Evid Based Mental Health: first published as 10.1136/ebmental-2018-300050 on 9 October 2018. Downloaded from http://ebmh.bmj.com/ on 10 October 2018 by guest.

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Twenty years of research on attention-deficit/hyperactivity
disorder (ADHD): looking back, looking forward
Samuele Cortese,1,2,3,4,5 David Coghill6,7,8
1
Academic Unit of Psychology, Center for Innovation in Mental Health, University of Southampton, Southampton, UK; 2Clinical and
Experimental Sciences (CNS and Psychiatry), Faculty of Medicine, University of Southampton, Southampton, UK; 3Solent NHS Trust,
Southampton, UK; 4New York University Child Study Center, New York City, New York, USA; 5Division of Psychiatry and Applied
Psychology, School of Medicine, University of Nottingham, Nottingham, UK; 6Departments of Paediatrics and Psychiatry, Faculty of
Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Victoria, Australia; 7Murdoch Children’s Research Institute,
Melbourne, Victoria, Australia; 8Royal Children’s Hospital, Melbourne, Victoria, Australia
Correspondence to Dr Samuele Cortese, Academic Unit of Psychology and Clinical and Experimental Sciences (CNS and Psychiatry),
University of Southampton, Southampton SO17 1BJ, UK; ​samuele.​cortese@​gmail.​com

Abstract
In this clinical review we summarise what in our view have been some the most important advances in the past two decades, in terms of diagnostic
definition, epidemiology, genetics and environmental causes, neuroimaging/cognition and treatment of attention-deficit/hyperactivity disorder (ADHD),
including: (1) the most recent changes to the diagnostic criteria in the Diagnostic and Statistical Manual of Mental Disorders and International
Classification of Diseases; (2) meta-analytic evidence showing that, after accounting for diagnostic methods, the rates of ADHD are fairly consistent
across Western countries; (3) the recent finding of the first genome-wide significant risk loci for ADHD; (4) the paradigm shift in the pathophysiological

Clinical review
conceptualisation of ADHD from alterations in individual brain regions to a complex dysfunction in brain networks; (5) evidence supporting the short-
term efficacy of ADHD pharmacological treatments, with a different profile of efficacy and tolerability in children/adolescents versus adults; (6) a series
of meta-analyses showing that, while non-pharmacological treatment may not be effective to target ADHD core symptoms, some of them effectively
address ADHD-related impairments (such as oppositional behaviours for parent training and working memory deficits for cognitive training). We also
discuss key priorities for future research in each of these areas of investigation. Overall, while many research questions have been answered, many
others need to be addressed. Strengthening multidisciplinary collaborations, relying on large data sets in the spirit of Open Science and supporting
research in less advantaged countries will be key to face the challenges ahead.

