Attention-deficit hyperactivity disorder

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Attention-Deficit Hyperactivity Disorder (ADHD) is a behavioral condition affecting about 2-5% of the world's population depending on the diagnostic criteria used. It typically presents during childhood, and is characterized by a persistent pattern of impulsiveness, hyperactivity, and inattention. ADHD occurs twice as commonly in boys as in girls.

ADHD diagnosed in childhood resolves in 40 to 90% of individuals by the time they reach adulthood. Those affected are likely to develope coping mechanisms as they mature thus compensating for their previous ADHD.

Though typically regarded as a diagnosis in children Adult ADHD has been increasingly recognized in the last few decades. ADHD has a strong genetic component. Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling. The American Academy of Pediatrics states that stimulant medications and/or behavior therapy are appropriate and generally safe treatments for ADHD. Long term safety of stimulants however has not been determined.

ADHD is a controversial disorder both within and outside the medical profession.



ADHD is usually classified by the Diagnostic and Statistical Manual of Mental Disorders (DSM IV). The DSM IV identifies three subtypes:

  • ADHD Primarily Inattentive (ADHD-I): previously known as ADD-H or Attention Deficit Disorder without Hyperactivity
  • Primarily Hyperactive/Impulsive (ADHD-HI): previously known as ADHD
  • combined type (ADHD-C): previously known as ADD+H or Attention Deficit Disorder with Hyperactivity

The majority of studies have looked at ADHD-C, with much less work done on ADHD-I.

ADHD has been classied as a developmental disorder, a behavior disorder and a neurological disorder.

ADHD is a developmental disorder where certain traits such as impulse control significantly lag in development when compared to the general population. Using magnetic resonance imaging, this developmental lag has been estimated to range between 3 to 5 years in the prefrontal cortex of ADHD patients in comparison to their peers. These delays are considered to cause the impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioral or neurodevelopmental disorders.


The most common symptoms of ADHD are:

  • Impulsiveness: a person who acts quickly without thinking things through.
  • Hyperactivity: a person who is unable to sit still.
  • Inattention: a person who daydreams or seems to be in another world.

The DSM IV categorises the symptoms of ADHD into two clusters: inattention symptoms and hyperactivity/impulsivity symptoms. Most ordinary people exhibit some of these behaviors but not to the point where they seriously interfere with the person's work, relationships, or studies or cause anxiety or depression.

Hyperactivity is common among children with ADHD but tends to disappear during adulthood. However, over half of children with ADHD continue to have symptoms of inattention throughout their lives.

Inattention and "hyperactive" behavior are not the only problems with children with ADHD. ADHD exists alone in only about 1/3 of the children diagnosed with it. Many of these co-existing conditions require other courses of treatment and should be diagnosed separately instead of being grouped in the ADHD diagnosis. Some of the associated conditions are:

  • Oppositional defiant disorder (35%) and Conduct disorder (26%). These are both characterized by anti-social behaviors such as aggression, frequent temper tantrums, deceitfulness, lying, or stealing.
  • Primary disorder of vigilance. Characterized by poor attention and concentration, as well as difficulties staying awake. These children tend to fidget, yawn and stretch, and appear to be hyperactive in order to remain alert and active.
  • Bipolar disorder. As many as 25% of children with ADHD have bipolar disorder. Children with this combination may demonstrate more aggression and behavioral problems than those with ADHD alone.
  • Anxiety Disorders. Commonly accompany ADHD, particularly Obsessive-Compulsive Disorder. OCD is believed to share a genetic component with ADHD, and shares many of its characteristics. Although children with ADHD have an inability to maintain attention, conversely, they may also fixate especially when the fixation is generated by a focused source (such as a computer, or a highly imaginative task such as reading).


ADHD is generally inherited, but it can also be caused by various problems, including difficulties with pregnancy, birth, early childhood severe illness, and environmental toxins.

Genetic factors

Twin studies indicate that the disorder is highly heritable and that genetics cause about 75% of ADHD cases. Hyperactivity also seems to be primarily a genetic condition however other causes do have an effect.

Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters. Candidate genes include dopamine transporter, dopamine receptor D4, dopamine beta-hydroxylase, monoamine oxidase A, catecholamine-methyl transferase, serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), 5-hydroxytryptamine 1B receptor (5-HT1B), the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI).

