Attention Deficit Disorder

Attention-deficit hyperactivity disorder (ADHD) (sometimes also referred to as ADD) is a psychiatric diagnosis that interprets divergent personality traits perceived to be distracting as symptoms of a mental disorder. Characteristics sometimes interpreted as symptoms include hyperfocus, hyperactivity, forgetfulness, mood shifts, poor impulse control, and distractibility.

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

The image on the left illustrates areas of activity in the brain of a person without ADHD. The image on the right illustrates the areas of activity of the brain of someone with ADHD. There is some controversy over the research by Dr. Alan Zametkin that produced these images.

Formal definitions

According to the U.S. Surgeon General, and ICD-9-CM (International Classification of Disease Revised Edition 2005), ADHD is a metabolic form of encephalopathy, impairing the release and homeostasis of neurological chemicals, and reducing the function of the limbic system.

According to the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders-IV (Text Revision) (DSM-IV-TR), there are three subtypes of ADHD: Predominantly Inattentive, Predominantly Hyperactive-Impulsive, and Combined Type.

Symptoms

In children the disorder is characterized as inattentiveness to external direction, underachievement, impulsive behavior, and restlessness. Hyperactivity is typically taken as an indication, however, children identified as inattentive are often sluggish and hypo-active.

In adults the problem is often seen as an inability to structure their lives and plan simple daily tasks. Thus, inattentiveness and restlessness often become secondary problems.

Diagnosis

A diagnosis of ADHD is based on a checklist of symptoms from DSM-IV-TR. See the External links section for the Centers for Disease Control and Prevention (CDC) web page summarizing these criteria.

The 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. In fact, ADHD is similar to manic episodes in bipolar patients and giving stimulants to an undiagnosed bipolar person can intensify and lengthen their manic episodes.

Comparative behavior

It is thought that ADHD adults are less noticeable than children because they have learned better coping skills and other forms of adaptive behavior.

Studies show that those with ADD/ADHD are very creative, as a number of famous actors, writers, and artists have been diagnosed with the disorder. It is speculated that they are probably so creative because they are very focused on their thoughts and love to explore their imagination.

ADD/ADHD behavior traits are often mistaken for hyperactivity. Many with the disorder can't concentrate on tasks given to them, but are not necessarily hyperactive. In recent years, a large number of those diagnosed with the disorder have shown to be rather calm and quiet, but are unable to pay attention in some contexts because of the focus on their own thoughts.

ADHD is sometimes associated with higher school drop-out rates, traffic accidents, on-the-job injuries, and 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 is seen all over the industrialized world, although it is most commonly diagnosed in the United States of America.

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 CDC's 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). 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 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 diagnostical 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. Because twin studies have shown ADHD to be highly inheritable, almost as much as height, this theory might merit further consideration. Other research points to the link between the 7-repeat allele of the Dopamine transporter gene and civilizations' migratory path -- the so-called "Out of Africa" theory. However, because at least 4-7 genes thus far are thought to be associated with ADHD, this is conjecture at this point. Individuals without ADHD also have the 7-repeat allele, though in smaller numbers. Some researchers refer to this allele as the "response ready" allele.

A study by Olfson (2003) reports that the ADHD treatment rate amongst 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, Ph.D. 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 testing for ADHD symptoms generally consists of obtaining multiple types of assessments. 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.

Finally, computerized tests of attention can be helpful in providing a further independent assessment. These different assessments may not be consistent, but do provide a view of the person's difficulties. Subjectivity of the analysis can be compounded by the fact that physicians generally need not order psychological testing in order to make the diagnosis of ADHD, but many doctors use this kind of assessment to avoid over-diagnosis and treatment. 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.

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, viral or bacterial infections, brain injury, or nutritional deficits. 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 believe that problems in prenatal development, birth complications, or later neurological damage may contribute to ADHD, although no satisfactory proof exists for this. The burgeoning field of epigenetics -- the study of what causes genes to express or not express -- is examining these questions. There has been a surge in alternative approaches to ADHD, but these have been vigorously disputed. Still, most practitioners agree that a multi-modal treatment strategy is optimum, incorporating medication, nutrition, exercise, and modalities such as yoga, mindfulness meditation, and even drumming.

