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Attention deficit hyperactivity disorder

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PET scans measure brain activity. The image on the left illustrates areas of activity in the brain of a person without ADHD while doing an assigned task. The image on the right illustrates the areas of activity of the brain of someone with ADHD when given that same task.[1]
Attention deficit hyperactivity disorder
SpecialtyPsychiatry, child and adolescent psychiatry Edit this on Wikidata

Attention-deficit/hyperactivity disorder (ADHD) (sometimes referred to as ADD) is thought to be a neurological disorder, usually diagnosed in childhood, which manifests itself with symptoms such as hyperactivity, forgetfulness, poor impulse control, and distractibility.[2] In neurological pathology, ADHD is currently considered to be a chronic syndrome for which no medical cure is available. Both children and adults may present with ADHD, which is believed to affect between 3-5% of the population.[3]

Much controversy surrounds the diagnosis of ADHD, such as over whether or not the diagnosis denotes a disability in its traditional sense, or simply describes a neurological property of an individual. There is also a sizable minority of clinicians who believe that the condition is not biological, but psychological in origin. Those who believe that ADHD is a traditional disability or disorder often debate over how it should be treated, if at all. According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded to be a non-curable neurological disorder for which, however, a wide range of effective treatments are available. Methods of treatment usually involve some combination of medication, psychotherapy, and other techniques. Some patients are able to control their symptoms over time, even without the use of medication. Other individuals who meet the diagnostic criteria of ADHD do not consider themselves to be handicapped by the disorder and therefore may remain undiagnosed or, after a positive diagnosis, untreated.

ADHD is most commonly diagnosed in children. When diagnosed in adults, it is regarded as adult attention-deficit disorder (AADD). It is believed that around 60% of children diagnosed with ADHD retain the disorder as adults.[4]

Terminology

The most appropriate designation of ADHD is currently disputed; the terms below are known to be used to describe the condition. A difficulty in the condition's nomenclature arises when some scientific research suggests that certain behaviors are directly attributable to ADHD, while other research concludes that the same behaviors constitute disorders that need to be classified independently 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" section, below.

  • Attention-deficit syndrome (ADS): Equivalent to ADHD, but used to avoid the connotations of "disorder".
  • 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. It 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.
  • Hyperkinetic disorders (F90) is the International Statistical Classification of Diseases and Related Health Problems (ICD) 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 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.

Definitions

From a developmental/behavioral standpoint, the DSM-IV states that ADHD is a developmental disorder that presents during childhood, in most cases before the age of seven, and is characterized by developmentally inappropriate levels of inattention and/or hyperactive-impulsive behavior. The DSM-IV also stipulates that in order to be diagnosed, the condition must also result in significant impairment of one or more major life activities, including interpersonal relations, educational or occupational goals, as well as cognitive or adaptive functioning. ADHD may be also diagnosed in adulthood, but symptoms must have been present prior to age seven in order to yield a positive diagnosis.

The ICD-10 differs from the DSM-IV in that it requires both inattention and hyperactive-impulsive behavior to be present before a diagnosis is warranted.[5]

The Amen classification is an informal definition and categorisation system which reorganises and extends the DSM-IV. It is not widely accepted as a formal classification, although it is still used by many doctors wordwide.

Symptoms

The symptoms of ADHD fall into the following two broad categories:[6]

Inattention:

  1. Failing to pay close attention to details or making careless mistakes when doing schoolwork or other activities
  2. Trouble keeping attention focused during play or tasks
  3. Appearing not to listen when spoken to
  4. Failing to follow instructions or finish tasks
  5. Avoiding tasks that require a high amount of mental effort and organization, such as school projects
  6. Frequently losing items required to facilitate tasks or activities, such as school supplies
  7. Excessive distractibility
  8. Forgetfulness

Hyperactivity-impulsive behavior

  1. Fidgeting with hands or feet or squirming in seat
  2. Leaving seat often, even when inappropriate
  3. Running or climbing at inappropriate times
  4. Difficulty in quiet play
  5. Frequently feeling restless
  6. Excessive speech
  7. Mood swings
  8. Answering a question before the speaker has finished
  9. Failing to await one's turn
  10. Interrupting the activities of others at inappropriate times

A positive diagnosis is usually only made if the patient has experienced six of the above symptoms for at least three months. Symptoms must appear consistently in varied environments (e.g., not only at home or only at school) and interfere with function. One of the difficulties in diagnosis is the incidence of co-morbid conditions, especially the presence of Bipolar Disorder which is being reported at earlier ages than previously described.

Children who grow up with ADHD often continue to have symptoms as they grow into adulthood. Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning (also known as working memory). If the patient is not treated appropriately, co-morbid conditions, such as depression, anxiety and self-medicating substance abuse may present as well. If a patient presents with such conditions as well, the co-morbid condition may be treated first, or simultaneously.

