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Attention-deficit hyperactivity disorder

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2], Haleigh Williams, B.S.

Synonyms and keywords: Adult attention-deficit disorder; AADD; ADD; ADD/ADHD; ADHD; ADHD predominantly hyperactive-impulsive; ADHD predominantly inattentive; hyperactiveness; other specified attention-deficit/hyperactivity disorder; short attention span; unspecified attention-deficit/hyperactivity disorder; hyperkinetic syndrome; ADDH; childhood hyperkinesis

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Haleigh Williams, B.S.

Overview

Attention-deficit hyperactivity disorder (ADHD) is a neurobehavioral brain disorder marked by an ongoing pattern of inattention and/or hyperactivity–impulsivity that interferes with functioning or development. It may negatively impact the patient’s academic or professional performance and/or social interactions. ADHD has a strong component of heritability. ADHD is more commonly diagnosed in boys than in girls, though this may be because the symptoms of the disorder are less easily recognized in girls.[1]

Clinical practice guidelines exist to guide diagnosis and treatment.

  • American Academy of Pediatrics (AAP), 2019[2][3]
  • Society of Developmental and Behavioral Pediatrics (SDBP)[4]

Historical Perspective

  • ADHD symptoms have been recognized in children and described in medical texts since the nineteenth century, though the formal diagnosis had not yet been devised.
  • ADHD was first included in some form in the DSM in its second edition, when it was referred to as “hyperkinetic reaction of childhood.” It was not until the third edition of the DSM was released in 1980 that the disorder was formally identified as “ADD (Attention-Deficit Disorder) with or without hyperactivity.”[5]
  • In 1937, Rhode Island physician Dr. Charles Bradley pioneered the use of medications to treat ADHD. The prescription of stimulants has since become a first-line treatment for ADHD.[6]

Classification

ADHD may be classified according to the DSM V criteria into three subgroups:

  • predominantly inattentive type;
  • predominantly hyperactive-impulsive type; and
  • combined type.[7]

Pathophysiology

  • ADHD is highly heritable, although one-fifth of all cases are estimated to be caused by trauma or exposure to toxins.
  • ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology.[8]
  • Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are a molecular abnormality of ADHD or a secondary consequence of ADHD.

Causes

There are no established causes of ADHD. Studies suggest that ADHD results from a complex interaction between genetic and environmental factors.[9]

Differentiating Attention Deficit Hyperactivity Disorder from other Diseases

Epidemiology and Demographics

  • The prevalence of attention-deficit hyperactivity disorder (ADHD) is estimated to be 5,000 per 100,000 (5%) children and 2,500 per 100,000 (2.5%) adults.[7]
  • Boys are more commonly affected by ADHD than girls. The male to female ratio is 2 to 1.[11]

Risk Factors

Common risk factors in the development of attention-deficit hyperactivity disorder (ADHD) are:[7]

Natural History, Complications and Prognosis

If left untreated, patients with ADHD may experience negative social consequences, such as isolation from and difficulty communicating with friends and loved ones. Patients are unlikely to experience any physical problems as a direct result of ADHD.[12]

Diagnosis

The diagnosis of ADHD is made based on the DSM V criteria, which can be found on the Attention-deficit hyperactivity disorder diagnostic criteria page.

Practice guidelines are available[13][14][15].

History and Symptoms

  • The most common symptoms of ADHD include chronic and long-lasting hyperactivity, impulsivity, and inattention.[1]
  • It is particularly important to collect a family history with regard to psychiatric disorders, as ADHD has a strong genetic component.[16]
  • It is also vital to understand how long the patient has been experiencing symptoms of ADHD, as the DSM V stipulates that symptoms must have been present for at least 6 months in order for a diagnosis of ADHD to be made. Similarly, an adult cannot be diagnosed with ADHD unless his/her symptoms were present prior to the age of 12 years.[7]

Physical Examination

  • A psychiatric evaluation of a patient who may be suffering from ADHD consists of a behavioral assessment.
  • It is common practice for clinicians to administer rating scales to those who have frequent contact with the patient, often including parents and teachers.[17] It is important that rating scales be completed by people who observe the patient in different settings, such as at home and at school, since ADHD symptoms can be situation-specific.[7]
  • Commonly used rating scales include the Vanderbilt Rating Scale, the Brown Rating Scale, and the Wender Utah Rating Scale.[17]
  • These rating scales are subjective, and informants regularly differ in their reports.[17]

Laboratory Findings

  • There are no laboratory findings associated with ADHD.

