Attention deficit hyperactivity disorder

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Attention deficit hyperactivity disorder
SpecialtyPsychiatry, child and adolescent psychiatry Edit this on Wikidata

Attention-Deficit/Hyperactivity Disorder (ADHD) previously known as Attention Deficit Disorder (ADD), 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. 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 disorder as adults.[7] 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 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.[8] 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. Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD.[8][9] Methods of treatment usually involve some combination of medication, behaviour modification, 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. 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, and many adverse life outcomes are associated with ADHD.

Classification

ADHD is a developmental disorder that is often said to be neurological in nature. The term "developmental" means that certain traits such as impulse control significantly lag in development when compared to the general population. This developmental lag has been estimated to range between 30-40 percent in ADHD sufferers in comparison to their peers; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioural or neurodevelopmental disorders. These compounded terms are now more frequently used in the field to describe the disorder.[citation needed] The behavioral classification for ADHD is not completely accurate in that those with Predominately Inattentive ADHD often display few or no overt behaviors.[citation needed]

Diagnosis

Based on DSM-IV criteria, three types of ADHD are identified:

  • 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.

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Causes

PET scans of glucose metabolism in the brains of a normal adult (left) compared to an adult diagnosed with ADHD (right).[10]

The exact cause of ADHD remains unknown and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology. 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.[11] Suspect genes include the 10-repeat allele of the DAT1 gene,[12] the 7-repeat allele of the DRD4 gene,[12] and the dopamine beta hydroxylase gene (DBH TaqI).[13] Additionally, SPECT scans found people with ADHD to have reduced blood circulation,[14] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.[15][16]

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.[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 right 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.[10] 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.[18] 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.[19] 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).[20] 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.[21] This could be related to the fact than 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,[22] 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".[23]

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.[24] 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."[25] 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 ADHD, studies have found that malnutrition is correlated with attention deficits.[26]

Treatment

Main article: Attention-deficit hyperactivity disorder treatments

There are several clinically proven effective options available to treat people diagnosed with ADHD. ADHD is treated most effectively, and cost efficiently, with medication.[27] 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]

Prognosis

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 underachievement". 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.[8] The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool.[32] 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. Their income level does not rise as quickly as their peers even when education level, IQ, and their neighborhood is accounted for. Thirty five percent of all those with ADHD will be self employed in their mid-thirties. Those with ADHD are at greater risk of: injury, abnormal risk taking, smoking, having learning disabilities, other mental disorders, teen pregnancy, substance abuse, involvement with the criminal justice system, and having a poorer driving record.[33]

Prevention

There is no known way to prevent ADHD. Some studies indicate an association between mothers who smoke during pregnancy and a higher rate of ADHD in their children. Avoiding smoking, alcohol, and drugs during pregnancy may help prevent a higher risk of developing ADHD or similar behaviour in offspring.

Epidemiology

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

Hippocrates

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/behavioural disabilities" or "hyperactivity".

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 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,[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] However, analysis of Still's descriptions by Palmer and Finger indicated that the qualities Still described are not "considered primary symptoms of ADHD".[40]

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.[41] 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.[42]

Controversy

Main article: Controversy about ADHD

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.[43] 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.

See also

General

Controversy

Related disorders

References

  1. ^ Attention Deficit Hyperactivity Disorder. National Institute of Mental Health (NIMH), October 26, 2006. Retrieved on 2007-08-13.
  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. ^ Attention-Deficit / Hyperactivity Disorder: ADHD in Adults. WebMd.com. Retrieved on December 11, 2006.
  8. ^ a b c d e f Barkley, Russell A. Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity. ContinuinedEdCourse.Net. Retrieved on 2007-08-12.
  9. ^ Barkley, Russell A. Treating Children and Adolescents with ADHD: An Overview of Empirically Based Treatments. ContinuingEdCourses.Net. Retrieved on 2007-08-13.
  10. ^ 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
  11. ^ 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
  12. ^ a b Swanson JM, Flodman P, Kennedy J, et al. "Dopamine Genes and ADHD." Neurosci Biobehav Rev. 2000 Jan;24(1):21–5. PMID 10654656
  13. ^ 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
  14. ^ 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
  15. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  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. ^ 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
  19. ^ Template:PDFlink SchwabLearning.org.
  20. ^ 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 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."
  21. ^ 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
  22. ^ 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
  23. ^ What Causes AD/HD. Attention Deficit Disorder Association. Retrieved on 2007-08-13.
  24. ^ Template:PDFlink
  25. ^ Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
  26. ^ Galler JR, Ramsey F. "A follow-up study of the influence of early malnutrition on development: behavior at home and at school." J Am Acad Child Adolesc Psychiatry. 1989 Mar;28(2):254–61. PMID 2494148
  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. ^ Template:PDFlink
  33. ^ Attention-Deficit / Hyperactivity Disorder (ADHD) Workshops. Public Health Issues in ADHD: Individual, System, and Cost Burden of the Disorder Workshop. Centers for Disease Control and Prevention. May 17, 1999. Retrieved on 2007-08-13.
  34. ^ Template:PDFlink. 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. ^ Palmer E, Finger S. 2001. "An Early Description of AD/HD: Dr. Alexander Crichton and ‘Mental Restlessness’". Child Psychology and Psychiatry Review 6(2):66–73.
  41. ^ Classification of ADHD through History. Retrieved on 2006-09-15.
  42. ^ 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
  43. ^ Special Education and the Concept of Neurodiversity New Horizons for Learning.

Further reading

  • A special issue of the journal Clinical Psychology Review focuses on ADHD. Includes such articles as Neuropsychological functioning in people with ADHD across the lifespan by L. Seidman, Evidence-based psychosocial treatments for children and adolescents with ADHD by A. Chronis, H. Jones and V. Raggi, et al.
  • 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
  • Carey,Benedict Debate Over Children and Psychiatric Drugs
  • 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
  • Timimi, Sami. (2005) Naughty Boys: Anti-Social Behaviour, ADHD and the Role of Culture London Palgrave McMillan ISBN 1-4039-4511-X

External links

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