The broad selection of targets indicates that ADHD does not follow the traditional model of a "genetic disease" and should be viewed as a complex interaction among genetic and environmental factors. Even though all these genes might play a role to date no single gene has been shown to make a major contribution to ADHD.

Environmental factors

The estimated contribution of non-genetic factors to all cases of ADHD is 20 percent.

The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure, believed to stress babies prenatally. Lead concentration below the Center for Disease Control's action level account for slightly more cases of ADHD than tobacco smoke (290 000 versus 270 000, in the USA, ages 4 to 15). Complications during pregnancy and birth—including premature birth—might also play a role. It has been observed that women who smoke while pregnant are more likely to have children with ADHD. This could be related to the fact that nicotine is known to cause hypoxia (lack of oxygen) in utero, but it could also be that ADHD women have more probabilities to smoke both in general and during pregnancy, being more likely to have children with ADHD due to genetic factors.

Current evidence does not support an association between head injuries and ADHD.


Studies have found that malnutrition is also correlated with attention deficits. Diet seems to cause ADHD symptoms or make them worse. Many studies point to synthetic preservatives and artificial coloring agents aggravating ADD & ADHD symptoms in those affected. Older studies were inconclusive quite possibly due to inadequate clinical methods of measuring offending behavior. Parental reports were more accurate indicators of the presence of additives than clinical tests. Several major studies show academic performance increased and disciplinary problems decreased in large non-ADD student populations when artificial ingredients, including artificial colors were eliminated from school food programs.. Professor John Warner stated, “significant changes in children’s hyperactive behaviour could be produced by the removal of artificial colourings and sodium benzoate from their diet.” and “you could halve the number of kids suffering the worst behavioural problems by cutting out additives”.

In 1982, the NIH had determined, based on research available at that time, that roughly 5% of children with ADHD could be helped significantly by removing additives from their diet. The vast majority of these children were believed to have food allergies. More recent studies have shown that approximately 60-70% of children with and without allergies improve when additives are removed from their diet, that up to almost 90% of them react when an appropriate amount of additive is used as a challenge in double blind tests, and that food additives may elicit hyperactive behavior and/or irritability in normal children as well.

A study from 2008 concludes that Omega-3/Omega-6 supplementation reduces ADHD symptoms for some, but for the majority it has little or no effect.

Social factors

There is no compelling evidence that social factors alone can cause ADHD. Many researchers believe that relationships with caregivers have a profound effects on attentional and self-regulatory abilities. A study of foster children found that a high number of them had symptoms closely resembling ADHD. Well other researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse. Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

Neurobiological mechanisms

The pathophysiology of ADHD is unclear and there are a number of competing theories.

In one study a delay in development of certain brain structures by an average of three years occurred in ADHD elementary school aged patients. The delay was most prominent in the frontal cortex and temporal lobe, which are believed to be responsible for the ability to control and focus thinking. In contrast, the motor cortex in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the fidgetiness that characterize an ADHD diagnosis.

The same laboratory had previously found involvement of the "7-repeat" variant of the dopamine D4 receptor gene, which accounts for about 30 percent of the genetic risk for ADHD, in unusual thinness of the cortex of the right side of the brain; however, in contrast to other variants of the gene found in ADHD patients, the region normalized in thickness during the teen years in these children, coinciding with clinical improvement.

Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity), and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. Medications focused on treating ADHD (such as methylphenidate) work by reducing dopamine reuptake in certain areas of the brain, such as those that control and regulate concentration. As dopamine is a stimulant, this increases neural activity and thus blood flow in these areas (blood flow is a marker for neural activity). A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain's ability to produce dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to "childhood learning problems" in healthy subjects as well.

Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are the molecular abnormality of ADHD or a secondary consequence of a problem elsewhere. Researchers have described a form of ADHD in which the abnormality appears to be sensory overstimulation resulting from a disorder of ion channels in the peripheral nervous system.

