Disease Site

Attention deficit hyperactivity disorder (ADHD) is a neuro-behavioural syndrome characterised by hyperactivityimpulsivity and/or inattention.1-4 While these symptoms are experienced by all people from time to time, they are severe and persistent in those with ADHD, and therefore interfere with these individuals’ normal functioning.1,2,4,5
Children with ADHD have difficulty carrying out tasks which require focus, such as homework, and have difficulty establishing positive relationships with others.3
Caring for children with the condition can also be disruptive to family life, often causing considerable stress for parents, siblings and others who live with children who have ADHD.5


Estimates of the incidence of ADHD in children and adolescents vary from 1.7% to 17.8%; however, most estimates lie within 5–10%.4 A recent epidemiological analysis of international data reported a global prevalence of 5.3%.6 Boys are significantly more likely to be diagnosed with ADHD than girls, with at least four of every five cases of ADHD occurring in boys.4 The incidence in different communities (e.g. Australia vs. United States) is thought to vary, although the variation in the reported incidence could be due to the method and criteria used to assess ADHD.4
The Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) sets out standard criteria for ADHD diagnosis, which are now recommended for use in Australian settings.5 Recent research which used the DSM-IV criteria has revealed that almost 9% of American children have ADHD. However, less than half had been diagnosed by a health professional and less than a third were receiving appropriate treatment. Thus, there are likely many undiagnosed cases in the community.1
In Australia, the National Survey of Mental Health and Wellbeing reported that 11% of the child and adolescent population fulfil the criteria for ADHD.7 On a national basis, 0.5% of 4– 17-year-olds were prescribed stimulant medications to treat the condition between June 2006 and May 2007. The proportion of children prescribed stimulants varied between states (e.g. in NSW, 1.5% of 4– 17-year-olds were prescribed stimulants in the period). Similar to other countries, the vast majority of ADHD cases treated were amongst boys. In the 2006–07 period, 15,466 males were prescribed stimulant medication, compared to 3872 females, a ratio of ~4:1.8
There has been an increase in the reported number of children with ADHD, and subsequently the prescription of stimulant medications, in the past decade.1,2 For example, in Australia from 1984 to 2000, the number of scripts issued for stimulant medications to treat ADHD increased by an average of 31% per year. However, the proportion of children prescribed stimulant medication remains below the proportion of children with ADHD; this apparent increase in the rate of reported cases of ADHD is due to increased awareness amongst health professionals and the public on the condition.9

Predisposing Factors

The exact cause of ADHD is unknown, but several factors have been implicated in their association with ADHD development.

Genetic factors

Genetic influence is possible, as ADHD is known to run in families. Identical twins are more likely to both be affected than non-identical twins.2,8
Family studies show that 10-35% of immediate family members of children with ADHD are likely to have the disorder, and the risk to siblings is 35%.10 Clinical data from over 20 international twin studies indicate that the heritability of ADHD is 76%.10 While the rate of ADHD is about 5% in the general population, about 25% of close relatives to families with ADHD children also have ADHD.2
ADHD is a complex trait which makes identifying specific genes associated with the disorder difficult. An example to highlight this complexity is the recent discovery that certain genes are associated with different ADHD subtypes. In addition, symptom severity is affected by interactions between certain ADHD risk genes and environmental factors. There have been over 215 genes associated with ADHD so far, yet none of the gene variations currently studied have presented as sole mediators of the disorder. Essentially a complex genetic architecture is strongly believed to underlie the aetiology of ADHD.11
That being said, some genes have been identified as predisposing factors to the disorder. Genetic research to date has focused largely on dopaminergic genes due to the hypothesised influence of dopamine in behavioural disorders and as a target for ADHD treatment. Increased levels of dopamine activity are also seen during neuroimaging of the ADHD brain.12 Underlying genetic mutations have also been evidenced, which explains why families can be significantly similar in their ADHD presentation. Meta-analyses have confirmed genetic associations to ADHD for the D4 dopamine receptor (DRD4), DBH and the D5 dopamine receptor (DRD5).13
Decreased serotonin is associated with poor arousal and, accordingly, a subset of serotonergic genes have also been identified as promising candidate genes, including the serotonin transporter gene and the serotonin 2A receptor gene.12
Not all individuals with the genetic predisposition to ADHD will develop the disorder; environmental factors are a critical mediating factor.14

