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Hyperkinetic disorders
ICD-10 F90
ICD-9 314.00 Inattentive, 314.01 Hyperactive-Impulsive and Combined
DiseasesDB {{{DiseasesDB}}}
MedlinePlus {{{MedlinePlus}}}
eMedicine {{{eMedicineSubj}}}/{{{eMedicineTopic}}}
MeSH {{{MeshNumber}}}
Attention-Deficit Hyperactivity Disorder
ICD-10 F90
ICD-9 314.00, 314.01
OMIM 143465
DiseasesDB 6158
MedlinePlus 001551
eMedicine med/3103 {eMedicine2
MeSH {{{MeshNumber}}}

Attention deficit disorder with hyperactivity redirect here

Attention-Deficit Hyperactivity Disorder (ADHD) or Hyperkinetic Disorder as officially known in the US, although ADHD is more commonly used, is generally considered to be a neurodevelopmental condition, largely neurological in nature, affecting about 5% of the world's population.[1][2][3][4] The disorder typically presents itself during childhood, and is characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility.[5][6]

ADHD is currently considered to be a persistent and chronic condition for which no medical cure is available. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults. About 60% of children diagnosed with ADHD retain the disorder as adults.[7] The disorder appears to be highly heritable, with contributions on occasion from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. Certain social critics are highly skeptical that the diagnosis denotes a genuine impairment and question virtually all that is known about ADHD. The symptoms of ADHD are not as profoundly different from normal behavior as are those of other chronic mental disorders. Still, ADHD has been shown to often impair functioning, and many adverse life outcomes are associated with ADHD.

ADHD is a developmental disorder that is often said to be neurological in nature. The term "developmental" means that certain traits such as impulse control significantly lag in development when compared to the general population. This developmental lag has been estimated to range between 30-40 percent in ADHD sufferers in comparison to their peers; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioural or neurodevelopmental disorders. These compounded terms are now more frequently used in the field to describe the disorder.[How to reference and link to summary or text] Those with Predominately Inattentive ADHD often display few or no overt behaviors.[How to reference and link to summary or text]


ADHD Word Cloud 2

ADHD word cloud

Diagnosis is based on a number of strict criteria, laid down in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV ), 4th edition. These criteria have been created for research purposes. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

  • 1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
  • 2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
  • 3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

The terminology of ADD expired with the revision of the most current version of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

DSM-IV Criteria for ADHD[]

I. Either A or B:

A. Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:

  1. Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
  2. Often has trouble keeping attention on tasks or play activities.
  3. Often does not seem to listen when spoken to directly.
  4. Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).
  5. Often has trouble organizing activities.
  6. Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
  7. Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
  8. Is often easily distracted.
  9. Often forgetful in daily activities.

B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:

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


  1. Often blurts out answers before questions have been finished.
  2. Often has trouble waiting one's turn.
  3. Often interrupts or intrudes on others (e.g., butts into conversations or games).

II. Some symptoms that cause impairment were present before age 7 years.

III. Some impairment from the symptoms is present in two or more settings (e.g. at school/work and at home).

IV. There must be clear evidence of significant impairment in social, school, or work functioning.

V. The symptoms do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The symptoms are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).

In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10[8]) 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".[8]

The American Academy of Pediatrics Clinical Practice Guideline for children with ADHD emphasizes that a reliable diagnosis is dependent upon the fulfillment of three criteria:[9]

  • The use of explicit criteria for the diagnosis using the DSM-IV-TR.
  • The importance of obtaining information about the child’s symptoms in more than one setting.
  • The search for coexisting conditions that may make the diagnosis more difficult or complicate treatment planning.

The first criterion can be satisfied by using an ADHD-specific instrument such as the Conners' Rating Scale.[10] The second criterion is best fulfilled by examining the individual's history. This history can be obtained from parents and teachers, or a patient's memory.[11] The requirement that symptoms be present in more than one setting is very important because the problem may not be with the child, but instead with teachers or parents who are too demanding. The use of intelligence testing, psychological testing, and neuropsychological testing (to satisfy the third criterion) is essential in order to find or rule out other factors that might be causing or complicating the problems experienced by the patient.[12]

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

Adults often continue to be impaired by ADD. Adults with ADD are diagnosed under the same criteria, including the stipulation that their symptoms must have been present prior to the age of seven.[13] Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning, usually having more symptoms of inattention and fewer of hyperactivity or impulsiveness than children do.[14]

Main article: ADHD - Genetic factors.
Main article: ADHD - Biological factors.
Main article: ADHD - Theoretical approaches.
Main article: ADHD - Assessment.
Main article: ADHD - Treatment.


A diagnosis of ADHD is based on a checklist of symptoms from DSM-IV-TR. DSM-IV-TR Criteria for ADHD

The Centers for Disease Control and Prevention (CDC) emphasizes that a diagnosis of ADHD should only be made by trained health care providers. This is important, as many of the criteria are shared between other disorders. Different psychiatric disorders may present with the symptoms of inattentiveness (depressive and anxiety disorders) or hyperactivity and distractability (manic phase of bipolar illness).It is also important to note that ADHD symptoms to a certain degree are present in many individuals, what makes it a disorder is a significant severity and pervasiveness of the symptoms leading to prominent functional impairment across different settings (school, work, social relationships).

Comparative behavior[]

It is thought that ADHD adults are less noticeable than children because they may have found certain occupational specialties or niches in which their symptoms are not as problematic, apparent, or impairing. Or, they may have learned better coping skills and other forms of adaptive behavior, such as relying on more organized partners, spouses, or co-workers and friends to help keep them focused on important goals.

While some advocates for ADHD believe that those with ADD/ADHD are very creative, scientific studies have not found this to be the case, finding that they are no more or less creative than other individuals. They may, however, be less productive in their daily lives and often under-achieve in their occupations because of the interference created by their disorder. While a number of famous actors, writers, artists and inventors have been diagnosed with the disorder, the disorder can be found in nearly all occupational specialties.

ADHD is associated with poorer school performance, especially low productivity, with higher occurrences of grade retention (25-50%), suspensions and expulsions (10-20%), and school drop-out rates(30-40%). It is also highly associated with increased difficulties with driving, including greater speeding citations, traffic accidents(2-4 times the risk), and worse accidents leading to a 2-3 fold increase in license suspensions. Those with ADHD are also more likely to be involved in a teen-age pregnancy (30-35%) and carry a greater risk for sexually transmitted disease due to a reduced use of contraception. At work, they may experience not only their usual problems with attention, time management, organization, and poor impulse control, but also have greater risks for on-the-job injuries (more than double the risk). They change jobs more often out of boredom and/or may be fired more often due to poor work performance or difficulties controlling their emotions in the workplace. ADHD is associated with a greater risk for financial difficulties, including over-use of credit, poor saving habits, and even bankruptcies. A conjectured positive aspect of medication is that the person with the disorder can then put into action their individual intelligence and interests.

On the other hand, symptoms are often identified in school or business settings, where individual interests are regarded as distractions and originality is discouraged. In this context, medication serves the purpose of normalizing the school or business atmosphere.


ADHD has been found to exist in every country and culture studied to date. While it is most commonly diagnosed in the United States of America, rates of diagnosis are rising in most industrialized countries as they become more aware of the disorder, its diagnosis, and its management.