Electrocardiogram

  • There are no ECG findings associated with ADHD.

Chest X Ray

  • There are no chest x-ray findings associated with ADHD.

CT Scan

  • There are no CT scan findings associated with ADHD.

Electrocardiography or Ultrasound

  • There are no echocardiography or ultrasound findings associated with ADHD.

Other Imaging Findings

  • Though the brains of ADHD patients follow a normal pattern of development, imaging findings indicative of ADHD may include delayed physical development of the brain. This may help explain why some adolescent ADHD patients do not experience symptoms into adulthood.[18]

Treatment

The mainstay of therapy for ADHD is the administration of such stimulants as Ritalin and Adderall. While there is no cure for ADHD, currently available treatments can help reduce symptoms and improve functioning. Other treatment options include psychotherapy, education and training, or a combination of therapies.[1]

Practice guidelines are available[13][14][15].

Medical Therapy

Surgery

Surgical intervention is not recommended for the management of ADHD.

Prevention

  • There is no established method for the prevention of ADHD. Although there is no proven way to prevent ADHD, early identification and treatment can prevent many of the problems associated with ADHD.[1]
  • Secondary prevention strategies following a diagnosis of ADHD include the administration of stimulants, cognitive behavioral therapy, regular psychiatric evaluations, and the maintenance of a healthy diet.[1]

Psychotherapy

  • Many psychological interventions can be used to manage symptoms of attention-deficit hyperactivity disorder.

Brain Stimulation Therapy

  • There is no brain stimulation therapy associated with attention-deficit hyperactivity disorder.