PET scans of glucose metabolism in the brains of a normal adult (left) compared to an adult diagnosed with ADHD (right). "This PET scan was taken from Zametkin's landmark 1990 study, which found lower glucose metabolism, in the brains of patients with ADHD who had never taken medication. Scans were taken while patients were engaging in tasks requiring focused attention. The greatest deficits were found in the premotor cortex and superior prefrontal cortex."
An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children. The image on the left illustrates glucose metabolism in the brain of a 'normal' adult while doing an assigned auditory attention task; the image on the right illustrates the areas of activity in the brain of an adult who had been diagnosed with ADHD as a child when given that same task; these are not pictures of individual brains, which would contain substantial overlap, these are images constructed to illustrate group-level differences. Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex. A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADHD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADHD patients (relative to the controls). Most notably, lower metabolic activity in one specific region of the left anterior frontal lobe was significantly inversely correlated with symptom severity. These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.


Many of the symptoms of ADHD occur from time to time in everyone. In patients with ADHD, however, the frequency of these symptoms is much higher and impairs regular life functionality, typically at school or at work. Not only will they perform poorly in task oriented settings but they will also have difficulty with social functioning with their peers. No objective physical test exists to diagnose ADHD in a patient. As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these critera are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

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

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

DSM-IV criteria

I. Either A or B:

A. Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:
  1. Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
  2. Often has trouble keeping attention on tasks or play activities.
  3. Often does not seem to listen when spoken to directly.
  4. Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).
  5. Often has trouble organizing activities.
  6. Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
  7. Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
  8. Is often easily distracted.
  9. Often forgetful in daily activities.
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:
  • Hyperactivity:
  1. Often fidgets with hands or feet or squirms in seat.
  2. Often gets up from seat when remaining in seat is expected.
  3. Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless).
  4. Often has trouble playing or enjoying leisure activities quietly.
  5. Is often "on the go" or often acts as if "driven by a motor".
  6. Often talks excessively.
  • Impulsiveness:
  1. Often blurts out answers before questions have been finished.
  2. Often has trouble waiting one's turn.
  3. Often interrupts or intrudes on others (e.g., butts into conversations or games).

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

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

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

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

Other diagnostic criteria

In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADHD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10) is present, the condition is referred to as "Hyperkinetic conduct disorder". Otherwise the disorder is classified as "Disturbance of Activity and Attention", "Other Hyperkinetic Disorders" or "Hyperkinetic Disorders, Unspecified". The latter is sometimes referred to as, "Hyperkinetic Syndrome".

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

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

All five criteria are proven using specifically designed test or using the patients history given by the parents, teachers or the patient's memory.

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

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

Common comorbid conditions are Oppositional Defiance Disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder. Learning disorders are more common when there are inattention symptoms.


Methods of treatment often involve some combination of medications, behaviour modifications, life style changes, and counselling. Stimulant medications are the most clinically effective and cost efficient method of treating ADHD. Behavior therapy aimed at parents to help them understand ADHD shown short term benefits.

Comorbid disorders or substance abuse can make the diagnosis and the treatment of ADHD more difficult. Psychosocial therapy is useful in treating some comorbid conditions.

Long term safety however has not been determined with no randomized controlled trials assessing the harms or benefits of treatment beyond two years.


ADHD diagnosed in childhood resolves in 40 to 90% of individuals by the time they reach adulthood. Those affected are likely to develop coping mechanisms as they mature thus compensating for their previous ADHD.

37% of those with ADHD do not get a high school diploma even though many of them will receive special education services. The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish high school. In the United States, less than 5% of individuals with ADHD get a college degree compared to 28% of the general population.


A review estimated ADHD's global prevalence in people under the age of 19 at 5%. There was however wide variability in prevalence estimates with North America children appearing to have a higher rate of ADHD than Africa and the Middle East children. There is also a gender discrepency in children diagnosed with ADHD. 10% of males and 4% of females have been diagnosed in the United States. This sex difference may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.


The clinical definition of "ADHD" dates to the mid-20th century, when physicians developed a diagnosis for a set of conditions variously referred to as "minimal brain damage", "minimal brain dysfunction", "learning/behavioural disabilities" and "hyperactivity". Researchers speculate that earlier references to the condition as mentioned in the examples below, have been made throughout history.

In 493 BCE, physician-scientist Hippocrates described a condition that seems to be compatible with what we now know as ADHD. He described patients who had "quickened responses to sensory experience, but also less tenaciousness because the soul moves on quickly to the next impression". Hippocrates attributed this condition to an "overbalance of fire over water”. His remedy for this "overbalance" was "barley rather than wheat bread, fish rather than meat, water drinks, and many natural and diverse physical activities." Shakespeare made reference to a "malady of attention", in King Henry VIII.