According to the 2000 edition of DSM-IV-TR, ADHD affects three to seven percent of all children in the U.S. According to 2002 data from the Centers for Disease Control and Prevention annual National Health Interview Survey, released in 2004, nearly 4 million children younger than 18 in the United States had been diagnosed with attention deficit hyperactivity disorder (ADHD). In general, 5-8% of children likely have ADHD while 4-5% of adults do so. The 2002 data indicated that twice as many boys were diagnosed with ADHD as girls (10% vs. 4%). Some experts theorize that ADHD is under-diagnosed in girls, since their symptoms tend to be less dramatic than those in boys and thus draw less attention from parents and teachers. This may be due to a lower likelihood of aggressive and antisocial behavior in girls and possibly a higher incidence of the inattentive-type of ADHD among girls. Even girls with hyperactivity, however, are under-detected because their hyperactivity might manifest in non-physical ways, such as excessive talking.

Speculation exists to explain the higher diagnostic quota in the U.S. One theory suggests that due to the high-risk traits of ADHD-affected people, it can be suggested that there was a higher prevalence for ADHD in the immigrants heading for America in former centuries than in the general population. No evidence exists at the moment to support such a popular idea. And it is becoming increasingly evident that ADHD can be found in equally high rates of countries with far less migratory patterns, such as in Japan and China.

A study by Olfson (2003) reports that the ADHD treatment rate among Caucasian children is significantly higher than among African Americans (4.4% versus 1.7% in 1997). On the other hand, it is also possible that social and other factors may prevail here. At the University of Florida Regina Bussing has conducted research showing that the obstacles to ADHD treatment are higher in the African-American and female populations. Cultural factors also inhibit treatment being sought.

A different, often related theory, links the statistical difference mainly to a higher problem awareness and competence in the U.S. due to the longer research and public acquaintance with ADHD. Although all of these theories have some support, many are debated.

Testing for ADHD[]

Psychological testing[]

Psychological or psychiatric evaluation for ADHD generally consists of obtaining multiple types of information from multiple sources along with a careful history that is then used in the process of differential diagnosis (differentiation from other mental disorders). These usually include a clinical interview reviewing the DSM-IV criteria for ADHD diagnosis. The interview also needs to rule out as much as possible other types of syndromes which can cause attention problems, such as depression, anxiety, allergies and psychosis. Rating scales can be administered which provide measurement of the person's own view of their symptoms, as well as the views of parents, teachers, and significant others. A review of prior records from school is also critical to establishing the presence of impairment in the educational setting. Psychological testing of intelligence is essential to rule out subnormal intelligence as a contributor to school problems or those in adaptive functioning. Achievement testing of reading, math, spelling, etc. is often necessary to determine if a comorbid learning disability is present, as it often is in 25-50% of clinical cases.

Some tests that may be useful as adjunctive and for confirmatory purposes are the following:

  1. Behavior Rating Inventory of Executive Function.[15] This screening tool has a teacher and parent version. The questionnaires consist of approximately 86 questions answered on a three point scale (Never, Sometimes, Often). A variety of scales are produced regarding executive functions such as planning, impulse control, working memory, etc.
  2. Child Behavior Checklist.[16] This questionnaire has parent and teacher versions for children 1.5-5 and 6-18, and other versions. Scales are produced that include one for attention problems.
  3. Conners' Rating Scales.[17] This instrument has both teacher and parent version and a long and short form. The instrument produces a number of scales focusing on Attention Deficit/Hyperactivity Disorder. Reliability and validity, as reported in the manuel, are good.

Computerized tests of attention are not especially helpful in providing a further independent assessment because they have a high rate of false negatives (real cases of ADHD can pass the tests in 35% or more of cases), they do not correlate well with actual behavioral problems at home or school, and are not especially helpful in determining treatments. Both the American Academy of Pediatrics and American Academy of Child and Adolescent Psychiatry have recommended against the use of such computerized tests for now in view of their lack of appropriate scientific validation as diagnostic tools. In the USA, the process of obtaining referrals for such assessments is being promoted vigorously by the President's New Freedom Commission on Mental Health.

Other forms of testing[]

Neurometrics, PET scans, or SPECT scans have been used for a more objective diagnosis. However, these are not usually suitable for very young children, may result in unacceptable exposure to radiation with no increase in benefit from the scan, and do not have acceptable data on their predictive power to detect ADHD to be used in clinical practice. Currently, the American Academy of Pediatrics and the American Academy of Child and Adolescent Psychiatry recommend against using these neuro-imaging methods for clinical diagnosis of individuals who may have ADHD. They remain useful research tools, however, when studying groups of patients with ADHD. A recent review of all of the scientific literature on scanning in ADHD by Alan Zametkin, M.D., an expert in neuro-imaging at the NIMH (see The ADHD Report, October 2005,, concluded as well that these methods should not be used for clinical diagnosis as they lack adequate scientific information on their accuracy in doing so.

Possible causes[]

ADHD is broadly defined and pervasive, and it is likely that the symptoms attributed to ADHD have a variety of different causes. The initial triggers could include genetic vulnerabilities,allergies,viral or bacterial infections, brain injury, or nutritional deficits. As a result, this seemingly intractable illness occasionally responds to a five day fast (see mainstream treatment section). A 1990 study at the U.S. National Institute of Mental Health correlated ADHD with a series of metabolic abnormalities in the brain, providing further evidence that ADHD is a neurological disorder. While heredity is often indicated, some cases may arise from problems in prenatal development, birth complications, or later neurological damage may contribute to ADHD. The most compelling evidence at the moment suggests some role for maternal smoking and alcohol use to contribute to risk for the disorder (2.5 times increased risk for each). the total number of pregnancy complications may also increase risk for disorder. Prematurity has been repeatedly established as being associated with markedly elevated risk for disorder (30-50%), apparently due to the traumatic effects of birth on the premature brain resulting in minor bleeding and brain immaturity itself. The burgeoning field of epigenetics—the study of what causes genes to express or not express—is examining the questions concerning the interaction of these and other risk factors with genes that also contribute to risk for the disorder. There has been a surge in alternative approaches to causation ADHD, such as excess sugar, TV-viewing, video-game use, etc. but these have little research in support of them and have been vigorously disputed.

Slower brain growth[]

Brain maturation in children with ADHD lags several years behind that of children with no psychiatric or neurological impairments.[18] The reported developmental delays hit a peak of five years in regions at the front of the cortex. The study showed that children with ADHD showed the same sequence of brain development as healthy children, but at a slower pace. A slight developmental speedup occurs in the motor cortex of children with ADAH while there is a late-maturing of the frontal cortex. This developmental mis-match is hypothesized by the study authors as accounting for restlessness and fidgety behavior. The group used MRI to gage the thickness of 40,000 sites in the cortex of 223 youth with ADHD and 223 youth without any impairments. The age range was from seven to thirteen at the start of the study.

Genetic vulnerabilities[]

It has been demonstrated that children who have at least one parent diagnosed with ADHD are more likely to be diagnosed with ADHD. Scientific evidence suggests most strongly that, in many cases, the disorder is genetically transmitted. If a parent has ADHD, their child is 8 times more likely to have ADHD, and a sibling is 5-7 times more likely to also have the same disorder. The concordance between identical twins if one has the disorder is 78-92%. Candidate genes have been identified as having some association with the disorder, as noted above. These genes imply that ADHD may result from an imbalance or deficiency in certain chemicals that regulate the efficiency with which the brain controls behavior. Current research is examining which genes may be involved. A team at the University of California suggest that genes contributing to (ADHD) overlap an area of chromosome 16p13, a marker that has repeatedly come up in genome-wide scans for autism genes. The two conditions appear related, with both (ADHD) and autism frequently involving inattentiveness and/or hyperactivity. Other studies have associated ADHD with the 10-repeat allele of the DAT1 gene and the 7-repeat allele of the DRD4 gene, both dopamine genes [5]. Several studies have now documented an association with the dopamine beta hydrozylase gene (DBH TaqI). Such research suggests that ADHD likely arises from a combination of these various risk genes rather than from a single gene. In the future it is likely that ADHD will be sub-typed according to which risk genes individuals possess as these subtypes are likely to have different risks, life courses, and responses to treatment, particularly to medications.

