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Attention-Deficit Hyperactivity Disorder (USA)
ICD-10 F90
ICD-9 314.00, 314.01
OMIM 143465
DiseasesDB 6158
MedlinePlus 001551
eMedicine med/3103  ped/177

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Editor-in-Chief: Laura Tommaso, M.D.

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Overview

Attention-Deficit Hyperactivity Disorder (ADHD), is a neurobehavioural developmental disorder[1] [2] [3] affecting about 3-5% of the world's population under the age of 19[4]. It typically presents itself during childhood, and is characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility.[5][6] ADHD is currently considered to be a persistent and chronic condition for which no medical cure is available. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults. About 60% of children diagnosed with ADHD retain the condition as adults.[7] It appears to be highly heritable, although one-fifth of all cases are estimated to be caused from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling.

The scientific consensus in the field, and the consensus of the national health institutes of the world, is that ADHD is a disorder which impairs functioning, and that many adverse life outcomes are associated with ADHD. It has been frequently said by a minority of news sources, social critics, certain religions, and individual medical professionals, to be a controversial disorder. These critics question its classification as a single syndrome, its causes, its treatment, and even the existence of ADHD. See Controversy about ADHD.

Classification

ADHD is a developmental disorder, in that, in the diagnosed population, certain traits such as impulse control significantly lag in development when compared to the general population[8]. Using magnetic resonance imaging, this developmental lag has been estimated to range between 3 years, to 5 years in the prefrontal cortex of those with ADHD patients in comparison to their peers[9]; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder [10] or combinations of these classifications such as neurobehavioral or neurodevelopmental disorders.

Symptoms

The most common symptoms of ADHD are distractibility, difficulty with concentration and focus, short term memory slippage, procrastination, problems organizing ideas and belongings, tardiness, impulsivity, and weak planning and execution. Not all people with ADHD have all the 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. Children do not often have to deal with deadlines, organization issues, and long term planning so these types of symptoms often become evident only during adolescence or adulthood when life demands become greater.

According to an advanced high-precision imaging study by researchers at the United States National Institutes of Health's National Institute of Mental Health, an actual delay in physical development in some brain structures, with a median value of three years, was observed in the brains of 223 ADHD patients beginning in elementary school, during the period when cortical thickening during childhood begins to change to thinning following puberty. The delay was most prominent in the frontal cortex and temporal cortex, which are believed responsible for the ability to control and focus thinking, attention and planning, suppress inappropriate actions and thoughts, remember things from moment to moment, and work for reward, all functions whose disturbance is associated with a diagnosis of ADHD; the region with the greatest average delay, the middle of the prefrontal cortex, lagged a full five years in development in the ADHD patients. 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 both be required for the restlessness and fidgetiness that characterise an ADHD diagnosis. Aside from the delay, both groups showed a similar back-to-front development of brain maturation with different areas peaking in thickness at different times. This contrasts with the pattern of development seen in other disorders such as autism, where the peak of cortical thickening occurs much earlier than normal.[11]

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.[12] 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: a. Oppositional-Defiance Disorder (35%) and Conduct Disorder(26%). These are both characterized by extreme anti-social behaviors. These disorders are frequently characterized by aggression, frequent temper tantrums, deceitfulness, lying, or stealing. b. 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. c. Bi-polar disorder. As many as 25% of children with ADHD may have bipolar disorder. Children with this combination may demonstrate more aggression and behavioral problems than those with ADHD alone. d. 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. </ref?[2]

Causes

According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there are some effective treatments, but no true cure.[13] Evidence suggests that hyperactivity has a strong heritable component, and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology.[14] Candidate genes include dopamine transporter (DAT), dopamine receptor D4 (DRD4), dopamine beta-hydroxylase (DBH), monoamine oxidase A (MAOA), catecholamine-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-HT1B). Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters.[15] Suspect genes include the 10-repeat allele of the DAT1 gene,[16] the 7-repeat allele of the DRD4 gene,[16] and the dopamine beta hydroxylase gene (DBH TaqI).[17]

Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17.[18] If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a "genetic disease" and is better viewed as a complex interaction among genetic and environmental factors. As the authors of a review of the question have noted, "Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified."[19]

Studies show that there is a familial transmission of the disorder which does not occur through adoptive relationships.[8] Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population.[8] While the majority of ADHD is believed to be genetic in nature,[8] roughly one-fifth of all ADHD cases are thought to be acquired after conception due to brain injury caused by either toxins or physical trauma prenatally or postnatally.[8]

Additionally, SPECT scans found people with ADHD to have reduced blood circulation,[20] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.[21][22] 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.[23]

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).[24] "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.[24] 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.[25] 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.

