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Attention deficit hyperactivity disorder
Specialty	Psychiatry, child and adolescent psychiatry

Attention-deficit hyperactivity disorder (ADHD) (sometimes also referred to as ADD, an earlier name many feel is still more applicable to many individuals) is a psychiatric diagnosis that identifies characteristics such as hyperactivity, forgetfulness, mood shifts, poor impulse control, and distractibility, when judged to be chronic, as symptoms of a neurological pathology.

ADHD is commonly diagnosed among children. When diagnosed in adults, it is regarded as adult attention-deficit disorder (AADD). It is believed that anywhere between 30 to 70% of children diagnosed with ADHD retain the disorder as adults.

Formal definitions

According to the U.S. Surgeon General and ICD-10-CM, ADHD is a metabolic form of encephalopathy, impairing the release and homeostasis of neurological chemicals, and thereby possibly reducing the function of the limbic system.

According to the Diagnostic and Statistical Manual of Mental Disorders-IV-TR, ADHD is a developmental disorder that arises in childhood, in most cases before the age of 7 years, is characterized by developmentally inappropriate levels of inattention and/or hyperactive-impulsive behavior, and results in impairment in one or more major life activities, such as family, peer, educational, occupational, social, or adaptive functioning. ADHD may be diagnosed in adulthood, but in order to make a positive diagnosis, the behavioral characteristics must have already been present prior to age 7.

Symptoms

In children the disorder is characterized by inattentiveness, impulsive behavior, and restlessness. The inattentiveness often appears as a difficulty with sustaining attention or persisting toward activities, particularly those that are not especially interesting or rewarding. This is often combined with problems inhibiting responding to distracting events that often draw the person off-task. Those with ADHD also have difficulties re-engaging the previous task once they have been distracted. The hyperactivity is typically most evident in early to middle childhood and declines significantly with age. By adulthood, it is most evident in a feeling of restlessness or inner or subjective hyperactivity as well as a need to be busy or engaged in physical activities. The impulsiveness or poor inhibition persists throughout childhood into adulthood and may be manifest verbally (excessive talking, interrupting others, blurting out answers before questions are finished, saying what's on your mind without regard to its consequences, etc.) or physically, as in doing things on impulse or a dare. Those with ADHD are often more involved in risk-taking activities and, as a consequence, suffer 2–4 times the rate of accidental injuries as do unaffected children or adults. A newly identified subset of children now classified as having ADHD are called the Predominantly Inattentive Type and may often appear to be day dreamy, spacey, confused, in a fog, staring frequently, slow moving, sluggish and hypo-active. Researchers call these children Sluggish Cognitive Tempo but this is not a commonly used diagnostic label. Some reserve the term ADD for those with Predominantly Inattentive Type due to the lack of hyperactivity in these individuals.

In adults the problem is often seen as a difficulty with time management, procrastination, organization, risk-taking, careless behavior, and distractible and impulsive behavior. They often show an inability to structure their lives and plan complex daily tasks. Their greatest difficulties are in self-control or executive functioning, which refers to inhibit off-task behavior, the ability to direct behavior toward future goals and tasks and to keep those tasks in mind until completed (typically called working memory), to self-motivate such behavior in the absence of rewards, to innovate or reorganize goal-directed behavior as obstacles arise, and to evaluate one's own performance.

Here are some symptoms of ADHD.

Diagnosis

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Traditional diagnosis of ADHD is based on a clinical interview and a checklist of symptoms from DSM-IV-TR. DSM-IV-TR Criteria for ADHD 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.

In recent times the Amen classification has subclassified the DSM-IV classification and this led to improved diagnostic accuracy, which leads to better selection of medication and treatment.

Clinical guidelines

The American Academy of Pediatrics Clinical Practice Guideline for children with ADHD emphasizes that a reliable diagnosis requires:

1. The use of explicit criteria for the diagnosis using the DSM-IV-TR.
2. The importance of obtaining information about the child’s symptoms in more than 1 setting (especially from schools).
3. The search for coexisting conditions that may make the diagnosis more difficult or complicate treatment planning.

