Sluggish cognitive tempo

Abstract

Sluggish cognitive tempo (SCT) is characterized by excessive daydreaming, mental confusion and fogginess, and slowed behavior/thinking. A brief history of the SCT construct is provided, followed by a review of the current research supporting SCT as distinct from attention-deficit/hyperactivity disorder (ADHD) and other psychopathologies. SCT is positively associated with ADHD inattentive symptoms, depression, anxiety, and daytime sleepiness, but unassociated or negatively associated with externalizing behaviors such as hyperactivity-impulsivity, oppositionality, and aggression. A growing body of research also demonstrates that SCT is uniquely associated with poorer functioning in various domains of major life activities, including academic difficulties (including poor organization, homework problems, and lower grade point average), social problems (especially peer withdrawal and isolation), and emotion dysregulation. SCT is less clearly associated with most neuropsychological performance outcomes with the possible exceptions of sustained attention, processing speed, and motor speed. SCT is more consistently related to deficits in daily life executive functioning, though perhaps more so in adults than in children. Key directions for future research are offered, and issues related to terminology are discussed.

Full text

CHAPTER15
Sluggish cognitivetempo
Stephen P. Becker and Russell A. Barkley
Introduction
ere has been longstanding interest in how best to categor-
ize the heterogeneity of children with ADHD (1, 2). In an eort
to understand the variability of inattention specically, there has
recently been a resurgence of interest in sluggish cognitive tempo
(SCT) (3– 6), a set of behavioural symptoms characterized by
daydreaming, mental fogginess/ confusion, and slowed behaviour/
thinking. is chapter provides a brief history of the SCT construct
and summarizes the rapidly accumulating research examining SCT
as distinct from ADHD and other psychopathologies and the extent
to which SCT is uniquely related to functioning in various domains
of major life activities. We conclude by commenting on issues of
terminology and oering key directions for future research.
History ofthe sluggish cognitive
tempo construct
e rst description of attentional problems characterized by
underarousal and daydreaming is believed to have appeared in
a textbook by Sir Alexander Crichton in 1798 (7). As Barkley
(5)observed, Crichton’s description of individuals with ‘low power’,
who are generally unsocial and insensible to external objects,
may align with current descriptions of SCT. Nevertheless, the
scientic study of SCT began in the 1980s when the third edition
of the Diagnostic and Statistical Manual of Mental Disorders (DSM)
(8)created two subtypes of attention decit disorder (ADD):one
with hyperactivity (ADD+H) and one without hyperactivity
(ADD– H). In turn, researchers began to investigate dierences
between children with ADD+H or ADD– H. A thorough review
of this research is beyond the scope of this chapter (see Barkley
[5] and Becker etal. [4] for more thorough reviews). It was during
this time that researchers rst began to evaluate the extent to which
a set of symptoms characterized by sluggishness, apathy, lethargy,
and being in a world of one’s own were part of, or distinct from,
inattention as dened in the DSM (9– 11). However, when SCT
symptoms showed poor predictive power for identifying ADHD in
the DSM- IV eld trials (12), the study of SCT largely stalled. at is
until an inuential review by Milich etal. (2)appeared as well as an
empirical article by McBurnett and colleagues (13), both published
in 2001. ese papers emphasized the importance of further study
of the SCT construct. In turn, a slow but steady increase in the
number of SCT studies began to enter the published literature
(4). Specically, since these two seminal papers were published in
2001, over 50 papers related to SCT have been published, most in
just the past 5years (14). As the ndings from these studies have
accumulated (and are reviewed next), the study of SCT has largely
shied away from eorts to identify dierences between subtypes
of ADHD to examine SCT in its own right, independent from and
in contrast toADHD.
Sluggish cognitive tempo is distinct
fromADHD
It is now clear that SCT symptoms are empirically distinct from
symptoms of ADHD. Becker etal. (14) recently conducted a meta-
analysis that included factor analytical studies with over 19,000 chil-
dren and adults, and found strong support for 13 SCT symptoms
that loaded consistently on an SCT factor as opposed to an ADHD
factor. ese 13 symptoms are listed in Box 15.1. Although add-
itional measurement work needs to be conducted now that these
13 items have been identied, it is important to note that parent,
teacher, adult self- report, and child self- report ratings scales (15–
20), as well as a semistructured clinical interview (21), have been
developed that include at least most of these 13 items. Studies using
these measures demonstrate that SCT can be reliability assessed,
with excellent internal consistency and test– retest reliability, and
moderate interrater reliability (14). Importantly, the internal
validity of SCT has been identied across a range of sample types
(clinical, community, epidemiological), age ranges (spanning ages
3– 96 years), and continents (North America, South America,
Europe, and Asia)(14).
Additional evidence for the distinctiveness of SCT from
ADHD comes from Barkley’s two nationally representative
studies examining SCT in children (16) and adults (15). As in
other studies, Barkley found evidence for an SCT factor that did
not load with ADHD. Further, Barkley classied participants as
meeting research criteria for SCT and/ or ADHD and found only
moderate overlap between the SCT and ADHD classications. In
both studies, approximately half of the participants with ADHD
were not classied with SCT, and vice versa. ese ndings led
Barkley (15) to conclude that the relation between SCT and ADHD
‘is similar to comorbidity between two disorders, such as between
anxiety and depression, than one of subtyping within a single dis-
order or in which subgroups share the same disorder of attention’
(p. 987). In line with this conclusion, two recent studies using
bifactor modelling found SCT to fall outside of a general ADHD or
disruptive behaviour factor (22, 23). SCT and ADHD also appear to
have dierent developmental trajectories, with ADHD hyperactive-
impulsive symptoms declining, ADHD inattentive symptoms
remaining relatively stable, and SCT symptoms showing a slight
increase across childhood and adolescence(24).