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, and is caused by 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 [1]. It would appear that not all cases of diagnosed ADHD can be attributed to a single gene.

This investigative path also suggests an associated hypothesis that environmental factors, handed down from generation to generation, may trigger the symptoms associated with ADHD. There also exists a possibility that a family with one diagnosed member may have a heightened awareness of the disorder, along with a willingness to seek formal diagnosis, which would make detection and diagnosis more likely, thus skewing the data on heritability. However, studies involving identical vs. fraternal twins are a strong indication that genetics are a fairly decisive factor.

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, 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).

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 pregnacy. 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, possibly related to drug use during pregnancy or environmental toxins may also be possible causes, but again, little proof seems to exist as yet, and it can again be pointed out that the parents of many if not most individuals with ADHD did not consume drugs during pregnancy.

Nutrition

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. Studies of changes in diets of children provide some anecdotal and scientific evidence for this, but current majority opinion seems to be that the available evidence is insufficient to either prove or disprove this. However, it has been noticed that 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.

It has, however, been established conclusively that a significant number of 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). Many other studies supporting the connection between diet and behavior can be found at diet-studies.com.

Nutritional data has been well summarized in a review article (Burgess et al., 2000, Am J Clin Nutr 71:327-330). Children with ADHD have lower levels of key fatty acids. 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 is especially 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.

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 (Richardson and Montgomery, Pediatrics, 2005, 115:1360-1366). 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.

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. (ScienceDaily)

Head injuries

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

Treatment

There are many options available to treat people diagnosed with ADHD. These options include a variety of medications, behavior-changing therapies, educational interventions, and dietary modification.

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. The stimulants used include:

• Methylphenidate -- Available in:
  • Regular formulation, sold as Ritalin, Metadate, 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: 8 hours per dose. Usually taken twice daily.
  • All-day formulation, sold as Ritalin LA, Metadate CD, Concerta. 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.
• Atomoxetine. A Selective Norepinephrine Reuptake Inhibitor (SNRI) introduced in 2002, 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 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 -- 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.^[2]

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.

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.

The Feingold Program eliminates several groups of synthetic food additives: Artificial colors, artificial flavors, BHA, BHT, TBHQ and (more recently) aspartame. 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 diet-studies.com

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

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. Many professionals consider the treatment promising, but state that there is not yet sufficient evidence that it works after the immediate treatment is complete.

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.

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[3] ) 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) [4]. 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 the lack of scientific evidence.

However, 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.

Moreover, independent research that is currently under way on the DORE program, yielded 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)

Parenting

A frequent assessment of ADHD children is that their parents are too lenient, or incompetent. But 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. Whereas, ADHD children might be more responsive to an enriched intellectual environment. 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.

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). Researchers have also shown that individuals labeled as either bipolar or ADHD often have variant dopamine receptor alleles. Researchers have reported, for example, that DRD4 7 repeat alleles appear more frequently in certain aboriginal cultures with low population densities such as the Amazon, whereas DRD4 2 repeat alleles are especially common in higher population density regions, including the Orient.

Positive aspects

Though ADHD is classified as a serious disorder, many people have a different perspective and note the positive aspects. ADHD children tend to look at situations in a different manner. They tend to look beyond the norm. "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). 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: "Compulsivity isn't always bad. Instead of dithering over a decision, they're willing to take risks" (Underwood). ADHD does not necessarily slow down a person's learning process. In fact, ADHD can contribute to a faster or more comprehensive learning process, especially if teachers implement effective teaching strategies geared specifically towards the ADHD learner. JetBlue founder David Neeleman believes that ADHD contributed to his business acumen and refuses to take medication for fear that he will lose his creativity. Experts agree this would not be the case. Unfortunately, few others with ADHD can afford the support that Neeleman can, hiring accountants and managers to handle his affairs.