Environmental and family factors

Children who have a genetic predisposition are more likely to express symptoms of the disorder when exposed to certain environments.5
Exposure during pregnancy to cigarettes, alcohol and other substances (e.g. cocaine) may increase the risk of ADHD. Preschool children with higher levels of lead in their bodies are also at a higher risk of developing ADHD.2
Chaotic parenting may increase the risk of developing ADHD, but the relationship between ADHD and parenting may result from both negative aspects of the child influencing the parents’ behaviour, as well as the parents influencing the child’s behaviour.  The behaviour of parents who are more demanding, aversive, negative, controlling, intrusive, disapproving, power assertive and less rewarding has been shown to exacerbate ADHD symptoms.5
Children from lower socioeconomic classes have higher rates of ADHD and are more likely to be undertreated for their disorder. The increased rates of ADHD in poorer children is thought to relate to varying exposure to certain risk factors (e.g. in utero tobacco exposure, childhood lead exposure, complications of pregnancy and delivery). In addition, the heritable nature of ADHD and its negative impact on social, academic and career outcomes may cause ADHD sufferers to cluster in lower socioeconomic groups.1
Addressing these predisposing factors should form part of future health prevention strategies.

Congenital factors

Studies have shown a possible link between the use of cigarettes and alcohol during pregnancy, and the risk of ADHD in offspring. Maternal substance abuse (e.g. cocaine, nicotine) may also be associated with ADHD-like symptoms.2
Pregnancy and delivery complications (e.g. prematurity) have been linked with increased rates of ADHD.1
Acquired brain injury can also increase the risk of ADHD.15

Brain structure factors

Some studies suggest that ADHD is caused by a compromised structure in areas of the brain that relate to inhibition and attention. Studies show that the brain circuits linking the prefrontal cortex, striatum and cerebellum are malfunctioning in children with ADHD.11
Another study, a case-control study of ADHD children matched by age and sex to non-ADHD controls, reported reduced brain size amongst ADHD children, mainly in the posterior but also in the anterior regions of the brain. The study used magnetic resonance imaging to map regional brain size and grey matter abnormalities. It also reported prominent increases in grey matter in the posterior temporal and inferior parietal cortices bilaterally.16

Neurophysiological factors

ADHD symptoms may be a result of cognitive deregulation, where the child’s behaviour results from insufficient forethought, planning and control, and leads to impulsive responses and higher error rates.5
Another explanation of the impulsive response is the ‘delay aversion’ hypothesis, in which the child makes a more impulsive response because it allows the faster completion of a task, and therefore avoids delay.5
In a situation where the child is not in control (e.g. in a classroom where he/she is expected to behave in a certain way), the child could achieve control by either daydreaming (inattention) or by fidgeting (hyperactivity).5

Dietary factors

ADHD has been linked to the intake of food additives, food colourings and refined sugar. These substances have been shown to exacerbate ADHD symptoms. Diets that exclude foods containing substances which exacerbate behavioural problems, such as the Australian-developed FAILSAFE diet, have been used to treat ADHD since the 1980s.17 While the association between diet and ADHD symptoms is clear, dietary interventions alone have proven insufficient to treat the symptoms of ADHD, and are best used in combination with pharmacological and educational interventions.5
Children with iron deficiency have more severe symptoms of ADHD than those without iron deficiency.18

Microscopic Features

ADHD brains differ significantly in level of brain activity, size and functioning.21Impairment or dysfunction, as evidenced by neuroimaging research of the prefrontal cortex, the basal ganglia and the cerebellum, results in deficits in attention and executive functioning.22

Natural History

ADHD usually begins before preschool age. Some parents may suspect it and seek help, but for most it goes unnoticed until the child experiences problems at school. Occasionally, teachers may be the first to recognise that the child has a problem, and subsequently point it out to the parents or school psychologist. Once developed, many children outgrow ADHD in adolescence or early adulthood, but for others it may persist as adult ADHD.2

For more information on ADHD in adults, see Adult ADHD.

Clinical History

The principal signs and symptoms of ADHD are:4

  • Impulsivity: Children seem unable to curb their immediate reactions or think before they act;
  • Hyperactivity: Children always seem to be “on the go” or constantly in motion;
  • Inattention: Children have a hard time keeping their minds on any one thing and may quickly become bored with a task.

These symptoms appear early in a child’s life and will occur over the course of many months. Often, impulsivity and hyperactivity precedes inattention, which may not emerge for a year or more. These symptoms appear in different settings (e.g. school, home, the play ground). Children with ADHD may show some or all of the symptomatic behaviours. Hence, there are three subtypes of ADHD:4

  • Predominantly hyperactive-impulsive type: Does not show significant inattention;
  • Predominantly inattentive type: Does not show significant hyperactive-impulsive behaviour;
  • Combined type: Displays both inattentive and hyperactive-impulsive behaviour.

The diagnosis of ADHD in children must meet the Diagnostic and Statistical Manual of Mental Disorders, 4thedition (DSM-IV) criteria.5 These are a minimum of six out of nine symptoms of inattention, and/or a minimum of six out of nine symptoms of hyperactivity/impulsivity. These symptoms must:4

  • Have persisted for at least six months;
  • Be present in two or more different settings;
  • Be present before the age of seven years;
  • Be evident that they are severe and maladaptive and inconsistent with development level;
  • Not be explained by other mental disorders.