Diagnosis

The Centers for Disease Control and Prevention (CDC) emphasize that a diagnosis of ADHD 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 physical disorders, such as hyperthyroidism. Further, 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.

Analytical Testing

Due to the lack of objectivity that surrounds the critical factors, many question the reliability of ADHD diagnosis. The American Academy of Pediatrics Clinical Practice publishes guidelines to aid providers in making an objective diagnosis, but even if strictly adhered to, doubt still remains among some patients, as well as providers. Other diagnostic methods, such as those involving magnetic resonance imaging (MRI), may detect the presence of ADHD by analyzing images of the patient's brain, are usually not recommended (see brain scans). In a majority of cases, diagnosis is therefore dependent upon the observations and opinions of those who are close to the patient; in many patients, especially as they approach adulthood, self-diagnosis is not uncommon.

Publications that are designed to analyze a person's behavior, such as the Brown Scale or the Conners Scale, for example, attempt to assist parents and providers in making a diagnosis by evaluating an individual on typical behaviors such as "Hums or makes other odd noises", "Daydreams" and "Acts 'smart'"; the scales rating the pervasiveness of these behaviors range from "never" to "very often". Connors states that, based on the scale, a valid diagnosis can be achieved; critics, however, counter Connors' proposition by pointing out the breadth with which these behaviors may be interpreted. This becomes especially relevant when family and cultural norms are taken into consideration; this premise leads to the assumption that a diagnosis based on such a scale may actually be more subjective than objective (see cultural subjectivism).

Clinical Testing

The American Academy of Pediatrics Clinical Practice Guideline for children with ADHD emphasizes that a reliable diagnosis requires:[7]

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

A proper diagnosis is dependant upon a physician fulfilling all three of these criteria. The first criteria can be satisfied by using an ADHD-specific instrument such as the Conners Scale. The second criteria is best fulfilled by examining the individual's history. This history can be obtained from parents and teachers, or a patient's memory.[8] 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 and psychological testing (to satisfy the third criteria) is essential in order to find or rule out other factors that might be causing or complicating the problems experienced by the patient.[9]

Computerized tests

Computerized tests of attention are not especially helpful in providing a further independent assessment because they have a high rate of false negatives (real cases of ADHD can pass the tests in 35% or more of cases) (Barkley, 2006) they do not correlate well with actual behavioral problems at home or school, and are not especially helpful in determining treatments. Both the American Academy of Pediatrics and American Academy of Child and Adolescent Psychiatry have recommended against the use of such computerized tests for now in view of their lack of appropriate scientific validation as diagnostic tools. In the USA, the process of obtaining referrals for such assessments is being promoted vigorously by the President's New Freedom Commission on Mental Health.

Brain scans

Neurometrics, PET scans, FMRI, or SPECT scans have the potential to provide a more objective diagnosis. However, these are not typically suitable for very young children, and PET and SPECT scans may unnecessarily expose the patient to small amounts of radiation. Because the etiology of the disorder is unknown, and a complete neurological definition of this disorder is lacking, a majority of clinicians doubt the current predictive power of these objective tests to detect ADHD to be used to direct clinical treatment. An October 2005 meta-analysis by Alan Zametkin, M.D., with the NIMH, concluded that these diagnostic methods lack adequate scientific research on accuracy and specificity to be used as a primary diagnostic tool.[10] They remain, however, useful research tools when studying groups of patients with ADHD.

Incidence

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

Nearly four million children younger than 18 in the United States had been diagnosed with attention deficit hyperactivity disorder (ADHD). The prevalence among children is estimated to be in the range of 5% to 8% in children, and 4% to 8% in adults. 10% of males, but only 4% of females have been diagnosed.[11]. This apparent sex difference may either reflect a difference is susceptibility or that females with ADHD are less likely to be diagnosed than males.[12][13]

The ADHD treatment rate among Caucasian children is significantly higher than among African and Hispanic Americans (4.4% Caucasian, 1.7% African, 1.5% Hispanic in 1997)[14]. The same study notes that outpatient treatment for ADHD has grown from 0.9 children per 100 (1987) to 3.4 per 100 (1997).

Possible causes

The exact cause of ADHD remains unknown, but there is no shortage of speculation concerning its etiology [15][16], most of which centers around the brain. The cerebellum in particular has been shown to be smaller in the brains of those with this disorder.[17] Another possible culprit is a region in the middle or medial aspect of the frontal lobe, known as the anterior cingulate cortex division.[18] The source of these differences is not yet known, but some hypotheses have been presented.