The estimated contribution of non genetic factors to the contribution of all cases of ADHD is 20 percent.[26] The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure. 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).[27] 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.[28] 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.

Head injuries can cause a person to present ADHD-like symptoms,[29] possibly because of damage done to the patient's frontal lobes. Because these types of symptoms can be attributable to brain damage, one earlier designation for ADHD was "Minimal Brain Damage".[30]

There is no compelling evidence that social factors alone can create ADHD.[8] Many researchers believe that attachments and relationships with caregivers and other features of a child's environment have profound effects on attentional and self-regulatory capacities. It is noteworthy that a study of foster children found that an inordinate number of them had symptoms closely resembling ADHD.[31] An editorial in a special edition of Clinical Psychology in 2004 stated that "our impression from spending time with young people, their families and indeed colleagues from other disciplines is that a medical diagnosis and medication is not enough. In our clinical experience, without exception, we are finding that the same conduct typically labelled ADHD is shown by children in the context of violence and abuse, impaired parental attachments and other experiences of emotional trauma."[32] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

It is believed that there are several different causes of ADHD. Roughly 80 percent of ADHD is considered genetic in nature and the estimated contribution of non genetic factors to the contribution of all cases of ADHD is believed to be 20 percent.[33]. Environmental agents also cause ADHD. These agents, such as alcohol, tobacco, and lead, are believed to stress babies prenatally and cause 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.[34][35] 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.[36] 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.[37][38]. 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. [39] More recent studies have shown that approximately 60-70% of children with and without allergies improve when additives are removed from their diet,[40] that up to almost 90% of them react when an appropriate amount of additive is used as a challenge in double blind tests,[41] and that food additives may elicit hyperactive behavior and/or irritability in normal children as well.[42]

Diagnosis

Many of the symptoms of ADHD occur from time to time in everyone. In those with ADHD the frequency of these symptoms occurs frequently and impairs regular life functioning 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 for ADHD

I. Either A or B:

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

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

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

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

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

In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10[43]) 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".[43]

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:[44]

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

The first criterion can be satisfied by using an ADHD-specific instrument such as the Conners' Rating Scale.[45] The second criterion is best fulfilled by examining the individual's history. This history can be obtained from parents and teachers, or a patient's memory.[46] The requirement that symptoms be present in more than one setting is very important because the problem may not be with the child, but instead with teachers or parents who are too demanding. The use of intelligence testing, psychological testing, and neuropsychological testing (to satisfy the third criterion) is essential in order to find or rule out other factors that might be causing or complicating the problems experienced by the patient.[47]

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.[48] 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.[49]

Common comorbid conditions are Oppositional Defiance Disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder.[50] Learning disorders are more common when there are inattention symptoms.[51]

Treatment

Main article: Attention-deficit hyperactivity disorder treatments

Singularly, stimulant medication is the most efficient and cost effective method of treating ADHD. [52] [53] Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD.[8][54] Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. Behavioral parent training, behavior therapy aimed at parents to help them understand ADHD has also shown short term benefits.[55] Omega-3 fatty acids, zinc and magnesium may have benefits with regard to ADHD symptoms.[56][57]

Comorbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming. Psychosocial therapy is useful in treating some comorbid conditions.[58]

Prognosis

The diagnosis of ADHD implies an impairment in life functioning. Many adverse life outcomes are associated with ADHD.