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 National Institute of Mental Health (NIH). (2016). “Attention Deficit Hyperactivity Disorder.”
  2. ↑ Wolraich, Mark L.; Hagan, Joseph F.; Allan, Carla; Chan, Eugenia; Davison, Dale; Earls, Marian; Evans, Steven W.; Flinn, Susan K.; Froehlich, Tanya; Frost, Jennifer; Holbrook, Joseph R.; Lehmann, Christoph Ulrich; Lessin, Herschel Robert; Okechukwu, Kymika; Pierce, Karen L.; Winner, Jonathan D.; Zurhellen, William; SUBCOMMITTEE ON CHILDREN AND ADOLESCENTS WITH ATTENTION-DEFICIT/HYPERACTIVE DISORDER (2019). “Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents”. Pediatrics. 144 (4): e20192528. doi:10.1542/peds.2019-2528. ISSN 1098-4275. PMC 7067282 Check |pmc= value (help). PMID 31570648. Retrieved 2025-12-06.
  3. ↑ Clinical Care of ADHD. CDC 2024 Available at https://www.cdc.gov/adhd/hcp/treatment-recommendations/index.html
  4. ↑ Barbaresi, William J.; Campbell, Lisa; Diekroger, Elizabeth A.; Froehlich, Tanya E.; Liu, Yi Hui; O’Malley, Eva; Pelham, William E.; Power, Thomas J.; Zinner, Samuel H.; Chan, Eugenia (2020). “The Society for Developmental and Behavioral Pediatrics Clinical Practice Guideline for the Assessment and Treatment of Children and Adolescents with Complex Attention-Deficit/Hyperactivity Disorder: Process of Care Algorithms”. Journal of developmental and behavioral pediatrics: JDBP. 41 Suppl 2S: S58–S74. doi:10.1097/DBP.0000000000000781. ISSN 1536-7312. PMID 31996578. Retrieved 2025-12-06.
  5. ↑ Lange, K. W., Reichl, S., Lange, K. M., Tucha, L., & Tucha, O. (2010). The history of attention deficit hyperactivity disorder. Attention Deficit and Hyperactivity Disorders, 2(4), 241–255. http://doi.org/10.1007/s12402-010-0045-8.
  6. ↑ Strohl, M. P. (2011). Bradley’s Benzedrine Studies on Children with Behavioral Disorders. The Yale Journal of Biology and Medicine, 84(1), 27–33.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  8. ↑ Barkley, Russel A. “Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity”. Retrieved 2006-06-26.
  9. ↑ OurMed. (2010). “Attention-deficit hyperactivity disorder.”
  10. ↑ Cross-Disorder Group of the Psychiatric Genomics Consortium. (2013). Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet, 381(9875), 1371–1379. http://doi.org/10.1016/S0140-6736(12)62129-1.
  11. ↑ Briars, L., & Todd, T. (2016). A Review of Pharmacological Management of Attention-Deficit/Hyperactivity Disorder. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 21(3), 192–206. http://doi.org/10.5863/1551-6776-21.3.192.
  12. ↑ Briars, L., & Todd, T. (2016). A Review of Pharmacological Management of Attention-Deficit/Hyperactivity Disorder. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 21(3), 192–206. http://doi.org/10.5863/1551-6776-21.3.192
  13. ↑ 13.0 13.1 May T, Birch E, Chaves K, Cranswick N, Culnane E, Delaney J; et al. (2023). “The Australian evidence-based clinical practice guideline for attention deficit hyperactivity disorder”. Aust N Z J Psychiatry. 57 (8): 1101–1116. doi:10.1177/00048674231166329. PMC 10363932 Check |pmc= value (help). PMID 37254562 Check |pmid= value (help).
  14. ↑ 14.0 14.1 Kooij JJS, Bijlenga D, Salerno L, Jaeschke R, Bitter I, Balázs J; et al. (2019). “Updated European Consensus Statement on diagnosis and treatment of adult ADHD”. Eur Psychiatry. 56: 14–34. doi:10.1016/j.eurpsy.2018.11.001. PMID 30453134.
  15. ↑ 15.0 15.1 Baughman DJ, Watson CM, Beich JW, Herboso MNJ, Cuttie LK, Marlyne AC (2023). “Recommendation for Long-term Management of Adult Attention-Deficit/Hyperactivity Disorder in Military Populations, Veterans, and Dependents: A Narrative Review”. Mil Med. doi:10.1093/milmed/usad403. PMID 37878798 Check |pmid= value (help).
  16. ↑ Cross-Disorder Group of the Psychiatric Genomics Consortium. “Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs.” Nat Genet. (2013). 45(9):984-94. doi: 10.1038/ng.2711. Epub 2013 Aug 11.
  17. ↑ 17.0 17.1 17.2 Gualtieri CT, Johnson LG (2005). “ADHD: Is Objective Diagnosis Possible?”. Psychiatry (Edgmont). 2 (11): 44–53. PMC 2993524. PMID 21120096.
  18. ↑ Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern NIMH Press Release, November 12, 2007

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Haleigh Williams, B.S.

Overview

ADHD symptoms have been recognized in children and described in medical texts since the nineteenth century, though the formal diagnosis had not yet been devised. ADHD was first included in some form in the DSM in its second edition, when it was referred to as “hyperkinetic reaction of childhood.” It was not until the third edition of the DSM was released in 1980 that the disorder was formally identified as “ADD (Attention-Deficit Disorder) with or without hyperactivity.”[1] In 1937, Rhode Island physician Dr. Charles Bradley pioneered the use of medications to treat ADHD. Since that time, the prescription of stimulants has become a first-line treatment for ADHD.[2]

Historical Perspective

Discovery

  • In 1798, Scottish physician Sir Alexander Crichton published “On Attention and its Diseases,” which contains one of the earliest recorded mentions of a disorder resembling our modern conception of ADHD. In his book, Crichton spoke of a disorder characterized by an “incapacity of attending with a necessary degree of constancy to any one object.”[1][3]
  • In 1844, the German physician Heinrich Hoffmann published a series of illustrated children’s stories including a character called “Fidgety Phil” (“Zappelphilipp”), who has become a popular representation of children with ADHD. Hoffmann was known for his efforts to improve the living conditions of psychiatric patients.[1][3]
  • In 1902, British pediatrician Sir George Frederic Still delivered a series of Goulstonian Lectures to the Royal College of Physicians of London “On Some Abnormal Psychical Conditions in Children,” in which he discussed ADHD extensively. In his Goulstonian Lectures, Still discussed “the particular psychical conditions (…) which are concerned with an abnormal defect of moral control in children.” He defined moral control as “the control of action in conformity with the idea of the good of all.”
  • Still divided these cases in two groups, children with a “morbid defect of moral control associated with physical disease,” such as a brain tumor, meningitis, epilepsy, head injury or typhoid fever, and children with a “defect of moral control as a morbid manifestation, without general impairment of intellect and without physical disease.” Some patients of the latter group, however, showed a “history of severe cerebral disturbance in early infancy.” This differentiation was the origin of later concepts of brain damage, minimal cerebral dysfunction, and hyperactivity as historical precursors to ADHD.
  • Further, Still observed the higher incidence of ADHD in boys as compared to girls that remains a hallmark of the disorder today.[1][3]