Some people find hints of ADHD in the lives of many famous people in history. Though such post mortem diagnosis is questionable, it is intriguing to ponder the evidence that people such as Thomas Edison might have been diagnosed as having ADHD if the current DSM criteria had been developed long ago. 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 and Dustin Hoffman. Robin Williams has sometimes been called "the poster child for ADD". At the same time, those representing the Asperger syndrome and bipolar camps also claim many of the above as their own. And, while many people with ADHD do succeed, many more remain underemployed, many times-divorced, absentee parents, and often incarcerated. Romantic views of ADHD "gifts" should be approached with caution.

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. 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

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.

Dr. Mary Megson, however, in her presentation to the House Government Reform Committee on Autism and Vaccines (2000) claims the increase in ADHD, as well as autism, are a result of the increasing use of vaccines that deplete vitamin A stores, combined with a G-protein defect. This is especially likely in a family where at least one parent suffers night-blindness, she says.

It has often been suggested that the causes of the apparent ADHD epidemic lie in cultural patterns that variously encourage or sanction the use of drugs as a simple and expeditious cure for complex problems that may stem primarily from social and environmental triggers rather than any innate disorder. Some critics assert that many children are diagnosed with ADHD and put on drugs as a substitute for parental attention, whereas many parents of ADHD children assert that the associated demand for attention goes beyond what can be humanly provided, causing massive disruption to other individuals and relationships, as well as to environments with dysfunctionally structured relationships such as are manifest in many classrooms. This criticism also includes the use of prescription drugs as a substitute for parental duties such as communication and supervision.

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 on their book Shadow Syndromes: The Mild Forms of Major Mental Disorders That Sabotage Us.

Another explanation comes from a common misconception of the symptoms that leads to an incorrect diagnosis. For example, an employee of a school might think that a student has ADHD simply because the child cannot be controlled in the classroom. A teacher may think a student whom they cannot control has ADD, but in reality the problem may be a lack of discipline. The same teacher might not notice a child who forgets their papers, stares (entranced) at the carpet for long periods of time, or shows many of the recognized symptoms.

However, the results achieved in clinical tests with medication and anecdotal evidence of parents, teachers, and both child and adult sufferers has been taken as proof that there is both a condition and successful treatment options for most people who meet the criteria for a diagnosis. But critics point out that neurological differences exist among individuals just as with any human trait, such as eye color or height; and that stimulants have an effect on anyone, not just those diagnosed with ADHD.

Another problem lies in misdiagnosis; critics believe many of those being treated for ADHD do not suffer from the disorder to such a point that potentially mind-altering drugs should be prescribed.

A further problem is that ADD and ADHD are syndromes, associations of symptoms. There is no well established cause for the condition. This means that it may actually be a blanket term covering a multitude of conditions with a variety of causes. In fact, genome scans have identified several gene alleles which are prevalent among individuals diagnosed with ADHD, but no single allele can account for all cases, and not all cases have been explained genetically.

Confusion may also arise from the fact that ADD/ADHD symptoms vary with each individual, and some mimic those of other causes. A known fact is that, as the body (and brain) matures and grows, the symptoms and adaptability of the individual also change. Many individuals diagnosed with ADD/ADHD successfully develop coping skills, while others may never do so.

Another view is that while there does exist a phenotype that corresponds roughly to the ADHD diagnostic criteria, this phenotype should not necessarily be described as a pathology. There are many phenotypes considered normal-variant, which have liabilities, and perhaps some advantages as well, such as homosexuality and left-handedness. In other words, ADHD may be better seen as a form of neurodiversity.

ADHD as pseudo-science and its falsifiability

Some experts have noted that the hypothesis "ADHD is a disorder" is unscientific, and point out that people generally assume that something is scientific just because it sounds scientific [5]. 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. Given that the neurobiological basis is often brought up, one criteria could be the following:

If individuals with ADHD behavior are shown to not have neuroanatomical differences compared to the average individual, then ADHD is not a disorder.