Hereditary dopamine deficiency

Research suggests that ADHD arises from a combination of various genes, many of which have something to do with dopamine transporters.[19] Suspect genes include the 10-repeat allele of the DAT1 gene,[20] the 7-repeat allele of the DRD4 gene,[21] and the dopamine beta hydroxylase gene (DBH TaqI).[22] Additionally, SPECT scans found people with ADHD to have reduced blood circulation,[23] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.[24]

Diet

It has long been suggested that ADHD could be the result of a nutritional problem. Recent studies have begun to find metabolic differences in these children, indicating that an inability to handle certain elements of one's diet might contribute to the development of ADHD, or at least ADHD-like symptoms. For example, in 1990 the English chemist, Neil Ward,[25] showed that children with ADHD lose zinc when exposed to a food dye. Some studies suggest that a lack of fatty acids, specifically omega-3 fatty acids can trigger the development of ADHD. Support for this theory comes from findings that children who are breastfed for six or more months seem to be less likely to have ADHD than their bottlefed counterparts and until very recently, infant formula did not contain any omega-3 fatty acids at all.[26] Time and futher investigation will perhaps tell whether this correlation is reliable or merely a coincidence.

Despite the uncertainty of nutrition as a cause of ADHD it does play a role in the diagnosis and treatment of the disorder. Certain dietary issues, most commonly a moderate to severe protein deficiency, can cause symptoms consistent with ADHD.[27]

External Factors

There is no compelling evidence that social factors, alone, can create ADHD. (However, see discussion of parental role in section below) The few environmental factors implicated fall in the realm of biohazards including alcohol, tobacco smoke, and lead poisoning. Allergies (including those to artificial additives)[28] as well as complications during pregnancy and birth--including premature birth--might also play a role.

Smoking during pregnancy

It has been observed that women who smoke while pregnant are more likely to have children with ADHD.[29]. Nicotine is known to cause hypoxia (lack of oxygen) in the uterus, which could lead to brain damage in the unborn child. Smoking could therefore play a major role in the child's development of the disorder prior to birth.

Head injuries

Head injuries may cause a person to present with ADHD-like symptoms, possibly because of damage done to the patient's frontal lobes. Because symptoms were attributable to brain damage, the earliest designation for ADHD was "Minimal Brain Damage". [30]

Treatment

There are many options available to treat people diagnosed with ADHD. The options with the greatest scientific support include a variety of medications, behavior modification, and educational interventions. The results of a large randomized controlled trial[31][32] suggested that medication alone is superior to behavioral therapy alone, but that the combination of behavioral therapy and medication has a small additional benefit over medication alone.

Mainstream treatments

File:Methylphenidate.png
The chemical structure of methylphenidate, better known as Ritalin. Ritalin is one of the most popular treatments for ADHD currently on the market.

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

  • Methylphenidate — Available in:
    • Regular formulation, sold as Ritalin, Metadate, Focalin (different in that it is derived from dexmethylphenidate, the d-isomer), or Methylin. Duration: 4–6 hours per dose. Usually taken morning, lunchtime, and in some cases, afternoon.
    • Long acting formulation, sold as Ritalin LA, Metadate ER. Duration: 6–8 hours per dose. Usually taken twice daily.
    • All-day formulation, sold as Ritalin SR, Metadate CD, Concerta (Methylphenidate Hydrochloride), Focalin XR. Duration: 10–12 hours per dose. Usually taken once a day.
  • Amphetamines —
    • Dextroamphetamine — Available in:
      • Regular formulation, sold as Dexedrine. Duration: 4–6 hours per dose. Usually taken 2–3 times daily.
      • Long-acting formulation, sold as Dexedrine Spansules. Duration: 8–12 hours per dose. Taken once a day.
    • Adderall, a trade name for a mixture of dextroamphetamine and laevoamphetamine salts. — Available in:
      • Regular formulation, Adderall. Duration: 4–6 hours a dose.
      • Long-acting formulation, Adderall XR. Duration: 12 hours. Taken once a day.
    • Methamphetamine — Available in:
      • Regular formulation, sold as Desoxyn by Ovation Pharmaceutical Company.
  • Bupropion. A dopamine and norepinephrine reuptake inhibitor, marketed under the brand name Wellbutrin.
  • Atomoxetine. A norepinephrine reuptake inhibitor (NRI) introduced in 2003, it is the newest class of drug used to treat ADHD, and the first non-stimulant medication to be used as a first-line treatment for ADHD. Available in:
    • Once daily formulation, sold by Eli Lilly and Company as Strattera. This medicine doesn't have an exact duration. It is to be taken once or twice a day, depending on the individual, every day, and takes up to 6 weeks to begin working fully. If the intake schedule is interrupted, it may take a few weeks to begin working correctly again.

