User:Jklin/sandbox

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Jklin/sandbox

Attention-Deficit Hyperactivity Disorder (ADHD), or Hyperkinetic Disorder as officially known in the UK though ADHD is more commonly used, is generally considered to be a developmental disorder, largely neurological in nature, affecting about 5% of the world's population.[1][2][3][4] The disorder 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.[citation needed] ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults.[citation needed] About 50% of children diagnosed with ADHD retain the disorder as adults.[citation needed] The disorder appears to be highly heritable, with contributions on occasion from trauma or toxic exposure.[citation needed] Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling.

Certain social critics are highly skeptical that the diagnosis denotes a genuine impairment and question virtually all that is known about ADHD.[citation needed] The symptoms of ADHD are not as profoundly different from normal behavior as are those of other chronic mental disorders.[citation needed]

Diagnosis[edit]

Formal diagnosis is based on a number of strict criteria, laid down in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV ), 4th edition. These criteria have been created for research purposes. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

  • 1. ADD, 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. ADD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

DSM-IV Criteria for ADHD[edit]

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.

Impulsiveness

  1. Often blurts out answers before questions have been finished.
  2. Often has trouble waiting one's turn.
  3. Often interrupts or intrudes on others (e.g., butts into conversations or games).

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

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

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

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

In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADHD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10[7]) 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".[7]

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:[8]

  • 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.[9] 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.[10] 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.[11]

The Centers for Disease Control and Prevention (CDC) state 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 physiological disorders, such as hyperthyroidism. 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 ADHD. Adults with ADHD are diagnosed under the same criteria, including the stipulation that their symptoms must have been present prior to the age of seven.[12] 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.[citation needed]

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

Causes[edit]

Studies show that there is a familial transmission of the disorder which does not occur through adoptive relationships.[citation needed]Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population.[citation needed] While the majority of ADHD is believed to be genetic in nature [citation needed], roughly 1/5 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.[citation needed] 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.[citation needed] Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD.[citation needed] Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling.[citation needed]

PET scans of glucose metabolism in the brains of a normal adult (left) compared to an adult diagnosed with ADHD (right).[13] Brain scans are valuable and raise questions for further study, but many published ADHD brain scan studies have serious flaws. Cohen deals directly with the shortcomings of the Zametkin study.[14]

The exact cause of ADHD remains unknown and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomatology. Still, there is a wide body of evidence which indicates that the overriding cause of ADHD is genetics. Research suggests 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, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI).[16] Additionally, SPECT scans found people with ADHD to have reduced blood circulation, and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.


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 ADD 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 ADD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor.[citation needed] 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.[17]

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.[13] A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADD 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.[citation needed] 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.[citation needed]

The estimated contribution of non genetic factors to the contribution of all cases of ADHD is 20 percent.[18] 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).[19] 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.[20] 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 ADD 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 ADD-like symptoms,[21] possibly because of damage done to the patient's frontal lobes. Because these types of symptoms can be attributable to brain damage, the earliest designation for ADHD was "Minimal Brain Damage".[22]

There is no compelling evidence that social factors alone can create ADHD. 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.[23] 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."[24] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

Despite the lack of evidence that nutrition causes ADD, studies have found that malnutrition is correlated with attention deficits.[citation needed]

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 that characterize 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.[25]

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.[26]

Treatment[edit]

Main article: Attention-deficit hyperactivity disorder treatments

There are several clinically proven effective options available to treat people diagnosed with ADHD. It has been believed that ADHD is treated most effectively, and cost efficiently, with medication.[27] However, recent long term studies now cast serious doubt to this assertion. "[D]rugs such as Ritalin and Concerta work no better than therapy after three years of treatment. The findings by an influential US study also suggested long-term use of the drugs could stunt children's growth. It said that the benefits of drugs had previously been exaggerated."[1] Psychotherapy is another option, with or without medication[28] Omega-3 fatty acids, zinc and magnesium may have benefits with regards to ADHD symptoms.[29][30]

Comorbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming.[31]

ADHD is a developmental disorder meaning that certain traits will be delayed in the ADHD individual. These traits will develop but just at a much slower rate than the average person. With ADHD it has been estimated that this lag could be as high as thirty to forty percent in the development of impulse control. Symptoms of ADHD are often seen by the time a child enters preschool. Those with ADHD typically have a greater degree of parent-child conflict and emotional reactivity. The incidence of speech problems, central auditory processing difficulties, and coordination problems are all higher than that of the general population. A marked decrease in academic skills such as reading, spelling, or math is common with children who have 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 behaviour 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.[citation needed] Thirty seven percent of those with ADHD do not get a high school diploma even though many of them will receive special education services.[32] The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool.[33] Only five percent of those with ADHD will get a college degree compared to twenty seven percent of the general population. (US Census, 2003)

Social impairment for those with ADHD are seen at both school and work. They often have more troubled relationships with peers or family members. At the workplace, they change jobs more often and are more likely to get fired. Thirty five percent of all those with ADHD will be self employed in their mid-thirties.[citation needed]

Epidemiology[edit]

ADHD's prevalence worldwide is estimated to be a bit over 5%, with most of the reported variability being due to methodological characteristics of studies.[4] 10% of males, and (only) 4% of females have been diagnosed in the U.S.[34] This apparent sex difference may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[35][36]

History[edit]

Main article: Controversy about ADHD

Some sources claim to have identified historical and literary references to ADHD before 1900. However, the condition we refer to as "ADHD" dates to the mid-twentieth century, when physicians developed a diagnosis for a set of conditions variously referred to as "minimal brain damage", "learning/behavioral disabilities" or "hyperactivity".