Item 1. is dealt with by using an ADHD-specific instrument such as the Connor's Scale. The use of methods such as questionnaires that attempt to identify other conditions as well as ADHD would not meet this requirement. Diagnosis based on a clinician's, teacher's or parent's opinion, without the use of a scale such as Conners would also be invalid.

Item 2. emphasizes that the DSM-IV requires that the behaviors be present in more than one setting, normally school and home. (This is a significant change from the DSM-III criteria - see Historical Background). A diagnosis based on the a Connors Scale completed only for one setting would therefore be invalid.

The requirement that it be present in two settings is important because in the majority of cases observers in different settings do not agree on the child's behaviour. In studies that used both teachers and parents in the United States, Canada and Australia the difference has been significant. For example, one of these studies (Wolraich, 2004) found American teachers identified ADHD in 25.5% of a group of 6,171 children but parents identified it in only 7.8%.

Careful assessment must include indices of IQ scores and adaptive functioning screens. This is essential since many children and adolescents are incorrectly diagnosed as having ADHD or ADD when, in fact, their principal problems are a direct result of Borderline Intellectual Functioning (IQ 70-85) and impaired adaptive skills. Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 8th Ed., 2005, devotes Chapter 26.3 to a detailed review with clinical illustrations and proposed treatments (Ninivaggi 1999, 2005).This precludes the use of psychostimulant medications, which often complicate the clinical presentation.

Computerized tests

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.

Brain scans

Neurometrics, PET scans, FMRI, or SPECT scans have been used to provide a more objective diagnosis. These are not typically suitable for very young children, and may unnecessarily expose the patient to harmful radiation. Because the etiology of the disorder is unknown, and a complete neurological definition of this disorder is lacking, a majority of clinicians doubt the current predictive power of these objective tests to detect ADHD to be used to direct clinical treatment. 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, however, useful research tools when studying groups of patients with ADHD. An October 2005 meta-analysis by Alan Zametkin, M.D., with the NIMH entitled "The ADHD Report", concluded that these diagnostic methods lack adequate scientific research on accuracy and specificity to be used as a primary diagnostic tool.

The role of teachers in diagnosis

The role of teachers in diagnosing ADHD is particularly significant. Teachers are very active in initiating ADHD diagnosis with a survey by physicians in the Washington D.C. finding that 46% of ADHD diagnoses were first suggested by teachers, with only 30% by parents and 11% by physicians. A survey of American teachers' knowledge of ADHD found that a high percentage of teachers have minimal or no formal training in identifying or teaching ADHD children, levels being typically 80 to 90% with no training and one Canadian study finding 99% untrained. The same study found that almost all teachers surveyed claimed to have read some articles or books on ADHD. However because this study failed to examine the origins of this knowledge, many question the sources these teachers cite as a basis of their knowledge on the matter. The answer is speculative, however between 1998 and 2004 The Reading Teacher, a specialist teachers' magazine, carried only 6 articles on ADHD while the New York Times carried 637. That is, teachers appear to be about 100 times more likely to read about ADHD in the popular media than in professional publications.

This evidence suggests that a teacher's opinion that a child has ADHD should be treated with considerable caution regardless of their specialist expertise in other areas.

Reliability of diagnosis

Even if the American Academy of Pediatrics Clinical Practice Guideline is followed rigorously, questions still remain about the reliability of diagnosis. Since methods that attempt to detect it directly are not recommended (see brain scans), diagnosis is dependent on the observation and opinion of adults. The Conners Scale, for example, asks adults to rate a child on behaviors such as "Hums or makes other odd noises", "Daydreams" and "Acts 'smart'". These are rated from "not at all" to "very much". Although Conners argues for the validity of the scale, the breadth of interpretation, particularly when family and cultural norms are considered indicates that it may be far more subjective rather than objective. A further criticism of the scale is that it was originally developed to measure the effectiveness of stimulant medication, not to detect ADHD. Consequently what it may be measuring is the potential for behavior modification with stimulants such as Ritalin rather than the presence of 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 distractibility (manic phase of bipolar illness). It is also important to note that ADHD symptoms to a certain degree are also present in a high proportion of "normal" 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). ADHD is, under no circumstances, a contagious disease, as the disorder is inside a person's mind and not outside of it.

Comparative behavior

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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.