Second-line medications include:

  • Benzphetamine — a less powerful stimulant. Research on the effectiveness of this drug is not yet complete.
  • Provigil/Alertec/modafinil — In the US, it is currently offlabel pending decision by the FDA on August 22, 2006. Was originally pending marketting on-label as Alertec but denied for a reported incidence of Stevens-Johnson Syndrome.
  • 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. In fact, this drug has been also withdrawn by the FDA from the market.
  • Amineptine/Survector/Maneon — a tricyclic antidepressant now illegal in many countries for being thought to have a small potential for abuse. It is still legal in some parts of the EU, such as Spain and Italy; it is no longer available in the US, Canada, France or the UK.
  • 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.[33]
  • Emsam/Selegiline — an MAOI currently being investigated for ADHD; Emsam is not a pill, but a patch.
  • Tianeptine/Stablon/Coaxil/Tatinol — an SSRE tricyclic antidepressant used primarily in Europe which is being investigated. It is currently off-patent in the United States and is therefore not likely to be approved by the FDA.
  • Amantadine — an anti-viral and dopamine agonist. There have been reports that low-dose amantadine has been successfully used off-label to treat ADHD.[34]

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 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.[35]

Alternative treatments

Many alternative treatments have been proposed for ADHD. There are few or no credible scientific studies to support these suggested interventions.

Nutrition

As noted above there are indications that children with ADHD are metabolically different from others, [36][37][38] and it has therefore been suggested that diet modification may play a role in the management of ADHD. Perhaps the best known of the dietary alternatives is the Feingold diet which involves removing salicylates, artificial colors and flavors, and certain synthetic preservatives from children's diets.[39] In the 1980s vitamin B6 was promoted as a helpful remedy for children with learning difficulties including inattentiveness. Later, zinc and multivitamins have been promoted as cures, and currently the addition of certain fatty acids such as omega-3 has been proposed as beneficial.[40] [41]

It is claimed by some ADHD patients that commonly available mild stimulants such as caffeine and theobromine have similar effects to the more powerful drugs commonly used in treating the disorder. Herbal supplements such as ginkgo biloba are also sometimes cited. There is some empirical data suggesting caffeine can improve the funcion of children suffering from ADHD.[42] [43]

Coaching

ADD Coaching is a program where coaches work with ADHD individuals to help them prioritize, organize, and develop life skills. Coaching is aimed at helping clients to be more realistic in setting goals for themselves by learning about their individual challenges and gifts, and emphasizes spending more time in areas of strength, while minimizing time spent dealing with areas of difficulty.

Other alternatives

Neurofeedback is a proposed ADHD remedy which involves teaching children to control their brain waves by the use of video-game technology. A thorough review by Sandra Loo and Russell Barkley of the research done on this in Developmental Neuropsychology 2005 concluded that neurofeedback does not have adequate support from appropriately conducted scientific studies to support it as an intervention at this time.[44]

Audio-visual entrainment uses light and sound stimulation to guide and change brainwave patterns.[45] While safe for most, it cannot be used by those suffering from photosensitive epilepsy due to the risk of triggering a seizure.

Cerebellar stimulation assumes that by improving the patient’s cerebellar function, many ADHD symptoms can be reduced or even eliminated permanently. As noted above, several studies have shown that the cerebellums of children with ADHD are notably smaller than their non-ADHD counterparts. Several programs of balance, coordination, eye and sensory exercises that specifically involve the functions of the cerebellum are used to treat ADHD, Asperger's syndrome, and many learning difficulties such as dyslexia and dyspraxia. Most prominent are the DORE program,[46] the Learning Breakthrough Program, and the Brain Gym.

Controversy

The ADHD diagnosis is controversial and has been questioned by some professionals, adults diagnosed with ADHD, and parents of diagnosed children. They point out the positive traits that people with ADHD have, such as "hyperfocusing." Others believe ADHD is a divergent or normal-variant human behavior, and use the term neurodiversity to describe it, emphasizing that there are an immense number of variations in genetics which could favor a greater or lesser ability to concentrate and/or to remain calm under varying circumstances.[47]

Skepticism towards ADHD as a diagnosis

The number of people diagnosed with ADHD in the U.S. and UK has grown dramatically over a short period of time. Critics of the diagnosis, such as Dan P. Hallahan and James M. Kauffman in their book Exceptional Learners: Introduction to Special Education, have argued that this increase is due to the ADHD diagnostic criteria being sufficiently general or vague to allow virtually anybody with persistent unwanted behaviors to be classified as having ADHD of one type or another, and that the symptoms are not supported by sufficient empirical data.[48] Additionally, a recent study by Adam Rafalovich has found that many doctors are no more confident in the diagnosis and treatment of ADHD than are many parents.[49] Another source of skepticism is that most people with ADHD have no difficulties concentrating when they are doing something that interests them, whether it is educational or entertainment.[50] However, these objections have been rejected by the American Psychiatric Association, the American Psychological Association, the American Medical Association, the American Academy of Pediatrics and the U.S. Surgeon General.[51]