However, this falsifiability criteria has a number of problems. For one, psychiatry doesn't define something as a disorder only if it has a neurobiological basis. But more importantly, human brains are not identical, so every single person could be said to have neuroanatomical differences compared to an average. For this criteria to be valid, there would need to be a clear distinction between which neuroanatomical differences constitute a disorder (e.g. a tumor) and which do not. Unless the specific neurobiological characteristics of ADHD are tautologically defined as a disorder, this task is clearly problematic, as behavior that is considered normal-variant (e.g. homosexuality, left-handedness, giftedness, being asleep, tired, etc.) likely has a neurochemical or neuroanatomical basis as well.

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 published in Proceedings of the National Academy of Sciences [6] 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 (Timimi, 2002) 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'.

Showing that people with ADHD show differences from others by the use of medical tests such as PET scans does not answer the social constructionist view since such differences could be expected to be found in people at one end of any behavioural spectrum. Nor does evidence of successful treatment undermine the social constructionist view; for example the American National Institute on Drug Abuse [7] reports that Ritalin is abused by non-ADHD students partly for its ability to increase their attention. To undermine the social construction explanation, it would need to be demonstrated that ADHD is a true disorder (rather than a collection of traits) and that there is a distinct sub-group who clearly fall into the category. Neither proof yet exists.

ADD/ADHD a hoax?

There are some claims that ADD/ADHD is simply a hoax. Some of these charges are that there has been a conspiracy between medical and counseling professionals and the pharmaceutical companies, or that the former have been misled by the latter, which have profited greatly from the sale of medication such as Ritalin and Adderall, and have advertised their products extensively. Since medications became available, there has been an increased number of persons diagnosed. This might be explained by increased awareness or easy solution for doctors.

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.[8] 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.

Concerns about the impact of labeling

Dr. Thomas Armstrong [9], 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 [10].

Thom Hartmann became interested in ADHD when his son was diagnosed; Hartmann has said that the brain disorder label is "a pretty wretched label for any child to have to bear" [11].

Others have expressed concern that the brain disorder label can negatively impact the self-esteem of a child and effectively become a self-fulfilling prophecy mainly through self-doubt.

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. See more studies on stimulant medication and heart disease and pay attention to the Brown 1989 study showing that African-Americans are more prone to increase in blood pressure and should be monitored closely.

A new concern, raised by a small scale 2005 study, is that methylphenidate might cause chromosome aberrations [13], 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. 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 [14] [15].

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. http://faculty.ashrosary.org/faculty/counseling/ADHDNotes.htm
• 1957 - the stimulant Methylphenidate (Ritalin) became available.
• 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)
• 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. 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, once a Professor of Allergy in San Francisco, claimed that hyperactivity was increasing in proportion to the level of food additives.
• 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." [16]
• 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.
• 2005 - the Italian campaign Giù le mani dai bambini launched the International Consensus: ADHD and Abuse in the Prescription of Psychofarmaceutical Drugs to Minors among experts in the field. A link is provided in the External Links section below.

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.

See also

• Adult attention-deficit disorder
• ADHD psychosis
• List of fictional characters with ADHD
• Anti-psychiatry
• Auditory processing disorder
• Chemical imbalance theory
• Hyperactivity
• Hyperfocus
• NIMH
• Sensory integration disorder
• Sluggish cognitive tempo
• Texas Medication Algorithm Project

References

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

• 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.)

• Hartmann, Thom (2003). The Edison Gene: ADHD and the Gift of the Hunter Child. ISBN 0892811285 Rochester, Vermont: Park Street.
• Hartmann, Thom (1998) Healing ADD: Simple Exercises That Will Change Your Daily Life. Underwood-Miller (1st ed.) ISBN 1887424377 (Uses Neuro-linguistic programming techniques)
• Hartmann, Thom (1997 rev.) ADD, a different perception ISBN 1887424148 ( hunter vs. farmer comparison)

• 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), 9-3