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Introduction can still present with impairment.2 The required age of onset was
Attention-deficit/hyperactivity disorder (ADHD) is the most common increased from ‘prior to 7’ to ‘prior to 12’. The purpose of these changes
neurodevelopmental disorder in children, with an estimated worldwide was well intended and designed to facilitate the diagnostic process in
prevalence around 5%.1 Although it has for a long time been considered a adults, who often have trouble pinpointing the exact age of onset, espe-
childhood disorder, it is now established that impairing ADHD symptoms cially if early in the development. Unfortunately, neither change was
persist in adulthood in a sizeable portion of cases (around 65%),2 although based on empirical evidence, and methods used for diagnostic ascertain-
there is variability in the estimate due to methodological heterogeneity ment in adults are still under debate.3 Another pivotal change in DSM-5
across studies.3 is the removal of the veto around the dual diagnosis of ADHD and autism
As for other mental health conditions there has, over the past two spectrum disorders (ASD) that was present in previous editions of the
decades, been an increasing body of research on ADHD. Reasons for this DSM. Unlike the age of onset and symptom number changes this change
increase include: increased recognition of the impact of ADHD on func- is supported by a significant body of research (see ref 6). Finally, the (sub)
tioning; advances in research methodology and technology; and interest types of ADHD defined in the DSM-IV-(TR) were replaced by the notion
from pharmaceutical companies. of different presentations. This acknowledges the instability in the pheno-
Here, we provide an overview of what we deem have been some the typic manifestation of inattention or hyperactive/impulsive symptoms
most important advances, in the past two decades, in ADHD research. over time,7 in contrast to the more static notion of a subtype.
We also discuss key areas for future research. With regard to the International Classification of Diseases (ICD),
it appears that the veto to diagnose ASD in the presence of ADHD
Methods will be retained in the upcoming ICD 11th Revision (https://​icd.​who.​
Given the large body of literature and space constraints, this review is int/​browse11/​l-​m/​en#/​http%​3a%​2f%​2fid.​who.​int%​2ficd%​2fentity%​
selective rather than systematic and comprehensive. We relied mostly 2f821852937).
on meta-analyses, retrieved with a search in PubMed using the following Overall, while these changes to a degree reflect recent empirical
syntax/terms (update: 8 August 2018): (ADHD OR Attention Deficit OR evidence and/or practical needs in the diagnostic process, there are still
Hyperkinetic Disorder) AND (meta-analy* OR metaanaly). issues that need to be addressed. First, current criteria still focus on the
number of symptoms rather than on a more precise definition of functional
impairment. This should be a priority for the field and efforts, such as the
Presentation development of the International Classification of Functioning, Disability
Diagnostic definition and Health: Child and Youth version, are already ongoing.8 Second, while
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition currently each of the symptoms listed in the DSM criterion A carries
(DSM-5),4 published in 2013, introduced several significant changes in the same weight, it has been argued that inattention should be more
relation to the DSM Fourth Edition Text Revision (DSM-IV-TR)5 criteria. heavily weighted than hyperactivity/impulsivity.9 Supporting evidence,
First, the threshold in the number of symptoms (criterion A) necessary for which comes from clinical samples, needs to be replicated in popula-
the diagnosis in older adolescents and adults was reduced from 6 to 5. tion-based studies. Third, from a practical standpoint, it is unclear on how
This change is in keeping with the notion that, despite a reduction in the to best integrate different information sources (eg, parents, teachers,
number of symptoms over development, adults with ADHD in childhood etc). Addressing this challenge is pivotal. Fourth, although proposed as a

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separate type of ADHD or even a separate diagnostic entity, the extent genes as having significant support,19 which together accounted for only
to which the construct of sluggish cognitive tempo (impairment of atten- a small fraction of the total ADHD heritability. The next major approach,
tion in hypoactive-appearing individuals) overlaps with ADHD inattentive ‘genome-wide association studies’ (GWAS), which allows the analysis
presentation remains still unclear.10 11 Finally, one of the most contro- of a large number of common (ie, present at greater than 5% frequency
versial topics in the entire field of ADHD research is currently around in the population) single-nucleotide polymorphisms across the entire
the possibility that ADHD can emerge de novo in adulthood, in contrast genome, was initially unsuccessful in ADHD, as the available sample was
to its conceptualisation as a neurodevelopmental disorder. Despite an too small to show a meaningful effect. However, in a major breakthrough,
increasing number of important studies, the controversy is far from being the first 12 independent loci have been recently identified through
solved12 and we expect it will be a major focus of research in the field in GWAS.20 Associations were enriched in loss-of-function intolerant genes
coming years. and brain-expressed regulatory marks, paving the way for a number of
We also expect that proposed radical, although controversial, changes novel lines of investigation on the neurobiology of ADHD.
in the nosographic approach to mental health conditions, such as the A further recently developed approach focuses on rare (ie, a frequency
Research Domain Criteria will significantly influence future research on in the general population below 1%) ‘copy number variants’ (CNV). These
ADHD.13 are defined as replications or deletions of the DNA with a length of at
least 1 kb. CNVs over-represented in ADHD have been detected, but their
contribution can so far only explain 0.2% of ADHD heritability.21
Epidemiology
As for environmental aetiological factors, there have been, over the
One of the most controversial questions in relation to the epidemiology
past years, considerable data suggesting that prenatal and postnatal
of ADHD has been around possible differences in the prevalence of the
factors, such as maternal smoking and alcohol use, low birth weight,
disorder in different countries. In particular, the differential rates of clinical
premature birth and exposure to environmental toxins, such as organo-
diagnosis in North America and Europe are cited by detractors of ADHD,
phosphate pesticides, polychlorinated biphenyls and zinc, are asso-
Clinical review