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Little is known regarding the aetiology of SCT, but again, there
is emerging evidence for the separateness of SCT from ADHD. e
only published twin study to date found SCT to be substantially
heritable, although SCT symptoms were less heritable than ADHD
and more strongly inuenced by shared and non- shared environ-
mental factors (25). e one neuroimaging study of SCT found an
association between SCT symptom severity and hypoactivity in the
le superior parietal lobe during a cued anker task, suggestive of
decits in reorientating or shiing of attention (26) that is dierent
from the attention networks implicated in ADHD (27). Although
these ndings are intriguing, much more research examining the
aetiology of SCT is clearly needed. Nevertheless, essentially all
available research points to SCT as a set of attentional symptoms
distinct from those captured byADHD.
Sluggish cognitive tempo inrelation
tofunctioning and impairment
In comparison to the number of studies examining the structure of
SCT, especially as related to ADHD, far fewer studies have examined
SCT in relation to functioning and impairment. Nevertheless,
a growing body of research indicates that SCT is associated with
poorer adjustment across a range of domains of major life activities,
with many associations remaining even aer controlling for ADHD
(for additional reviews, see [5,14]).
Mental health functioning
Multiple studies have documented a signicant association
between SCT and internalizing symptoms such as anxiety and
depression (20, 28– 30), although it should be noted that SCT is dis-
tinct from both anxiety and depression (18, 31, 32). In considering
specic internalizing comorbidities, SCT seems to be more strongly
related to depression than to anxiety (16, 31, 33, 34). However,
this may be more true in children than in adults (14) and could
therefore simply reect the increased rates of depression as chil-
dren transition to adolescence and adulthood. In any event, SCT
is clearly more strongly related to internalizing problems than
with externalizing problems such as hyperactivity- impulsivity and
oppositionality (14). In fact, although SCT and ADHD inattention
are themselves strongly correlated, these two attention domains
evince dierential associations with hyperactive- impulsive and
externalizing symptoms when controlling for each other. When
controlling for ADHD inattention, SCT is unassociated with, or
is negatively associated with, externalizing behaviours, whereas
ADHD inattention remains strongly positively associated with
externalizing behaviours (18– 20, 31, 32). Crucially, recent
longitudinal studies have found the same pattern whereby SCT
predicted greater internalizing behaviours and fewer hyperactive-
impulsive and oppositional behaviours up to 2years later (35– 37).
Further, children with ADHD who also have high levels of SCT
show lower rates of externalizing behaviours such as aggression
than other children with ADHD (38,39).
ese ndings provide additional compelling evidence for the
separation of SCT and ADHD. It would be even more so if add-
itional research supports the hypothesis that SCT falls under the
internalizing umbrella of psychopathology whereas ADHD falls
under the externalizing domain (40). As Barkley has noted (41), it
remains important to identify functioning domains on which SCT
may have a negative impact, as well as domains that are unlikely to
be impacted by SCT or for which SCT may actually play a buering
role. Future studies should therefore continue to examine SCT
in relation to internalizing- salient domains while also testing the
hypothesis that SCT would be unrelated to externalizing- salient
domains characterized by impulsivity and risk- taking, including
substance use, delinquency and antisocial behaviours, speedy and
reckless driving, and accidental injuries.
Academic functioning
Somewhat discrepant ndings have been reported in studies
examining SCT in relation to academic functioning. Several studies
did not nd the presence of SCT to predict academic impairment
or negatively impact academic achievement aer accounting
for ADHD (29, 38, 39, 42, 43). is may be due to these studies
examining the relation between SCT and academics in samples of
children diagnosed with ADHD, which may confound ndings
specic to SCT. It could also result from using very short measures
of SCT comprised of just a few items. In line with this possibility,
the most recent studies that have used longer, validated measures
of SCT have repeatedly found SCT symptoms to be uniquely
associated with poorer academic functioning, even in ADHD
samples (30, 33, 44) or aer controlling for ADHD symptom
severity (17, 18, 32, 34, 45– 47). In particular, it appears that SCT
is associated with problems in organization and homework com-
pletion (16, 39, 44). In terms of academic achievement, SCT may
be uniquely associated with lower achievement in mathematics,
word reading, and written language (28, 32). Nevertheless, there
is some indication even from these recent studies that ADHD is
a stronger contributor than SCT to academic problems (16, 18,
19, 48), although more research needs to be done using real world
measures of academic functioning and success. Of note, the three
studies that have examined overall grade point average (GPA) each
found SCT to signicantly predict lower GPA aer accounting for
ADHD symptoms (30, 32, 44). Indeed, two of these studies found
ADHD symptoms to no longer remain associated with GPA when
SCT was added to the model (30, 44). In sum, additional research
is needed to determine the precise relation between SCT and
Box 15.1 Sluggish cognitive tempoitems
1. Apathetic/ unmotivated
2. Daydreams
3. Easily confused
4. Inafog
5. Loses train of thought/ cognitiveset
6. Lost in thoughts
7. Sluggish
8. Sleepy/ drowsy
9. Slow thinking/ processing
10. Spacey
11. Stares blankly
12. Tired/ lethargic
13. Underactive/ slowmoving
Note: ese 13 items were identied in a meta- analysis as having a mean
factor loading >.70 on a sluggish cognitive tempo factor; see Becker etal.(14).
Data from Becker SP, Leopold DR, Burns GL, Jarrett MA, Langberg JM,
Marshall SA, et al. e internal, external, and diagnostic validity of sluggish
cognitive tempo: A meta-analysis and critical review. J Am Acad Child
Adolesc Psychiatry. 2015. Advance online publication. DOI: http://dx.doi.
org/10.1016/j.jaac.2015.12.006

