behaviors.[170] As of June 2015, the long-term effects of ADHD medication have yet to be fully determined.[172][173] 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.[174][175][176]

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.[23] Medications are not recommended for preschool children.[25][177] Underdosing of stimulants can occur and result in a lack of response or later loss of effectiveness.[178] 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.[179][180][181] 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 citation needed][182]

While stimulants and atomoxetine are usually safe, there are side-effects and contraindications to their use.[164] 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.[183] Careful monitoring of children while taking this medication is recommended.[183] A large overdose on ADHD stimulants is commonly associated with symptoms such as stimulant psychosis and mania.[184] 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.[184][185][186] Administration of an antipsychotic medication has been found to effectively resolve the symptoms of acute amphetamine psychosis.[184] Regular monitoring has been recommended in those on long-term treatment.[187] Stimulant therapy should be stopped periodically to assess continuing need for medication, decrease possible growth delay, and reduce tolerance.[188][189] Long-term misuse of stimulant medications at doses above the therapeutic range for ADHD treatment is associated with addiction and dependence.[190][191] Untreated ADHD, however, is also associated with elevated risk of substance use disorders and conduct disorders.[190] The use of stimulants appears to either reduce this risk or have no effect on it.[19][172][190] The safety of these medications in pregnancy is unclear.[192]

Improvement of Sleep[edit]

Main article: Sleep-Related Breathing Disorders (SRBDs) or attention deficit hyperactivity disorder

The Pediatric Sleep Questionnaire (PSQ) developed from the University of Michighan is a questionnaire for parents to fill out on their child. There are 22 questions relating to various behaviors. The final 6 questions specifically relate to behaviors that may not be distinguished from an ADHD diagnosis. These scales for childhood SRBDs, snoring, sleepiness, and behavior are valid and reliable instruments that can be used to identify SRBDs or associated symptom-constructs in clinical research when polysomnography is not feasible.[193]

Diet[edit]

Main article: Diet and attention deficit hyperactivity disorder

Dietary modifications may be of benefit to a small proportion of children with ADHD.[194] 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.[102] These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications.[102] This review also found that evidence does not support removing other foods from the diet to treat ADHD.[102] A 2014 review found that an elimination diet results in a small overall benefit.[105] A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is discouraged.[70] Iron, magnesium and iodine may also have an effect on ADHD symptoms.[195] There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD.[196] In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD.[197] However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD.[198] There is evidence of a modest benefit of omega 3 fatty acid supplementation, but it is not recommended in place of traditional medication.[199][200]

Prognosis[edit]

ADHD persists into adulthood in about 30–50% of cases.[20] Those affected are likely to develop coping mechanisms as they mature, thus compensating to some extent for their previous symptoms.[29] Children with ADHD have a higher risk of unintentional injuries.[168] 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.[201]

Epidemiology[edit]

Main article: Epidemiology of attention deficit hyperactive disorder

ADHD is estimated to affect about 6–7% of people aged 18 and under when diagnosed via the DSM-IV criteria.[13] When diagnosed via the ICD-10 criteria rates in this age group are estimated at 1–2%.[14] 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.[202] If the same diagnostic methods are used, the rates are more or less the same between countries.[15] It is diagnosed approximately three times more often in boys than in girls.[17][18] This difference between sexes may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[203]

Rates of diagnosis and treatment have increased in both the United Kingdom and the United States since the 1970s.[204] This is believed to be primarily due to changes in how the condition is diagnosed[204] and how readily people are willing to treat it with medications rather than a true change in how common the condition is.[14] 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.[205]

History[edit]

Timeline of ADHD diagnostic criteria, prevalence, and treatment
Main article: History of attention deficit hyperactivity disorder

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.[206][207][page needed] ADHD was first clearly described by George Still in 1902.[204]

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."[204] 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.[208] These terms were kept in the DSM-5 in 2013.[2] Other terms have included "minimal brain damage" used in the 1930s.[209]

The use of stimulants to treat ADHD was first described in 1937.[210] In 1934, Benzedrine became the first amphetamine medication approved for use in the United States.[211] Methylphenidate was introduced in the 1950s, and enantiopure dextroamphetamine in the 1970s.[204]

Society and culture[edit]