as supporting the notion that ADHD is not a ‘real’ disorder but rather a
ciated with increased risk for ADHD.17 22 However, except for preterm
social construct.14 However, a meta-analysis published in 20071 found
birth, genetics studies have implicated unmeasured familial confounding
that diagnostic criteria, source of information, requirement of impairment
factors, which are not in line with a causal role of environmental factors.23
for diagnosis and geographic origin of the studies significantly impacted
Severe maternal deprivation has also been related to the development
on the estimated pooled rate of ADHD (5.29%). A significant difference
of ADHD-like symptoms.24
in prevalence emerged only between North America and both Africa and
The study of the causes of ADHD still has many unanswered questions.
the Middle East, although evidence from non-Western countries was
We need a better understanding of how genes interact with each other,
limited. However, as there were only a limited number of studies avail-
and of the interplay between environmental factors and genes. Genetics
able for Africa and Middle East, these findings should be considered with
has the potential to offer many other exciting future avenues of research

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caution. By contrast, no significant differences emerged between Europe
in ADHD. We will only mention briefly here: (1) the use of induced plurip-
and North America, suggesting that when using the same diagnostic
otent stem cell derived from peripheral tissue of patients with ADHD and
approach the rates of the disorder are fairly consistent in Western coun-
used to generate brain cells with the aim to model brain circuits and
tries, with variability in the prevalence accounted for primarily by methods
responses to medications or other stressors; (2) the use of zebrafish and
used to diagnose ADHD. Another more recent meta-analysis15 found no
fruit fly models to augment currently available animal models of ADHD.
evidence to support an increase in the epidemiological prevalence of
ADHD over the past three decades when standardised diagnostic proce-
dures are followed. This implies that the trend for increased rates of diag-
Neuroimaging and neurocognition
nosis16 are not accounted for by actual increases in prevalence. Rather,
Initial pathophysiological models of ADHD published 20 years ago25 were
the mismatch between administrative and epidemiological rates of the
based on dysfunctions in a limited number of brain areas, namely the
disorder, which varies between the USA and Europe, is likely accounted
frontal cortex and the basal ganglia. Over the past two decades, and
for by cultural and social factors.16
similar to other mental health conditions, a major paradigm shift from
As the bulk of the available epidemiological studies focus on school-age
alterations in individual brain regions to dysfunction in brain networks has
children from North America and Europe, further population-based studies
begun to reshape our understanding of the pathophysiology of ADHD.
from other continents as well as in preschoolers and adults should be
Structurally, meta-analyses and mega-analyses of the structural MRI
encouraged. Additionally, longitudinal epidemiological studies aimed at
studies conducted over the past two decades pointed to consistently
better understanding the developmental trajectories and predictors of
replicated alterations in the basal ganglia,26 and in a number of other
remission/persistence of ADHD in adulthood will be instrumental, along-
subcortical areas.27 Functionally, a comprehensive meta-analysis28 found
side other clinical, neuropsychological, genetic and neuroimaging studies,
that the majority of the ADHD-related hypoactivated areas were related
to inform prevention programmes. Development of a standardised defi-
to the ventral attention and the frontoparietal networks. By contrast, the
nition of caseness and remission will be pivotal for this body of research
majority of ADHD-related hyperactivated areas fell within the default
to be fruitful.
mode network and other hyperactivated areas were within the visual
network. This is in line with the hypothesis that the attentional lapses that
Genetics and environmental causes of ADHD characterise ADHD result from an inappropriate intrusion of the default
Studies of twins and adopted children indicate a high heritability for ADHD network in the activity of task-positive networks frontoparietal, ventral or
(60%–90%).17 Efforts to find the genes underpinning this heritability have dorsal attention networks,28 according to the default network hypothesis
been more challenging than initially anticipated. As for other mental of ADHD,29 which has been arguably one of the most inspiring proposals
health conditions, it became clear that ADHD aetiology is accounted for in the neuroscience of ADHD over the past two decades.
by a complex interaction of many genes each with a relatively small effect While we have gained insight into the brain networks that are dysfunc-
and by gene × environment interactions.18 tional in ADHD and in the delay in cortical maturation,30 we look forward
The first approach to finding the genes involved in ADHD was the to the next generation of neuroimaging studies which we hope will start
‘candidate gene’ approach. This approach focuses on identifying the vari- to translate these findings into the clinical practice. The introduction
ants in genes coding for proteins hypothesised, a priori, to be involved of machine learning approaches, such as support vector machine, has
in the pathophysiology of ADHD. These studies identified only about 10 been welcomed in the field of clinical neuroscience as a way to translate