CHAPTER15   149
academic functioning, as well as the mechanisms and develop-
mental progression of this association.
Socioemotional functioning
Studies have repeatedly found a link between SCT and problems/
impairment in social functioning (17, 18, 29, 31, 45, 47). One recent
study found SCT symptoms to predict increased peer problems
across the duration of a school year even aer controlling for other
psychopathology symptoms and initial levels of peer functioning
(49). In terms of specic domains of social functioning, both
Bauermeister etal. (28) and McBurnett etal. (19) found SCT to
predict poorer social skills in children even aer controlling for
ADHD severity, though only when teacher ratings were used and
not parent ratings. is is perhaps because teachers have ample op-
portunity to observe children’s interactions with peers and the spe-
cic types of peer diculties related to SCT. In a novel computer
chat room experiment, SCT symptoms were found to be associated
with a poorer perception of subtle social cues and less memory for
the chat room conversation (50). Further, whereas children with
ADHD are oen disliked or actively rejected by peers owing to nox-
ious and annoying behaviours (51), children with SCT are likely to
be socially withdrawn and isolated (32, 38, 39, 52). Whether or not
this is primarily due to shyness or social disinterest has not yet been
specically examined. It seems likely due to shyness as opposed to
lack of interest, since SCT is also associated with parent reports
of children’s fear/ shyness as part of the ght– ight– freeze motiv-
ational system (40) and children’s own ratings of loneliness (17).
Additional studies supporting this conclusion would have clear
implications for intervention (e.g. social skills training).
Since SCT is associated with both social problems and depres-
sive symptoms, it is not surprising that it has also been linked to
problems in emotion regulation, although ndings are not fully
consistent across studies. In his nationally representative sample
of youth, Barkley (16) found SCT to be signicantly associated
with children’s self- regulation of emotion decits, but SCT was
a much smaller contributor than either ADHD inattention or
hyperactivity- impulsivity to these decits. Conversely, SCT was the
strongest predictor of self- regulation of emotion decits in Barkley’s
representative sample of adults (15). Does this mean the association
between SCT and emotion regulation diculties grows stronger
across development? is is unknown, and no longitudinal studies
examining the association between SCT and emotion regulation
exist. However, there is some evidence that SCT is in fact associated
with poorer emotion regulation in youth. Specically, Becker etal.
(17) found both child- and teacher- rated SCT symptoms to predict
poorer child- rated emotion regulation coping (ability to cope with
and control emotional experiences appropriately) and lower self-
esteem even aer controlling for ADHD, anxiety, and depressive
symptoms. Likewise, Araujo Jiménez etal. (53) found SCT to be
signicantly associated with poorer parent- rated emotional con-
trol in a sample of children and adolescents with ADHD, even
aer controlling for both ADHD inattention and hyperactivity-
impulsivity. ese ndings converge with other studies of college
students that consistently document a link between SCT and
emotion dysregulation (54– 56). Interestingly, Willcutt etal. (32)
hypothesized that regulation diculties may account for the asso-
ciation between SCT and social isolation, whereby ‘individuals
with SCT may become overwhelmed by the rapid ow of complex
information that must be processed continuously to successfully
navigate social interactions, which may then lead to avoidance of
social situations and subsequent isolation’ (pp.32– 3). In line with
this possibility, Flannery etal. (54) directly tested and found support
for emotion dysregulation mediating the association between SCT
and social problems, albeit with a cross- sectional design making
longitudinal studies that are better suited for testing indirect and
developmental pathways a clear research priority. Also important
to distinguish in future research is whether such dysregulation
actually reects greater emotional distress, more emotional lability,
or poor self- regulation of elicited emotions.
Neuropsychological and executive functioning
Only a handful of studies have examined neuropsychological
decits associated with SCT, and most of these studies have used
samples (and, thus, neuropsychological test batteries) specic to,
or oversampled for, ADHD (28, 32, 43, 57, 58). In general, these
studies demonstrate that SCT is unassociated with pervasive
neuropsychological decits, whereas a large literature links
ADHD to wideranging neuropsychological impairments (59,
60). In particular, ADHD is clearly associated with decits in
response inhibition, working memory, and response variability.
In contrast, SCT does not seem to be associated with any of these
decits when accounting for the contribution of ADHD symptoms
(28, 32, 43). However, there is some indication that SCT may be
uniquely related to problems with early information processing
or selective attention (58). Furthermore, two of the larger studies
examining SCT in relation to neuropsychological test performance
both found SCT to be related to poorer sustained attention aer
controlling for ADHD inattention (32, 43). ere is mixed evi-
dence in terms of whether or not SCT remains associated with
slower motor or processing speed aer controlling for ADHD (28,
32, 61). One study found SCT to be associated with variability of
spatial memory performance specically (57). Replication will
be needed to draw conclusions regarding any of these ndings. It
will be especially important for future studies examining SCT in
relation to neuropsychological functioning to do so in non- ADHD
samples, as well as to use neuropsychological and cognitive tests
more specic to the nature of SCT that may not be frequently used
in studies of ADHD. In addition, only one study has examined SCT
in relation to neuropsychological test performance in adults. is
study found neither SCT nor ADHD to predict test performance,
which is likely due to this study’s use of a college student sample
(55). In sum, although more studies are needed, it seems clear
that SCT is not associated with substantial or pervasive executive
functioning (EF) decits. is is yet one more indication that SCT
is best conceptualized as distinct fromADHD.
When ratings of EF in daily life are used, as opposed to
neuropsychological tests of EF, there appear to be dierent
conclusions between studies of youth or adults. is can be seen
most clearly in Barkley’s national studies (15, 16), which did not
suer from possible ascertainment bias by using previously ADHD
dened samples. In the study of children and adolescents, SCT
accounted for very little variance across all EF dimensions when
controlling for ADHD symptoms in youth, though SCT did contrib-
ute somewhat to decits in self- organization and problem- solving.
ADHD inattention was far and away the strongest predictor of EF
decits across all EF dimensions (16). In contrast, in the national
study of adults, ADHD inattention remained the strongest predictor
of self- management to time and self- motivation EF dimensions,
but SCT accounted for the most variance in the self- organization