There is no compelling evidence that social factors, alone, can create ADHD. What environmental factors have been identified to date fall in the realm of bio-hazards such as alcohol, tobacco smoke, lead poisoning, premature birth, excessively complicated pregnancy, etc.

Neuro-chemical imbalance[]

There is increasing evidence that variants in the gene for the dopamine transporter are related to the development of ADHD (Roman et al., 2004, American Journal of Pharmacogenomics 4:83-92). This evidence is consonant with the theory of inefficacy of dopamine in people with ADD/ADHD; according to other recent studies, some people with ADHD usually have relatively high dopamine transporter levels, which clears dopamine from between neurons before the full effect is gained from dopamine. Stimulant medications used to treat ADHD are all capable of either inhibiting the action of dopamine transporter (as methylphenidate does) or promoting the release of dopamine itself (as the amphetamine-class medications do). Therefore, it is theorized that stimulant medication allows the brain to enhance the effect of dopamine by blocking dopamine transporters or increasing the release of dopamine. Currently this is the most widely accepted model of ADD/ADHD etiology in the scientific and medical community.

New studies consider the possibility that norepinephrine also plays a role. (see Krause, Dresel, Krause in Psycho 26/2000 p.199ff). Drugs that manipulate norepinephrine levels in certain brain regions, such as atomoxetine, have shown effectiveness for managing the disorder.

Smoking during pregnancy[]

The finding of another possible cause stemmed from the observation that children of women who smoked during pregnancy are more likely to be diagnosed with ADHD (Kotimaa et al., 2003, J Am Acad Child Adol Psychiatry 42, 826-833). Given that nicotine is known to cause hypoxia (too little oxygen) in the uterus, and that hypoxia causes brain damage, smoking during pregnancy could be an important contributing factor leading to ADHD (or a phenocopy). It may even help explain in part the increase in ADHD diagnoses, as the number of women smokers has increased. However, there are not nearly enough women smoking during pregnancy to account for all the ADHD diagnoses, and the mothers of many of those diagnosed with ADHD did not smoke during or before pregnancy. It is also possible that cause and effect could be confounded in this study, since many mothers who smoke during pregnancy may be ADHD suffers themselves; therefore the cause may simply be the shared genetic material of mother and child, rather than the mother's smoking.

Brain development in the uterus and during the first year of life may be compromised by drug use during pregnancy or environmental toxins.


It has also been suggested that ADHD may be the result of a poor diet and other external factors, rather than from any physiological source. Recent studies have begun to find metabolic differences in these children, indicating that it is not so much a poor diet, as it may be an inability to handle certain elements of the diet. For example, in 1990 the English chemist [19] showed that children with ADHD lose zinc when exposed to a food dye.,[20] and others have shown that children with autism or ADHD are low in sulfation metabolism, in particular the enzyme Phenol Sulfotransferase-P.

A recent study in the Lancet [21] found that certain food colorings and preservatives (sodium benzoate) in soft drinks, candy, and other foods can increase a child's activity level. This was a double blind study using 300 children in England, half age three years and half age eight years old, over a seven week period. Each child got two different mixes of food colorings, together with sodium benzoate on two randomly assigned weeks. The report stated that this increase, "fosters hyperactivity and inattentiveness, potentially diminishing a child's ability to learn." (p. 349). The heightened activity level did not persist once the additives were stopped. The increase in activity level was measured by survey's filled out by parents, teachers and researchers. The average increase attributable to the additives was about one tenth as large as the scores separating normal children from those with a diagnosis of ADHD.

It has, however, been established conclusively that some children are sensitive to dyes and other food additives, while a few may be sensitive to sugar, caffeine, etc.[22] More than 30 double-blind studies support this.[23]

Nutritional data has been well summarized in a review article.[24] A few studies suggest that children with ADHD may have lower levels of key fatty acids but this remains to be replicated convincingly. In fact, one study found that the lower the levels, the worse the symptoms. The possibility that fatty acid deficiency is a trigger for ADHD may be plausible as nutrition scientists have recently demonstrated that the American diet is extremely deficient in omega-3 fatty acids. At the same time, ADHD diagnoses are rapidly increasing. More support for this idea comes from findings that breast-fed children have much lower levels of ADHD, and that until quite recently, infant formula contained NO omega-3 fatty acids. These remain purely correlational findings, however, that cannot be used to infer cause or the exact direction of the effects between these agents and ADHD symptoms. At present, experts do not accept the involvement of fatty acids as significant to the disorder or to its treatment.

A recent randomized double-blind experiment compared a fatty acid supplement with placebo in children with developmental coordination disorder (which exhibits a high degree of overlap with ADHD diagnoses). Fatty acid supplements improved spelling, reading, and behaviour after three months.[25] Numerous studies have shown an improvement in cognitive function, in mood, and in vision when omega 3 fatty acid supplements are given. While not directly showing a causal link between ADHD and fatty acids, increased levels of fatty acids has a beneficial effect on related behaviour.

Furthermore, creating a deficiency of omega-3 fatty acids in pregnant rats produces pups that are hyperactive and that have altered brain levels of dopamine in the same brain regions as seen in humans and other rat models of hyperactivity. More research, however, is clearly needed before dietary supplements, such as those involving fatty acids can be recommended for clinical use.

Sleep apnea[]

There is also new evidence that brief pauses in breathing (apnea) during infancy may be a cause of ADHD. Dr. Glenda Keating of Emory University presented data at the Society for Neuroscience annual meeting in October 2004, showing that repetitive drops in blood oxygen levels in newborn rats similar to that caused by apnea in some human infants is followed by a long-lasting reduction in dopamine levels, associated with ADHD. Apnea occurs in up to 85% of prematurely born human infants. [6] Though intriguing, these findings with rats must be replicated in humans.

Head injuries[]

It has been known for some decades that head injuries can cause a person to experience and display ADHD-like symptoms.

Head injuries often result in damage to the frontal lobe, causing difficulty with executive function, a key element of ADD.

Brain scan technology has revealed differences in the size, symmetry, metabolism, and chemistry of the brain in those who have ADHD. However, it should be noted that there is yet no clear determination of the source of these differences. Some recent studies, such as that by Loo and colleagues at UCLA Medical School (Journal of the American Academy of Child and Adolescent Psychiatry, 2005) suggest that they are likely to be associated with the differences in genes discussed above. For instances, differences in the length of the DAT1 gene have been found to be linked to both differences in EEG patterns and to likelihood of responding to methylphenidate.


There are many options available to treat people diagnosed with ADHD. The options with the greatest scientific support include a variety of medications, behavior-changing therapies, and educational interventions.