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 dropout 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 teenage 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 overuse 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.

Incidence

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.

Others (e.g. Singh ) explain the difference as being due to a lower tolerance of the normal range of boys' behavior that has developed in the past fifty years. That is, they claim that many boys are diagnosed with ADHD who do not, in fact, meet the diagnostic criteria but have attracted attention for other reasons. More rigorous diagnosis would lower the incidence in boys to that of girls.

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.

Another explanation put forward by the United Nations International Narcotics Control Board is that the increased incidence in the U.S. can, in part, be explained by the fact that the U.S. permits direct marketing of ADHD drugs to the general public whereas most other countries do not.

The ADHD treatment rate among Caucasian children is significantly higher than among African and Hispanic Americans (4.4% Caucasian, 1.7% African, 1.5% Hispanic in 1997). The same study notes that outpatient treatment for ADHD has grown from 0.9 children per 100 (1987) to 3.4 per 100 (1997).

It is also possible that social and other factors may underlie ethnic and gender differences. For example, obstacles to ADHD treatment are higher in the African-American and female populations. Cultural factors also inhibit treatment being sought.

Since most explanations of the disorder are expressed in biological terms (see #Possible causes) the incidence should not vary between communities or countries when adjusted for possible factors such as smoking during pregnancy. However some research has, found that such differences do exist. Jensen et al studied children in four U.S. communities finding that only 12.5% of children diagnosed with ADHD had been treated with stimulants but that the incidence of diagnosis, while averaging 5.1% (roughly the DSM-IV prediction) varied from 9.4% in Atlanta, Georgia to 1.6% in Puerto Rico. They also found that the incidence was higher in urban than rural communities and higher in more affluent than less affluent.

Yet another 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. At present most research focuses on broadly medical issues with very little probing possible social and economic explanations of the observed differences.

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 disorder 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. Research indicates that the frontal lobes, their connections to the basal ganglia, and the central aspects of the cerebellum (vermis) are most likely to be involved in this disorder, as may be a region in the middle or medial aspect of the frontal lobe, known as the anterior cingulate.

While heredity is often indicated, some cases may arise from problems in prenatal development, birth complications, or later neurological damage. 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 attributing causation of 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.

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%. "Based on interviews with the biological mothers, the investigators concluded that ADHD in the children was associated with a 24-fold increase in rates of maternal and paternal childhood ADHD compared with rates in parents of control children. ADHD+Oppositional Defiant Disorder/Conduct Disorder was associated with maternal mood disorders, anxiety disorders, and dependence on stimulants or cocaine, as well as childhood disruptive behavior disorders and alcohol problems in the biological fathers." <<Excerpted from Parents of Children With ADHD May Have ADHD Themselves

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 . 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 biohazards such as alcohol, tobacco smoke, lead poisoning, premature birth, excessively complicated pregnancy, etc.

Neural changes

There is increasing evidence that variants in the gene for the dopamine transporter are related to the development of ADHD . 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. 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 . 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.

Nutrition

It has also been suggested that ADHD may be the result of a poor diet and other external factors. 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 N.I. Ward showed that children with ADHD lose zinc when exposed to a food dye. Waring, McFadden, and others have shown that children with autism or ADHD are low in sulfation metabolism, in particular the enzyme Phenol Sulfotransferase-P.

Some children with ADHD seem to be addicted to milk. It has been proposed by Norwegian and British scientists that this is due to the casomorphins, peptides formed by incomplete digestion of the casein protein. While interesting, there is no compelling evidence that this in fact contributes to risk for the disorder.

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. (Jacobson and Schardt, 1999, Diet, ADHD & Behavior, Center for Science in the Public Interest, Washington, DC). More studies supporting the connection between diet and behavior, including more than 30 double-blind studies, can be found at diet-studies.com.

Critics of dietary intervention for ADHD continue to claim that fewer than 5% of ADHD children appear to be diet sensitive. They say that the available evidence is insufficient to either prove or disprove a dietary connection.

Nutritional data has been well summarized in a review article. 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 . 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 and Dr. Michael Decker 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. Though intriguing, these findings with rats would have to be replicated in humans to form any conclusive data.