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neuroscientific findings at the individual patient level, thus overcoming clinical impact of these treatments on ADHD core symptoms is, at the
the main limitation of current studies that can only provide results valid at group level, modest.
the group, rather than individual, level.31 An increasing number of studies Subsequent EAGG meta-analyses focused on ADHD core symptoms
have used machine learning based on MRI data to validate the diagnosis and on ADHD-related problems. A meta-analysis38 specifically focusing
of ADHD with varying degrees of success.32 33 on behavioural interventions showed that, even when considering prob-
Neurocognitive studies have made a considerable contribution to ably blinded ratings, the behavioural interventions were efficacious at
our understanding of ADHD. In recent years, the field has moved away improving important aspects related to ADHD, namely parenting (SMD
from linear single-cause models of ADHD towards multipathway models for positive parenting 0.63; SMD for negative parenting 0.43) and
that emphasise the heterogeneity inherent to ADHD and provide a link conduct problems (SMD 0.31). Another updated meta-analysis39 on
between individual differences at the brain level and clinical presenta- cognitive training, which was found efficacious in improving verbal and
tion.34 35 visual working memory, which are impaired in a sizeable portion of chil-
We believe that an interesting line of research for the future will be dren with ADHD and have been demonstrated to dissociate from ADHD
to combine genetics, clinical, neurocognitive and neuroimaging data to symptoms.40 These meta-analyses also suggest that training which
define, via machine learning approaches, response to treatment, toler- targets several neuropsychological aspects may be more efficacious at
ability profiles and functional trajectory of the disorder over time. This improving ADHD symptoms, than training targeting only one aspect of
will be a crucial step towards personalised and precision approaches to cognitive functioning. The most recent meta-analysis41 by the EAGG on
treatment. neurofeedback did not provide support for the efficacy of neurofeedback
on any of the neuropsychological and academic outcomes. Overall, this
body of research does not provide solid evidence to routinely recom-
Treatment mend non-pharmacological interventions as highly effective treatments
Over the past two decades, there has been a marked increase in the for ADHD core symptoms, although some of them (eg, behavioural inter-

Clinical review
number of randomised controlled trials (RCT) aimed at testing the ventions or cognitive training) may be effective for important associated
short-term efficacy and tolerability of pharmacological treatments for impairments (oppositional behaviours and working memory deficits,
ADHD (both stimulant and non-stimulant medications). Most have respectively). The role of fatty acid supplementation and artificial food
been sponsored by Big Pharma and were designed to support the colours exclusion as possible treatment strategies should be considered
licence of the medication. In parallel, due to concerns around possible cautiously given the small effect size, with CIs close to non-significance.
side effects of medications and lack of clarity around their long-term Probably, the most crucial area of future treatment research in ADHD
effects, several lines of research on non-pharmacological interven- will be to gain insight into the long-term positive and negative effects of
tions have been developed. Recent important methodologically sound treatments, using randomised trials with withdrawn designs, as well as
meta-analyses allow us to summarise and critically discuss this large additional population-based studies with self-controlled methodologies

