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ADHD: a True Neurodevelopmental Disorder? Medical Journalism ADHD: A true neurodevelopmental disorder? Medical Journalism 1 2 Melanie Price , Diana Raffelsbauer Correspondence to: 1 Write-on Editing: Scientific Writing and Editing, Av. du Grey 1, Diana Raffelsbauer, 1004 Lausanne, Switzerland PharmaWrite Medical 2 Communications Freelance Medical Writer and Journalist, Network, Giebelstadt, PharmaWrite Medical Communications Network, Germany Germany diana.raffelsbauer@ pharmawrite.de; www.pharmawrite.de Abstract Attention-deficit/hyperactivity disorder (ADHD) is 1.4–6% of school children, and probably the most one of the most common childhood disorders. First controversial.3 described in 1798 by Alexander Crichton, ADHD The major clinical features are severe impulsive- became widely known outside the medical pro- ness, lack of concentration, and motor hyperactivity, fession with the publication of the story of Fidgety observed in at least two distinct settings, for Phil (‘Zappelphilipp’) in Heinrich Hoffman’sbook example, home, school, and social settings. ADHD ‘Struwwelpeter’ in 1846. Since then, scientists and is often accompanied by other psychiatric and devel- clinicians have been struggling to understand its opmental disorders, including learning impair- causes. To date, there is neither a genetic test nor a ments, oppositional defiant disorder, conduct brain scan to diagnose ADHD due to the fact that disorder, autism, and dyslexia.1 These impairing it is a heterogeneous collection of behaviours that symptoms put children at risk of education failure appear to have different causes and symptoms. In and can severely disrupt family, teacher, and peer view of the lack of an objective diagnostic method, relationships. the major difficulty that specialists face is to decide From a public health perspective, the cost of ADHD where to set the threshold between behaviours and is significant in terms of academic underachievement, states of mind that require medication or behavioural later unemployment, and often comorbid substance treatment and differences that can be left alone. The abuse and antisocial behaviour.4 In England and increased rate in diagnosis and stimulant use in Wales, children with ADHD place a significant cost ADHD recently raises several issues, notably, are we on health, social, and education services, reaching setting lower diagnostic thresholds because of £23 million for initial specialist assessment and £14 societies’ intolerance of behaviours and impairments million annually for follow-up care. In 2006, the total associated with ADHD? This article discusses some of annual cost of prescribed stimulants and other drugs the controversies in ADHD diagnosis and treatment, for ADHD in England was roughly £29 million.5 including many medical, social, and ethical aspects. And the costs keep rising…. Keywords: Attention deficit hyperactivity disorder, ADHD, Impulsivity, Stimulant, Methylphenidate, Molecular genetics of ADHD Atomoxetine Given the impact of ADHD on society as a whole and particularly on children’s quality of life, it is imperative to understand the aetiology and pathophysiology of this disorder. At present, little is known about either the causes or the mechanisms Attention-deficit/hyperactivity disorder (ADHD) is of ADHD, but family, twin, and adoption studies a highly disruptive childhood-onset disorder, provided strong evidence that ADHD is heredi- characterized by inappropriate hyperactivity, inat- tary.1,6 Twin studies showed that disease concor- tention, and impulsivity that onsets before the age dance was much higher in identical twins of seven and often persists into adolescence and compared to non-identical twins, with 60–90% of adulthood.1,2 It is the most common neurodevelop- the phenotypic variance being explained by inher- mental disorder of childhood, estimated to affect ited factors. There is evidence for shared inherited © The European Medical Writers Association 2012 114 DOI: 10.1179/2047480612Z.00000000023 Medical Writing 2012 VOL. 21 NO. 2 Price and Raffelsbauer – ADHD: A true neurodevelopmental disorder factors with a wide range of psychiatric disorders. greater that vary in number when the genomes of Another interesting aspect is that ADHD prevalence different individuals are compared. They can be is higher in males than in females, but at present a copy number gains (insertions and duplications) or genetic explanation for this phenomenon is lacking.1 subtractions (deletions) when compared to the Interestingly, the high-heritability estimates are control genome. Large and rare CNVs have been similar to those found in other psychiatric disorders associated with neurodevelopmental disorders such as schizophrenia and autism. As with these such as schizophrenia and autism.8,9 A UK study disorders, genetic