Another argument which has been offered against the diagnosis is that the behavior of putative ADHD sufferers is the "natural" way for children to behave in a situation which does not engage them. It has never been a simple task to teach children how to behave in a "grown up" fashion, and therefore great amounts of time and energy have traditonally been spent by parents and educators trying to inspire, cajole, threaten, lecture, bribe (and every other imaginable strategy) in the service of teaching a child how to gain self control, act with consideration for others, and do tasks that are not fun. In other words, it is argued, a child who is not successfully taught how to behave, obey the rules and stay on task will display all of the symptoms of ADHD. Those who place emphasis on the parental role in ADHD claim that while neurological impairments, or innate tendencies, can be a factor in the ability to stay focused on tasks being demanded, the "nature" (or biological) aspects of the nature vs.nurture controversy have been greatly exaggerated. They claim millions of children being diagnosed with this condition have nothing physically wrong with their brains. [52]

A believer that ADHD is a biological condition, Xavier Castellanos M.D., then head of ADHD research at the National Institute of Mental Health, (NIMH), [53] has also expressed reservations about the extent of available biological information about that condition in an interview on Frontline in 2000:

Frontline: "How does ADHD work on the brain? What do we know about it?"
Castellanos: "We don't yet know what's going on in ADHD..."
Frontline: "Give me one true fact about ADHD."
Castellanos "The posterior inferior vermis of the cerebellum is smaller in ADHD. I think that that is a true fact. It's taken about five years to convince myself that that's the case. That's about as much as I know--that I'm confident about..."

Parental role

Many clinicians believe that attachments and relationships with caregivers and other features of a child's environment have profound effects on attentional and self-regulatory capacities. An editorial in a special editon 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."[54]

While no compelling evidence has been offered that parenting methods can cause ADHD in otherwise normal children a sizable minority of clinicians believe this is the case. A different perspective holds that while evidence shows that parents of ADHD children experience more stress and give more commands,[55] further research has suggested that such parenting behavior is in large part a reaction to the child's ADHD and related disruptive and oppositional behavior, and to a minor extent the result of the parent's own ADHD.[56]

Positive aspects

Although ADHD is considered a disorder, some view it in a neutral or positive light. Rather than assuming that ADHD is inherently negative, some argue that ADHD is simply a different method of learning as opposed to an inferior one. "While the A students are learning the details of photosynthesis, the ADHD kids are staring out the window and pondering if it still works on a cloudy day" (Underwood). The aspects of ADHD which are generally viewed negatively can be a potential source of strength, such as willingness to take risks. "Impulsivity isn't always bad. Instead of dithering over a decision, they're willing to take risks" (Underwood). Both a proponent and an example of this point is JetBlue Airways founder David Neeleman. He considers ADHD one of his greatest assets and refuses to take medication. [57][58] There has been little serious research into either the intellectual advantages it can provide, or into conditions which might be necessary for taking advantage of ADHD traits.

Many professional counselors emphasize to persons diagnosed with ADHD and their families the perspective that the condition does not necessarily block, and may even facilitate, great accomplishments. Most frequently cited as potentially useful is the mental state of hyperfocus. Lists of famous persons either diagnosed with ADHD or suspected (but not necessarily known to have had ADHD) are numerous, such as Albert Einstein and Thomas Edison, but currently lack scientific proof because ADHD was not a documented medical condition until its appearance in the DSM-III in 1980.

Timeline

There is considerable evidence to suggest that ADHD is not a recent phenomenon.