Some signs of inattention are when the patient often:2

  • Has difficulty focusing on any one thing;
  • Gets bored with a task in only a few minutes;
  • Does not seem to listen when spoken to directly;
  • Is easily distracted by irrelevant sights and sounds;
  • Has difficulty focusing consciously (e.g. on an activity that they do not like) or learning something new;
  • Has difficulty organising tasks and activities;
  • Avoids or dislikes, or is reluctant to engage in, tasks that require sustained mental effort (e.g. schoolwork or homework);
  • Loses things necessary for tasks (e.g. toys, assignments, pencils, books, tools);
  • Is easily distracted by extraneous stimuli;
  • Is forgetful in daily activities.

Hyperactivity and impulsivity

Some signs of hyperactivity are when the patient often:2

  • Feels restless, fidgets with hands or feet, or squirms while seated;
  • Runs, climbs, or leaves a seat in situations where sitting or quiet behaviour is expected;
  • Has difficulty playing or engaging in leisure activities quietly;
  • Is “on the go”, or acts as if “driven by a motor”.


Some signs of impulsivity are when the patient often:2

  • Blurts out answers before question has been completed;
  • Has difficulty awaiting turns;
  • Interrupts or intrudes on others (e.g. “blurts into” conversations or games);
  • Has difficulty restraining emotions (e.g. anger).


ADHD is associated with other psychiatric conditions, which may occur together. These include:4,8

Clinical Examination

The diagnosis of ADHD must be made by a professional with training in ADHD (e.g. child psychiatrists and psychologists, developmental/behavioural paediatricians, behavioural neurologists). Health professionals should be aware of the symptoms of ADHD and the need for specialist referral, as ADHD has been both under-diagnosed in children in general,  as well as misdiagnosed in children with other behavioural problems (e.g. learning disabilities).2
The diagnosis is based on very specific symptoms which must be present in more than one setting, must have started before 7 years of age, and must have lasted for at least 6 months. The child should have a clinical evaluation if ADHD is suspected.2
Evaluation may include:2

  • Parent and teacher questionnaires (Burks23; Connors,24);
  • Psychological evaluation of the child AND family, including IQ testing and psychological testing;
  • Complete developmental, mental, nutritional, physical and psychosocial examination.

These are done through:2

  • Parent and teacher interviews;
  • Parent and teacher rating scales;
  • Direct observations of behaviour;
  • Academic performance data.

A comprehensive assessment of a child with suspected ADHD should include the following elements:5

  • History: Family, past and current medical, psychosocial;
  • Medical: Physical and neurological examination, and any appropriate investigations;
  • Developmental: To exclude significant specific and/or global problems, hearing and vision difficulties, and to make further referrals as appropriate;
  • Behavioural: Description of behaviour in various settings, especially home and school; and
  • Educational: A review of classroom observations and prior testing, including estimates of intellectual capabilities, strengths and weaknesses and measure of academic achievement, including language development.

Attention-Deficit/Hyperactivity Disorder (ADHD) Evaluation Tool

  1. Does your child fail to pay attention to details during tasks? For example, a teacher may have reported careless errors in schoolwork.
    1. Yes
    2. Not more than other children of the same age
  2. Does your child have trouble sustaining attention during tasks or games? For example, they appear to easily lose interest and become distracted.
    1. Yes
    2. Not more than other children of the same age
Click here to complete the survey
This information will be collected for educational purposes, however, it will remain anonymous.

Symptoms of This Disease:

Specific Investigations

Further investigations, such as brain imaging and neurophysiological tests, are not recommended as part of the routine assessment of ADHD.5


ADHD is a long-term chronic condition for some children. For other children and adolescents, ADHD improves as they grow up. 30-70% of children with ADHD will continue to have troublesome symptoms of inattention or impulsivity as adults.2