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and problem- solving, self- restraint, and self- regulation of emotion
dimensions (15). In line with these studies, Araujo Jiménez (53) found
ADHD symptoms to be a stronger predictor than SCT symptoms of
most EF dimensions in a sample of youth aged 6– 17years, though
SCT did contribute meaningful variance in predicting emotional
control, working memory, and planning/ organization. Similarly,
Becker and Langberg (62) found SCT to be signicantly associated
with metacognitive EF decits in a sample of young adolescents
diagnosed with ADHD. However, this was only true when parent
ratings of SCT were used and not teacher ratings. As hypothesized,
SCT was not signicantly associated with behavioural regulation
EF decits that are more strongly linked to poor inhibition (62).
In line with ndings from Barkley’s nationally representative study
of adults (15), two studies conducted with college students suggest
SCT to be more clearly related to EF ratings in adults, with the
strongest associations apparent for the organization and problem-
solving, self- motivation, and self- regulation of emotion dimensions,
with signicant, albeit weaker, associations also found for the time
management and self- restraint dimensions (55, 56). Once again,
longitudinal and developmentally informed studies are needed
to evaluate the developmental pathways and mechanisms of the
linkage between SCT and daily life EF decits.
Functional impairment
In addition to studies examining SCT in relation to aspects of ad-
justment, several studies have examined SCT in relation to global
and specic domains of functional impairment. SCT is related to
global impairment (14), though likely to a lesser degree and less
pervasively so than ADHD (15, 16). Nevertheless, it is clear that
SCT is associated with functional impairment not explained by any
overlap with ADHD (15, 16, 19, 32, 56). It is thus not surprising
that SCT is also linked to increased stress (63) and a poorer
quality of life (64), as well as lower educational attainment and
socioeconomic status (14– 16). As such, SCT is clearly not benign
and so is deserving of both research inquiry and clinical attention.
Key directions forfuture research
roughout this chapter we have pointed out key directions for fu-
ture research, but it is important to mention a few additional areas
(see also 3, 14). First, there is a clear need for additional longitu-
dinal research. Such studies would allow for a better understanding
of the developmental course of SCT, longitudinal correlates, and
pathways by which SCT is associated with developmental outcomes
and functional impairments. Second, and relatedly, the vast ma-
jority of extant SCT studies have focused on school- aged children
and college students, making research in other developmental
periods, as well as in other samples of young adults, a necessity.
ird, very little is known regarding the aetiology of SCT, including
either biological and/ or environmental contributions to the SCT
phenotype. In particular, social adversities may be more relevant
for the aetiology of SCT than for ADHD (3, 14). Pathological mind
wandering is another intriguing possibility for the aetiology of
SCT (3, 65). As we have discussed elsewhere (5, 6, 17), it is also
possible that dierent attentional networks are implicated in SCT
versus ADHD. Moreover, SCT is only modestly associated with
nighttime sleep problems (66– 68), but is moderately related to both
sleep quality and daytime sleepiness (66, 69). It would be fruitful
for studies to evaluate whether similar mechanisms contribute to
SCT and hypersomnia, including use of methodologies such as the
multiple sleep latency test and default mode network connectivity.
Finally, it is important to examine whether the presence of SCT
symptoms predicts or moderates treatment response to currently
established evidence- based interventions for ADHD as well as
other psychiatric disorders (e.g. anxiety, mood, sleep disorders). It
is likewise important to evaluate interventions that might be e-
cacious for treating SCT, including both pharmacological and psy-
chosocial interventions. Initial evidence indicates that atomoxetine
may eectively reduce SCT symptoms (70), and selective serotonin
reuptake inhibitors may also be eective given the strong asso-
ciation between SCT and internalizing problems such as anxiety
and depression (5). In terms of psychosocial interventions, Pner
and colleagues (71) found evidence- based parent- and teacher-
mediated behavioural interventions to reduce SCT symptoms in
children with ADHD predominantly inattentive type. Given SCT’s
associations with internalizing problems (especially depression)
and social withdrawal, we have also hypothesized that cognitive–
behavioural treatment (CBT), social skills training, and behav-
ioural activation may be eective for treating SCT (3, 5, 14, 72).
However, each of these possibilities has yet to be examined empir-
ically. Of course, it will be important to do so in samples that are
not restricted to individuals diagnosed with ADHD but instead use
a broader sampling strategy (e.g. including individuals with anx-
iety, depression, and/ or sleep disorders) or are selected based on
SCT specically.
A comment onterminology
Before concluding, we believe one additional point regarding
terminology is warranted. In coauthoring this chapter, we hope
it is clear that we (SPB and RAB) agree on the vast majority of
conclusions that can be drawn regarding the current state of SCT, as
well as the very clear need for additional research that can ultimately
shed light on the aetiology, course, and clinical implications of SCT.
Nevertheless, we also acknowledge one area of professional dis-
agreement; namely, the best term to be used to describe this con-
stellation of symptoms.
Barkley has advocated moving away from the SCT terminology
and suggests the term concentration decit disorder (CDD) (3, 5,
41, 73)for various reasons, ‘not the least of which is that SCT can be
viewed by the public as pejorative, derogatory, or frankly oensive’
(5)(p.435). It is important to note that Becker agrees that the SCT
term is far from optimal and ‘shares with Barkley the overarching
concerns he has for the SCT label’ (17) (p.1038). In fact, this is why
Becker avoided the SCT term when naming his youth self- report
scale, calling it the Child Concentration Inventory (17). However,
Becker has also expressed concerns that it may be ‘premature to use
terminology suggesting that the SCT construct is a diagnostic entity
(e.g. Concentration Decit Disorder)’ (14). Just as the SCT label
may be perceived as pejorative and oensive, premature use of the
term ‘disorder’ may create confusion for families and professionals
while also drawing unfavourable media attention that detracts from
the important value of SCT research (74, 75). Further, terminology
suggestive of a ‘disorder’ casts SCT in a dichotomous light, and
Becker believes it is important to consider other options, espe-
cially the possibility that SCT is best viewed as a transdiagnostic
construct as opposed to a categorical diagnosis (4, 76). is latter
possibility aligns with the broader shi in psychiatry as outlined

CHAPTER15   151
by the United States National Institute of Mental Health research
domain criteria (RDoC) initiative (77, 78). us, Becker would cur-
rently favour a term that focuses more on ‘symptoms’ as opposed
to ‘diagnosis’ and is actively considering possible alternatives as
research continues to emerge, even though he has so far continued
to use the SCT terminology.
However, as Barkley has appropriately noted, ‘the mere fact that
SCT has existed for 35years and so should continue to be used
out of mere historical tradition is not a convincing reason to retain
a term that research participants and other consumers likely will
nd oensive’ (41). Becker agrees fully with this point, but for him
the issue is one of timing:a new term is needed but much more
remains to be learned before we can settle on an ideal term. ere
is no easy solution to this dilemma, as the introduction of a new
term earlier may likely spur the very research needed to determine
an even better term. Barkley has clearly acknowledged that he is
not wedded to his proposed CDD terminology (41). He suggests
here that perhaps the term ‘syndrome’ might be a better modier
of ‘concentration decit’ so as not to convey ocial sanctioning of
it as a recognized clinical disorder. Where does this leave us? We
both agree that we need a new term that:1) accurately describes the
constellation of symptoms and state of the science; and 2)is not o-
putting to either the scientic community or general population.
We hope we can nd consensus around such a term in the near
future. In the meantime, we are certainly in agreement that there is
a crucial need for much more research on SCT/ CDD, and we hope
our colleagues will join us in pursuing this theoretically and clinic-
ally important area ofstudy.
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CHAPTER15   153
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Oxford Textbook of
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Hyperactivity
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Oxford Textbook of
Attention Deficit
Hyperactivity
Disorder
Editedby
Tobias Banaschewski
Department of Psychiatry and Psychotherapy of Childhood and Adolescence,
The Central Institute of Mental Health,
Mannheim, Germany
David Coghill
Department of Paediatrics and Department of Psychiatry,
The University of Melbourne, Australia;
Murdoch Children’s Research Institute, Melbourne, Australia;
The Royal Children’s Hospital, Melbourne, Australia
and
AlessandroZuddas
Child & Adolescent Neuropsychiatry, Section of Neuroscience & Clinical Pharmacology,
Department of Biomedical Science, University of Cagliari; ‘G.Brotzu’ Hospital Trust,
Cagliari,Italy

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Foreword
TO COME

Contents
Abbreviations xv
Contributors xi
SECTION 1
Introduction
1 Development of the concept 3
EricTaylor
2 ADHD in the twenty- first century:biology,
context, policy, and the need for
integrative perspective 9
Stephen P. Hinshaw and Richard M. Scheffler
SECTION 2
Aetiology and pathophysiology
3 ADHD genetics 19
Kate Langley
4 Conceptualizing and investigating the role of
the environment in ADHD:correlate, cause,
consequence, context, and treatment 25
Edmund Sonuga- Barke and GordonHarold
5 Gene– environment interactions 35
Barbara Franke and Jan K. Buitelaar
6 Brain volumes and intrinsic brain
connectivity in ADHD 57
Kerstin Konrad, Adriana Di Martino, and YutaAoki
7 ADHD brain function 64
KatyaRubia
8 Insights from neuroanatomical imaging
into ADHD throughout the lifespan 73
Philip Shaw and Eszter Szekely
9 Neurophysiology 82
Daniel Brandeis, Sandra K. Loo, Grainne McLoughlin,
Hartmut Heinrich, and Tobias Banaschewski
10 Cognitive functioning in ADHD:inhibition,
memory, temporal discounting, decision-
making, timing, and reaction time variability 94
David Coghill, Maggie Toplak, Sinead Rhodes,
and NicolettaAdamo
11 Emotional dysregulation and ADHD 103
Celine Ryckaert, Jonna Kuntsi, and Philip Asherson
12 Neuropsychological functioning and
ADHD:a developmental perspective 118
Sarah O’Neill, Jeffrey M. Halperin, and David Coghill
SECTION 3
Epidemiology
13 Epidemiology 131
Guilherme V. Polanczyk
SECTION 4
Clinical presentation
14 Current diagnostic criteria:DSM,
ICD, and future perspectives 139
Luis Augusto Rohde, Christian Kieling,
and Giovanni AbrahãoSalum
15 Sluggish cognitive tempo 147
Stephen P. Becker and Russell A. Barkley
16 Sex differences in ADHD 154
Corina U. Greven, Jennifer S. Richards, and Jan K. Buitelaar
17 Quality of life and impairment in ADHD 161
Melissa Mulraney and David Coghill
18 Adult ADHD and employment 170
MariosAdamou
19 Adult ADHD:clinical presentation
and assessment 178
Philip Asherson, Josep Antoni Ramos- Quiroga,
and SusanYoung