  • 493 BC years ago, the great 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."[59]
  • 1845. ADHD was alluded to by Dr. Heinrich Hoffmann, a physician who wrote books on medicine and psychiatry, Dr. Hoffman was also a poet who became interested in writing for children when he couldn't find suitable materials to read to his 3-year-old son. The result was a book of poems, complete with illustrations, about children and their 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.[60] Alternatively, it may be seen as merely a moral fable to amuse young children at the same time as encouraging them to behave properly.
  • 1902 – The English pediatrician George Still, in a series of lectures to the Royal College of Physicians in England, described a condition which some have claimed is analogous to ADHD. Still described a group of children with significant behavioral problems, caused, he believed, by an innate genetic dysfunction and not by poor child rearing or environment.[61]. Analysis of Still's descriptions by Palmer and Finger indicated that the qualities Still described are not "considered primary symptoms of ADHD".[62]
  • 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.[63]
  • 1957 – The stimulant Methylphenidate (Ritalin) became available. It remains one of the most widely prescribed medications for ADHD in its various forms (Ritalin, Focalin, Concerta, Metadate, and Methylin).
  • 1960 – Stella Chess described "Hyperactive Child Syndrome" introducing the concept of hyperactivity not being caused by brain damage.[64]
  • 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.[65]
  • 1973 – Dr Ben F. Feingold, Chief of Allergy at Kaiser Permanente Medical Center in San Francisco, claimed that hyperactivity was increasing in proportion to the level of food additives.
  • 1975 – Pemoline (Cylert) is approved by the FDA for use in the treatment of ADHD. While an effective agent for managing the symptoms, the development of liver failure in at least 14 cases over the next 27 years would result in the manufacturer withdrawing this medication from the market.
  • 1980 – The name Attention Deficit Disorder (ADD) was first introduced in DSM-III, the 1980 edition.
  • 1987 – The DSM-IIIR was released changing the diagnosis to "Undifferentiated Attention Deficit Disorder." [66]
  • 1994 – DSM-IV described three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination.
  • 1996 – ADHD accounted for at least 40% of child psychiatry references.[67]
  • 1999 – New delivery systems for medications are invented that eliminate the need for multiple doses across the day or taking medication at school. These new systems include pellets of medication coated with various time release substances to permit medications to dissolve hourly across an 8–12 hour period (Medadate CD, Adderall XR, Focalin XR) and an osmotic pump that extrudes a liquid methylphenidate sludge across an 8–12 hour period after ingestion (Concerta).
  • 1999 – The largest study of treatment for ADHD in history is published in the American Journal of Psychiatry. Known as the Multimodal Treatment Study of ADHD (MTA Study), it involved more than 570 ADHD children at 6 sites in the United States and Canada randomly assigned to 4 treatment groups. Results generally showed that medication alone was more effective than psychosocial treatments alone but that their combination was beneficial for some subsets of ADHD children beyond the improvement achieved only by medication. More than 40 studies have subsequently been published from this massive dataset.
  • 2001 – The International Consensus Statement on ADHD is published and signed by more than 80 of the world's leading experts on ADHD to counteract periodic media misrepresentation that ADHD is a real disorder and that medications are justified as a treatment for the disorder. In 2005, another 100 European experts on ADHD added their signatures to this historic document certifying the validity of ADHD as a valid mental disorder.
  • 2003 – Atomoxetine, the first new medication for ADHD in 25 years, receives FDA approval for use in children, teens, and adults with ADHD.