Hippocrates

In 493 BC, 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."[37] 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 behaviors. "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,[38] 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.[39]

The 1918–1919 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.[40] 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) became available. In its various forms (Ritalin, Focalin, Concerta, Metadate, and Methylin), it remains one of the most widely prescribed medications for ADHD. Ritalin was first produced in 1950. 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. 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). 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.

Psychiatry first 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. During 1996, ADHD accounted for at least 40% of child psychiatry references.[41]

The ADHD diagnosis has been questioned on many fronts. Some critics focus upon the positive traits that people with ADHD are thought to have, such as "hyperfocusing." Others believe ADHD is a divergent or normal-variant human behavior (using the term neurodiversity to describe this idea), emphasizing that human behaviour is immensely variable and "ADHD" may simply represent one part of the spectrum.[42] Such critics sometimes allege that ADHD is not actually a discrete condition and question why it should be treated with drugs. Others dispute the alleged genetic basis of ADHD.

==Controversy Certain social critics are highly skeptical that the diagnosis denotes a genuine impairment and question virtually all that is known about ADHD.[citation needed] The symptoms of ADHD are not as profoundly different from normal behavior as are those of other chronic mental disorders. Still, ADHD has been shown to often impair functioning.

See also[edit]

General

Controversy

Related disorders

References[edit]

  1. ^ Attention Deficit Hyperactivity Disorder. National Institute of Mental Health (NIMH), November 17, 2007. Retrieved on 2007-11-17.
  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. ^ ADHD - A Guide for Families. American Academy of Child Adolescent Psychiatry. Retrieved on 2007-08-13.
  4. ^ a b 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Diagnostic and Statistical Manual of the American Psychiatric Association, Fourth Edition, American Psychiatric Association, 2000.
  6. ^ Attention-Deficit/Hyperactivity Disorder (ADHD). Behavenet.com. Retrieved on December 11, 2006.
  7. ^ a b ICD Version 2006: F91. World Health Organization. Retrieved on December 11, 2006.
  8. ^ 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
  9. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Ratey, John; Hallowell, Edward. Driven to Distraction first edition, p. 42
  11. ^ 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.
  12. ^ Attention-Deficit/Hyperactivity Disorder. Psychiatry Online. Retrieved on 2007-08-13.
  13. ^ a b 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
  14. ^ Leo J, Cohen D. "Broken Brains or Flawed Studies? A Critical Review of ADHD Neuroimaging Research." The Journal of Mind and Behavior. Vol. 24 No. 1 Winter 2003 P29–56
  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. ^ 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
  17. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ "Barkley presentaiton" (PDF). (779 KiB) SchwabLearning.org.
  19. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link): "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 ADD 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."
  20. ^ 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
  21. ^ 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
  22. ^ What Causes ADD. Attention Deficit Disorder Association. Retrieved on 2007-08-13.
  23. ^ "What Keeps Children in Foster Care from Succeeding in School" (PDF). (661 KiB)
  24. ^ Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
  25. ^ Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern NIMH Press Release, November 12, 2007
  26. ^ Gene Predicts Better Outcome as Cortex Normalizes in Teens with ADHD NIMH Press Release, August 6, 2007
  27. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help) Free full text
  28. ^ Barkley, R. (2005) Take Charge of ADHD: The Complete Authoritative Guide for Parents. NY: Guilford Publications
  29. ^ 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.
  30. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)
  32. ^ Barkley, Russell A. Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity. ContinuinedEdCourse.Net. Retrieved on 2007-08-12.
  33. ^ http://eric.ed.gov/ERICDocs/data/ericdocs2/content_storage_01/0000000b/80/22/94/d6.pdf. {{cite web}}: Missing or empty |title= (help)
  34. ^ ""National Health Interview survey, 2002"" (PDF). (3.71 MiB). Centers for Disease Control (March, 2004). Retrieved on December 11, 2006.
  35. ^ Staller J, Faraone SV. (2006) "Attention-deficit hyperactivity disorder in girls: epidemiology and management." CNS Drugs. 2006;20(2):107–23. PMID 16478287
  36. ^ 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
  37. ^ What is ADHD? ADHD.org.nz. Retrieved on 2007-08-13.
  38. ^ Heinrich Hoffmann. The Story of Fidgety Philip. Virginia Commonwealth University. Retrieved on 2007-08-13.
  39. ^ Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008-1012
  40. ^ Classification of ADHD through History. Retrieved on 2006-09-15.
  41. ^ 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
  42. ^ Special Education and the Concept of Neurodiversity New Horizons for Learning.

Further reading[edit]

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