viii
SECTION 5
Comorbidity
20 Conduct disorder in ADHD 193
Anita apar and Stephanie vanGoozen
21 Irritability, disruptive mood, and ADHD 200
Melissa Mulraney, Argyris Stringaris, and EricTaylor
22 Comorbidity:depression and anxiety 206
Cristal Oxley and Argyris Stringaris
23 ADHD and substance misuse 215
Timothy Wilens, Nicholas Carrellas,
and Joseph Biederman
24 Autism spectrum disorder 227
Sven Bölte, Luise Poustka, and HildeGeurts
25 Intellectual impairment and
neurogenetic disorders 235
Emily Simonoff
26 Influence of tics and/ or obsessive- compulsive
behaviour on the phenomenology
of coexisting ADHD 247
Aribert Rothenberger, Andreas Becker,
Lillian- Geza Rothenberger, and Veit Roessner
27 Developmental coordination disorder 254
Christopher Gillberg, Elisabeth Fernell, I.
Carina Gillberg, and Björn Kadesjö
28 ADHD and communication disorders 261
Rosemary Tannock
29 ADHD and reading disorder 273
Erik G. Willcutt
30 ADHD and sleep 280
Melissa Mulraney, Emma Sciberras,
and Michel Lecendreux
31 e relationship of ADHD to
obesity and asthma 289
Samuele Cortese and Marcel Romanos
SECTION 6
Clinical assessment 295
32 Children and adolescents:assessment
in everyday clinical practice 297
Marina Danckaerts and David Coghill
33 ADHD in adults; assessment issues 307
Sandra Kooij, Philip Asherson, and MichaelRösler
SECTION 7
Interventions
34 Long- term outcomes in the Multimodal
Treatment study of Children with ADHD 315
James M. Swanson, L. Eugene Arnold, Peter S. Jensen,
Stephen P. Hinshaw, Lily T. Hechtman, William E. Pelham,
Laurence L. Greenhill, C. Keith Conners, Helena C.
Kraemer, Timothy Wigal, Benedetto Vitiello, Glen R.
Elliott, Howard B. Abikoff, Betsy Hoza, Jeffrey H. Newcorn,
Karen Wells, Marc Lerner, Brooke S.G. Molina, Jeffery N.
Epstein, Elizabeth B. Owens, James Waxmonsky, Desiree
W. Murray, Margaret H. Sibley, John T. Mitchell, Arunima
Roy, Annamaire Stehli for the MTA CooperativeGroup
35 Behavioural interventions for
preschool ADHD 333
David Daley and Saskia Van derOord
36 Cognitive– behavioural treatment in
childhood and adolescence 340
Manfred Döpfner and Saskia van derOord
37 Behavioural therapy (adolescent/ adult) 348
Alexandra Philomena Lam and Alexandra Philipsen
38 Cognitive training approaches for ADHD:can
they be made more effective? 358
Edmund Sonuga- Barke and Samuele Cortese
39 Neurofeedback 366
Martin Holtmann, Björn Albrecht, and Daniel Brandeis
40 Nutritional intervention for ADHD 373
Jan K. Buitelaar, Nanda Rommelse,
Verena Ly, and Julia J. Rucklidge
41 ADHD treatment:psychostimulants 379
Alessandro Zuddas, Tobias Banaschewski,
David Coghill, and Mark A.Stein
42 Non- stimulants in the treatment of ADHD 393
Ralf W. Dittmann, Alexander Häge, Juan
D. Pedraza, and Jeffrey H. Newcorn
43 ADHD and transitions to adult
mental health services 402
ChrisHollis
44 ADHD and school 408
Christine Merrell and KapilSayal

 ix
SECTION 8
Clinical management
45 Organizing and delivering
treatment for ADHD 417
David Coghill and Marina Danckaerts
46 Treatment in adult ADHD 426
Philip Asherson and Josep Antoni Ramos- Quiroga
47 e next steps:future clinical and
research developments in ADHD 437
David Coghill, Alessandro Zuddas, Luis
Augusto Rohde, and Tobias Banaschewski
Index 445