See also

Footnotes

  1. ^ Zametkin AJ, Nordahl TE, Gross M, King AC, Semple WE, Rumsey J, Hamburger S, Cohen RM. Cerebral glucose metabolism in adults with hyperactivity of childhood onset. N Engl J Med. 1990 Nov 15;323(20):1361-6. PMID 2233902
  2. ^ Behavenet.com Attention-Deficit/Hyperactivity Disorder (ADHD)
  3. ^ ADHD Health Center
  4. ^ Attention-Deficit / Hyperactivity Disorder: ADHD in Adults Accessed 9/15/06
  5. ^ Attention deficit hyperactivity disorder in children. Accessed 9/15/06
  6. ^ http://www.help4adhd.org/en/about/what/WWK1 What we know
  7. ^ Perrin, James. M., Martin T. Stein, Robert W. Amler, and Thomas A. Blondius. 2001. Clinical practice guideline: treatment of school-aged children with Attention Deficit/Hyperactivity Disorder. Pediatrics 108 (4):1033-1044. PMID: 11581465
  8. ^ John Ratey; Edward Hallowell, Driven to Distraction first edition, pg 42
  9. ^ Ninivaggi, F. J. Borderline intellectual functioning and academic problem. In: Sadock B.J. Sadock, V.A., eds. Kaplan & Sadock's Comprehensive Textbook of psychiatry. 8th ed. Vol. II. Baltimore: Lippincott William and Wilkins; 2005: 2272-2276.
  10. ^ Role of Brain Imaging in the Diagnosis and Management of ADHD
  11. ^ CDC "National Health Interview, 2002" http://www.cdc.gov/nchs/data/series/sr_10/sr10_221.pdf (March, 2004)
  12. ^ Staller J, Faraone SV. (2006) Attention-deficit hyperactivity disorder in girls: epidemiology and management. CNS Drugs. 2006;20(2):107-23. PMID 16478287
  13. ^ Biederman J, Faraone SV. The Massachusetts General Hospital studies of gender influences on attention-deficit/hyperactivity disorder in youth and relatives. Psychiatr Clin North Am. 2004 Jun;27(2):225-32. PMID 15063995
  14. ^ Olfson M, Gameroff MJ, Marcus SC, & Jensen PS. (2003). National trends in the treatment of attention deficit hyperactivity disorder. American Journal of Psychiatry, 160 (6): 1071-1077 PMID: 10326176
  15. ^ [http://consensus.nih.gov/1998/1998AttentionDeficitHyperactivityDisorder110html.htm Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder National Institutes of Health Consensus Development Conference Statement November 16-18, 1998
  16. ^ Mental Health: A Report of the Surgeon General (ADHD)
  17. ^ Xavier Castellanos, Judith Rapaport, "Scientific America" (August, 2003)
  18. ^ Anterior cingulate cortex dysfunction in attention-deficit/hyperactivity disorder revealed by fMRI and the Counting Stroop. Biol Psychiatry. 1999 Jun 15;45(12):1542-52. Bush G, Frazier JA, Rauch SL, et. al. PMID: 10376114
  19. ^ Roman et al., 2004, American Journal of Pharmacogenomics 4:83-92
  20. ^ Swanson JM, Flodman P, Kennedy J, Spence MA, Moyzis R, Schuck S, Murias M, Moriarity J, Barr C, Smith M, Posner M. Dopamine Genes and ADHD. Neurosci Biobehav Rev. 2000 Jan;24(1):21-5. PMID 10654656
  21. ^ ibid
  22. ^ Smith KM, Daly M, Fischer M, Yiannoutsos CT, Bauer L, Barkley R, Navia BA. 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
  23. ^ 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
  24. ^ Dougherty et al. in Lancet 354 (1999) 2132-2133; Dresel et al. in Eur. J.Nucl. Med. 25 (1998) 31-39
  25. ^ The influence of the chemical additive tartrazine on the zinc status of hyperactive children: A double-blind placebo-controlled study.
  26. ^ The duration of breastfeeding and attention deficit hyperactivity disorder. Kadziela-Olech H, Piotrowska-Jastrzebska Rocz Akad Med Bialymst. 2005;50:302-6. PMID: 16358988
  27. ^ A follow-up study of the influence of early malnutrition on development: behavior at home and at school. Galler JR, Ramsey F. J Am Acad Child Adolesc Psychiatry 1991 Jan;30(1):157. PMID: 2494148
  28. ^ Neal L. Rojas and Eugenia Chan. (2005). Old and new controversies in the alternative treatment of attention deficit hyperactivity disorder. Mental Retardation and Developmental Disabilities, 11, 116-130. PMID: 15977318
  29. ^ Kotimaa et al.,Maternal smoking and hyperactivity in 8-year-old children. 2003, J Am Acad Child Adol Psychiatry 42, 826-833 PMID: 12819442
  30. ^ What Causes AD/HD Attention Deficit Disorder Association website
  31. ^ [No authors listed] Moderators and mediators of treatment response for children with attention-deficit/hyperactivity disorder: the Multimodal Treatment Study of children with Attention-deficit/hyperactivity disorder. Arch Gen Psychiatry. 1999 Dec;56(12):1088-96. PMID 10591284. Free Full Text.
  32. ^ Associated Counselors & Therapists. ADHD: Current Status of What We Know. URL: http://www.beachpsych.com/pages/cc34.html. Accessed on: April 12, 2006.
  33. ^ Methylphenidate and Clonidine Help Children With ADHD and Tics
  34. ^ Hallowell and Ratey, Delivered from Distraction: Getting the Most out of Life with Attention Deficit Disorder (2005), pp. 253-5. 0345442318
  35. ^ Wilens, T. E. Straight Talk about Psychiatric Medications for Kids (Revised Edition--2004). ISBN 1-57230-945-8.
  36. ^ Ward NI et al. (1990). The influence of the chemical additive tartrazine on the zinc status of hyperactive children: A double-blind placebo-controlled study. J Nutr Med; 1 (1). 51-58.
  37. ^ Ward NI (1997)Assessment of chemical factors in relation to child hyperactivity. Journal of Nutritional & Environmental Medicine (Abingdon); 7 (4). 333-342.
  38. ^ Oades RD, Daniels R, Rascher W. Plasma neuropeptide-Y levels, monoamine metabolism, electrolyte excretion and drinking behavior in children with attention-deficit hyperactivity disorder. Psychiatry Res. 1998; Aug 17;80(2):177-86 PMID 9754697
  39. ^ Schnoll R, Burshteyn D, Cea-Aravena (2003). Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect, J. Appl Psychophysiol Biofeedback Mar;28(1):63-75 PMID 12737097
  40. ^ Joshi K, Lad S, Kale M, Patwardhan B, Mahadik SP, Patni B, Chaudhary A, Bhave S, Pandit A. Supplementation with flax oil and vitamin C improves the outcome of Attention Deficit Hyperactivity Disorder (ADHD) Prostaglandins Leukot Essent Fatty Acids. 2006 Jan;74(1):17-21. PMID 16314082
  41. ^ Singh M (2005) Essential fatty acids, DHA and human brain. Indian J Pediatr. Mar;72(3):239-42. PMID 15812120]
  42. ^ [http://ajp.psychiatryonline.org/cgi/content/abstract/130/7/796 M. R. Leon Effects of caffeine on cognitive, psychomotor, and affective performance of children with Attention-Deficit/Hyperactivity Disorder J Atten Disord, April 1, 2000; 4(1): 27 - 47.
  43. ^ [http://apa.org/monitor/jun01/dangersip.html Eileen O'CONNOR A sip into dangerous territory, Monitor on Psychology, Volume 32, No. 5 June 2001
  44. ^ go to www.russellbarkley.org and see Research to Read subpage
  45. ^ Joyce, Michael & Siever, Dave Audio-Visual Entrainment (AVE) Program as a Treatment for Behavior Disorders in a School Setting, , 1997, Journal of Neurotherapy, vol 4 (2), 9-32.
  46. ^ *“How does the DORE programme work?” Dore Achievement Centres, UK, retrieved November 28th, 2005.
  47. ^ http://www.newhorizons.org/spneeds/inclusion/information/armstrong.htm Special Education and the Concept of Neurodiversity
  48. ^ Hallahn, Dan P.; Kauffman, James M.. Exceptional Learners : Introduction to Special Education Allyn & Bacon; 10 edition (April 8, 2005) ISBN: 0205444210
  49. ^ Rafalovich, Adam. 2005. Exploring clinician uncertainty in the diagnosis and treatment of attention deficit hyperactivity disorder. Sociology of Health and Illness. 27(3). PMID: 15953210
  50. ^ ADHD and Other Sins of Our Children
  51. ^ Skeptical Enquirer magazine; May/June 2006
  52. ^ ADHD and Other Sins of Our Children
  53. ^ interviewed October 10, 2000 on Frontline
  54. ^ Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
  55. ^ ADHD Parental Stress The University of Sydney School of Behavioural & Community Health Sciences
  56. ^ Andrea Englander (2005)Childhood ADHD and Its Effects on Parents and the Family System Journal of Student Award Winners
  57. ^ Eileen Bailey The ADHD Entrepreneur
  58. ^ Anne Underwood The Gift Of ADHD?
  59. ^ http://www.adhd.org.nz/define1.html What is ADHD
  60. ^ http://www.fln.vcu.edu/struwwel/philipp_e.html
  61. ^ Still GF. Some abnormal psychical conditions in children: the Goulstonian lectures. Lancet, 1902;1:1008-1012
  62. ^ Palmer, E. and S. Finger. 2001. “An Early Description of AD/HD: Dr. Alexander Crichton and ‘Mental Restlessness’.” Child Psychology and Psychiatry Review 6(2):66–73.
  63. ^ Notes from Dr. Ned Hallowell's Workshop on ADHD
  64. ^ Classification of ADHD through History accessed 9/15/06
  65. ^ Oxford English Dictionary Online
  66. ^ ADHD History
  67. ^ Castellanos, F. X., Giedd, J. N., Marsh, W. L., Hamburger, S. D., Vaituzis, A. C., Dickstein, D. P., Sarfatti, S. E., Vauss, V. C., Snell, J. W., Lange, N., Kaysen, D., Krain, A. L., Ritchie, G. F., Rajapakse, J. C., & Rapoport, J. L. (1996). Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder. Archives of General Psychiatry, 53, 607–616. PMID: 14765004