Mainstream treatments[]


Currently, there is a consensus that the best pharmacological treatments available for patients with attention-deficit/hyperactivity disorder (ADHD) with clinical impairment include one or another formulation of the psychostimulants methylphenidate and amphetamine, or the noradrenergic reuptake inhibitor atomoxetine.[26][27] A good clinical improvement in approximately 70% of patients receiving one of the psychostimulants rises to more than 80% after treatment with the other.[28] This percentage is difficult to improve in psychopharmacology, however, which still leaves at least 20% who are nonresponders. Furthermore, for many responders, clinical improvement may not extend beyond approximately 25-30%, and the youngsters' academic impairment may show no long-term improvement at all. As the NIMH Collaborative Multisite Multimodal Treatment Study of Children with Attention-Deficit/Hyperactivity Disorder (MTA) study demonstrated, the positive effects of medication may continue for some months, but can deteriorate markedly over 2 years.[29]

The first-line medication used to treat ADHD are mostly stimulants, which work by stimulating the areas of the brain responsible for focus, attention, and impulse control. The use of stimulants to treat a syndrome often characterized by hyperactivity is sometimes referred to as a paradoxical effect. But there is no real paradox in that stimulants activate brain inhibitory and self-organizing mechanisms permitting the individual to have greater self-regulation. The stimulants used include:

  • Methylphenidate—Available in:
    • Regular formulation, sold as Ritalin, Metadate, Focalin,or Methylin. Duration: 4–6 hours per dose. Usually taken morning, lunchtime, and in some cases, afternoon.
    • Long acting formulation, sold as Ritalin SR, Metadate ER. Duration: 6–8 hours per dose. Usually taken twice daily.
    • All-day formulation, sold as Ritalin LA, Metadate CD, Concerta, Focalin XR. Duration: 10–12 hours per dose. Usually taken once a day.
  • Amphetamines --
    • Dextroamphetamine—Available in:
      • Regular formulation, sold as Dexedrine. Duration: 4–6 hours per dose. Usually taken 2-3 times daily.
      • Long-acting formulation, sold as Dexedrine Spansules. Duration: 8–12 hours per dose. Taken once a day. Also known as dexamphetamine in Australia.
    • Adderall, a trade name for a mixture of dextroamphetamine and laevoamphetamine salts. -- Available in:
      • Regular formulation, Adderall. Duration: 4–6 hours a dose.
      • Long-acting formulation, Adderall XR. Duration: 12 hours. Taken once a day.
    • Methamphetamine—Available in:
      • Regular formulation, sold as Desoxyn by Ovation Pharmaceutical Company. Usually taken twice daily.
  • Wellbutrin (buproprion hydrochloride) is a selective catecholamine (dopamine and norepinephrine) reuptake inhibitor that is used to treat depression as well as ADHD. It has also been approved as a smoking cessation aid, and is marketed for this purpose under the name Zyban.
    • Wellbutrin is available in Sustained Release (SR) form, taken twice daily and Extended Release (XL), taken once daily. Usual doses begin at 150 mg, then proceed to 300 mg. Dosage should not exceed 450 mg.
  • Atomoxetine. A Selective Norepinephrine Reuptake Inhibitor (SNRI) introduced in 2003, it is the newest class of drug used to treat ADHD, and the first non-stimulant medication to be used as a first-line treatment for ADHD. Available in:
    • Once daily formulation, sold by Eli Lilly and Company as Strattera. Duration: 24 hours per dose. Taken once or twice a day.

Second-line medications include:

  • Benzphetamine—a less powerful stimulant. Research on the effectiveness of this drug is not yet complete.
  • Provigil/Alertec/modafinil—promotes vigilance and is used as a treatment for narcolepsy, though it has also been used in other contexts to promote wakefulness. Research on this drug is not yet complete.
  • Cylert/Pemoline—a stimulant used with great success until the late 1980s when it was discovered that this medication could cause liver damage. Although some physicians do continue to prescribe Cylert, it can no longer be considered a first-line medicine. In March 2005 the makers of Cylert announced that it would discontinue the medication's production.
  • Clonidine—Initially developed as a treatment for high blood pressure, low doses in evenings and/or afternoons are sometimes used in conjunction with stimulants to help with sleep and because Clonidine sometimes helps moderate impulsive and oppositional behavior and may reduce tics.article

Because most of the medications used to treat ADHD are Schedule II under the U.S. DEA schedule system, and are considered powerful stimulants with a potential for diversion and abuse, there is controversy surrounding prescribing these drugs for children and adolescents. However, research studying ADHD sufferers who either receive treatment with stimulants or go untreated has indicated that those treated with stimulants are in fact much less likely to abuse any substance than ADHD sufferers who are not treated with stimulants.[7]


There are also psychotherapeutic interventions that can be used in conjunction with or instead of medication. One such approach is the Parent Training Program [30]

Alternative treatments[]

There are many alternative treatments for ADHD, most of them heavily disputed or relegated to adjunct status with medication treatment. This section attempts to deal with the most prominent of the alternative treatments. Bear in mind that the term "alternative" often means unscientific because there simply are little or no credible scientific studies to support these suggested interventions. If there were, they would be called scientifically based interventions, not alternative ones.

Feingold diet[]

Dr. Benjamin F. Feingold was both a pediatrician and allergist and was considered a pioneer in the fields of allergy and immunology. He served as the Chief of Allergy at the Kaiser Permanente Medical Center in San Francisco. In treating patients at the clinic, Dr. Feingold found that certain synthetic food additives were triggering not only allergic-type reactions, but also behavioral changes in some of his patients.

By the 1970s pediatricians in the United States were becoming alarmed by the growing numbers of children they saw who had difficulty behaving, focusing and functioning normally. Based on his successful clinical work, Dr. Feingold developed what he called the K-P Diet, named for Kaiser-Permanente. The media soon dubbed it the "Feingold diet," and it became best known for helping hyperactive and learning disabled children.

As parents began using this diet for their children, many saw dramatic success and formed grass roots support groups. In 1976 they gathered to form a non-profit national organization and chose the name "Feingold Association" to honor the man who had so helped their children. As the structure of the Feingold Association evolved, the national offices took on many of the tasks that had once been done locally.

The Feingold Program eliminates several groups of synthetic food additives:

Most of these additives are derived from petroleum.

During the initial weeks of the Program, a group of foods referred to as "salicylates" are removed and may later be reintroduced. Most of the salicylate foods are common fruits. During this early period (called Stage One) foods like pears, pineapple and banana are used instead of foods like apples, oranges and grapes.

The Feingold Association provides information and support for those starting the program. They receive comprehensive materials including books listing thousands of brand name foods that have been researched by the Association and are free of the unwanted additives. Newsletters, updates, phone and email support are also provided.

All types of food may be used on the Feingold Program. This includes processed foods, convenience foods, snacks and even junk food. The suitable brands are included in the Foodlist and Shopping Guide. Contrary to a popular misconception, soft drinks, chocolate and sugar have never been eliminated on the Feingold Program, although moderation is suggested when consuming sweets. Families can continue to eat the types of food to which they are accustomed, including desserts. Most of the suitable foods are available at supermarkets.

Early studies showed mixed results, but newer studies have been more carefully designed. They show that about 75% of the children respond positively to the removal of the synthetic additives. Abstracts of these studies can be found at

The Institutes for The Achievement of Human Potential[]

Established in 1955, IAHP is a non-profit organization dedicated to improving the health and development of children who have some form of brain injury, including children diagnosed with Attention-deficit hyperactivity disorder. The IAHP claims that with a home program consisting of a healthy diet, clean air, and respiratory programs many of these children can be well without the need for medication. The IAHP publishes the results of its treatment for over 1700 children on its website. (IAHP website [8].

Vitamin B6[]

In the 1980s the vitamin B6 promoted as a helpful remedy for children with learning difficulties including inattentiveness. After that, zinc was promoted for ADD and autism. Multivitamins later became the claimed solution. Thus far, no reputable research has appeared to support any of these claims, except in cases of malnutrition.


