Assignment: Journal Article On ADHD
Assignment: Journal Article On ADHD
1240 www.thelancet.com Vol 387 March 19, 2016
Attention defi cit hyperactivity disorder Anita Thapar, Miriam Cooper
Attention defi cit hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder with a prevalence of 1·4–3·0%. It is more common in boys than girls. Comorbidity with childhood-onset neurodevelopmental disorders and psychiatric disorders is substantial. ADHD is highly heritable and multifactorial; multiple genes and non-inherited factors contribute to the disorder. Prenatal and perinatal factors have been implicated as risks, but defi nite causes remain unknown. Most guidelines recommend a stepwise approach to treatment, beginning with non-drug interventions and then moving to pharmacological treatment in those most severely aff ected. Randomised controlled trials show short-term benefi ts of stimulant medication and atomoxetine. Meta-analyses of blinded trials of non-drug treatments have not yet proven the effi cacy of such interventions. Longitudinal studies of ADHD show heightened risk of multiple mental health and social diffi culties as well as premature mortality in adult life.
Introduction Attention defi cit hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder char ac- terised by developmentally inappropriate and impairing inattention, motor hyperactivity, and impulsivity, with diffi culties often continuing into adulthood. In this Seminar, we aim to update and inform early career clinicians on issues relevant to clinical practice and discuss some controversies and misunderstandings.
Defi nitions of ADHD ADHD is a diagnostic category in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders 4th edition (DSM-IV)1 and the more recent DSM-5.2 The broadly equivalent diagnosis used predominantly in Europe is hyperkinetic disorder, which is defi ned in WHO’s International Classifi cation of Diseases (10th edition; ICD-10).3 This defi nition captures a more severely aff ected group of individuals, since reported prevalence of hyperkinetic disorder is lower than that of DSM-IV ADHD, even
within the same population.4 Key diagnostic criteria are listed in the panel. DSM-5 has longer symptom descriptors than those used in DSM-IV; these descriptors also capture how symptoms can manifest in older adolescents and adults. DSM-IV distinguished between inattentive, hyperactive–impulsive, and combined sub- types of ADHD; a diagnosis of the combined subtype required the presence of symptoms across the domains of inattention and hyperactivity–impulsivity. However, ADHD subtypes are not stable across time,5 and DSM-5 has de-emphasised their distinctions. ICD-10 does not distinguish subtypes; symptoms need to be present from the three separate domains of inattention, hyperactivity, and impulsivity for a diagnosis of hyperkinetic disorder.
The diagnosis of ADHD or hyperkinetic disorder also requires the presence of symptoms across more than one setting (eg, home and school) and requires that the symptoms needed for diagnosis result in impairment, for example in academic, social, or occupational functioning. Onset must be early, although DSM-5 has changed the age of onset from before age 7 years (ICD-10 and DSM-IV) to before age 12 years.
Like all complex medical and psychiatric disorders, ADHD shows marked heterogeneity at clinical, aetiological, and pathophysiological levels. Individuals with a diagnosis of ADHD diff er from each other in terms of their core symptom combinations, level of impairment and comorbidities, as well as on other background individual, family, and social factors.