During the elementary years an ADHD student will have more difficulties with work completion, productivity, planning, remembering things needed for school, and meeting deadlines. Oppositional and socially aggressive behavior is seen in 40-70 percent of children at this age. Even ADHD kids with average to above average intelligence show "chronic and severe under achievement". Fully 46% of those with ADHD have been suspended and 11% expelled.[59] Thirty seven percent of those with ADHD do not get a high school diploma even though many of them will receive special education services.[8] The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool.[60] Only five percent of those with ADHD will get a college degree compared to twenty seven percent of the general population. (US Census, 2003)

Epidemiology

A review of 102 studies estimated ADHD's worldwide prevalence in people under the age of 19 to be 5.29%. There was wide variability in prevalence estimates, mostly due to the methodological characteristics of studies (for example, diagnostic criteria used) and, to a lesser extent, geographic location (North America having a significantly higher rate of ADHD than Africa and the Middle East).[4] 10% of males, and (only) 4% of females have been diagnosed in the U.S.[61] This apparent sex difference may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[62][63]

History

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.

Hippocrates

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."[64] Shakespeare made reference to a "malady of attention", in King Henry VIII.

In 1845, Dr. Heinrich Hoffmann (a German physician and poet who wrote books on medicine and psychiatry) 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 undesirable behaviours. "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,[65] or as merely a moral fable to amuse young children and encourage them to behave properly.

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.[66]

In 1918–19, the world-wide influenza pandemic left many survivors with encephalitis, affecting their neurological functions. Some of these exhibited immediate behavioral problems which may correspond to ADHD (although no diagnosis for such a disorder existed at the time). This caused many later commentators to believe that the condition was the result of injury rather than heredity. (The concept of hyperactivity not being caused by brain damage was first described by Stella Chess as, ""Hyperactive Child Syndrome" in 1960.[67]) This caused a significant rift in the understanding of the disorder. Europeans saw hyperkinesis as unusual and often associated it with retardation, brain damage, and conduct disorders, and changes to the ICD were not made until 1994. In the USA 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.)

In 1937, a Dr. Bradley in Providence, RI reported that a group of children with behavioral problems improved after being treated with stimulant medication. 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 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 (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).

During 1996, ADHD accounted for at least 40% of child psychiatry references.[68]

In 2003, Atomoxetine (Strattera) received the first FDA approval for a nonstimulant drug to be used specifically for ADHD. In 2007 Lisdexamfetamine 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

A study by two anthropologists looked at the way laypersons talk about ADHD, and found five thematic patterns: "(1) appropriating the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) descriptors; (2) schools as identity-construction sites; (3) resistance: biology versus moral culpability; (4) alternative solutions to a real problem; and (5) relief and hope in naming experience."[69]