Head injuries

One of the original etiologies of ADHD was that it was caused by either prenatal hypoxia, or some form of a head injury. In fact, one of the original terms for ADD/ADHD was "Minimal Brain Damage". It has been known for some decades that head injuries can cause a person to experience and display ADHD-like symptoms. This is likely due to the effect on the frontal lobe.

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.

Treatment

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.

Findings of a large randomized controlled trial suggest that:

• Medication alone is superior to behavioral therapy alone.
• The combination of behavioral therapy and medication has a small benefit over medication alone.

Mainstream treatments

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 (Methylphenidate Hydrochloride), 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.
  • 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.
• Bupropion. A dopamine and norepinephrine reuptake inhibitor, marketed under the brand name Wellbutrin.
• Atomoxetine. A norepinephrine reuptake inhibitor (NRI) 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. This medicine doesn't have an exact duration. It is to be taken once or twice a day, depending on the individual, every day, and takes up to 6 weeks to begin working fully. If the intake schedule is interrupted, it may take a few weeks to begin working correctly again.

Second-line medications include:

• Benzphetamine — a less powerful stimulant. Research on the effectiveness of this drug is not yet complete.
• Provigil/Alertec/modafinil — 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.

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" may mean unscientific because there are little or no credible scientific studies to support these suggested interventions, rather than there being experimental evidence against the intervention.

Feingold diet

The Feingold diet involves removing salicylates, artificial colors, artificial flavors, and three synthetic preservatives from children's diets. According to a recent meta-analysis, there is little scientific evidence for the efficacy of diet in treating ADHD, but there is some evidence that the elimination of certain additives may be helpful for some children, not only those with ADHD . A recent literature review notes that a possible reason for the lack of evidence for the Feingold Diet may be because research has focused on food dyes, despite the diet eliminating a wide variety of foods, some preservatives, and thousands of synthetic flavoring additives.. Thus, diet modification may play a major role in the management of ADHD, but individualised plans may be required, as not all children are sensitive to the same foods . Others have found indication that children with ADHD are metabolically different from other children, in zinc response to food dye, water/electrolyte handling and an increased need of essential fatty acids

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.

Vitamin B₆

In the 1980s vitamin B₆ was 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

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.

Neurofeedback

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 www.russellbarkley.org 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, Asperger's syndrome and many learning difficulties like dyslexia, dyspraxia, etc. Most prominent are the DORE program, the Learning Breakthrough Program™ 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 Asperger's syndrome is underdeveloped. The medical professionals at DORE call this Cerebellar Developmental Delay (CDD) . 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)

Other Stimulants

It is claimed by some with ADHD that commonly available mild stimulants such as caffeine and theobromine have similar effects to the more powerful drugs commonly used in treating the disorder. Herbal supplements such as Gingko biloba are also sometimes cited. While there is no scientific evidence to support this claim, it is widely accepted by those who wish to avoid strong medication.

Views on neurodiversity

The ADHD diagnosis is controversial and has been questioned by some professionals, adults diagnosed with ADHD, and parents of diagnosed children. They point out the positive traits that children with ADD have, such as "hyperfocusing." Others believe ADHD is a divergent or normal-variant human behavior, and use the term neurodiversity to describe it.

Views on parenting

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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 suggests 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. Many clinicians observe and assert, however, that attachments and relationships with caregivers and other features of the environment in which the child's development occurs, have profound effects on attentional and self-regulatory capacities. While challenging to measure and prove, many believe that the focus on psychopharmacological approaches to treatment fails to address this etiological complexity.

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 .