Further reading

  • Peter Conrad, Identifying Hyperactive Children (Ashgate, 2006).
  • Taking Charge of ADHD: The Complete Authoritative Guide for Parents (2005) by Russell A. Barkley, Ph.D. New York: Guilford Publications.
  • Understanding ADD by Dr Christopher Green & Dr Kit Chee, ISBN 0-86824-587-9, Doubleday 1994
  • The ADHD-Autism Connection: A Step toward more accurate diagnosis and effective treatment, by Diane M. Kennedy, ISBN 1-57856-498-0 (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.)
  • Kate Kelly and Peggy Ramundo: You Mean I'm Not Lazy, Stupid, or Crazy?! A Self-Help Book for Adults with Attention Deficit Disorder (1993). ISBN 0-684-81531-1
  • Edward M. Hallowell, M.D. and John J. Ratey, M.D. (2005). Delivered from Distraction: Getting the Most out of Life with Attention Deficit Disorder. Ballantine Books. ISBN 0-345-44230-X
  • Bellak L, Kay SR, Opler LA. (1987) Attention deficit disorder psychosis as a diagnostic category. Psychiatric Developments, 5 (3), 239-63.
  • Ninivaggi, F.J., "Attention-Deficit/Hyperactivity Disorder in Children and Adolescents: Rethinking Diagnosis and Treatment Implications for Complicated Cases," Connecticut Medicine. September 1999; Vol. 63, No. 9, 515-521.