Main article: Attention deficit hyperactivity disorder controversies

ADHD, its diagnosis, and its treatment have been controversial since the 1970s.[31][32][212] The controversies involve clinicians, teachers, policymakers, parents, and the media. Positions range from the view that ADHD is within the normal range of behavior[53][213] to the hypothesis that ADHD is a genetic condition.[214] Other areas of controversy include the use of stimulant medications in children,[32][215] the method of diagnosis, and the possibility of overdiagnosis.[215] 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.[130] 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.[216] In contrast, a 2014 peer-reviewed medical literature review indicated that ADHD is underdiagnosed in adults.[21]

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.[109] Some sociologists consider ADHD to be an example of the medicalization of deviant behavior, that is, the turning of the previously non-medical issue of school performance into a medical one.[31][100] Most healthcare providers accept ADHD as a genuine disorder, at least in the small number of people with severe symptoms.[100] Among healthcare providers the debate mainly centers on diagnosis and treatment in the much greater number of people with mild symptoms.[34][35][100][216][217][218]

References[edit]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 "Attention Deficit Hyperactivity Disorder". National Institute of Mental Health. March 2016. Archived from the original on 23 July 2016. Retrieved 5 March 2016.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington: American Psychiatric Publishing. pp. 59–65. ISBN 978-0-89042-555-8. Search this book on
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 "Symptoms and Diagnosis". Attention-Deficit / Hyperactivity Disorder (ADHD). Division of Human Development, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention. 29 September 2014. Archived from the original on 7 November 2014. Retrieved 3 November 2014.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 NIMH (2013). "Attention Deficit Hyperactivity Disorder (Easy-to-Read)". National Institute of Mental Health. Archived from the original on 14 April 2016. Retrieved 17 April 2016.
  5. ↑ Ferri FF (2010). Ferri's differential diagnosis : a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders (2nd ed.). Philadelphia, PA: Elsevier/Mosby. pp. Chapter A. ISBN 978-0323076999. Search this book on
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  69. ↑ Instanes JT, Klungsøyr K, Halmøy A, Fasmer OB, Haavik J (February 2018). "Adult ADHD and Comorbid Somatic Disease: A Systematic Literature Review". Journal of Attention Disorders (Systematic Review). 22 (3): 203–228. doi:10.1177/1087054716669589. PMC 5987989. PMID 27664125. Archived from the original on 7 February 2017.open access
  70. ↑ 70.0 70.1 70.2 Ertürk E, Wouters S, Imeraj L, Lampo A (January 2016). "Association of ADHD and Celiac Disease: What Is the Evidence? A Systematic Review of the Literature". Journal of Attention Disorders (Review): 108705471561149. doi:10.1177/1087054715611493. PMID 26825336. Up till now, there is no conclusive evidence for a relationship between ADHD and CD. Therefore, it is not advised to perform routine screening of CD when assessing ADHD (and vice versa) or to implement GFD as a standard treatment in ADHD. Nevertheless, the possibility of untreated CD predisposing to ADHD-like behavior should be kept in mind. ... It is possible that in untreated patients with CD, neurologic symptoms such as chronic fatigue, inattention, pain, and headache could predispose patients to ADHD-like behavior (mainly symptoms of inattentive type), which may be alleviated after GFD treatment. (CD: celiac disease; GFD: gluten-free diet)
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  76. ↑ 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. PMID 19586164.
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  78. ↑ Franke B, Faraone SV, Asherson P, Buitelaar J, Bau CH, Ramos-Quiroga JA, et al. (October 2012). "The genetics of attention deficit/hyperactivity disorder in adults, a review". Molecular Psychiatry. 17 (10): 960–87. doi:10.1038/mp.2011.138. PMC 3449233. PMID 22105624.
  79. ↑ 79.0 79.1 Gizer IR, Ficks C, Waldman ID (July 2009). "Candidate gene studies of ADHD: a meta-analytic review". Human Genetics. 126 (1): 51–90. doi:10.1007/s00439-009-0694-x. PMID 19506906.