In 1902, the English pediatrician George Still gave a series of lectures to the Royal College of Physicians in England, and 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 hereditary dysfunction and not by poor child rearing or environment.

In 1937, Dr. Charles Bradley in Providence, RI reported that a group of children with behavioral problems improved after being treated with the stimulant Benzedrine. In 1957, the stimulant methylphenidate (Ritalin, which was first produced in 1950) became available under various names (including Focalin, Concerta, Metadate, and Methylin); it remains one of the most widely prescribed medications for ADHD. Initially the drug was used to treat narcolepsy, chronic fatigue, depression, and to counter the sedating effects of other medications. The drug began to be used for ADHD in the 1960s and steadily rose in use.

Psychiatry officially codified a condition called “hyperkinetic reaction of childhood” in 1968, displaying the psychoanalytical influences of that time. The name Attention Deficit Disorder (ADD) was first introduced in DSM-III, the 1980 edition. By 1987 – The DSM-IIIR was released changing the diagnosis to "Undifferentiated Attention Deficit Disorder." Further revisions to the DSM were made in 1994 – DSM-IV described three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination.

In the 1970s researchers began to realize that the condition now known as ADHD did not always disappear in adolescence, as was once thought. At about the same time, some of the symptoms were also noted in many parents of the children under treatment. The condition was formally recognized as afflicting adults in 1978, often informally called Adult ADD, since symptoms associated with hyperactivity are generally less pronounced. Current research indicates that up to 60% of children with ADHD carry their symptoms into adulthood.

In 1975, pemoline (Cylert) was 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 14 cases over the next 27 years would result in the manufacturer withdrawing this medication from the market. New delivery systems for medications were invented in 1999 that eliminated 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 (Metadate CD, Adderall XR, Focalin XR) and an osmotic pump that extrudes a liquid methylphenidate sludge across an 8–12 hour period after ingestion (Concerta).

It has also been suggested that the disparities in diagnosis levels per capita between countries are affected by differences in knowledge and understanding of the condition. For example, more widespread knowledge and greater acceptance of the condition amongst both doctors and teaching professionals within a region will increase the likelihood of identification and subsequent diagnosis of the condition.

During 1996, ADHD accounted for at least 40% of child psychiatry references.

In 2003, atomoxetine (Strattera) received the first FDA approval for a nonstimulant drug to be used specifically for ADHD. In 2007, lisdexamfetamine (Vyvanse) becomes the first prodrug to receive FDA approval for ADHD. The landmark study of 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 children with ADHD 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.

Cultural aspects

People talk about ADHD in 5 different ways:

  • appropriating the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) descriptors;
  • schools as identity-construction sites
  • resistance: biology versus moral culpability
  • alternative solutions to a real problem
  • relief and hope in naming experience

Another study looked at Colombian and Castillejos, Zambales schoolchildren to examine whether ADHD is merely a cultural phenomenon, or a cultural phenomenon with a biological basis. The authors conclude: “If ADHD were explicable as a culturally formulated psychiatric phenomenon, then it would be predicted that the same hyperactive and inattentive behaviors displayed in different cultural contexts would be associated with differing degrees of harmful dysfunction. In this study we found that children's hyperactive and inattentive behavior were similarly expressed in diverse populations and systematically related to children's social and academic wellbeing across those varied cultural contexts.” This study was later criticized for assuming a homogenous culture for the United States population, failing to mention the socioeconomic backgrounds of the populations, and using two study populations that share European cultural origins.

Concerns and alternative theories

Despite being well-validated Attention deficit–hyperactivity disorder (ADHD) is a controversial diagnosis. Many professionals have concerns about the effects of an ADHD diagnosis on the mental state of patients and its effects on self-esteem. Social critics point out that there is disagreement over the cause of ADHD, questions about research methodologies, and skepticism toward its classification as a mental disorder. Social critics point to changing standards of diagnosis, such as the American Academy of Pediatrics (AAP) issuing a more careful set of standards in 2000 to aid clinicians than merely using DSM-IV.