Landmark Events in the Development of Treatment Strategies

  • In 1937, Dr. Charles Bradley of Providence, RI was the first to discover that children with behavioral problems improved after being treated with stimulants.[3] In 1954, the stimulant methylphenidate was marketed as (Ritalin); it remains one of the most widely prescribed medications for ADHD. Initially, the drug was used to treat narcolepsy, fatigue, depression, and to counter the sedative effect of certain other medications. Use of the drug to treat ADHD steadily rose over time.[2][3]
  • In 1975, Pemoline (Cylert) was approved by the FDA for use in the treatment of ADHD. While Pemoline proved effective for managing the symptoms associated with ADHD, the development of liver failure in 14 cases over the next 27 years caused the manufacturer to withdraw this medication from the market. In 1999, new delivery systems for medications were invented that eliminated the need for multiple doses across the day. 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 liquid methylphenidate 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 treating ADHD. In 2007, Lisdexamfetamine became the first prodrug to receive FDA approval for ADHD. The Multimodal Treatment Study of ADHD (MTA Study) 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.
  • The use of stimulants to treat ADHD rose slowly but steadily between 1996 and 2008, going from a prevalence rate among youth of 0.6 percent in 1987 to 2.7 percent in 1997, with the rate stabilizing around 2.9 percent in 2002. Overall, prescription use among 6-12-year-olds was found to be the highest, going from 4.2 percent in 1996 to 5.1 percent in 2008. But the fastest growth of prescribed use occurred among 13-18-year-olds, going from 2.3 percent in 1996 to 4.9 percent in 2008.[4]

Impact on Cultural History

  • In 1918–19, the world-wide influenza pandemic left many survivors with encephalitis, which affected their neurological functions. Some survivors exhibited immediate behavioral problems which may correspond to our modern conception of 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.[5]) This caused a significant rift in the understanding of the disorder. Europeans saw hyperkinesis as unusual and often associated it with mental retardation, brain damage, and conduct disorder, and changes to the ICD were not made until 1994. In 1966,, following observations that the condition existed without any objectively observed pathological disorder or injury, researchers in the United States changed the terminology from Minimal Brain Damage to Minimal Brain Dysfunction. A study by two anthropologists looked at the way laypersons talk about ADHD, and found five thematic patterns: “(1) appropriating the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) descriptors; (2) schools as identity-construction sites; (3) resistance: biology versus moral culpability; (4) alternative solutions to a real problem; and (5) relief and hope in naming experience.”[6]

Famous Cases

  • Many famous people have shared their experiences after being diagnosed with ADHD. Such celebrities include Terry Bradshaw, Richard Branson, Jim Carrey, James Carville, Ryan Gosling, Woody Harrelson, Michael Phelps, and Solange Knowles.[7]

References

  1. ↑ 1.0 1.1 1.2 1.3 Lange, K. W., Reichl, S., Lange, K. M., Tucha, L., & Tucha, O. (2010). The history of attention deficit hyperactivity disorder. Attention Deficit and Hyperactivity Disorders, 2(4), 241–255. http://doi.org/10.1007/s12402-010-0045-8.
  2. ↑ 2.0 2.1 Strohl, M. P. (2011). Bradley’s Benzedrine Studies on Children with Behavioral Disorders. The Yale Journal of Biology and Medicine, 84(1), 27–33.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Lange KW, Reichl S, Lange KM, Tucha L, Tucha O (2010). “The history of attention deficit hyperactivity disorder”. Atten Defic Hyperact Disord. 2 (4): 241–55. doi:10.1007/s12402-010-0045-8. PMC 3000907. PMID 21258430.
  4. ↑ Zuvekas, S. H., & Vitiello, B. (2012). Stimulant Medication Use among U.S. Children: A Twelve-Year Perspective. The American Journal of Psychiatry, 169(2), 160–166.
  5. ↑ Classification of ADHD through History. Retrieved on 2006-09-15.
  6. ↑ Danforth, Scot (2001). “Hyper Talk: Sampling the Social Construction of ADHD in Everyday Language”. Anthropology & Education Quarterly. 32 (2): 167–190. Retrieved 2008-04-07. Unknown parameter |coauthors= ignored (help)
  7. ↑ “Famous People with ADHD.” (2016). Adult Attention Deficit Disorder Center of Maryland.