  80. ↑ 80.0 80.1 80.2 Kebir O, Tabbane K, Sengupta S, Joober R (March 2009). "Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies". Journal of Psychiatry & Neuroscience. 34 (2): 88–101. PMC 2647566. PMID 19270759.
  81. ↑ 81.0 81.1 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. CiteSeerX 10.1.1.329.563. doi:10.2174/157488707779318107. PMID 18473983. 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.
  82. ↑ Sotnikova TD, Caron MG, Gainetdinov RR (August 2009). "Trace amine-associated receptors as emerging therapeutic targets". Molecular Pharmacology. 76 (2): 229–35. doi:10.1124/mol.109.055970. PMC 2713119. PMID 19389919.
  83. ↑ Arcos-Burgos M, Muenke M (November 2010). "Toward a better understanding of ADHD: LPHN3 gene variants and the susceptibility to develop ADHD". Attention Deficit and Hyperactivity Disorders. 2 (3): 139–47. doi:10.1007/s12402-010-0030-2. PMC 3280610. PMID 21432600.
  84. ↑ Nikolaidis A, Gray JR (June 2010). "ADHD and the DRD4 exon III 7-repeat polymorphism: an international meta-analysis". Social Cognitive and Affective Neuroscience. 5 (2–3): 188–93. doi:10.1093/scan/nsp049. PMC 2894686. PMID 20019071.
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  86. ↑ 86.0 86.1 86.2 Williams J, Taylor E (June 2006). "The evolution of hyperactivity, impulsivity and cognitive diversity". Journal of the Royal Society, Interface. 3 (8): 399–413. doi:10.1098/rsif.2005.0102. PMC 1578754. PMID 16849269.
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  89. ↑ Ekstein S, Glick B, Weill M, Kay B, Berger I (October 2011). "Down syndrome and attention-deficit/hyperactivity disorder (ADHD)". Journal of Child Neurology. 26 (10): 1290–5. doi:10.1177/0883073811405201. PMID 21628698. Archived from the original on 20 November 2015.
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  91. ↑ 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. PMID 21739408.CS1 maint: Unrecognized language (link)
  92. ↑ Eubig PA, Aguiar A, Schantz SL (December 2010). "Lead and PCBs as risk factors for attention deficit/hyperactivity disorder". Environmental Health Perspectives (Review. Research Support, N.I.H., Extramural. Research Support, U.S. Gov't, Non-P.H.S.). 118 (12): 1654–67. doi:10.1289/ehp.0901852. PMC 3002184. PMID 20829149.
  93. ↑ 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. PMID 22458970.
  94. ↑ 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. PMID 22394313.
  95. ↑ Thapar A, Cooper M, Jefferies R, Stergiakouli E (March 2012). "What causes attention deficit hyperactivity disorder?". Archives of Disease in Childhood (Review. Research Support, Non-U.S. Gov't). 97 (3): 260–5. doi:10.1136/archdischild-2011-300482. PMC 3927422. PMID 21903599.
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  97. ↑ Ystrom E, Gustavson K, Brandlistuen RE, Knudsen GP, Magnus P, Susser E, Davey Smith G, Stoltenberg C, Surén P, Håberg SE, Hornig M, Lipkin WI, Nordeng H, Reichborn-Kjennerud T (November 2017). "Prenatal Exposure to Acetaminophen and Risk of ADHD". Pediatrics. 140 (5): e20163840. doi:10.1542/peds.2016-3840. hdl:11250/2465905. PMC 5654387. PMID 29084830.
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  99. ↑ Eme R (April 2012). "ADHD: an integration with pediatric traumatic brain injury". Expert Review of Neurotherapeutics (Review). 12 (4): 475–83. doi:10.1586/ern.12.15. PMID 22449218.
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  101. ↑ 101.0 101.1 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. Archived from the original on 11 September 2015.
  102. ↑ 102.0 102.1 102.2 102.3 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". The American Journal of Psychiatry. 170 (3): 275–89. doi:10.1176/appi.ajp.2012.12070991. PMID 23360949. 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...
  103. ↑ 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. ISBN 978-0-12-378613-5. OCLC 865335120.
  104. ↑ FDA (March 2011), Background Document for the Food Advisory Committee: Certified Color Additives in Food and Possible Association with Attention Deficit Hyperactivity Disorder in Children (PDF), U.S. Food and Drug Administration, archived (PDF) from the original on 6 November 2015