effects are not 100%, indicating analysing rare CNVs and ADHD found a signifi- additional contribution from non-shared environ- cantly increased rate in ADHD cases compared to mental factors, epigenetic effects, random events, controls and also reported an overlap of CNVs or measurement inaccuracies. ADHD, like other found in ADHD with both schizophrenia and common medical and psychiatric disorders, is autism, further supporting ADHD as a neurodeve- considered a complex genetic trait, influenced by lopmental disorder.10,11 multiple genes, non-inherited factors, and the inter- Molecular genetic studies at best account for less action between them. than 5% of the estimated heritability in ADHD With this high heritability, much effort has been, symptoms due in a large part to the heterogeneity and still is being, directed towards searching for of the clinical phenotype and the genetic architec- specific susceptibility genes. The search has ture. Thus, future directions include finding ways consisted of identifying common DNA variation. of dividing subjects into more homogenous sub- Whole-genome linkage studies were not able to groups for use in genetic studies12 and using point to regions harbouring susceptibility genes, intermediate phenotypes or endophenotypes. probably reflecting the fact that there are no Endophenotypes are stable, heritable measurements common susceptibility genes of large effect sizes that are closer to the biological aetiology of a dis- for ADHD. order (e.g. the gene) than the clinical diagnosis Candidate gene association studies have been itself. Examples of endophenotypes that measure more promising, and a small number have been simpler traits, likely to be influenced by a smaller shown to consistently withstand replication and number of genes, are magnetic resonance (MR)- meta-analysis, including genes involved in the based measured effects on brain structure.13 dopaminergic pathway, long hypothesized to be Importantly, some MR imaging studies provide involved in ADHD; the 7-repeat allele of the D4 evidence for differences in brain structure and/or dopamine receptor gene (DRD4), a microsatellite function that may facilitate linkage studies as well repeat in the D5 dopamine receptor gene (DRD5), as provide neurobiological mechanisms for how and a 480 bp variable number tandem repeat in gene variants impact on the brain.14,15 the dopamine transporter gene, DAT1.1 There is considerable sample heterogeneity reported for the Environmental impact on ADHD DAT1 allele, which could be the result of multiple polymorphisms in this gene. There is also evidence There are a number of environmental risk factors that the gene encoding a protein responsible for that have been associated with ADHD. Major associ- the degradation of dopamine (COMT) could have ations have been seen with maternal-related prena- a modifying effect on the ADHD phenotype tal risk (alcohol, smoking, drug use, stress in (reviewed by Thapar et al.7). pregnancy), pregnancy and birth complications, Genome-wide association studies are still at an including prematurity and low birth weight, and early stage for ADHD and have provided some environmental exposures, including toxins (pesti- interesting genes to investigate further. However, cides, polychlorinated biphenyl, and lead) and all association studies have failed to find a some virus infections. At present, although some common gene variant and have not provided studies have found positive association with an support for previous candidate genes. This is agent and ADHD, for example, an association probably a reflection of the extremely large sample between low-level prenatal organochlorine exposure sizes required for the small effect size expected and ADHD-like behaviours in childhood,16 no firm and sample heterogeneity. Another possibility is conclusions can yet be made for a link to ADHD that disorders such as ADHD may be better behaviour outcome, with the exception of extreme explained by the effect of rare genetic variants, for situations including extreme prematurity, very low example, rare copy number variants (CNVs). birth weight, and foetal alcohol syndrome. CNVs are part of the normal variation of the Similarly, despite many studies of diet and ADHD human genome and are DNA segments of 1 Kb or symptoms, there is no evidence yet to show that Medical Writing 2012 VOL. 21 NO. 2 115 Price and Raffelsbauer – ADHD: A true neurodevelopmental disorder diet plays a causal role, although some nutritional within a given species) may not just be ‘symptoms’ changes may help relieve some symptoms in chil- of disorders, but they might instead reflect adaptive dren diagnosed with ADHD (see below). Adverse responses of the organism to environmental social and family environments have also been demands’.20 Gallagher
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