Contributors
Howard B. Abikoff, NewYork University, NewYork,USA
Nicoletta Adamo, MRC Social, Genetic and Developmental
Psychiatry Centre, Institute of Psychiatry, Psychology and
Neuroscience, King’s College London,UK
Marios Adamou, South West Yorkshire NHS Partnership
Foundation Trust, Manygates Clinic, Wakeeld, UK; Visiting
Professor, School of Human and Health Sciences, University of
Hudderseld,UK
Björn Albrecht, Child and Adolescent Psychiatry, University
Medical Center Göttingen, Germany
Yuta Aoki, Department of Child and Adolescent Psychiatry,
NewYork University, NewYork, NY,USA
L. Eugene Arnold, Ohio State University University, Columbus,
OH,USA
Philip Asherson, Social Genetic and Developmental Psychiatry,
King’s College London, London,UK
Tobias Banaschewski, Department of Psychiatry and
Psychotherapy of Childhood and Adolescence, e Central
Institute of Mental Health, Mannheim, Germany
Russell A. Barkley, Virginia Treatment Center for Children and
Virginia Commonwealth University Medical Center, Richmond,
VA,USA
Andreas Becker, Department of Childhood and Adolescent
Psychotherapy, University Medical Centre Gottingeny, Germany
Stephen P. Becker, Division of Behavioral Medicine and Clinical
Psychology, Cincinnati Children’s Hospital Medical Center,
Cincinnati, OH,USA
Joseph Biederman, Clinical and Research Programs in Pediatric
Psychopharmacology and Adult ADHD, Massachusetts General
Hospital, Boston, MA,USA
Sven Bölte, Center of Neurodevelopmental Disorders (KIND),
Department of Women’s and Children’s Health, Karolinska
Institute, Center for Psychiatry Research, Stockholm County
Council, Stockholm,Sweden
Daniel Brandeis, Department of Child and Adolescent Psychiatry
and Psychotherapy, Central Institute of Mental Health, Medical
Faculty Mannheim, Heidelberg University, Mannheim,
Germany
Jan K. Buitelaar, Department of Cognitive Neurosciences, Donders
Institute for Brain, Cognition and Behaviour, Radboud
University Medical Center, Nijmegen, e Netherlands
Nicholas Carrellas, Clinical and Research Programs in Pediatric
Psychopharmacology and Adult ADHD, Massachusetts General
Hospital, Boston, MA,USA
David Coghill, Department of Paediatrics and Department of
Psychiatry, e University of Melbourne, Australia; Murdoch
Children’s Research Institute, Melbourne, Australia; e Royal
Children’s Hospital, Melbourne, Australia
C. Keith Conners, Duke University, Durham, NC,USA
Samuele Cortese, Academic Unit of Psychology, Developmental
Brain- Behaviour Laboratory, Southampton, UK; Clinical
and Experimental Sciences (CNS and Psychiatry), Faculty of
Medicine, University of Southampton, UK; e Child Study
Center, Hassenfeld Children’s Hospital of NewYork, NYU
Langone Medical Center, NewYork, NY,USA
David Daley, Professor of Psychological Intervention and
Behaviour Change, Division of Psychiatry and Applied
Psychology, School of Medicine, University of Nottingham,UK
Marina Danckaerts, Department of Child and Adolescent
Psychiatry, UPC KU Leuven, Belgium and Department of
Neurosciences, KU Leuven, Belgium
Adriana di Martino, NewYork University Child Study Center,
NewYork, NY,USA
Ralf W. Dittmann, Department of Child and Adolescent Psychiatry
and Psychotherapy, Central Institute of Mental Health, Medical
Faculty Mannheim, University of Heidelberg, Germany
Manfred Döpfner, Department of Child and Adolescent
Psychiatry, Psychosomatics and Psychotherapy, Medical Faculty
of the University of Cologne, Germany
Glen R. Elliott, Children’s Health Council, Palo Alto, CA,USA

xii
Jeffery N. Epstein, Cincinnati Children’s Medical Center,
Cincinnati, OH,USA
Elisabeth Fernell, Gillberg Neuropsychiatry Centre, University of
Gothenburg,Sweden
Barbara Franke, Departments of Human Genetics and Psychiatry,
Donders Institute for Brain, Cognition and Behaviour, Radboud
University Medical Center, Nijmegen, e Netherlands
Hilde Geurts, University of Amsterdam, Department of
Psychology, Dutch Autism and ADHD Research Center,
Amsterdam, e Netherlands
Christopher Gillberg, Institute of Health and Wellbeing, University
of Glasgow, UK; Gillberg Neuropsychiatry Centre, University of
Gothenburg,Sweden
I. Carina Gillberg, Gillberg Neuropsychiatry Centre, University of
Gothenburg, Gothenburg,Sweden
Laurence L. Greenhill, Columbia University, NewYork, NY,USA
Corina U. Greven, Radboud University Medical Centre, Donders
Institute for Brain, Cognition and Behaviour, Department of
Cognitive Neuroscience, Nijmegen, e Netherlands
Alexander Häge, Department of Child and Adolescent Psychiatry
and Psychotherapy, Central Institute of Mental Health, Medical
Faculty Mannheim, University of Heidelberg, Germany
Jeffrey M. Halperin, Department of Psychology, Queens College
and e Graduate Center, City University of NewYork,
NY,USA
Gordon Harold, Andrew and Virginia Rudd Professor of Child and
Adolescent Mental Health, School of Psychology, University of
Sussex, UK; School of Psychology, University of Dublin, Ireland
Lily T. Hechtman, McGill University, Montreal Children’s Hospital,
Montreal, QC,Canada
Hartmut Heinrich, Department of Child and Adolescent Mental
Health, University Hospital Erlangen, Erlangen, Germany; kbo-
Heckscher- Klinikum, Munich, Germany
Stephen P. Hinshaw, University of California, Berkeley, CA,USA
Chris Hollis, University of Nottingham and Institute of Mental
Health, Developmental Psychiatry, Queen’s Medical Centre,
Nottingham,UK
Martin Holtmann, LWL- University- Hospital for Child and
Adolescent Psychiatry of the Ruhr- University Bochum, Hamm,
Germany
Betsy Hoza, University of Vermont, Burlington, VT,USA
Peter S. Jensen, University of Arkansas for Medical Sciences, Little
Rock, AR,USA
Björn Kadesjö, Gillberg Neuropsychiatry Centre, University of
Gothenburg,Sweden
Christian Kieling, Department of Psychiatry, Universidade Federal
do Rio Grande do Sul, Porto Alegre,Brazil
Kerstin Konrad, Child Neuropsychology Section, Department of
Child and Adolescent Psychiatry of RTWH Aachen, Germany;
JARA- Brain Institute (INM 11), Research Centre Juelich,
Germany
Sandra Kooij, Associate Professor of Psychiatry, VUMc
Amsterdam, PsyQ Psycho- Medical Programs, Expertise Center
Adult ADHD, e Hague, e Netherlands
Helena C. Kraemer, Stanford University, Palo Alto, CA,USA
Jonna Kuntsi, Social Genetic and Developmental Psychiatry, King’s
College London,UK
Alexandra Philomena Lam, Medical Campus University of
Oldenburg, School of Medicine and Health Sciences, Psychiatry
and Psychotherapy— University Hospital, Karl- Jaspers- Klinik,
Bad Zwischenahn, Germany
Kate Langley, School of Psychology, Cardi University, UK and
MRC Centre for Psychiatric Genetics and Genomics, School of
Medicine, Cardi University,UK
Michel Lecendreux, AP- HP, Pediatric Sleep Center, Hospital
Robert- Debré, Paris, France; National Reference Centre for
Orphan Diseases, Narcolepsy, Idiopathic Hypersomnia and
Kleine- Levin Syndrome (CNR Narcolepsie- Hypersomnie),
Paris,France
Marc Lerner, University of California, Irvine, CA,USA
Sandra K. Loo, Department of Psychiatry and Biobehavioral
Sciences, David Geen School of Medicine, University of
California, Los Angeles, CA,USA
Verena Ly, Department of Clinical Psychology, Leiden University,
the Netherlands
Gráinne McLoughlin, MRC Social Genetic & Developmental
Psychiatry Centre, Institute of Psychiatry, Psychology and
Neuroscience, King’s College London,UK
Christine Merrell, Durham University,UK
John T. Mitchell, Department of Psychiatry and Behavioral
Sciences, Duke University Medical Center, NC,USA
Brooke S.G. Molina, Departments of Psychiatry, Psychology, and
Pediatrics, University of Pittsburgh, Pittsburgh, PA,USA
Melissa Mulraney, Department of Paediatrics, e University of
Melbourne, Australia; Murdoch Children’s Research Institute,
Melbourne, Australia
Desiree W. Murray, Frank Porter Graham Child Development
Institute, University of North Carolina, NC,USA
Jeffrey H. Newcorn, Associate Professor of Psychiatry and
Pediatrics, Director, Division of ADHD and Learning
Disorders, Icahn School of Medicine at Mount Sinai, Director,
Pediatric Psychopharmacology, Mount Sinai Health System,
NewYork, NY,USA
Sarah O’Neill, Department of Psychology, e City College and
e Graduate Center, City University of NewYork, NY,USA