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

Though ADHD is classified as a serious disorder, some people have a different perspective and note the positive aspects. They argue that ADHD children tend to look at situations in a different manner, and that those with ADD tend to look beyond the norm. "While the A 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). Some children might be uneasy about getting into a situation. One positive side of impulsive behavior is the ability to try new things without trepidation. This can be a strength and a weakness: "Impulsivity isn't always bad. Instead of dithering over a decision, they're willing to take risks" (Underwood). Some argue that ADHD does not necessarily slow down a person's learning process. However, all longitudinal studies of ADHD children followed to adulthood find them, on the aggregate, 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, guilford.com). Some argue this is due to an educational system which focus on organization and long lectures that handicap ADHD individuals, which may lead one with ADHD to receive less formal education despite possessing high intellect. Clearly certain individuals have benefited greatly from ADHD. Michael Flatley, originator of Riverdance, was diagnosed with ADHD during his childhood in Chicago. He was also a golden glove boxer. He has also repeatedly walked out on situations where people in charge tried to tell him what to do. jetBlue Airways founder David Neeleman believes that ADHD contributed to his business acumen and refuses to take medication for fear that he will lose his creativity. Unfortunately, few others with ADHD can afford the support that Neeleman can, hiring accountants and managers to handle his affairs. It should be kept in mind that more than 6000 studies have been done in this field and not a single one has found ADHD to convey any advantage over normal or control groups in these studies. However, this result can be predicted as it has long been a scientific assumption that ADHD is disadvantageous, and therefore there has been little serious research into the intellectual advantages it can provide.

To see ADHD positively may seem somewhat problematic to anxious parents but it is at least a perspective that should be kept in mind. With or without hyperfocus, a common manifestation, ADD/ADHD in combination with successful coping skills may be utilized to achieve remarkable accomplishments in some people. Of course, favorable socioeconomic conditions and the home environment play key roles.

Controversy

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. Some denial in families may also relate to the negative perception of the condition as a hereditary brain disorder.

Skepticism towards ADHD as a diagnosis

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Critics have complained that the ADHD diagnostic criteria are sufficiently general or vague to allow virtually any child with persistent unwanted behaviors to be classified as having ADHD of one type or another.

A growing number of critics have wondered why the number of children diagnosed with ADHD in the U.S. and UK has grown so dramatically over a short period of time. However, doctors often claim that improving methods of diagnosis and greater awareness are probably in part, if not mostly the reason for this increase.

One critic points out that most children with ADHD have no difficulties concentrating when they are doing activities that are fun. Many, for instance, do quite well with video games, spending hours completely focused. They also do well with charismatic teachers. This critic argues that the symptoms of ADHD describe children when they are bored and unconnected to a task. Since many factors can contribute to a child's inability to focus on material that they are not buying into and thus, approach as drudgery, biological shortcomings cannot be completely dismissed. However the biological evidence, though repeated and repeated, (this article is a perfect example) when scrutinized more closely is not what it seems. For example Zametkin's impressive looking brain image at the beginning of this article, contrasting differences in brain activity in those with the diagnosis is a picture of those with and without the diagnosis while doing an assigned task. Thus a person (with ADHD) who is not doing the assigned task will have a different looking picture of the brain's activity on that basis alone. If brain imaging is done while one person moves their arm and another doesn't there will also be a demonstrable difference. In this particular case the so-called biological evidence may turn out to be inconclusive. Yet this brain image and many similar pictures of the brain have been repeatedly displayed with full knowledge of the weakness of the evidence. This lack of intellectual integrity by self proclaimed "experts" in this field is an issue in itself.

Contrasting sharply with the confident tone of those in this article who assume biological causality, a different perspective is very plausible . While a believer that ADHD is a biological condition, it is noteworthy that Xavier Castellanos M.D.,then head of ADHD research at the National Institute of Mental Health (NIMH) (interviewed October 10, 2000 on Frontline ) was very explicit about the extent of our biological information.

Frontline:

"How does ADHD work on the brain? What do we know about it?"

Castellanos:

"We don't yet know what's going on in ADHD..."

Frontline:

"Give me one true fact about ADHD."

Castellanos

"The posterior inferior vermis of the cerebellum is smaller in ADHD. I think that that is a true fact. It's taken about five years to convince myself that that's the case. That's about as much as I know--that I'm confident about..."

Or: Frontline: "Are you uncomfortable with how little you know about this?"

Castellanos

"Yes. But I'm also glad that I know more than I used to. It's both half full and half empty. It's not even half full. It's about a tenth full..."

It also should be noted that despite the repeated references to the genetics of ADHD being unequivocal, according to Joseph Glenmullen, M.D., clinical instructor in psychiatry at Harvard Medical School "no claim of a gene for a psychiatric condition has stood the test of time, in spite of popular misinformation."