  105. ↑ 105.0 105.1 Nigg JT, Holton K (October 2014). "Restriction and elimination diets in ADHD treatment". Child and Adolescent Psychiatric Clinics of North America (Review). 23 (4): 937–53. doi:10.1016/j.chc.2014.05.010. PMC 4322780. PMID 25220094. an elimination diet produces a small aggregate effect but may have greater benefit among some children. Very few studies enable proper evaluation of the likelihood of response in children with ADHD who are not already preselected based on prior diet response.
  106. ↑ "Mental health of children and adolescents" (PDF). 15 January 2005. Archived from the original (PDF) on 24 October 2009. Retrieved 13 October 2011.
  107. ↑ Parens E, Johnston J (January 2009). "Facts, values, and attention-deficit hyperactivity disorder (ADHD): an update on the controversies". Child and Adolescent Psychiatry and Mental Health. 3 (1): 1. doi:10.1186/1753-2000-3-1. PMC 2637252. PMID 19152690.
  108. ↑ Szasz T (2001). "Psychiatric Medicine: Disorder". Pharmacracy: medicine and politics in America. Westport, CT: Praeger. pp. 101. ISBN 978-0-275-97196-0 – via Google Books. Mental diseases are invented and then given a name, for example attention deficit hyperactivity disorder (ADHD). Search this book on
  109. ↑ 109.0 109.1 Elder TE (September 2010). "The importance of relative standards in ADHD diagnoses: evidence based on exact birth dates". Journal of Health Economics. 29 (5): 641–56. doi:10.1016/j.jhealeco.2010.06.003. PMC 2933294. PMID 20638739.
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  112. ↑ Stockman JA (2016). Year Book of Pediatrics 2014 E-Book. Elsevier Health Sciences. p. 163. ISBN 9780323265270. Search this book on
  113. ↑ 113.0 113.1 113.2 113.3 113.4 Chandler DJ, Waterhouse BD, Gao WJ (May 2014). "New perspectives on catecholaminergic regulation of executive circuits: evidence for independent modulation of prefrontal functions by midbrain dopaminergic and noradrenergic neurons". Frontiers in Neural Circuits. 8: 53. doi:10.3389/fncir.2014.00053. PMC 4033238. PMID 24904299.
  114. ↑ 114.00 114.01 114.02 114.03 114.04 114.05 114.06 114.07 114.08 114.09 114.10 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, 315, 318–323. ISBN 978-0-07-148127-4. 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. Search this book on
  115. ↑ 115.0 115.1 115.2 115.3 115.4 115.5 115.6 115.7 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 978-0-07-148127-4. 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. Search this book on
    NOTE: DA: dopamine, LC: locus coeruleus, VTA: ventral tegmental area, 5HT: serotonin (5-hydroxytryptamine)
  116. ↑ 116.0 116.1 116.2 Castellanos FX, Proal E (January 2012). "Large-scale brain systems in ADHD: beyond the prefrontal-striatal model". Trends in Cognitive Sciences. 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 [10].
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  119. ↑ Hoogman, Martine (2017). "Subcortical brain volume differences in participants with attention deficit hyperactivity disorder in children and adults: a cross-sectional mega-analysis". Lancet Psychiatry. 4 (4): 310–319. doi:10.1016/S2215-0366(17)30049-4. PMC 5933934. PMID 28219628.
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  123. ↑ 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. PMID 22306277.
  124. ↑ 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. PMID 22939004.
  125. ↑ 125.0 125.1 Diamond A (2013). "Executive functions". Annual Review of Psychology. 64: 135–68. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641. 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.
  126. ↑ Skodzik T, Holling H, Pedersen A (February 2017). "Long-Term Memory Performance in Adult ADHD". Journal of Attention Disorders. 21 (4): 267–283. doi:10.1177/1087054713510561. PMID 24232170.
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  129. ↑ 129.0 129.1 129.2 129.3 Modesto-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. 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.
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  131. ↑ "MerckMedicus Modules: ADHD –Pathophysiology". August 2002. Archived from the original on 1 May 2010.
  132. ↑ Wiener JM, Dulcan MK (2004). Textbook Of Child and Adolescent Psychiatry (illustrated ed.). American Psychiatric Publishing. ISBN 978-1-58562-057-9. Archived from the original on 6 May 2016. Retrieved 2 November 2014. Search this book on