Pycnogenol, a flavinoid extract of pine tree bark with potent antioxidant activity has anecdotally been reported to have a beneficial effect on attention span in children with ADHD. Experimental tests, while not ruling out a possible effect, have been inconsistent.


There has been a lot of interesting work done with neurofeedback and ADHD. Children are taught, using video game-like technology, how to control their brain waves. Some clinical professionals may consider the treatment promising, but state that there is not yet sufficient evidence that it works after the immediate treatment is complete. A thorough review of the scientific research by Sandra Loo, Ph.D. and Russell Barkley, Ph.D. (Developmental Neuropsychology 2005) concluded that neurofeedback does not have adequate support from appropriately conducted scientific studies to support it as an intervention at this time. While many papers have been published, they have fallen short of scientific standards. Only two studies have used randomized assignment to treatment and placebo groups and neither found significant results from this treatment (to read this article, go to and see Research to Read subpage).

Audio visual entrainment[]

Audio visual entrainment uses light and sound stimulation to guide and change brainwave patterns. It is claimed that the success rate is very high, although the method is not widely used (see Joyce study in reference section). The technology is inexpensive compared to most treatments, but for many people it is not covered by health insurance. The technology is safe but unfortunately it cannot be used with those suffering from photosensitive epilepsy due to the risk of triggering a seizure. The technology is currently being used in the New Visions charter school in Minneapolis along with approximately 50 other schools. However, there is no scientific evidence to support this treatment at this time nor does it appear to be consistent with current evidence on the causes of ADHD.

Cerebellar Stimulation[]

There exist several exercise programs based on cerebellar stimulation that are used to treat ADHD, Aspergers and many learning difficulties like dyslexia, dyspraxia, etc. Most prominent are the DORE program, the Learning Breakthrough Program™ (which served as the basis for the DORE program[9] ) and the Brain Gym®, based on Educational Kinesiology.

These drug-free programs include balance, coordination, eye and sensory exercises that specifically stimulate the cerebellum. For instance, it is assumed by the creators of the DORE program that the cerebellum of people with learning difficulties or disorders like ADHD and Aspergers is underdeveloped. The medical professionals at DORE call this Cerebellar Developmental Delay (CDD) [10]. By improving the patient’s cerebellar function many of the symptoms can be reduced or even eliminated permanently.

Although some of the above mentioned exercise programs (claim to) have a high success rate, they are still controversial and not widely accepted due to a substantial lack of scientific evidence.

Recent brain science has provided new data on the cerebellum. According to Bower and Parsons(2003) “the cerebellum may play important roles in short-term memory, attention, impulse control, emotion, higher cognition, the ability to schedule and plan tasks“. Some researchers directly link the cerebellum to ADHD and dyslexia, e.g. a neuroimaging study conducted in 2002 by Xavier Castellanos and Judith L. Rapoport and published in August 2003 in Scientific American, revealed that in children with ADHD the cerebellum is reduced in size. Such evidence however supports the role of the cerebellum in ADHD but does not support treatments like the DORE program that claim to alter functioning of the cerebellum.

Moreover, independent research that is currently under way on the DORE program, yielded only suggestive results that the method works. However, more research is necessary in order to prove the validity of this alternative treatment. As Dr. Hallowell states in Delivered from Distraction, “we must remain critical, even sceptical, until we have a full body of research to give us a definite answer”(p. 238)

Views on neurodiversity[]

The ADHD diagnosis is controversial and has been questioned by some professionals, adults diagnosed with ADHD, and parents of children diagnosed as such. Some assert there are positive aspects to ADHD, such as hyperfocus, even though this has not been addressed in the scientific literature. Others believe ADHD is a divergent or normal-variant human behavior, and use the term neurodiversity to describe it.

Views on parenting[]

There is no compelling evidence that parenting methods can cause ADHD in otherwise normal children. Evidence does show that parents of ADHD children experience more stress and depression, give more commands, spend less leisure time with their children, and vacillate between lax and harsh punishment. But further research shows that such parenting behavior is in large part a reaction to the child's ADHD and related disruptive and oppositional behavior and in a small part the result of the parent's own ADHD. According to parents, parenting an ADHD child is an onerous task. The children are often willfully disobedient. Psychiatry offers the option that deficient regulatory processes in the brain are responsible for the child's poor impulse control. Medications such as Ritalin thus treat the child and assure parents that the child's behavior is not caused by their lack of parenting skills.

On the other hand, parents often try to guide their children by emphasizing obedience and adherence to rules. Parenting is often a balance between overindulgence of children and teaching responsibility. Circumstances might force a parent to rely on school, or TV for their children's education. When a thoughtful child needs more intellectual stimulation than they are offered, they might be more cooperative if their personal interests are accommodated.

A significant source of stress for parents, though, comes from outside assumptions that poor parenting is the cause of the child's misbehaviour. Parents have to cope with comments from friends, family, and teachers. The family runs the risk of becoming isolated. This is where support groups and connections with other families with children with ADHD can be helpful. Organizations such as CHADD (Children and Adults with Attention Deficit Hyperactivity Disorder) in the U.S Chadd US and Canada Chadd Canada and ADDERS in the UK Adders can help parents to feel less alone, and offer information and strategies for coping with the disorder.

Evidence for ADHD as an organic phenomenon[]

Brain imaging research using magnetic resonance imaging (MRI) has shown that differences exist between the brains of children with and without ADHD, though these differences have not been shown in any way to be pathological in nature. Additionally PET studies have shown there might be a link between a person's ability to pay continued attention to external directives and the use of glucose - the body's major fuel - in the brain. In adults diagnosed with ADHD, the brain areas that control attention use less glucose and appear to be less active, suggesting that a lower level of activity in some parts of the brain may cause inattention (Zametkin et al.).

Also worth noting are the results of some studies using SPECT (Single Photon Emission Computed Tomography). One study (Lou et al. in Arch. Neurol. 46(1989) 48-52) found people labeled as ADHD have reduced blood circulation in the striatum. But even more significant may be the discovery that people with ADHD seem to have a significantly higher concentration of dopamine transporters in the striatum (Dougherty et al. in Lancet 354 (1999) 2132-2133; Dresel et al. in Eur. J.Nucl. Med. 25 (1998) 31-39).

The various neuro-imaging studies have converged to suggest that at least three areas are involved in ADHD, these being the frontal lobes (particularly the orbital frontal region, more on the right side than the left), the basal ganglia (in particular the striatum), and the central cerebellum (vermis). Some research also implicates the anterior cingulate as possibly involved in ADHD. These various regions appear to be between 3-10% smaller than normal and between 10-20% less active than normal.

Genetic research was discussed above and is also supportive of neurotransmitter problems being associated with ADHD.

Positive aspects[]

It has been widely observed that people with ADD tend to look at situations in a different manner. "While students are learning the details of photosynthesis, the ADHD kids are staring out the window and pondering if it still works on a cloudy day" (Underwood). One positive side of impulsive behavior is the ability to try new things without trepidation. This can be a strength and a weakness: "Compulsivity isn't always bad. Instead of dithering over a decision, they're willing to take risks" (Underwood).

In contrast to this view of ADHD, longitudinal studies of ADHD children followed to adulthood find them to be significantly less educated than control groups of children followed over the same period of time(see Weiss and Hechtman, 1993, Hyperactive Children Grown Up, New York: Guilford, JetBlue founder David Neeleman believes that ADHD contributed to his business acumen and has been cited as saying that he refuses medication for fear that he will lose his creativity. However, little scientific evidence supports the argument that medications affect creativity.