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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Haleigh Williams, B.S.

Overview

ADHD may be classified according to the DSM V criteria into three subgroups: predominantly inattentive type, predominantly hyperactive-impulsive type, and combined type.[1]

Classification

ADHD may be classified according to the DSM V criteria into three subgroups: predominantly inattentive type, predominantly hyperactive-impulsive type, and combined type. Distinctions are made according to the following criteria:[1]

  1. ADHD Combined Type: ≥6 symptoms of hyperactivity/impulsivity and inattention have been observed for ≥6 months
  2. ADHD Predominantly Inattentive Type: ≥6 symptoms of inattention (but <6 symptoms of hyperactivity/impulsivity) have been present for ≥6 months
  3. ADHD Predominantly Hyperactive-Impulsive Type: ≥6 symptoms of hyperactivity/impulsivity (but <6 symptoms of inattention) have been present for ≥6 months

For detailed descriptions of the symptoms of hyperactivity/impulsivity and inattention used in the diagnosis of ADHD, refer to the Attention-deficit hyperactivity disorder diagnostic criteria page.

The terminology of ADD expired with the release of the fifth edition of the DSM in 2013. ADHD is the term currently used to describe one distinct disorder which can manifest itself as hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type), inattention (ADHD predominately inattentive type), or both (ADHD combined type).

Classification Based on Neurological and Psychiatric Factors

References

  1. ↑ 1.0 1.1 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. ↑ Brain Matures A Few Years Late In ADHD, But Follows Normal Pattern
  3. ↑ LONI: Laboratory of Neuro Imaging
  4. ↑ 4.0 4.1 ICD Version 2006: F91. World Health Organization. Retrieved on December 11, 2006.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Haleigh Williams, B.S.

Overview

ADHD appears to be highly heritable, although one-fifth of all cases are caused by trauma or exposure to toxins. Evidence suggests that ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology.[1] Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are a molecular abnormality of ADHD or a secondary consequence of ADHD.

Pathophysiology

Pathogenesis

  • The exact pathogenesis of ADHD is not fully understood. It is believed that ADHD is caused by a complex interaction between genetic and environmental factors.[2] A meta-analysis of studies of functional and structural magnetic resonance imaging has identified several pathologies[3].

Genetics

  • Common genetic variation accounts for around 75% of cases of ADHD.[4] Loci on chromosomes 7, 11, 12, 15, 16, and 17 are associated with ADHD, likely indicating that ADHD does not follow the traditional model of an hereditary disease.[2]

Dopamine Levels and Blood Circulation

  • It is likely not the dopamine transporter levels that indicate the presence of ADHD, but the brain’s ability to produce dopamine itself. ADHD patients show lower levels of dopamine than healthy subjects across the board. Further, plasma homovanillic acid, an index of dopamine levels, is inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to “childhood learning problems” in healthy subjects as well.[10]

Glucose Metabolism

  • 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, but rather 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.[11] ADHD symptoms are likely the result of impaired activity in specific regions of the brain, rather than a broad, global deficit.
PET scans of glucose metabolism in the brains of a normal adult (left) compared to an adult diagnosed with ADHD (right).[11] “This PET scan was taken from Zametkin’s landmark 1990 study, which found lower glucose metabolism, in the brains of patients with ADHD who had never taken medication. Scans were taken while patients were engaging in tasks requiring focused attention. The greatest deficits were found in the premotor cortex and superior prefrontal cortex.”