See also

General

Controversy

Related disorders

References

  1. ↑ LONI: Laboratory of Neuro Imaging
  2. ↑ NINDS Attention Deficit-Hyperactivity Disorder Information Page. National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.
  3. ↑ Dr. Russell A. Barkley Official Site, Authority ADHD, Attention Deficit Hyperactivity Disorder
  4. ↑ 4.0 4.1 Polanczyk G, de Lima MS, Horta BL, Biederman J, Rohde LA (2007). "The worldwide prevalence of ADHD: a systematic review and metaregression analysis". Am J Psychiatry. 164 (6): 942–48. doi:10.1176/appi.ajp.164.6.942. PMID 17541055.
  5. ↑ Diagnostic and Statistical Manual of [American Psychiatric Association, 2000.
  6. ↑ Psychiatric Association|the American Psychiatric Association, Fourth Edition, htm Attention-Deficit/Hyperactivity Disorder (ADHD).] Behavenet.com. Retrieved on December 11, 2006.
  7. ↑ Attention-Deficit / Hyperactivity Disorder: ADHD in Adults. WebMd.com. Retrieved on December 11, 2006.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 Barkley, Russell A. Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity. ContinuinedEdCourse.Net. Retrieved on 2007-08-12.
  9. ↑ Brain Matures A Few Years Late In ADHD, But Follows Normal Pattern
  10. ↑ LONI: Laboratory of Neuro Imaging
  11. ↑ Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern NIMH Press Release, November 12, 2007
  12. ↑ Gene Predicts Better Outcome as Cortex Normalizes in Teens with ADHD NIMH Press Release, August 6, 2007
  13. ↑ NINDS Attention Deficit-Hyperactivity Disorder Information Page. National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.
  14. ↑ Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26.
  15. ↑ Roman T, Rohde LA, Hutz MH. (2004). "Polymorphisms of the dopamine transporter gene: influence on response to methylphenidate in attention deficit-hyperactivity disorder." American Journal of Pharmacogenomics 4(2):83–92 PMID 15059031
  16. ↑ 16.0 16.1 Swanson JM, Flodman P, Kennedy J, et al. "Dopamine Genes and ADHD." Neurosci Biobehav Rev. 2000 Jan;24(1):21–5. PMID 10654656
  17. ↑ Smith KM, Daly M, Fischer M, et al. "Association of the dopamine beta hydroxylase gene with attention deficit hyperactivity disorder: genetic analysis of the Milwaukee longitudinal study." Am J Med Genet B Neuropsychiatr Genet. 2003 May 15;119(1):77–85. PMID 12707943
  18. ↑ M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine. 6 (1): 1–15.
  19. ↑ M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine. 6 (1): 1–15.
  20. ↑ Lou HC, Andresen J, Steinberg B, McLaughlin T, Friberg L. "The striatum in a putative cerebral network activated by verbal awareness in normals and in ADHD children." Eur J Neurol. 1998 Jan;5(1):67–74. PMID 10210814
  21. ↑ Dougherty DD, Bonab AA, Spencer TJ, Rauch SL, Madras BK, Fischman AJ (1999). "Dopamine transporter density in patients with attention deficit hyperactivity disorder". Lancet. 354 (9196): 2132–-33. PMID 10609822.
  22. ↑ Dresel SH, Kung MP, Plössl K, Meegalla SK, Kung HF (1998). "Pharmacological effects of dopaminergic drugs on in vivo binding of [99mTc]TRODAT-1 to the central dopamine transporters in rats". European journal of nuclear medicine. 25 (1): 31–9. PMID 9396872.
  23. ↑ Coccaro EF, Hirsch SL, Stein MA (2007). "Plasma homovanillic acid correlates inversely with history of learning problems in healthy volunteer and personality disordered subjects". Psychiatry research. 149 (1–3): 297–302. doi:10.1016/j.psychres.2006.05.009. PMID 17113158.
  24. ↑ 24.0 24.1 Zametkin AJ, Nordahl TE, Gross M, et al. "Cerebral glucose metabolism in adults with hyperactivity of childhood onset." N Engl J Med. 1990 November 15;323(20):1361–6. PMID 2233902
  25. ↑ Zametkin AJ, Liebenauer LL, Fitzgerald GA,, et al. "Brain metabolism in teenagers with attention-deficit hyperactivity disorder." Arch Gen Psychiatry.. 1993 May 50;333(5). PMID 2233902
  26. ↑ Template:PDFlink SchwabLearning.org.