Famous people and ADHD[]

Many professional counselors find it useful to emphasize to persons diagnosed with ADHD and their families the perspective that the condition does not necessarily block, and may even facilitate, great accomplishments. Most frequently cited as potentially useful is the mental state of hyperfocus. A number of lists of famous persons either diagnosed with ADHD, it predecessor ADD, or suspected (but not necessarily known to have had ADHD) are numerous.

Among the individuals often listed is comedian Robin Williams, whose spontaneous humor, hyperactive manner, and other noted behavior (not all constructive) have combined to earn the him the label "Poster child for ADD (or ADHD)." Notwithstanding inspirational value, cited by critics is the fact that Williams' personal medical records are not public information, so including him and many others found on such lists falls below reasonable criteria for validity. List of famous peoples with ADD or ADHD

Some other famous contributors may have had ADD, although a post-mortem diagnosis is questionable. Other historical figures who have been proposed as ADHD candidates include: Hans Christian Andersen, Ludwig van Beethoven, Winston Spencer Churchill, Walt Disney, Benjamin Franklin, Robert and John F. Kennedy, Theodore Roosevelt, Jules Verne, Woodrow Wilson, and the Wright brothers. Some contemporary ADHD candidates have also been proposed, including Whoopi Goldberg, Emma Watson, Dustin Hoffman, and The Olsen Twins At the same time, those representing the Asperger syndrome and bipolar camps also claim many of the above as their own. No evidence has been presented, however, that these individuals actually qualified for or received a clinical diagnosis of the disorder. And, while many people with ADHD do succeed, views of ADHD as a "gift" should not be seen as excluding the possibility of benefit from medical intervention.


While ADD/ADHD is a known psychiatric condition, there are various theories about the cause and some controversy over the number of persons diagnosed and the cost of medications.

Skepticism towards ADHD as a diagnosis[]

Dr. Mary Megson[31] claims the increase in ADHD, as well as the alleged increase in autism, are a result of the increasing use of vaccines that deplete vitamin A stores, combined with a G-protein defect.

Another source of skepticism towards making the diagnosis of "ADHD or not ADHD" may arise from the rising diagnosis of subclinical forms of ADHD. So called 'Shadow-syndromes' or 'sub-syndromes' stand for weaker forms of ADHD and are described in various degrees by John J. Ratey and Catherine Johnson[32]

Hunter in a Farmer's Society theory[]

Main article: Hunter vs. farmer theory

Proposed by Thom Hartmann, this evolutionary psychology theory holds that ADHD was an adaptive behavior for the "restless" hunter before agriculture became widespread. Scientific concern around Hartmann's theory revolves around the mismatch between the behaviours symptomatic of ADHD, and those he describes as being adaptive for hunters, which better fit a diagnosis of hypomania (Mota-Castillo, 2005). A positive feature of the theory is the idea that thinking in terms of attentional 'differences' rather than attentional 'disorders' may direct effort toward utilizing an affected individual's strengths and uniqueness. Conversely, it could also reinforce a person's denial and refusal to seek treatment.

A 2001 study [33] on the seven-repeat (7R) allele of the human dopamine receptor D4 (DRD4) gene (known to be linked to ADHD) has been cited as support for Hartmann's theory. The study concludes that "this allele originated as a rare mutational event that nevertheless increased to high frequency in human populations by positive selection." Some scientists point out that mutations may survive without conferring any benefit (see genetic drift) simply because the individuals mature and procreate. In other words, the gene causes no early mortality and does not reduce the fitness to procreate.

ADHD as a social construct[]

Following from the Hunter-versus-farmer theory, as with many conditions in the field of psychiatry, ADHD can be explained as a social construct[34] rather than an objective 'disorder'.

In this view, in societies where passivity and order are highly valued, those on the active end of the active-passive spectrum may be seen as 'problems'. Medically defining their behaviour (by giving a label such as ADHD) serves the purpose of removing blame from those 'causing the problem'.

Evidence presented against the social constructionist view comes from a number of studies that demonstrate significant differences between ADHD and typical individuals across a wide range of social, psychological, and neurological measures as well as those assessing various areas of functioning in major life activities. More recently, studies have been able to clearly differentiate ADHD from other psychiatric disorders in its symptoms, associated features, life course, comorbidity, and adult outcome adding further evidence to its view as a true disorder.

Invocation of this evidence is seen by proponents of the social construct theory as a misunderstanding, nonetheless. The theory does not state that individuals across a behavioral spectrum are identical neurologically and that their life outcomes are equivalent. It is not surprising for PET scan differences to be found in people at one end of any behavioral spectrum. The theory simply says that the boundary between normal and abnormal is arbitrary and subjective, and hence ADHD does not exist as an objective entity, but only as a 'construct'.

Nor does evidence of successful treatment persuade the social constructionist; for example the American National Institute on Drug Abuse [11] reports that Ritalin is abused by non-ADHD students partly for its ability to increase their attention. Evidence showing that ADHD is associated with certain liabilities does not appear to undermine this view either; normal-variant behavior could have certain liabilities as well, and a life outcome cannot be predicted with certainty for any given diagnosed individual.

Critics of the social constructionist view contend that it presents no evidence in support of its own position. Theories must present their details and mechanisms in as precise a manner as possible so that they are testable and falsifiable, and this theory is said to provide no such details. But proponents of the view disagree that criteria for falsifiability is lacking. One way, for example, is to show that there exists an objective characteristic possessed by virtually all diagnosed individuals which does not exist in any non-diagnosed individual. Current candidates for falsifiability include PET scans, genes, neuroanatomical differences, and life outcomes. However, none of these have been shown to be precise predictors of a diagnosis or lack thereof. (Such criteria is generally fulfilled by well-understood medical diseases).

Critics of this view also assert that it is not consistent with known findings. For instance, ADHD is as frequent in Japan and China as in the US, yet in such societies that favor child obedience and passivity one would expect higher rates of ADHD if this theory were correct. Timimi's view has been seriously criticized by Russell Barkley and numerous experts in Child and Family Psychology Review (2005).

Significant differences in the prevalence of ADHD across different countries have been reported, however (Dwivedi, 2005). Timimi himself cites a range of prevalence that goes from 0.5% to 26% as support for his theory.

ADHD as pseudo-science and its falsifiability[]

Critics have noted that the hypothesis "ADHD exists as an objective disorder" is unscientific. In other words, ADHD does not have good Popperian criteria for falsifiability. To be falsifiable, there would need to be a possible empirical observation which could show that the hypothesis is false.

As indicated in the previous section, the opposing theory (i.e. "ADHD exists only as a social construct") is falsifiable and thus scientific. That is, it could be shown that ADHD exists as an objective entity by finding an objective characteristic which separates all diagnosable individuals from all undiagnosable ones. In contrast, to prove that ADHD does not exist as an objective entity, it would need to be shown that said objective characteristic does not exist. This task, which consists of proving a negative, is clearly not feasible.