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. Lists of famous persons either diagnosed with ADHD, its 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 AD(H)D." 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. (More to the point, the public behavior of Robin Williams does not resemble ADHD. The pressured speech, punning, and flight of ideas found in mania are a closer fit, but the above considerations apply.)

Ozzy Osbourne has said he has been diagnosed as having ADD and dyslexia

Timeline

• 1845. ADHD was first alluded to by Dr. Heinrich Hoffmann, a physician who wrote books on medicine and psychiatry, Dr. Hoffman was also a poet who became interested in writing for children when he couldn't find suitable materials to read to his 3-year-old son. The result was a book of poems, complete with illustrations, about children and their characteristics. "Die Geschichte vom Zappel-Philipp" (The Story of Fidgety Philip) in Der Struwwelpeter was a description of a little boy who could be interpreted as having attention deficit hyperactivity disorder.http://www.fln.vcu.edu/struwwel/philipp_e.html
• 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, in a series of lectures to the Royal College of Physicians in England, described a condition which some have claimed is analogous to ADHD. Still described a group of children with significant behavioral problems, caused, he believed, by an innate genetic dysfunction and not by poor child rearing or environment.. Analysis of Still's descriptions by Palmer and Finger indicated that the qualities Still described are not "considered primary symptoms of ADHD".
• 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. (http://campus.houghton.edu/orgs/psychology/student/adhd/sld004.htm)
• 1961 – Ritalin first indicated for "various behaviour problems in children".
• 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)
• 1970 – News reports that Ritalin was being prescribed to 5-10% of children in Omaha lead to national outcry and a Congressional inquiry.
• 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. http://faculty.ashrosary.org/faculty/counseling/ADHDNotes.htm
• ~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."
• 1991 – The U.S. 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.
• 1996 – ADHD accounted for at least 40% of child psychiatry references.
• 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 – Atomoxetine, the first new medication for ADHD in 25 years, receives FDA approval for use in children, teens, and adults with ADHD.

Terminology

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.