  1. Froehlich TE, Lanphear BP, Epstein JN, et al. Prevalence, recognition, and treatment of attention-deficit/hyperactivity disorder in a national sample of US children.Arch Pediatr Adolesc Med. 2007;161(9):857-64. [Abstract | Full text]
  2. Attention deficit hyperactivity disorder (ADHD): NIH Publication No. 08-3572 [online]. Bethesda, MD: National Institutes of Health; 3 April 2008 [cited 24 December 2008]. Available from: URL link
  3. Medication management for attention deficit hyperactivity disorder: A brief guide for parents and non health professionals [online]. Sydney, NSW: Royal Australasian College of Physicians; 10 July 2006 [cited 24 December 2008]. Available from: URL link
  4. Attention deficit and hyperkinetic disorders in children and young people: A national clinical guidline [online]. Edinburgh, UK: Scottish Intercollegiate Guidelines Network; 29 June 2001 [cited 24 December 2008]. Available from: URL link
  5. Criteria for diagnosis and management of attention deficit hyperactivity disorder in children and adolescents [online]. North Sydney, NSW: New South Wales Government Health; 1 February 2008 [cited 24 December 2008]. Available from: URL link
  6. Polanczyk G, de Lima MS, Horta BL, et al. The worldwide prevalence of ADHD: A systematic review and metaregression analysis. Am J Psychiatry. 2007;164(6):942-8. [AbstractFull text]
  7. Sawyer MG, Kosky RJ, Graetz BW, et al. The National Survey of Mental Health and Wellbeing: The child and adolescent component. Aust NZ J Psychiatry. 2000;34(2):214-20. [Abstract]
  8. Attention deficit hyperactivity disorder in children and adults in New South Wales 2007: Final report of the special review [online]. Sydney, NSW: Clinical Excellence Commission; 2 May 2008 [cited 24 December 2008]. Available from: URL link
  9. Buckmaster L. Research brief no. 2 200405: Medication for attention/deficit hyperactivity disorder (ADHD): An analysis by Federal Electorate (200103) [online]. Canberra, ACT: Australian Parliamentary Library; 16 November 2004 [cited 21 September 2009]. Available from: URL link
  10. Faraone SV, Perlis RH, Doyle AE, et al. Molecular genetics of attention deficit/hyperactivity disorder. Biol Psychiatry. 2005;57(11):1313-23. [Abstract]
  11. Wallis D, Russell HF, Muenke M. Review: Genetics of attention deficit/hyperactivity disorder. J Pediatr Psychol. 2008;33(10):1085-99. [AbstractFull text]
  12. Larsson H, Lichtenstein P, Larsson JO. Genetic contributions to the development of ADHD subtypes from childhood to adolescence. J Am Acad Child Adolesc Psychiatry. 2006;45(8):973-81. [Abstract]
  13. Lowe N, Kirley A, Hawi Z, et al. Joint analysis of the DRD5 marker concludes association with attention-deficit/hyperactivity disorder confined to the predominantly inattentive and combined subtypes. Am J Hum Genet. 2004;74(2):348-56. [AbstractFull text]
  14. Smalley SL, McCracken J, McGough J. Refining the ADHD phenotype using affected sibling pair families. Am J Med Genet. 2001;105(1):31-3. [Abstract]
  15. Gerring JP, Brady KD, Chen A, et al. Premorbid prevalence of ADHD and development of secondary ADHD after closed head injury. J Am Acad Child Adolesc Psychiatry. 1998;37(6):647-54. [Abstract]
  16. Sowell ER, Thompson PM, Welcome SE, et al. Cortical abnormalities in children and adolescents with attention-deficit hyperactivity disorder. Lancet. 2003;362(9397):1699-707. [Abstract]
  17. Swain A, Soutter V, Loblay R, Truswell AS. Salicylates, oligoantigenic diets and behaviour. Lancet. 1985;326(8445):41-2. [Abstract]
  18. Konofal E, Lecendreux M, Arnulf I, Mouren M. Iron deficiency in children with attention-deficit/hyperactivity disorder. Arch Pediatr Adolesc Med. 2004;158(12):1113-5. [AbstractFull text]
  19. Brown TE. Executive functions and attention deficit hyperactivity disorder: Implications of two conflicting views. Int J Disabil Develop Edu. 2006;53(1):35-46. [Abstract]
  20. Pliszka S. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(7):894-921. [AbstractFull text]
  21. Faraone SV. Advances in the genetics and neurobiology of attention deficit hyperactivity disorder. Biol Psychiatry. 2006;60(10):1025-7. [Abstract]
  22. Kieling C, Goncalves RR, Tannock R, Castellanos FX. Neurobiology of attention deficit hyperactivity disorder. Child Adolesc Psychiatr Clin N Am. 2008;17(2):285-307. [Abstract]
  23. Burks HF. Burks’ Behavior Rating Scale: Manual. Los Angeles: Western Psychological Services; 1996. [Publisher]
  24. Conners CK, Sitarenios G, Parker JDA, Epstein JN. The revised Conners’ Parent Rating Scale (CPRS-R): Factor structure, reliability and criterion validity. J Abnorm Child Psychol. 1998;26(4):257-68. [Abstract]
  25. Lubar JF, Swartwood MO, Swartwood JN, O’Donnell PH. Evaluation of the effectiveness of EEG neurofeedback training for ADHD in a clinical setting as measured by changes in T.O.V.A. scores, behavioral ratings, and WISC-R performance. Biofeedback Self Regul. 1995;20(1):83-99. [Abstract]

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