Concerns about the impact of labeling[]

Dr. Thomas Armstrong,[35] a prominent critic of ADHD as an objective disorder, has said that the ADHD label is a "tragic decoy" which erodes away the potential to see the best in every child. Armstrong is a proponent of the idea that there are many types of "smarts" and has adopted the term neurodiversity (first used by autistic rights activists) as an alternative, less damaging, label [36]

Concerns about medication[]

Many parents and professionals have raised questions about the safety of drugs used to treat ADHD, particularly methylphenidate (Ritalin). Despite belief to the contrary, no significant effects have been observed on stature or the emergence of tics [12]. Deaths attributed to methylphenidate are believed to be caused by interactions with other drugs, and are extremely rare. Medical Examiner Ljubisa Dragovic does not agree, however, and in the case of the death of 14-year-old Matthew Smith he said, "There is an ocean-sized problem out there that needs to be looked at very carefully by multidisciplinary teams for careful reassessment of the use of this drug." He discussed the type of disorder called "small vessel disease" which is caused only by stimulant drugs - including Ritalin - and the likelihood that diabetic children were at higher risk for cardiac problems. The web page Stimulant medication and heart disease lists a number of relevant studies. In particular, Brown (1989) showed that African-Americans are more prone to increase in blood pressure and should be monitored closely.

The Pediatric Advisory Committee of the Food and Drug Administration (FDA) released a statement on June 30, 2005 identifying two possible safety concerns regarding Concerta and methylphenidate: Psychiatric adverse events and cardiovascular adverse events [13]. On February 9, 2006 the FDA's advisory panel voted in favor of having Ritalin and other stimulant drugs carry a strong "black box" warning after looking into the deaths of 25 people, including 19 children [14].

A new concern, raised by a small scale 2005 study, is that methylphenidate might cause chromosome aberrations [15], and suggested that further research is warranted considering the established link between chromosome aberrations and cancer and considering that all the children in this study showed suspicious DNA changes within a very short time. A team from the Food and Drug Administration (FDA), the National Institutes of Health (NIH) and the Environmental Protection Agency (EPA) went to Texas on May 23, 2005 to evaluate the methodology of the study. Dr. David Jacobson-Kram of the FDA said that the study had flaws in its methods but that its results could not be dismissed. Flaws cited are (1) that the study did not include a control group on placebo, and (2) that it is too small. Several research teams will attempt to replicate the study on a larger scale.

Studies on rats have suggested there could be plastic changes in personality and brain functioning after chronic use into adulthood, including changes in sensitivity to reward [16] [17]. But, again, studies in humans are lacking and so such results cannot be automatically extrapolated to humans.

ADD/ADHD a hoax?[]

There are some claims that ADD/ADHD is simply a hoax; a conspiracy between pharmaceutical companies and psychiatrists to make money.

A major proponent of this theory, although not the only one, is the Church of Scientology, which is opposed to the field of psychiatry in general, citing ADHD as one example in which psychiatrists "harm" patients. Scientology maintains several satellite organizations like the Citizens Commission on Human Rights which have been outspoken critics of the biological basis of ADHD and medications used to treat it.[18] There may exist a conflict of interest as Scientology advocates and sells an alternative and expensive non-pharmacological treatment known as Dianetics. To complicate matters, The Church of Scientology is associated with other organizations, many of which do not openly declare themselves to be connected in any way. This makes the work of other opponents of the ADHD diagnosis difficult, because they are under false suspicion of being undeclared Scientology agents.

Nevertheless, evidence for any such grand conspiracy theory is lacking. Moreover, many studies show numerous differences/deficits between those with ADHD and the general population that contradict this view that ADHD is simply a fiction or hoax. The Church also has a conflict of interest in their position given that organized psychiatry and psychology are their competitors against their own therapies and course work through their Church.

Twentieth century history[]

  • 1867 The term "hyperactive" is first used in reference to the "condition of the brain in acute mania." (Source: Oxford English Dictionary Online)
  • 1902 - the English pediatrician George Still described a condition analogous to ADHD. He regarded it as innate and not caused by the environment.
  • The 1918–1919 influenza pandemic left many survivors with encephalitis, affecting their neurological functions. Some of these exhibited immediate behavioral problems which correspond to ADD. This caused many to believe that the condition was the result of injury rather than genetics.
  • 1937 - Dr. Bradley in Providence RI reported that a group of children with behavioral problems improved after being treated with stimulant medication.
  • 1957 - the stimulant Methylphenidate (Ritalin) became available. It remains one of the most widely prescribed medications for ADHD in its various forms (Ritalin, Focalin, Concerta, Medadate, and Methylin).
  • 1960 - Stella Chess described "Hyperactive Child Syndrome" introducing the concept of hyperactivity not being caused by brain damage. (
  • By 1966, following observations that the condition existed without any objectively observed pathological disorder or injury, researchers changed the terminology from Minimal Brain Damage to Minimal Brain Dysfunction. (Source: Oxford English Dictionary Online)
  • 1970s - Canadian Virginia Douglas released various publications to promote the idea that attention deficit was of more significance than the hyperactivity, influencing the American Psychiatric Association.
  • ~1971 - the Church of Scientology set up the Citizen's Commission on Human Rights (CCHR), which lobbied using the media against psychiatric medication in general, and Ritalin in particular.
  • 1973 - Dr Ben F. Feingold, Chief of Allergy at Kaiser Permanente Medical Center in San Francisco, claimed that hyperactivity was increasing in proportion to the level of food additives.
  • 1975 - pemoline (Cylert) is approved by the FDA for use in the treatment of ADHD. While an effective agent for managing the symptoms, the development of liver failure in at least 14 cases over the next 27 years would result in the manufacturer withdrawing this medication from the market.
  • 1980 - the name Attention Deficit Disorder (ADD) was first introduced in DSM-III, the 1980 edition.
  • 1987 - the DSM-IIIR was released changing the diagnosis to "Undifferentiated Attention Deficit Disorder." [19]
  • 1991 - The US Department of Education rules that ADHD is an eligible condition for receipt of special educational services provided that it interferes with academic functioning. Most cases are dealt with under the "Other Health Impaired" category of special education while others qualify under the categories for learning and emotional disorders.
  • 1994 - DSM-IV described three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination.
  • 1998 - the NIH developed and issued a Consensus Statement attesting to the existence of ADHD. A link is provided in the External Links section below.
  • 1999 - New delivery systems for medications are invented that eliminate the need for multiple doses across the day or taking medication at school. These new systems include pellets of medication coated with various time release substances to permit medications to dissolve hourly across an 8-12 hour period (Medadate CD, Adderall XR, Focalin XR) and an osmotic pump that extrudes a liquid methylphenidate sludge across an 8-12 hour period after ingestion (Concerta).
  • 1999 - The largest study of treatment for ADHD in history is published in the American Journal of Psychiatry. Known as the Multimodal Treatment Study of ADHD (MTA Study), it involved more than 570 ADHD children at 6 sites in the United States and Canada randomly assigned to 4 treatment groups. Results generally showed that medication alone was more effective than psychosocial treatments alone but that their combination was beneficial for some subsets of ADHD children beyond the improvement achieved only by medication. More than 40 studies have subsequently been published from this massive dataset.
  • 2001 - The International Consensus Statement on ADHD is published (Clinical Child and Family Psychology Review) and signed by more than 80 of the world's leading experts on ADHD to counteract periodic media misrepresentation that ADHD is not a real disorder and that medications are not justified as a treatment for the disorder. In 2005, another 100 European experts on ADHD added their signatures to this historic document certifying the validity of ADHD as a valid mental disorder.
  • 2003 - the first new medication for ADHD in the past 25 years receives FDA approval for use in children, teens, and adults with ADHD. The drug is atomoxetine.


There is not yet a naming consensus. Below are listed several terms that have been used, past and present. One challenge in taxonomy is that some patterns of behavior are labeled by experts symptoms or sub-types of ADHD, while other experts label those same patterns as their own disorders, independent of ADHD. For the purposes of this article, the "Terminology" section will be used only to name ADHD and its near equivalents, while the names for its manifestations and subtypes will be listed in 'Symptoms', below.