Footnotes

1. Perrin, James. M., Martin T. Stein, Robert W. Amler, and Thomas A. Blondius. 2001. Clinical practice guideline: treatment of school-aged children with Attention Deficit/Hyperactivity Disorder. Pediatrics 108 (4):1033-1044.
2. Molin, B.S., W.E. Pelham, J. Blumenthal, and E. Galiszewski. 1998. Agreement among teachers' behavior ratings of adolescents with a childhood history of ADHD. Journal of Clinical Child Psychology 27 (3):330-339.
3. Wolraich, Mark L., E. Warren Lambert, Leonard Bickman, Tonya Simmons, Melissa A. Doffing, and Kim A. Worley. 2004. Assessing the Impact of Parent and Teacher Agreement on Diagnosing Attention-Deficit Hyperactivity Disorder. Journal of developmental and behavioral pediatrics 25 (1):41-47.
4. Gomez, R., J. Harvey, C. Quick, I. Scharer, and G. Harris. 1999. DSM-IV AD/HD: Confirmatory Factor Models, Prevalence, and Gender and Age Differences Based on Parent and Teacher Ratings of Australian Primary School Children. Journal of Child Psychology and Psychiatry 40 (2):265-274.
5. Breton, Jean-Jacques, Lise Bergeron, Jean-Pierre Valla, Claude Berthiaume, and Nathalie Gaudet. 1999. Quebec Child Mental Health Survey: Prevalence of DSM-III-R Mental Health Disorders. Journal of Child Psychology and Psychiatry 40 (3):375-384.
6. Sax, Leonard, and Kathleen J. Kautz. 2003. Who First Suggests the Diagnosis of Attention-Deficit/Hyperactivity Disorder? Annals of Family Medicine 1 (3):171-174.
7. Bussing, Regina, Faye A. Gary, Christina E. Leon, and Cynthia Wilson Garvan. 2002. General classroom teachers' information and perceptions about attention deficit hyperactivity disorder. Behavioral Disorders 27 (4):327-339.
8. Singh, Ilina. 2002. Bad Boys, Good Mothers, and the "Miracle" of Ritalin. Science in context 15 (4):577-603.
9. Olfson M, Gameroff MJ, Marcus SC, & Jensen PS. (2003). National trends in the treatment of attention deficit hyperactivity disorder. American Journal of Psychiatry, 160 (6): 1071-1077
10. Bussing R, Zima BT, Gary FA, & Garvan CW. (2003). Barriers to detection, help-seeking, and service use for children with ADHD symptoms. Journal of Behavioral Health Services & Research, 30 (2): 176-189.
11. Jensen, Peter S., Lori Kettle, Margaret T. Roper, Michael T. Sloan, Mina K. Dulcan, Christina Hoven, Hector R. Bird, Jose J. Bauermeister, and Jennifer D. Payne. 1999. Are stimulants overprescribed? Treatment of ADHD in four U.S. communities. Journal of the American Academy of Child and Adolescent Psychiatry 38 (7):797-804.
12. Roman et al., 2004, American Journal of Pharmacogenomics 4:83-92
13. Michelson D, Faries D, Wernicke J, Kelsey D, Kendrick K, Sallee FR, Spencer T (2001): Atomoxetine in the treatment of children and adolescents with Attention-Deficit/Hyperactivity Disorder: a randomized, placebo-controlled, dose-response study. Pediatrics 108:e83 PubMed
14. Spencer T, Biederman J, Heiligenstein J, Wilens T, Faries D, Prince J, Faraone SV, Rea J, Witcher J, Zervas S (2001): An open-label, dose-ranging study of atomoxetine in children with attention deficit hyperactivity disorder. J Child Adolesc Psychopharmacol 11:251-265
15. Kotimaa et al., 2003, J Am Acad Child Adol Psychiatry 42, 826-833
16. Burgess et al., 2000, Am J Clin Nutr 71:327-330
17. Richardson and Montgomery, Pediatrics, 2005, 115:1360-1366)
18. ScienceDaily (2004) Reductions In Blood Oxygen Levels In Newborns Could Contribute To ADHD Development
19. Moderators and mediators of treatment response for children with attention-deficit/hyperactivity disorder: the Multimodal Treatment Study of children with Attention-deficit/hyperactivity disorder. Arch Gen Psychiatry. 1999 Dec;56(12):1088-96. PMID 10591284. Free Full Text.
20. Associated Counselors & Therapists. ADHD: Current Status of What We Know. URL: http://www.beachpsych.com/pages/cc34.html. Accessed on: April 12, 2006.
21. Wilens, T. E. Straight Talk about Psychiatric Medications for Kids (Revised Edition--2004). ISBN 1-57230-945-8.
22. Neal L. Rojas and Eugenia Chan. (2005). Old and new controversies in the alternative treatment of attention deficit hyperactivity disorder. Mental Retardation and Developmental Disabilities, 11, 116-130.
23. ^ Schnoll R, Burshteyn D, Cea-Aravena (2003). Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect, J. Appl Psychophysiol Biofeedback Mar;28(1):63-75
24. Ward NI et al. (1990). The influence of the chemical additive tartrazine on the zinc status of hyperactive children: A double-blind placebo-controlled study. J Nutr Med; 1 (1). 51-58
25. Ward NI (1997). Assessment of chemical factors in relation to child hyperactivity. Journal of Nutritional & Environmental Medicine (Abingdon); 7 (4). 333-342.
26. Oades et al (1998). Plasma neuropeptide-Y levels, monoamine metabolism, electrolyte excretion and drinking behavior in children with attention-deficit hyperactivity disorder. Psychiatry Res. 1998 Aug 17;80(2):177-86. Note: When the author was contacted by email re the children drinking more but urinating less, and asked "where is the water going?" he said that he did not know, but assumed that there was something metabolic going on that was using it.
27. Joshi et al. (2006). Supplementation with flax oil and vitamin C improves the outcome of Attention Deficit Hyperactivity Disorder (ADHD). Prostaglandins Leukot Essent Fatty Acids. 2006 Jan;74(1):17-21. Epub 2005 Nov 28.
28. Singh M (2005). Essential fatty acids, DHA and human brain. Indian J Pediatr. 2005 Mar;72(3):239-42.
29. Dougherty et al. in Lancet 354 (1999) 2132-2133
30. Dresel et al. in Eur. J.Nucl. Med. 25 (1998) 31-39
31. Still GF. Some abnormal psychical conditions in children: the Goulstonian lectures. Lancet, 1902;1:1008-1012
32. Palmer, E. and S. Finger. 2001. “An Early Description of AD/HD: Dr. Alexander Crichton and ‘Mental Restlessness’.” Child Psychology and Psychiatry Review 6(2):66–73.
33. Castellanos, F. X., Giedd, J. N., Marsh, W. L., Hamburger, S. D., Vaituzis, A. C., Dickstein, D. P., Sarfatti, S. E., Vauss, V. C., Snell, J. W., Lange, N., Kaysen, D., Krain, A. L., Ritchie, G. F., Rajapakse, J. C., & Rapoport, J. L. (1996). Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder. Archives of General Psychiatry, 53, 607–616.