While studies indicate that ADHD is in fact under diagnosed, social critics continue to state that the disorder is diagnosed far too often. The National Institute of Mental Health states that, "stimulant drugs, when used with medical supervision, are usually considered quite safe." Still, individual parents and individual professionals have raised questions about the side effects of drugs and their long term use. Calls for greater scrutiny are made by some news sources, social critics, religions, and individual medical professionals. Ethical and legal issues with regard to treatment have been key areas of concern for these critics. "Alternative theory" critics contend that the symptoms of ADHD can be better explained by the Hunter vs. farmer theory, Neurodiversity, or the social construct theory of ADHD. Fringe critics question if ADHD exists at all as a disorder. Scientologists and certain factions of the Antipsychiatry movement are against almost all aspects of psychiatric practice, and are highly skeptical that the diagnosis denotes a genuine impairment. (Conversely, those critical of Scientology believe that much of the controversy generated about ADHD is manufactured).

Concerns about the impact of labeling

Parents are generally concerned that telling children they have a brain disorder could possibly harm their self-esteem. Dr. Russell Barkley believes labeling is a double-edged sword; there are many pitfalls to labeling but that by using a precise label, services can be accessed. He also believes that labeling can help the individual understand and make an informed decision how best to deal with the disorder using evidence based knowledge. Furthermore studies also show that the education of the siblings and parents has at least a short term impact on the outcome of treatment. Dr. Russell Barkley states this about ADHD rights: "..because of various legislation that has been passed to protect them. There are special education laws with the Americans with Disabilities Act, for example, mentioning ADHD as an eligible condition. If you change the label, and again refer to it as just some variation in normal temperament, these people will lose access to these services, and will lose these hard-won protections that keep them from being discriminated against. . . ." Psychiatrist Harvey Parker, who founded CHAAD, states, "we should be celebrating the fact that school districts across the country are beginning to understand and recognize kids with ADHD, and are finding ways of treating them. We should celebrate the fact that the general public doesn't look at ADHD kids as "b-a-d" kids, as brats, but as kids who have a problem that they can overcome".

Social critics believe that this knowledge can effectively become a self-fulfilling prophecy mainly through self-doubt. Dr. Thomas Armstrong states that the ADHD label is a "tragic decoy" which severely erodes the potential to see the best in a 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. Thom Hartmann has said that the brain disorder label is "a pretty wretched label for any child to have to bear."

Hunter vs. farmer theory of ADHD

The hunter vs. farmer theory is a hypothesis proposed by Thom Hartmann, a radio host, about the origins of attention-deficit hyperactivity disorder (ADHD). He believes that these conditions may be a result of adaptive behavior of the species. His theory believes that those with ADHD retained some of the older hunter characteristics.


Proponents of this theory assert that atypical (neurodivergent) neurological development is a normal human difference that is to be tolerated and respected as any other human difference. Social critics argue that while biological factors may obviously play a large role in difficulties sitting still and/or concentrating on schoolwork in some children, for a variety of reasons they have failed to integrate into the social expectations that others have of them.

Social construct theory of ADHD

Social critics question whether ADHD is wholly or even predominantly a biological illness. A minority of these critics maintain that ADHD was, "invented and not discovered". They believe that no disorder exists and that the behaviour observed is not abnormal and can be better explained by environmental causes or just the personality of the "patient."

See also


Related disorders


Further reading

  • Barkley, Russell A. Take Charge of ADHD: The Complete Authoritative Guide for Parents (2005) New York: Guilford Publications.
  • Conrad, Peter Identifying Hyperactive Children (Ashgate, 2006).
  • Crawford, Teresa I'm Not Stupid! I'm ADHD!
  • Green, Christopher, Kit Chee, Understanding ADD; Doubleday 1994; ISBN 0-86824-587-9
  • Hanna, Mohab. (2006) Making the Connection: A Parent's Guide to Medication in AD/HD, Washington D.C.: Ladner-Drysdale.
  • Kelly, Kate, Peggy Ramundo. (1993) You Mean I'm Not Lazy, Stupid or Crazy?! A Self-Help Book for Adults with Attention deficit Disorder. ISBN 0-684-81531-1
  • Matlen, Terry. (2005) "Survival Tips for Women with AD/HD". ISBN 1886941599
  • 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. PMID 10531701

External links

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