  133. ↑ 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): 1007–22. doi:10.1542/peds.2011-2654. PMC 4500647. PMID 22003063.
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  155. ↑ 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. PMID 19715181.
  156. ↑ Daley D, Van Der Oord S, Ferrin M, Cortese S, Danckaerts M, Doepfner M, Van den Hoofdakker BJ, Coghill D, Thompson M, Asherson P, Banaschewski T, Brandeis D, Buitelaar J, Dittmann RW, Hollis C, Holtmann M, Konofal E, Lecendreux M, Rothenberger A, Santosh P, Simonoff E, Soutullo C, Steinhausen HC, Stringaris A, Taylor E, Wong IC, Zuddas A, Sonuga-Barke EJ (October 2017). "Practitioner Review: Current best practice in the use of parent training and other behavioural interventions in the treatment of children and adolescents with attention deficit hyperactivity disorder". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 59 (9): 932–947. doi:10.1111/jcpp.12825. PMID 29083042.
  157. ↑ 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. PMID 27238063.
  158. ↑ 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. PMID 15846741.
  159. ↑ Turkington, Carol; Harris, Joseph (2009). "attention deficit hyperactivity disorder (ADHD)". The Encyclopedia of the Brain and Brain Disorders. Infobase Publishing. pp. 47. ISBN 978-1-4381-2703-3 – via Google Books.
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  161. ↑ 161.0 161.1 161.2 161.3 161.4 Den Heijer AE, Groen Y, Tucha L, Fuermaier AB, Koerts J, Lange KW, Thome J, Tucha O (February 2017). "Sweat it out? The effects of physical exercise on cognition and behavior in children and adults with ADHD: a systematic literature review". Journal of Neural Transmission. 124 (Suppl 1): 3–26. doi:10.1007/s00702-016-1593-7. PMC 5281644. PMID 27400928. Beneficial chronic effects of cardio exercise were found on various functions as well, including executive functions, attention and behavior.
  162. ↑ 162.0 162.1 Kamp 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. PMID 24612421. 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
  163. ↑ 163.0 163.1 Rommel AS, Halperin JM, Mill J, Asherson P, Kuntsi J (September 2013). "Protection from genetic diathesis in attention-deficit/hyperactivity disorder: possible complementary roles of exercise". Journal of the American Academy of Child and Adolescent Psychiatry. 52 (9): 900–10. doi:10.1016/j.jaac.2013.05.018. PMC 4257065. PMID 23972692. The findings from these studies provide some support for the notion that exercise has the potential to act as a protective factor for ADHD.
  164. ↑ 164.0 164.1 164.2 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.
  165. ↑ Castells 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. PMID 21678370.
  166. ↑ Castells, Xavier; Blanco-Silvente, Lídia; Cunill, Ruth (2018-08-09). "Amphetamines for attention deficit hyperactivity disorder (ADHD) in adults". The Cochrane Database of Systematic Reviews. 8: CD007813. doi:10.1002/14651858.CD007813.pub3. ISSN 1469-493X. PMID 30091808.
  167. ↑ Storebø OJ, Ramstad E, Krogh HB, Nilausen TD, Skoog M, Holmskov M, Rosendal S, Groth C, Magnusson FL, Moreira-Maia CR, Gillies D, Buch Rasmussen K, Gauci D, Zwi M, Kirubakaran R, Forsbøl B, Simonsen E, Gluud C (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. PMID 26599576.
  168. ↑ 168.0 168.1 Ruiz-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. PMID 29162520.
  169. ↑ Childress AC, Sallee FR (March 2012). "Revisiting clonidine: an innovative add-on option for attention-deficit/hyperactivity disorder". Drugs of Today. 48 (3): 207–17. doi:10.1358/dot.2012.48.3.1750904. PMID 22462040.
  170. ↑ 170.0 170.1 McDonagh MS, Peterson K, Thakurta S, Low A (December 2011). "Drug Class Review: Pharmacologic Treatments for Attention Deficit Hyperactivity Disorder". Drug Class Reviews. United States Library of Medicine. PMID 22420008. Archived from the original on 31 August 2016.
  171. ↑ 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. PMID 23179416.
  172. ↑ 172.0 172.1 Kiely 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. PMID 25888152. 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.
  173. ↑ Hazell P (July 2011). "The challenges to demonstrating long-term effects of psychostimulant treatment for attention-deficit/hyperactivity disorder". Current Opinion in Psychiatry (Submitted manuscript). 24 (4): 286–90. doi:10.1097/YCO.0b013e32834742db. PMID 21519262.