For clinical purposes, defi ning ADHD categorically is useful given that clinical decisions tend to be categorical in nature—eg, whether to refer to specialist services or to treat. However, like many medical disorders (such as hypertension and diabetes), in terms of causes and outcomes, ADHD can be viewed as a continuously distributed risk dimension. In common with other continuously distributed phenotypes (eg, blood pressure), it could be argued that there is a lack of an objective cut-point that defi nes the diagnostic threshold. Indeed, individuals with subthreshold symptoms are at heightened risk of adverse outcomes6 (as is seen in hypertension). However, ultimately, categorical decisions on resource allocation and treatment have to be made,
Lancet 2016; 387: 1240–50
Published Online September 17, 2015
Child & Adolescent Psychiatry Section, Institute of
Psychological Medicine and Clinical Neurosciences, and
MRC Centre for Neuropsychiatric Genetics and
Genomics, Cardiff University School of Medicine, Cardiff , UK
(Prof A Thapar FRPsych, M Cooper MRCPsych)
Correspondence to: Prof Anita Thapar, Institute of
Psychological Medicine and Clinical Neurosciences, Cardiff
University School of Medicine, Hadyn Ellis Building, Maindy
Road, Cathays, Cardiff CF24 4HQ, UK
Search strategy and selection criteria
To identify studies for this Seminar, we searched PubMed for papers published between Jan 1, 2010, and March 31, 2015, using the search terms “ADHD”, “aetiology”, “epidemiology”, “prevalence”, “gender”, “time trends”, “prescribing”, “genetic”, “prenatal”, “psychosocial”, “toxins”, “institutional rearing”, “longitudinal”, “prognosis”, “animal model”, “biological pathway”, “cognition”, “neuroimaging”, “comorbidity”, “neuropsychological”, “medication”, “stimulants”, “behavioural interventions”, “nonpharmacological interventions”, “diet”, and “outcomes”. Only articles published in English were included. Key recent reviews and book chapters were also examined. To reduce the number of papers cited, the most up-to-date review papers and meta-analyses were used where possible. We selected papers according to our judgment of the quality of the study or review paper, the relevance to controversial or commonly misunderstood issues, and whether fi ndings had clinical relevance. We included older papers that we judged to be important.
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and ICD-defi ned or DSM-defi ned diagnosis provides a reliable way of balancing the risks and benefi ts of giving an individual a diagnostic label and providing treatments that are not free of adverse eff ects. A further challenge, which occurs in all psychiatric disorders and some neurological disorders (eg, migraine), comes from the diagnosis being based on reported symptoms alone; there are no biological tests. This diffi culty means that even with clear-cut diagnostic criteria, there is potential risk of overdiagnosis and underdiagnosis, which underscores the importance of careful and rigorous expert assessment.7 Concerns about underdiagnosis and overdiagnosis are not restricted to ADHD or psychiatric disorders.8
Epidemiology In the general population, the estimated prevalence of ADHD in children is 3·4% (95% CI 2·6–4·5) according to the most recent meta-analysis,9 with lower rates of around 1·4% reported for hyperkinetic disorder from European studies.10 International comparisons show that prevalence does not vary by geographical location but is aff ected by heterogeneity in assessment methods (eg, use of an additional informant to the parent or carer) and diagnostic conventions (eg, ICD vs DSM).11 Notably, there is a marked under-representation of studies on ADHD from low-income and middle-income countries.
One common assumption is that ADHD must be a modern occurrence. However, a case series of children presenting with the characteristic clinical features was published by the British paediatrician Sir George Still in The Lancet in 1902,12 and there are descriptions that pre-date this publication by several centuries. Time trends studies of non-referred population cohorts in the late 20th and early 21st centuries show no evidence of a rise in rates of ADHD symptoms or diagnosis across time.13,14 However, there has been a very marked rise in the number of prescriptions issued for ADHD pharma- cological treatment across high-income countries in the past decade.15–17 Rises in clinic incidence and treatment could simply indicate increased parent and teacher awareness of ADHD or changes in the impact of symptoms on children’s functioning, or both.18,19 Never- theless, European studies have repeatedly reported that despite the rise in ADHD treatment, the admin is trative prevalence is lower than the population fi gure, highlighting that in these countries there is still underdiagnosis.17,20,21 However, in the USA, similar types of studies show geographical variation in patterns of underdiagnosis and overdiagnosis or in ADHD medication prescribing.22,23 Such fi ndings highlight that there is the potential for misdiagnosis and inappropriate use of pharmacological interventions if safeguards are not in place. These safeguards include ensuring full, good-quality clinical assessments are undertaken, even though these require time, and adherence to national
and international treatment guidelines. However, there is no evidence of rising population rates of ADHD explained by social change, contrary to the opinion of some people.
An excess of aff ected male individuals is a strongly consistent epidemiological fi nding, although the male:female ratio of 3–4:1 recorded in epidemiological samples is increased in clinic populations to around 7–8:1, suggesting referral bias in relation to female patients with ADHD.24 The same male preponderance is seen for other neurodevelopmental disorders such as autism spectrum disorder, intellectual disability (intelligence quotient [IQ] <70), and communication disorders.25