Attention deficit disorders

Attention-deficit hyperactivity disorder (ADHD), otherwise known as hyperkinetic disorder, is a neurodevelopmental condition characterised by problems with impulsivity, hyperactivity, and/or inattention^1,2. For example, children with ADHD may blurt out answers in the classroom, fidget and find it impossible to keep still and struggle to focus on what a person is saying.

For a diagnosis of ADHD to be given, the symptoms must be functionally impairing and occur in at least two distinct settings (e.g. at home, and at school).

ADHD is the most common psychiatric disorder of childhood, affecting at least 5% of children globally. Symptoms persist into adulthood in up to 60% of childhood cases³.

Considerable research has examined the long-term consequences of ADHD, highlighting its global importance for society. In a systematic review of the data, untreated ADHD was associated with poorer long-term outcomes across all categories considered: these included academic performance, job performance/employment status, self-esteem, quality of life, and risk of driving accidents⁴.

The disorder is economically costly: the national annual incremental cost of ADHD in the USA has been estimated at $143 to $266 billion; most of these costs are in adult patients, including loss of productivity and income⁵.

 

Pathology and functional impact of ADHD

As with most psychiatric disorders, the brain basis of ADHD is incompletely understood. The heritability of ADHD is quite high, around 70-80%, suggesting that genetic factors are very important⁶. There is no singular ‘genetic cause’, but rather multiple genes are likely to confer risk or vulnerability towards developing the condition, especially genes involved in the regulation of cognition and fronto-striatal brain circuitry, such as those relating to the dopamine and noradrenaline/norepinephrine neurochemical pathways⁷.

Current biological models for ADHD emphasise dysregulation of brain regions including the prefrontal cortex, anterior cingulate cortex, superior parietal cortex, caudate, and cerebellum^8,9.

The core symptom domains of ADHD, namely inattention, hyperactivity, and impulsivity, implicate cognitive dysfunction. Given the implicated brain regions above, it is perhaps not surprising that patients often experience problems across a range of cognitive functions as measured by objective tests10.

In terms of neurochemical involvement in ADHD, the dopamine and noradrenaline/norepinephrine systems have been particularly implicated, not only as a consequence of gene studies but also in terms of why certain treatments are effective but others are not^11,12.

 

Research and development in ADHD

ADHD is a treatable psychiatric disorder, with medium to large effect sizes in terms of symptomatic improvement, versus control conditions, over the short-medium term⁷.

Affected individuals should be offered a multidisciplinary approach, by a team specialising in the disorder. In-depth specialist assessment is vital, as ADHD is often misdiagnosed, and is frequently comorbid with other mental (and physical health) disorders. First-line treatment options for ADHD can include consideration of psychotherapy and/or medication, but these should always be offered as part of a comprehensive package of care. The most appropriate treatment options and sequencing of treatment options can vary considerably depending on factors such as the age of the individual, severity of disease, and patient/family preference. 

For example, NICE guidelines16 recommend group-based parent-training/education programmes for parents and carers of school-aged children with moderately severe ADHD. Younger school-aged children with moderate ADHD may benefit from group psychological treatment with cognitive behavioural therapy (CBT) and/or social skills training; while older school-aged children with moderate ADHD may benefit from individual psychological treatment if group approaches are not preferred, or are ineffective. For school-aged children with severe ADHD, psychostimulant medication (e.g. methylphenidate) is regarded as the first-line treatment, with parents also being offered a group-based intervention. Medication is recommended as first-line treatment in adults with ADHD unless the person would prefer a psychological treatment.

While effective treatments are available for ADHD, many individuals cannot tolerate particular medications due to side effects and/or the need for physical health monitoring, or symptoms do not improve sufficiently¹³. Another limitation is that while the negative longer-term consequences of ADHD can be reduced by optimal treatment, currently available treatments do not completely normalise these risks, and hence there is scope for further improvement⁴. For example, current treatments may ameliorate cognitive impairment in people with ADHD, but not remove it completely. Another key area of ongoing research is the search for objective markers capable of identifying, for a given individual, treatment options that are most likely to be effective and well-tolerated. 

 

You might also be interested in…

Shaw M., et al (2012). A systematic review and analysis of long-term outcomes in attention deficit hyperactivity disorder: effects of treatment and non-treatment. BMC Med. 2012 Sep 4;10:99.

Biederman J., et al (2005). Attention-deficit hyperactivity disorder. Lancet. 2005 Jul 16-22;366(9481):237-48.

Chamberlain S.R., et al (2011). Translational approaches to frontostriatal dysfunction in attention-deficit/hyperactivity disorder using a computerized neuropsychological battery. Biol Psychiatry. 2011 Jun 15;69(12):1192-203.

Seixas M., et al (2012). Systematic review of national and international guidelines on attention-deficit hyperactivity disorder. J Psychopharmacol. 2012 Jun;26(6):753-65.

 

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1. _{American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-5. Washington, D.C: American Psychiatric Association.}
2. _{World Health Organization. (1992). The ICD-10 classification of mental and behavioural disorders: clinical descriptions and diagnostic guidelines. Geneva, World Health Organization.}
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4. _{Shaw M, Hodgkins P, Caci H, Young S, Kahle J, Woods AG, Arnold LE. A systematic review and analysis of long-term outcomes in attention deficit hyperactivity disorder: effects of treatment and non-treatment. BMC Med. 2012 Sep 4;10:99.}
5. _{Doshi JA, Hodgkins P, Kahle J, Sikirica V, Cangelosi MJ, Setyawan J, Erder MH, Neumann PJ. Economic impact of childhood and adult attention-deficit/hyperactivity disorder in the United States. J Am Acad Child Adolesc Psychiatry. 2012 Oct;51(10):990-1002.e2.}
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9. _{Kasparek T, Theiner P, Filova A. Neurobiology of ADHD From Childhood to Adulthood: Findings of Imaging Methods. J Atten Disord. 2015 Nov;19(11):931-43. 2013 Oct 4.}
10. _{Chamberlain SR, Robbins TW, Winder-Rhodes S, Müller U, Sahakian BJ, Blackwell AD, Barnett JH. Translational approaches to frontostriatal dysfunction in attention-deficit/hyperactivity disorder using a computerized neuropsychological battery. Biol Psychiatry. 2011 Jun 15;69(12):1192-203.}
11. _{Brennan AR, Arnsten AF. Neuronal mechanisms underlying attention deficit hyperactivity disorder: the influence of arousal on prefrontal cortical function. Ann N Y Acad Sci. 2008;1129:236-45.}
12. _{Del Campo N, Chamberlain SR, Sahakian BJ, Robbins TW. The roles of dopamine and noradrenaline in the pathophysiology and treatment of attention-deficit/hyperactivity disorder. Biol Psychiatry. 2011 Jun 15;69(12):e145-57.}
13. _{Sharma A, Couture J. A review of the pathophysiology, etiology, and treatment of attention-deficit hyperactivity disorder (ADHD). Ann Pharmacother. 2014 Feb;48(2):209-25.}