 xiii
Elizabeth B. Owens, Institute of Human Development, University
of California, Berkeley, CA,USA
Cristal Oxley, National and Specialist CAMHS Bipolar and
Depression Clinic, Maudsley Hospital, London,UK
Juan D. Pedraza, Child and Adolescent Psychiatry— Icahn
School of Medicine at Mount Sinai Medical Center, NewYork,
NY,USA
William E. Pelham, Florida International University, Miami,
FL,USA
Alexandra Philipsen, Medical Campus University of Oldenburg,
School of Medicine and Health Sciences, Psychiatry and
Psychotherapy— University Hospital, Karl- Jaspers- Klinik,
Bad Zwischenahn, Germany
Guilherme V. Polanczyk, Division of Child and Adolescent
Psychiatry, Department of Psychiatry, University of São Paulo
Medical School, São Paulo,Brazil
Luise Poustka, Department of Child and Adolescent Psychiatry/
Psychotherapy, University Medical Center Göttingen,
Göttingen, Germany
Josep Antoni Ramos- Quiroga, Department of Psychiatry,
OBERSAM, Hospital Universitari Vall d’Hebron,
Barcelona,Spain
Sinead Rhodes, Salvesen Mindroom Centre, University of
Edinburgh,UK
Jennifer S. Richards, Radboud University Medical Centre, Donders
Institute for Brain, Cognition and Behaviour, Department of
Cognitive Neuroscience, Nijmegen, e Netherlands; Karakter
Child and Adolescent Psychiatry. University Centre Nijmegen,
e Netherlands; University of Groningen, University Medical
Center Groningen, Department of Psychiatry, Groningen,
e Netherlands
Veit Roessner, Department of Child and Adolescent Psychiatry
and Psychotherapy, University Hospital Carl Gustav Carus at
the Technical University Dresden, Dresden, Germany
Luis Augusto Rohde, ADHD Program, Child and Adolescent
Psychiatric Division, Hospital de Clinicas de Porto Alegre,
Porto Alegre,Brazil
Marcel Romanos, University Hospital of Würzburg, Department
of Child and Adolescent Psychiatry, Psychosomatics and
Psychotherapy, Würzburg, Germany
Nanda Rommelse, Radboud University, Nijmegen, the
Netherlands
Michael Rösler, Neurozentrum, Universitätsklinikum des
Saarlandes, Hamburg, Germany
Aribert Rothenberger, Department of Childhood and Adolescent
Psychotherapy, University Medical Centre Gottingeny, Germany
Lillian- Geza Rothenberger, Institute of Ethics and History in
Medicine, Center for Medicine, Society and Prevention,
University of Tuebingen, Germany
Arunima Roy, Divison of Molecular Psychiatry, University
Hospital Würzburg, Germany
Katya Rubia, Department of Child and Adolescent Psychiatry,
Institute of Psychiatry, Psychology and Neuroscience,
King’s College London,UK
Julia J. Rucklidge, Department of Psychology, University of
Canterbury, Christchurch, New Zealand
Celine Ryckaert, Social Genetic and Developmental Psychiatry,
King’s College London,UK
Giovanni Abrahão Salum, Department of Psychiatry, Universidade
Federal do Rio Grande do Sul,Brazil
Kapil Sayal, Division of Psychiatry and Applied Psychology, School
of Medicine, University of Nottingham, UK; Centre for ADHD
and Neuro- developmental Disorders across the Lifespan
(CANDAL), Institute of Mental Health, Nottingham,UK
Richard M. Scheffler, Goldman School of Public Policy, School of
Public Health, University of California, Berkeley, CA,USA
Emma Sciberras, School of Psychology, Faculty of Health, Deakin
University, Geelong, Australia
Philip Shaw, Child Psychiatry Branch, National Institute of Mental
Health, Bethesda, MD,USA
Margaret H. Sibley, Department of Psychiatry and Behavioral
Health, Florida Internatiuonal University, FL,USA
Emily Simonoff, Department of Child and Adolescent Psychiatry,
King’s College London, Institute of Psychiatry, Psychology and
Neuroscience, London,UK
Edmund Sonuga- Barke, Department of Child and Adolescent
Psychiatry, Institute of Psychiatry, Psychology and
Neuroscience, King’s College London, Department of
Experimental Clinical and Health Psychology, Ghent University,
Belgium
Annamaire Stehli, Department of Pediatrics, University of
California, Irvine, CA,USA
Mark A. Stein, Seattle Children’s Hospital, Seattle, WA,USA
Argyris Stringaris, Chief Mood Brain and Development Unit,
National Institutes of Health, Bethesda, MD,USA
James M. Swanson, University of California, Irvine, CA,USA
Eszter Szekely, Department of Psychiatry, McGill University
Faculty of Medicine, Montreal,Canada
Rosemary Tannock, Neuroscience and Mental Health Research
Program, Research Institute of the Hospital for Sick Children,
Toronto, ON,Canada
Eric Taylor, King’s College London, Institute of Psychiatry,
Psychology and Neuroscience, London,UK
Anita apar, Institute of Psychological Medicine and Clinical
Neurosciences, Cardi University School of Medicine,
Cardi,UK

xiv
Maggie Toplak, Clinical Developmental Program, Core Member,
LaMarsh Centre for Child and Youth Research, Department of
Psychology, York University, York,UK
Saskia Van der Oord, Associate Professor, Research Group Clinical
Psychology, Department of Psychology and Educational
Sciences, KU Leuven, Belgium
Stephanie van Goozen, School of Psychology, Cardi
University,UK
Benedetto Vitiello, National Institute of Mental Health, Bethesda,
MD,USA
James Waxmonsky, Department of Psychiatry, Penn State College
of Medicine, PA,USA
Karen Wells, Duke University, Durham, NC,USA
Timothy Wigal, Avida, Inc., Newport Beach, CA,USA
Timothy Wilens, Clinical and Research Programs in Pediatric
Psychopharmacology and Adult ADHD, Massachusetts General
Hospital, Boston, MA,USA
Erik G. Willcutt, Department of Psychology and Neuroscience,
University of Colorado Boulder, CO,USA
Susan Young, Centre for Psychiatry, Imperial College, London,UK
Alessandro Zuddas, Child and Adolescent Neuropsychiatry,
Sect Neuroscience and Clinical Pharmacology, Department
of Biomedical Science, University of Cagliari, and ‘G.Brotzu’
Hospital Trust, Cagliari,Italy