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body of evidence. and longitudinal follow-up studies. These should clarify the conclusions
For the pharmacological interventions, a comprehensive network from the various follow-up waves of the Multimodal Treatment of ADHD
meta-analysis36 of 133 double-blind RCTs demonstrated high to moderate (MTA) study, showing that neither the type and intensity of treatment
effect sizes (in terms of efficacy) for the different medications versus received during the initial 15-month randomised phase of the study (treat-
placebo. Standardised mean differences (SMD) ranged from −1.02 ment as usual medication (MED), behavioural therapy (BEH), medication
(95% CI −1.19 to −0.85) for amphetamines to −0.56 (95% CI −0.66 plus behavioural therapy (COMB)) nor exposure to medication over the
to −0.45) for atomoxetine (methylphenidate: −0.78, 95% CI −0.93 to subsequent observational periods predicted the functional outcome at
−0.62). In children/adolescents, methylphenidate was the only drug with follow-up which has now extended to 16 years. Of note, in the MTA, the
better acceptability than placebo; in adults this was the case only for treatments received in the three experimental arms (MED, BEH, COMB)
amphetamines (with no difference between placebo and other active during initial 15-month randomised phase were carefully crafted in an
drugs). Taking into account both efficacy and safety, evidence from this attempt to achieve optimal outcomes. After this initial phase all partici-
meta-analysis supported methylphenidate as preferred first-choice medi- pants were free to choose the type of treatment they received from their
cation for the short-term treatment of ADHD in children/adolescents and regular provider. As it is likely that these treatments were not as carefully
amphetamines for adults. optimised and monitored as the three experimental groups during the
As for non-pharmacological options, a comprehensive synthesis on randomised  phase, these  longer term findings of the MTA are not easily
non-pharmacological treatments for children and adolescents with ADHD interpretable and might be, to some extent, misleading.
has been provided in a series of meta-analyses by the European ADHD
Guidelines Group (EAGG). In 2013, they published a first systematic
review/meta-analysis37 addressing the efficacy of behavioural interven- Conclusions
tions, diet interventions (restricted elimination diets, artificial food colour Many questions have been successfully answered in the field of ADHD.
exclusions and free fatty acid supplementation), cognitive training and Many others remain to be addressed. Additional multidisciplinary collab-
neurofeedback on ADHD core symptoms (ie, inattention, hyperactivity orations, use of large data sets in the spirit of Open Science and support
and impulsivity). The systematic review included only RCTs and consid- of research activities in less advantaged countries are key to address the
ered two contrasting outcomes: those rated by individuals not blinded to challenge.
the treatment condition (active vs control) and those rated by individuals
Contributors  SC drafted the paper. DC revised the first draft.
who were probably blinded to treatment (eg, teachers in trials assessing
a behavioural intervention implemented with parents). The results were Funding  The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
strikingly different depending on the type rater. When considering not
blinded ratings, all interventions resulted significantly more efficacious Competing interests  SC declares reimbursement for travel and accommodation
expenses from the Association for Child and Adolescent Central Health (ACAMH)
than the control condition in terms of reduction of ADHD core symptoms. in relation to lectures delivered for ACAMH, and from Healthcare Convention for
However, when considering the more rigorous probably blinded ratings, educational activity on ADHD. DC declares grants and personal fees from Shire and
only free fatty acid supplementation and artificial food colour exclusion Servier; personal fees from Eli Lilly, Novartis and Oxford University Press; and grants
remained significantly more efficacious than the control conditions, with from Vifor.
small effect sizes (SMD=0.16 and 0.42, respectively), indicating that the Patient consent  Not required.

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 Evid Based Mental Health: first published as 10.1136/ebmental-2018-300050 on 9 October 2018. Downloaded from http://ebmh.bmj.com/ on 10 October 2018 by guest. Protected by
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