Associated Conditions

References

  1. ↑ Barkley, Russel A. “Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity”. Retrieved 2006-06-26.
  2. ↑ 2.0 2.1 M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). “Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?”. Genetics in Medicine 6 (1): 1–15.
  3. ↑ Norman LJ, Carlisi C, Lukito S, Hart H, Mataix-Cols D, Radua J; et al. (2016). “Structural and Functional Brain Abnormalities in Attention-Deficit/Hyperactivity Disorder and Obsessive-Compulsive Disorder: A Comparative Meta-analysis”. JAMA Psychiatry. 73 (8): 815–825. doi:10.1001/jamapsychiatry.2016.0700. PMID 27276220.
  4. ↑ 4.0 4.1 Cross-Disorder Group of the Psychiatric Genomics Consortium. “Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs.” Nat Genet. (2013). 45(9):984-94. doi: 10.1038/ng.2711. Epub 2013 Aug 11.
  5. ↑ Briars, L., & Todd, T. (2016). A Review of Pharmacological Management of Attention-Deficit/Hyperactivity Disorder. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 21(3), 192–206. http://doi.org/10.5863/1551-6776-21.3.192
  6. ↑ M. F. Wells, R. D. Wimmer, L. I. Schmitt, G. Feng, M. M. Halassa. (2016). “Thalamic reticular impairment underlies attention deficit in Ptchd1Y/− mice.” Nature 532: 58-63.
  7. ↑ 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
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 11.0 11.1 Zametkin AJ, Nordahl TE, Gross M, et al. “Cerebral glucose metabolism in adults with hyperactivity of childhood onset.” N Engl J Med. 1990 November 15;323(20):1361–6. PMID 2233902
  12. ↑ National Institute of Mental Health (NIH). (2016). “Attention Deficit Hyperactivity Disorder.”

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Haleigh Williams, B.S.

Overview

There are no established causes of ADHD. Studies suggest that ADHD results from a complex interaction between genetic and environmental factors.[1]

Causes

  • There are no established causes of ADHD. ADHD likely results from an interaction between genetic factors and external factors, including trauma or exposure to toxins. The genetic component of the disease has been demonstrated by the increased likelihood that a person for whom ADHD runs in his/her family is more likely to have ADHD than a person with no family history of ADHD. There is also a familial transmission of ADHD which does not occur through adoptive relationships. Twin studies indicate that the disorder is highly heritable and that genetics account for about three quarters of the total ADHD population, leaving the contribution of non-genetic factors at around 25%.[1]
  • A link has been identified between traumatic brain injury and the onset of ADHD-like symptoms in some adults. Brain injury may be one possible non-genetic cause of ADHD.[2]

References

  1. ↑ 1.0 1.1 OurMed. (2010). “Attention-deficit hyperactivity disorder.”
  2. ↑ Ilie G, Vingilis ER, Mann RE, Hamilton H, Toplak M, Adlaf EM; et al. (2015). “The association between traumatic brain injury and ADHD in a Canadian adult sample”. J Psychiatr Res. 69: 174–9. doi:10.1016/j.jpsychires.2015.08.004. PMID 26343610.

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Differentiation Attention-Deficit Hyperactivity Disorder from Other Diseases

Differentiation Attention-Deficit Hyperactivity Disorder from Other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Kiran Singh, M.D. [3], Haleigh Williams, B.S.

Overview

ADHD must be differentiated from other diseases that cause behavioral issues and anxiety such as anxiety disorder, dissociative disorder, conduct disorder, and oppositional defiant disorder. ADHD must also be differentiated from the other psychiatric disorders with which it shares common genetic roots, including autism, bipolar disorder, major depression, and schizophrenia.[1]

Differential Diagnosis

ADHD must be differentiated from:[1][2]

References

  1. ↑ 1.0 1.1 Cross-Disorder Group of the Psychiatric Genomics Consortium. (2013). Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet, 381(9875), 1371–1379. http://doi.org/10.1016/S0140-6736(12)62129-1.
  2. ↑ Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2], Haleigh Williams, B.S.

Overview

The prevalence of attention-deficit hyperactivity disorder (ADHD) is estimated to be 5,000 per 100,000 (5%) children and 2,500 per 100,000 (2.5%) adults.[1] Boys are more commonly affected by ADHD than girls. The male to female ratio is 2 to 1.[2]

Epidemiology and Demographics

Prevalence

  • The prevalence of ADHD in children is 5,000 per 100,000 (5%) of the overall population.[1]
  • The prevalence of ADHD in adults is 2,500 per 100,000 (2.5%) of the overall population.[1] The prevalence of diagnosis is increasing in adults to 354 per 1000,000 in 2011[3].