  27. ↑ Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP (2006). "Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children". Environ. Health Perspect. 114 (12): 1904–9. PMID 17185283.: "Compared with the lowest quintile of blood lead levels, children with blood lead levels > 2.0 µg/dL were at a 4.1-fold increased risk of ADHD. When we limited the analysis to children with blood lead levels ≤ 5 µg/dL, the association between increased blood lead levels and ADHD remained. These results are consistent with previous reports that have found significant associations between blood or dentin lead levels and behavior problems .... Our results further indicate that blood lead levels below the CDC action level of 10 µg/dL are associated with an increased risk for ADHD in children. This result is consistent with previous studies that have found cognitive deficits in children with blood lead levels < 10 µg/dL."
  28. ↑ Kotimaa AJ, Moilanen I, Taanila A, et al. ,"Maternal smoking and hyperactivity in 8-year-old children". 2003, J Am Acad Child Adol Psychiatry Jul;42(7):826–33. PMID 12819442
  29. ↑ McAvinue L, O'Keeffe F, McMackin D, Robertson IH, et al. "Impaired sustained attention and error awareness in traumatic brain injury: implications for insight" Neuropsychological Rehabilitation. 2005 Dec;15(5):569–87. PMID 16381141
  30. ↑ What Causes ADD. Attention Deficit Disorder Association. Retrieved on 2007-08-13.
  31. ↑ Template:PDFlink
  32. ↑ Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
  33. ↑ Template:PDFlink SchwabLearning.org.
  34. ↑ Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomized, double-blinded, placebo-controlled trial”, Lancet, Sept 2007
  35. ↑ 1997 Graduate Student Research Project conducted at the University of South Florida. Author- Richard W. Pressinger M.Ed.
  36. ↑ "Food Additives May Affect Kids' Hyperactivity", WebMD Medical News, May 24, 2004
  37. ↑ A different kind of school lunch", PURE FACTS October 2002
  38. ↑ The Impact of a Low Food Additive and Sucrose Diet on Academic Performance in 803 New York City Public Schools, Schoenthaler SJ, Doraz WE, Wakefield JA, Int J Biosocial Res., 1986, 8(2); 185-195
  39. ↑ http://www.nimh.nih.gov/health/publications/adhd/complete-publication.shtml#pub4
  40. ↑ Rowe KS, Rowe KJ (1994). "Synthetic food coloring and behavior: A dose response effect in a double-blind, placebo-controlled, repeated-measures study". Journal of Pediatrics. 125: 691&ndash, 698. 7965420.
  41. ↑ Pollock, I. and Warner, J.O. (1990). "Effect of artificial food colours on childhood behaviour". Arch Dis Child. 65 (1): 74–77. PMID 2301986. Unknown parameter |month= ignored (help)
  42. ↑ McCann D, Barrett A, Cooper A, Crumpler D, Dalen L, Grimshaw K, Kitchin E, Lok K, Porteous L, Prince E, Sonuga-Barke E, Warner JO, Stevenson J. (2007 Nov). "Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial". Lancet. 3;370(9598): 1560–7. PMID 17825405. Check date values in: |year= (help)
  43. ↑ 43.0 43.1 ICD Version 2006: F91. World Health Organization. Retrieved on December 11, 2006.
  44. ↑ Perrin JM, Stein MT, Amler RW, Blondius TA. 2001. "Clinical practice guideline: treatment of school-aged children with Attention Deficit/Hyperactivity Disorder". Pediatrics 108 (4):1033-1044. PMID 11581465
  45. ↑ Conners CK, Sitarenios G, Parker JD, Epstein JN (1998). "Revision and restandardization of the Conners Teacher Rating Scale (CTRS-R): factor structure, reliability, and criterion validity". Journal of abnormal child psychology. 26 (4): 279–91. PMID 9700520.
  46. ↑ Ratey, John; Hallowell, Edward. Driven to Distraction first edition, p. 42
  47. ↑ Ninivaggi, F. J. "Borderline intellectual functioning and academic problem." In: Sadock B.J. Sadock, V.A., eds. Kaplan & Sadock's Comprehensive Textbook of psychiatry. 8th ed. Vol. II. Baltimore: Lippincott William and Wilkins; 2005: 2272–76.
  48. ↑ Attention-Deficit/Hyperactivity Disorder. Psychiatry Online. Retrieved on 2007-08-13.
  49. ↑ Jensen, PS. Exploring the Neurocircuitry of the Brain and Its Impact on Treatment Selections in ADD. Medscape. Retrieved on 2007-08-13.
  50. ↑ Pliszka S (2000). "Patterns of psychiatric comorbidity with attention-deficit/hyperactivity disorder". Child Adolesc Psychiatr Clin N Am. 9 (3): 525–40, vii. PMID 10944655.