Abbreviations
ACC anterior cingulatecortex
ACG anterior cingulategyrus
ADD attention decit disorder
ADHD- RS ADHD ratingscale
AERS Adverse Event ReportingSystem
AHI apnea– hypopneaindex
AIM ADHD plus impairments inmood
AMHS adult mental health services
APA American Psychiatric Association
ARI aective reactivityindex
ASD autism spectrum disorder
ATX atomoxetine
BADDS Brown Attention Decit DisorderScale
BDNF brain- derived neurotropicfactor
BMI body massindex
BOLD blood oxygen level- dependent
BPD borderline personality disorder
BPT behavioural parent training
CAADID Conners Adult ADHD Diagnostic Interview
CAARS Conners Adult ADHD RatingScale
CAI computer- assisted instruction
CAMHS child and adolescent mental health services
CAPA Child and Adolescent Psychiatric Assessment
CBCL childhood behaviour checklist
CBT cognitive– behavioural therapy/ treatment
CD conduct disorder
CDD concentration decit disorder
CDI child- directed intervention
CELF Clinical Evaluation of Language Fundamentals
CEN central executive network
CGAS Child Global AssessmentScale
CGH comparative genome hybridization
CGI Clinical Global Impressions
CHMP Committee for Medicinal Products for HumanUse
CHP Challenging Horizons Programme
CI condence interval
CLAS Child Life and AttentionSkills
CNV contingent negative variation
CNV copy number variant
CoT children- of- twins
CSD current source density
CWPT classwide peer tutoring
CXR clonidine extended- release
DA dopamine
DAMP decits in attention, motor control + perception
DAWBA development and wellbeing assessment
DCD developmental coordination disorder
DESR decient emotional self- regulation
DIVA 2.0 Diagnostic Interview for ADHD foradults
DLMO dim light melatoninonset
DMDD disruptive mood dysregulation disorder
DMN default mode network
DN default network
DPFC dorsolateral prefrontalcortex
DSM Diagnostic and Statistical Manual of Mental Disorders
DTI diusion tensor imaging
DZ dizygotic
EAGG European ADHD GuidelinesGroup
EC eortful control
EDS excessive daytime sleepiness
EEG electroencephalogram/ electroencephalography
EF executive functioning
EIS emotional impulsivenessscale
EMA European MedicinesAgency
EMG electromyogram/ electromyography
EMR electronic medicalrecord
EPSC excitatory postsynaptic current
ERA English and Romanian Adopteesstudy
ERN error- related negativity
ERP event- related potential
ES eectsize
ESM experience samplingmethod
ESSENCE early symptomatic syndromes eliciting
neurodevelopmental clinical examinations
FAS fetal alcohol syndrome
FDA Food and Drug Administration
fMRI functional magnetic resonance imaging
FR familial riskindex
GABA gamma- aminobutyricacid
GCTA genome- wide complex trait analysis
GREML genomic- relationship- matrix restricted maximum
likelihood
GWAS genome- wide association studies
GXR guanfacine extended- release
HKD hyperkinetic disorder
HRQoL health- related quality oflife
ICA independent component analysis
ICD International Classication of Diseases

xvi
ID intellectual disability
IFC inferior prefrontalcortex
IFG inferior frontalgyrus
IPC inferior parietalcortex
iPSC induced pluripotent stemcells
ITT intention totreat
K- SADS Kiddie- Schedule of Aective Disorders
LDX lisdexamphetamine
LI language impairment
LMIC lower- and middle- income countries
LNCG local normative comparisongroup
MAP mindful awareness practice
MAS mixed amfetaminesalts
MBCT mindfulness- based cognitive therapy
MBD minimal brain dysfunction
MDD major depressive disorder
MEG magnetoencephalography
MEP motor- evoked potential
MET motivational enhancement therapy
MI motivational interviewing
MMN mismatch negativity
MND minor neurological dysfunction
MPFC medial prefrontalcortex
MPH methylphenidate
MRI magnetic resonance imaging
MRR mortality rateratio
MSLT multiple sleep latencytest
MTA Multimodal Treatment sudy of children withADHD
MZ monozygotic
NCLB No Child LeBehind
NE negative emotionality
NE norepinephrine
NIDA National Institute of DrugAbuse
NIMH National Institute of MentalHealth
NIRS near- infrared spectroscopy
NMDA N- methyl- D- aspartate
NREM non- rapid eye movement
NSCH National Survey for Children’sHealth
OCB obsessive- compulsive behaviour
OCD obsessive- compulsive disorder
ODD oppositional deant disorder
OEST other early standard therapy
OFC orbitofrontalcortex
OR oddsratio
OSA obstructive sleepapnea
PAS- ADD Psychiatric Assessment Schedule for Adults with
Developmental Disabilities
PCC posterior cingulatecortex
PCIT parent– child interaction therapy
PD pharmacodynamic
PDD pervasive development disorder
PDI parent- directed intervention
PET positron emission tomography
PFC prefrontalcortex
PK pharmacokinetic
PLMD periodic limb movement disorder
PSG polysomnography
PUFA polyunsaturated fattyacids
QoL quality oflife
RAI resource allocationindex
RCT randomized controlledtrial
RD reading disorder
RDoC research domain criteria
REM rapid eye movement
rGE gene– environment interaction
RLS restless leg syndrome
ROI region of interest
RR relative riskratio
RTV response time variability
SCID- 5 Structured Clinical Interview forDSM- 5
SCN suprachiasmatic nucleus
SCP shared care protocol
SCP slow cortical potential
SCT sluggish cognitivetempo
SD standard deviation
SDB sleep- disordered breathing
SDQ Strengths and Diculties Questionnaire
SES socioeconomicstatus
SFC superior frontalcortex
SFT solution- focused treatment
SICI short- interval intracortical inhibition
SMA supplementary motorarea
SMD severe mood dysregulation
SMD standardized mean dierence
SMR sensorimotorrhythm
SNAP Swanson, Nolan, and Pelham ratingscale
SNP single nucleotide polymorphism
SNRI serotonin- norepinephrine reuptake inhibitors
SPCD social pragmatic communication disorder
SPECT single- photon emission computed tomography
SSD speech sound disorder
SSRI selective serotonin reuptake inhibitor
SSRT stop signal reactiontime
SST social skills training
SUD substance use disorder
SWA slow- wave activity
tACS transcranial alternating current stimulation
TAU treatment asusual
TBR theta to beta powerratio
TCA tricyclic antidepressant
TD tic disorders
TDC typically developing control
tDCS transcranial direct current stimulation
TMS transcranial magnetic stimulation
ToM theory ofmind
VAN ventral attention network
VBM voxel- based morphometry
VNTR variable number of tandem repeats
WCC weak central coherence
WHO World Health Organization