Incidence

  • The percentage of children age 4-17 years diagnosed with ADHD increased from 7.8 percent in 2003 to 11 percent in 2011.[4][5]

Age

  • ADHD is usually first diagnosed in school-aged children. For an adult to be diagnosed with ADHD, the patient’s symptoms must have been present prior to the age of 12.[6] However, the average age at diagnosis is 7 years.[5]

Gender

  • ADHD is more prevalent in males than in females. The male to female ratio is approximately 2 to 1.[2]

Race

  • ADHD is observed in patients of all racial/ethnic backgrounds, but does appear to be most common in non-Hispanic Caucasians.[2]

References

  1. ↑ 1.0 1.1 1.2 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. ↑ 2.0 2.1 2.2 Briars, L., & Todd, T. (2016). A Review of Pharmacological Management of Attention-Deficit/Hyperactivity Disorder. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 21(3), 192–206. http://doi.org/10.5863/1551-6776-21.3.192.
  3. ↑ Polyzoi M, Ahnemark E, Medin E, Ginsberg Y (2018). “Estimated prevalence and incidence of diagnosed ADHD and health care utilization in adults in Sweden – a longitudinal population-based register study”. Neuropsychiatr Dis Treat. 14: 1149–1161. doi:10.2147/NDT.S155838. PMC 5944447. PMID 29765219.
  4. ↑ Zuvekas SH, Vitiello B (2012). “Stimulant medication use in children: a 12-year perspective”. Am J Psychiatry. 169 (2): 160–6. doi:10.1176/appi.ajp.2011.11030387. PMC 3548321. PMID 22420039.
  5. ↑ 5.0 5.1 Center for Disease Control and Prevention http://www.cdc.gov/ncbddd/adhd/data.html Accessed on Oct 14, 2016.
  6. ↑ National Institute of Mental Health (NIH). (2016). “Attention Deficit Hyperactivity Disorder.”

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2], Haleigh Williams, B.S.

Overview

Common risk factors in the development of attention-deficit hyperactivity disorder (ADHD) are child abuse, infections of the central nervous system, epilepsy, and traumatic brain injury.

Risk Factors

Common risk factors in the development of ADHD are:[1][2]

References

  1. ↑ Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. ↑ National Institute of Mental Health (NIH). (2016). “Attention Deficit Hyperactivity Disorder.”

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2], Haleigh Williams, B.S.

Overview

If left untreated, patients with ADHD may experience negative social consequences, such as isolation from and difficulty communicating with friends and loved ones. Patients are unlikely to experience any physical problems as a direct result of ADHD.[1]

Natural History

  • The symptoms of ADHD usually develop in the first decade of life, and can appear as early as between the ages of 3 and 6. The symptoms of ADHD often continue through adolescence and adulthood.[2] The average age of onset of ADHD is 7 years.[3]
  • Military recruits who do not require medications to finish high school or to hold a job may have similar military performance as recruits without ADHD.[4]

Negative consequences

  • If left untreated, ADHD may cause negative social consequences, such as isolation from and difficulty communicating with friends and loved ones. ADHD patients are unlikely to experience any physical problems as a direct result of ADHD.[1]
  • Without treatment, the patient will likely continue exhibiting symptoms of hyperactivity, impulsivity, and inattention, which can bear negative academic, professional, and social consequences. Adolescents with untreated ADHD have a higher incidence of drug abuse and law-breaking than healthy children.[1]
  • There are significant adverse socioeconomic outcomes from ADHD.[5][6][7] Young adults with ADHD have more financial dependence on family members and public assistance. They may earn $543,000-$616,000 less over their lifetimes[7]. Teenage males are more likely to have automobile accidents.[8]
  • Employees with ADHD may experience less meaningfulness at work[9].
  • Mortality may be increased.[10]f>

Positive consequences

Employees with ADHD may have improved idea generation at work, but this is offset by less feeling of meaningfulness at work[9].