  51. ↑ Lamminmäky T ; et al. (1995). "Attention deficit hyperactivity disorder subtypes: Are there differences in academic problems?". Dev neuropsychology (11): 297–310.
  52. ↑ Practice Parameter for the Assessment and Treatment of Children and Adolescents With Attention-Deficit/Hyperactivity Disorder http://www.aacap.org/galleries/PracticeParameters/JAACAP_ADHD_2007.pdf
  53. ↑ Jensen; et al. (2005). "Cost-Effectiveness of ADHD Treatments: Findings from the Multimodal Treatment Study of Children With ADHD". American Journal of Psychiatry. 162: 1628–1636 (Page:1633). doi:10.1176/appi.ajp.162.9.1628. PMID 16135621. Free full text
  54. ↑ Barkley, Russell A. Treating Children and Adolescents with ADHD: An Overview of Empirically Based Treatments. ContinuingEdCourses.Net. Retrieved on 2007-08-13.
  55. ↑ Practice Parameter for the Assessment and Treatment of Children and Adolescents With Attention-Deficit/Hyperactivity Disorder http://www.aacap.org/galleries/PracticeParameters/JAACAP_ADHD_2007.pdf
  56. ↑ Arnold LE, DiSilvestro RA (2005). "Zinc in attention-deficit/hyperactivity disorder". Journal of child and adolescent psychopharmacology. 15 (4): 619–27. doi:10.1089/cap.2005.15.619. PMID 16190793.
  57. ↑ Antalis CJ, Stevens LJ, Campbell M, Pazdro R, Ericson K, Burgess JR (2006). "Omega-3 fatty acid status in attention-deficit/hyperactivity disorder". Prostaglandins Leukot. Essent. Fatty Acids. 75 (4–5): 299–308. doi:10.1016/j.plefa.2006.07.004. PMID 16962757.
  58. ↑ Foster; et al. (2007). "Treatment of ADHD: Is More Complex Treatment Cost-Effective for More Complex Cases?". HSR: Health Services Research. 42 (1): 165–182 (Page:177). PMID 17355587.
  59. ↑ U.S. Department of Education "How Does ADHD Affect School Performance?", 2007
  60. ↑ Template:PDFlink
  61. ↑ Template:PDFlink. Centers for Disease Control (March, 2004). Retrieved on December 11, 2006.
  62. ↑ Staller J, Faraone SV. (2006) "Attention-deficit hyperactivity disorder in girls: epidemiology and management." CNS Drugs. 2006;20(2):107–23. PMID 16478287
  63. ↑ Biederman J, Faraone SV. (2004) "The Massachusetts General Hospital studies of gender influences on attention-deficit/hyperactivity disorder in youth and relatives." Psychiatr Clin North Am. Jun;27(2):225–32. PMID 15063995
  64. ↑ What is ADHD? ADHD.org.nz. Retrieved on 2007-08-13.
  65. ↑ Heinrich Hoffmann. The Story of Fidgety Philip. Virginia Commonwealth University. Retrieved on 2007-08-13.
  66. ↑ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008-1012
  67. ↑ Classification of ADHD through History. Retrieved on 2006-09-15.
  68. ↑ Castellanos FX, Giedd JN, Marsh WL, et al. (1996). "Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder". Archives of General Psychiatry, 53, 607–616. PMID 14765004
  69. ↑ Danforth, Scot (2001). "Hyper Talk: Sampling the Social Construction of ADHD in Everyday Language". Anthropology & Education Quarterly. 32 (2): 167–190. Retrieved 2008-04-07. Unknown parameter |coauthors= ignored (help)

National Institute of Health http://www.nlm.nih.gov/medlineplus/ency/article/001551.htm

Further reading

  • Hartmann,Thom "Attention Deficit Disorder, A Different Perception" subtitled "A Hunter in a Farmers World".
  • Barkley, Russell A. Take Charge of ADHD: The Complete Authoritative Guide for Parents (2005) New York: Guilford Publications.
  • Bellak L, Kay SR, Opler LA. (1987) "Attention deficit disorder psychosis as a diagnostic category". Psychiatric Developments, 5 (3), 239-63. PMID 3454965
  • Conrad, Peter Identifying Hyperactive Children (Ashgate, 2006).
  • 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.
  • Joseph, J. (2000). "Not in Their Genes: A Critical View of the Genetics of Attention-Deficit Hyperactivity Disorder", Developmental Review 20, 539-567.
  • 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
  • Attention-Deficit / Hyperactivity Disorder (ADHD) at the Center for Disease Control
  • Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder at NIH
  • National Institute of Mental Health on ADHD

External links

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