See also

• Adult attention-deficit disorder
• ADHD psychosis
• List of famous people with attention-deficit hyperactivity disorder
• List of fictional characters with ADHD
• Anti-psychiatry
• Auditory processing disorder
• Chemical imbalance theory
• Educational psychology
• Hyperactivity
• Hyperfocus
• National Institute of Mental Health
• Sensory integration disorder
• Sluggish cognitive tempo
• Texas Medication Algorithm Project

References

Pine 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.
³Bellak L, Kay SR, Opler LA. (1987) Attention deficit disorder psychosis as a diagnostic category. Psychiatric Developments, 5 (3), 239-63.

• Ninivaggi, F.J., "Attention-Deficit/Hyperactivity Disorder in Children and Adolescents: Rethinking Diagnosis and Treatment Implications for Complicated Cases," Connecticut Medicine. September 1999; Vol. 63, No. 9, 515-521.

• 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: 2272-2276.

• Attention Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment (2006) by Russell A. Barkley, Ph.D. New York: Guilford Publications (guilford.com) (see also russellbarkley.org)

• Taking Charge of ADHD: The Complete Authoritative Guide for Parents (2005) by Russell A. Barkley, Ph.D. New York: Guilford Publications.

• Understanding ADD by Dr Christopher Green & Dr Kit Chee, ISBN 0-86824-587-9, Doubleday 1994
• The ADHD-Autism Connection: A Step toward more accurate diagnosis and effective treatment, by Diane M. Kennedy, ISBN 1578564980 (The aim of this book is to explore the similarities that attention deficit hyperactivity disorder (ADHD) shares with a spectrum of disorders currently known as pervasive developmental disorders.)
• Joyce, Michael & Siever, Dave Audio-Visual Entrainment (AVE) Program as a Treatment for Behavior Disorders in a School Setting, , 1997, Journal of Neurotherapy, vol 4 (2), 9-32.
• Kate Kelly and Peggy Ramundo: You Mean I'm Not Lazy, Stupid, or Crazy?! A Self-Help Book for Adults with Attention Deficit Disorder (1993). ISBN 0-684-81531-1
• Center for Neurobehavioral Genetics and Department of Psychiatry and Biobehavioral Sciences, University of California
• James M. Bower and Lawerence M. Parsons (2003). “Rethinking the ‘Lesser Brain’”. Scientific American August, 40-47.
• Edward M. Hallowell, M.D. and John J. Ratey, M.D. (2005). Delivered from Distraction: Getting the Most out of Life with Attention Deficit Disorder. Ballantine Books. ISBN 0-345-44230-X
• “Evaluation of an exercise-based treatment for children with reading difficulties" by David Reynolds, Roderick I. Nicolson and Helen Hambly, Version 3.4. Final (2003), retrieved December 1st, 2005.
• “How does the DORE programme work?”Dore Achievement Centres, UK, retrieved November 28th, 2005.

External links

• NIMH's ADHD page
• National Resource Center on ADHD Information & Resource Sheets for Adults with ADHD
• NIH - Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder
• CDC's ADHD page
• ADD/ADHD/ODD & Behavioral Problems - features some nutritional causes and their treatments.
• Basic Information on Attention Deficit Hyperactivity Disorder for the lay person
• Template:Dmoz

• Attention
• Attention disorders
• Childhood psychiatric disorders
• Educational psychology
• Special education