  174. ↑ 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. PMID 23247506.
  175. ↑ 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". The Journal of Clinical Psychiatry. 74 (9): 902–17. doi:10.4088/JCP.12r08287. PMC 3801446. PMID 24107764.
  176. ↑ 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. 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.
  177. ↑ 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. PMID 18295150.
  178. ↑ Stevens JR, Wilens TE, Stern TA (2013). "Using stimulants for attention-deficit/hyperactivity disorder: clinical approaches and challenges". The Primary Care Companion for CNS Disorders. 15 (2). doi:10.4088/PCC.12f01472. PMC 3733520. PMID 23930227.
  179. ↑ Young, Joel L. (2010). "Individualizing Treatment for Adult ADHD: An Evidence-Based Guideline". Medscape. Archived from the original on 8 May 2015. Retrieved 19 June 2016.
  180. ↑ 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 19 June 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.
  181. ↑ Kessler S (January 1996). "Drug therapy in attention-deficit hyperactivity disorder". Southern Medical Journal. 89 (1): 33–8. doi:10.1097/00007611-199601000-00005. PMID 8545689.
  182. ↑ [non-primary source needed]"2008-12: ADHD drugs prescribed for young women rose 85%". UPI. Retrieved 2018-04-03.
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  184. ↑ 184.0 184.1 184.2 Shoptaw 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. PMID 19160215. 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.
  185. ↑ "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 30 December 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.
  186. ↑ 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. PMID 19171629.
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  188. ↑ 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. PMID 21530185.
  189. ↑ Ibrahim K, Donyai P (July 2015). "Drug Holidays From ADHD Medication: International Experience Over the Past Four Decades". Journal of Attention Disorders. 19 (7): 551–68. doi:10.1177/1087054714548035. PMID 25253684. Archived (PDF) from the original on 30 June 2016.
  190. ↑ 190.0 190.1 190.2 Malenka 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. ISBN 978-0-07-148127-4. 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 Search this book on
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  195. ↑ Konikowska K, Regulska-Ilow B, Rózańska D (2012). "The influence of components of diet on the symptoms of ADHD in children". Roczniki Panstwowego Zakladu Higieny. 63 (2): 127–34. PMID 22928358.
  196. ↑ Arnold LE, DiSilvestro RA (August 2005). "Zinc in attention-deficit/hyperactivity disorder". Journal of Child and Adolescent Psychopharmacology. 15 (4): 619–27. doi:10.1089/cap.2005.15.619. hdl:1811/51593. PMID 16190793.
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  198. ↑ 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:10.1586/14737175.8.4.611. PMID 18416663. Zinc binds at ... extracellular sites of the DAT [103], 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.
  199. ↑ 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". Journal of the American Academy of Child and Adolescent Psychiatry. 50 (10): 991–1000. doi:10.1016/j.jaac.2011.06.008. PMC 3625948. PMID 21961774.
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  205. ↑ 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. (Subscription required (help)). Cite uses deprecated parameter |subscription= (help)
  206. ↑ 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. (Subscription required (help)). Cite uses deprecated parameter |subscription= (help)
  207. ↑ Crichton A (1976) [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 978-0-404-08212-3. Retrieved 17 January 2014 – via Google Books. Search this book on
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  214. ↑ Boseley, Sarah (30 September 2010). "Hyperactive children may suffer from genetic disorder, says study". The Guardian. Archived from the original on 8 July 2017.
  215. ↑ 215.0 215.1 Cormier E (October 2008). "Attention deficit/hyperactivity disorder: a review and update". Journal of Pediatric Nursing. 23 (5): 345–57. doi:10.1016/j.pedn.2008.01.003. PMID 18804015.
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