  • Attention-deficit hyperactivity disorder (ADHD): In 1987, ADD was in effect renamed to ADHD in the DSM-III-R. In it, ADHD was broken down into three subtypes (see 'symptoms' for more details):
    • predominantly inattentive ADHD
    • predominantly hyperactive-impulsive ADHD
    • combined type ADHD
  • Attention deficit disorder (ADD): This term was first introduced in DSM-III, the 1980 edition. Is considered by some to be obsolete, and by others to be a synonym for the predominantly inattentive type of ADHD.
  • Undifferentiated attention-deficit disorder (UADD): This term was first introduced in the DSM-III-R, the 1987 edition. This was a miscellaneous category, and no formal diagnostic criteria were provided. UADD is approximately the predominantly inattentive type of ADHD in the DSM-IV-TR. The DSM-III-R diagnosis of attention-deficit hyperactivity disorder required hyperactive-impulsive symptoms in addition to the inattentive symptoms.
  • Attention-deficit syndrome (ADS): Equivalent to ADHD, but used to avoid the connotations of "disorder".
  • Hyperkinetic disorders (F90) is the ICD-10 equivalent to ADHD. The ICD-10 does not include a predominantly inattentive type of ADHD because the editors of Chapter V of the ICD-10 believe the inattentivity syndrome may constitute a nosologically distinct disorder.
    • Disturbance of activity and attention (F90.0)
    • Hyperkinetic conduct disorder (F90.1) is a mixed disorder involving hyperkinetic symptoms along with presence of conduct disorder
    • Other hyperkinetic disorders (F90.8)
    • Hyperkinetic disorder, unspecified (F90.9)
  • Hyperkinetic syndrome (HKS): Equivalent to ADHD, but largely obsolete in the United States, still used in some places world wide.
  • Minimal cerebral dysfunction (MCD): Equivalent to ADHD, but largely obsolete in the United States, though still commonly used internationally.
  • Minimal brain dysfunction or Minimal brain damage (MBD): Similar to ADHD, now obsolete.


  1. ^  ScienceDaily (2004) Reductions In Blood Oxygen Levels In Newborns Could Contribute To ADHD Development

See also[]

References & Bibliography[]

  1. Attention Deficit Hyperactivity Disorder. National Institute of Mental Health (NIMH), October 26, 2006. Retrieved on 2007-08-13.
  2. NINDS Attention Deficit-Hyperactivity Disorder Information Page. National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.
  3. ADHD - A Guide for Families. American Academy of Child Adolescent Psychiatry. Retrieved on 2007-08-13.
  4. Cite error: Invalid <ref> tag; no text was provided for refs named Polanczyk
  5. Diagnostic and Statistical Manual of the American Psychiatric Association, Fourth Edition, American Psychiatric Association, 2000.
  6. Attention-Deficit/Hyperactivity Disorder (ADHD). Retrieved on December 11, 2006.
  7. Attention-Deficit / Hyperactivity Disorder: ADHD in Adults. Retrieved on December 11, 2006.
  8. 8.0 8.1 ICD Version 2006: F91. World Health Organization. Retrieved on December 11, 2006.
  9. Perrin JM, Stein MT, Amler RW, Blondius TA. 2001. "Clinical practice guideline: treatment of school-aged children with Attention Deficit/Hyperactivity Disorder". Pediatrics 108 (4):1033-1044. PMID 11581465
  10. Conners CK, Sitarenios G, Parker JD, Epstein JN (1998). Revision and restandardization of the Conners Teacher Rating Scale (CTRS-R): factor structure, reliability, and criterion validity. Journal of abnormal child psychology 26 (4): 279–91.
  11. Ratey, John; Hallowell, Edward. Driven to Distraction first edition, p. 42
  12. Ninivaggi, F. J. "Borderline intellectual functioning and academic problem." In: Sadock B.J. Sadock, V.A., eds. Kaplan & Sadock's Comprehensive Textbook of psychiatry. 8th ed. Vol. II. Baltimore: Lippincott William and Wilkins; 2005: 2272–76.
  13. Attention-Deficit/Hyperactivity Disorder. Psychiatry Online. Retrieved on 2007-08-13.
  14. Jensen, PS. Exploring the Neurocircuitry of the Brain and Its Impact on Treatment Selections in ADD. Medscape. Retrieved on 2007-08-13.
  15. BRIEF, Psychological Assessment Resources, Lutz, FL, (2000)
  16. Achenback, T., (2001), ASEBA, University of Vermont, Burlington, VT,
  17. Conners, C., (1997) Multi-Health Systems Inc., North Tonawanda, NY,
  18. Shaw, Proceedings of the National Academy of Sciences, as reported in Science News, 172(22), p. 349
  19. N.I. Ward
  20. Waring, McFadden
  21. Stevenson, J., Lancet, November 3, 2007, as reported in Science News, December 1, 2007, 172(22), p. 349
  22. Jacobson and Schardt, 1999, Diet, ADHD & Behavior, Center for Science in the Public Interest, Washington, DC
  24. Burgess et al., 2000, Am J Clin Nutr 71:327-330
  25. Richardson and Montgomery, Pediatrics, 2005, 115:1360-1366
  26. Banaschewski T, Coghill DR, Santosh PJ et al. Long-acting medications for the hyperkinetic disorders: a systematic review and European treatment guidelines. Eur. Child Adolesc. Psychiatry 15, 476-495 (2006).
  27. Asherson P. Clinical assessment and treatment of attention deficit hyperactivity disorder in adults. Expert Rev. Neurother. 5, 525-539 (2005).
  28. Medication for children with attentional disorders. Committee of Children with Disabilities and Committee on Drugs. Pediatrics 98, 301-304 (1996).
  29. Jensen PS, Arnold LE. National institute of mental health multimodal treatment study of ADHD follow-up: 24-month outcomes of treatment strategies for attention-deficit/hyperactivity disorder. Pediatrics 113, 754-761 (2004).
  30. Anastopoulos, A., Smith, J., & Wien, E., Counseling and Training Parents, in Russell A. Barkley (Ed.) 1998 Attention-Deficit Hyperactivity Disorder, 2nd. Ed., The Guilford Press, NY., pp. 373-393.
  31. [1] presentation to the House Government Reform Committee on Autism and Vaccines (2000)
  32. Ratey, J., & Johnson, C., Shadow Syndromes: The Mild Forms of Major Mental Disorders That Sabotage Us
  33. Proceedings of the National Academy of Sciences
  34. [2] (Timimi, 2002)
  35. [3]
  36. [4]

1Pine DS, Klein RG, Lindy DC, Marshall RD. (1993) Attention-deficit hyperactivity disorder and comorbid psychosis: a review and two clinical presentations. Journal of Clinical Psychiatry, 54 (4), 140-5.
²Opler LA, Frank DM, Ramirez PM. (2001) Psychostimulants in the treatment of adults with psychosis and attention deficit disorder. Annals of the New York Academy of Sciences, 931, 297-301.
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  • Attention Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment (2006) by Russell A. Barkley, Ph.D. New York: Guilford Publications ( also
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  • ^  Dr. Timothy E. Wilens, MD Straight Talk about Psychiatric Medications for Kids (Revised Edition—2004). ISBN 1-57230-945-8.
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Shaywitz, S. E., Shaywitz, B. A. (1991). Introduction to the special series on attention- deficit disorder. Journal of Learning Disabilities, 24, 68-71.

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