Complications

  • Complications that can develop as a result of ADHD are poor grades for schoolchildren or poor progress reports/possible termination for working adults.[1]

Prognosis

  • The prognosis of ADHD is poor with treatment. Without treatment, ADHD often results in negative social and academic/professional consequences. Approximately 70% of patients who are diagnosed with ADHD as children continue to experience severe symptoms throughout adolescence and sometimes into adulthood.[1]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Briars, L., & Todd, T. (2016). A Review of Pharmacological Management of Attention-Deficit/Hyperactivity Disorder. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 21(3), 192–206. http://doi.org/10.5863/1551-6776-21.3.192
  2. ↑ National Institute of Mental Health (NIH). (2016). “Attention Deficit Hyperactivity Disorder.”
  3. ↑ Kessler RC, Chiu WT, Demler O, Walters EE. (2005). Prevalence, severity, and comorbidity of twelve-month DSM-IV disorders in the National Comorbidity Survey Replication (NCS-R). Archives of General Psychiatry, 62(6):617-27.
  4. ↑ Wingo AP, Ghaemi SN (2007). “A systematic review of rates and diagnostic validity of comorbid adult attention-deficit/hyperactivity disorder and bipolar disorder”. J Clin Psychiatry. 68 (11): 1776–84. PMID 18052572.
  5. ↑ Biederman J, Faraone SV (2006). “The effects of attention-deficit/hyperactivity disorder on employment and household income”. MedGenMed. 8 (3): 12. PMID 17406154.
  6. ↑ Mannuzza S, Klein RG, Bessler A, Malloy P, Hynes ME (1997). “Educational and occupational outcome of hyperactive boys grown up”. J Am Acad Child Adolesc Psychiatry. 36 (9): 1222–7. PMID 9291723.
  7. ↑ 7.0 7.1 Altszuler AR, Page TF, Gnagy EM, Coxe S, Arrieta A, Molina BS; et al. (2016). “Financial Dependence of Young Adults with Childhood ADHD”. J Abnorm Child Psychol. 44 (6): 1217–29. doi:10.1007/s10802-015-0093-9. PMC 4887412. PMID 26542688.
  8. ↑ Redelmeier DA, Chan WK, Lu H, 2010 Road Trauma in Teenage Male Youth with Childhood Disruptive Behavior Disorders: A Population Based Analysis. PLoS Med 7(11): e1000369. doi:10.1371/journal.pmed.1000369
  9. ↑ 9.0 9.1 Steele, Logan M.; Pindek, Shani; Margalit, Ofra (2021). “The Advantage of Disadvantage: Is ADHD Associated with Idea Generation at Work?”. Creativity Research Journal: 1–9. doi:10.1080/10400419.2021.1916368. ISSN 1040-0419.
  10. ↑ Dalsgaard, Søren; Øtergaard, Søren Dinesen; Leckman, James F; Mortensen, Preben Bo; Pedersen, Marianne Giørtz. “Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study”. The Lancet. doi:10.1016/S0140-6736(14)61684-6.
  11. ↑ Vitiello B, Elliott GR, Swanson JM, Arnold LE, Hechtman L, Abikoff H; et al. (2012). “Blood pressure and heart rate over 10 years in the multimodal treatment study of children with ADHD”. Am J Psychiatry. 169 (2): 167–77. doi:10.1176/appi.ajp.2011.10111705. PMC 4132884. PMID 21890793.
  12. ↑ “DrugBank: Methylphenidate”.
  13. ↑ “DrugBank: Guanfacine”.
  14. ↑ “DrugBank: Clonidine”.
  15. ↑ Garnock-Jones KP, Keating GM (2009). “Atomoxetine: a review of its use in attention-deficit hyperactivity disorder in children and adolescents”. Paediatr Drugs. 11 (3): 203–26. doi:10.2165/00148581-200911030-00005. PMID 19445548.
  16. ↑ Michelson D, Adler L, Spencer T, Reimherr FW, West SA, Allen AJ, Kelsey D, Wernicke J, Dietrich A, Milton D (2003). “Atomoxetine in adults with ADHD: two randomized, placebo-controlled studies”. Biol. Psychiatry. 53 (2): 112–20. PMID 12547466.

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Diagnosis

Diagnosis

Diagnostic Criteria | Rating scales for diagnosis | History and Symptoms | Physical Examination | Laboratory Findings | Imaging Findings

Treatment

Treatment

Combination Therapy | Medical Therapy | Psychotherapy | Brain Stimulation Therapy | Future or Investigational Therapies | Cost-Effectiveness of Therapy | Monitoring Response to Therapy

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