Behavioural Brain Research 130 (2002) 29 – 36

www.elsevier.com/locate/bbr

Psychological heterogeneity in AD/HD—a dual pathway model of

behaviour and cognition
Edmund J.S. Sonuga-Barke *
Centre for Research into Psychological De6elopment, Department of Psychology, Uni6ersity of Southampton, Southampton SO17 1BJ, UK

Received 23 December 2000; accepted 13 August 2001

Abstract

Psychological accounts have characterised attention-deficit/hyperactivity disorder (AD/HD) as either a neuro-cognitive disorder
of regulation or a motivational style. Poor inhibitory control is thought to underpin AD/HD children’s dysregulation while delay
aversion is a dominant characteristic of their motivational style. A recent ‘head to head’ study of these two accounts suggest that
delay aversion and poor inhibitory control are independent co-existing characteristics of AD/HD (combined type). In the present
paper we build on these findings to propose a dual pathway model of AD/HD that recognises two quite distinct sub-types of the
disorder. In one AD/HD is the result of the dysregulation of action and thought resulting from poor inhibitory control associated
with the meso-cortical branch of the dopamine system projecting in the cortical control centres (e.g. pre-frontal cortex). In the
other AD/HD is a motivational style characterised by an altered delay of reward gradient linked to the meso-limbic dopamine
branch associated with the reward circuits (e.g. nucleus accumbens). The two pathways are further distinguished at the levels of
symptoms, cognitive and motivation profiles and genetic and non-genetic origins. © 2002 Elsevier Science B.V. All rights reserved.

Keywords: Attention deficit/hyperactivity disorder; Heterogeneity; Inhibitory control; Executive function; Delay aversion; Dopamine; Meso-limbic;
Meso-cortical; Birth complications

1. Introduction counter findings relating to the involvement of particu-

Despite the great scientific interest it has aroused,
attention-deficit/hyperactivity disorder (AD/HD) re-
mains among the least well characterised of mental
disorders. Historically, there have been difficulties in
precisely specifying the symptom structure of a disorder
that is heterogeneous in nature and has close associa-
tions with other problems of childhood [44,53]. Many
of these nosological and definitional ambiguities have
been resolved in the most recent diagnostic formula-
tions with the specification of separate diagnoses for
sub-types of the disorder [26,14]. A refined phenotype,
which limits diagnosis to more severe and pervasive
patterns of symptoms, has also been proposed [55].
Despite these developments, there are still inconsisten-
cies in findings regarding the underlying psychological
mechanisms responsible for AD/HD. Findings and
* Tel.: +44-23-80594604.
E-mail address: ejb3@soton.ac.uk (E.J.S. Sonuga-Barke).
lar psychological mechanisms in the disorder are regu-
larly published and even where some consistency of
findings is observed the size of statistical effects is often
only small to moderate. One possible contributory fac-
tor to this situation is the way that theoretical develop-
ments tend to be driven by the search for one
underlying mechanism that could provide the basis for
a ‘grand theory’ of AD/HD. This tendency has been
encouraged by currently dominant cognitive neuro-psy-
chological models of AD/HD. These accounts first reify
AD/HD as an ontological and psychological reality [17]
(rather than just a useful clinical construct) and then
attempt to explain it by reference to endogenous psy-
chological dysfunction caused by impairments in spe-
cific brain modules [19]. Even those theorists, who have
rejected the modular accounts of dysfunction proposed
by the neuro-psychological model, have tended to
search for grand theories. The heterogeneity of its
clinical expression and its multi-factorially determined
aetiology makes achieving the sort of theoretical unity
required by such models of AD/HD unlikely [58].

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30 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36
In the current paper, we describe a recent study
which provides a strong impetus for a dual pathway
model of combined type AD/HD. Two pathways are
proposed. In one, AD/HD is a disorder of dysregula-
tion of thought and action associated with diminished
inhibitory control. In the other, it is a motivational
style (delay aversion) associated with fundamental al-
terations in reward mechanisms. In part one of the
paper we review research on inhibitory control in, and
the effects of delay on, AD/HD children. In part two
we describe a ‘head to head’ study contrasting disinhi-
bition and delay aversion as characteristics of AD/HD.
The dual pathway model is developed in part three. The
final part extends the discussion of the model by mak-
ing predictions about the distinctive characteristics of
AD/HD arising from the two pathways.
1.1. AD/HD — deficient inhibitory control or delay
a6ersion
Neuro-psychological studies converge on the view
that AD/HD is associated with problems of executive
or higher order control functions [4]. AD/HD children
lack attentional and strategic flexibility, display poor
planning and working memory and fail to effectively
monitor their behaviour [12,11]. While such difficulties
are shared with a range of psychopathologies [8] the
primary role of deficient inhibitory control in the emer-
gence of this pattern of dysregulation seems to distin-
guish AD/HD from other disorders [3,5,35]. The best
evidence in support of this assertion comes from the
now large number of studies using the stop signal
paradigm (SSP [42]). This paradigm tests an individu-
al’s ability to inhibit an already initiated pre-potent
response to a ‘go signal’ (typically visual) when sig-
nalled to do so by a ‘stop signal’ (typically auditory)
presented at varying intervals prior to the expected time
of the individuals ‘go’ response. Both the slope of the
probability of inhibition given different stop intervals
and the stop signal reaction time (SSRT) provide mea-
sures of the efficiency of inhibitory processes. A recent
meta-analysis [30] and a number of subsequent studies
[41,28] show that AD/HD children have a flatter proba-
bility of inhibition slope and longer SSRTs. These
effects are of moderate to large size and appear consis-
tent at least across clinical samples [22]. The association
of AD/HD with deficient inhibitory control seems more
robust than that with other executive functions (e.g.
working memory [31]).
While models emphasising disinhibtion and dysregu-
lation dominate the current literature, a number of
alternative accounts have been proposed that emphasise
the motivational basis of AD/HD [15,63,18]. The delay
aversion hypothesis represents the most radical depar-
ture from the dominant neuro-psychological paradigm
[46]. This model is based on the assumption that AD/
HD behaviours are functional expressions of an under-
lying motivational style rather than the result of
dysfunctioning regulatory systems. According to this
hypothesis AD/HD children are motivated to escape or
avoid delay. Their inattentive, overactive and impulsive
behaviours therefore represent functional expressions of
what has been termed delay aversion. The model pre-
dicts that when faced with a choice between immediacy
and delay AD/HD children will choose immediacy [50],
when no choice is available they will act on their
environment to reduce their perception of time during
delay by either creating or attending to non-temporal
feature of the environment [1]. The resulting behaviour,
because of its likely task incompatibility, is labelled as
inattentive and overactive. In this model cognitive
deficits associated with the provision, protection and
use of time, such as working memory and planning,
arise as secondary effects of delay aversion associated
with patterns of reduced task engagement [52].
The majority of research on delay aversion in AD/
HD has concentrated on AD/HD children’s unwilling-
ness to wait for delayed rewards and events. There is
now good evidence that AD/HD children prefer imme-
diate over large delayed rewards under many circum-
stances [23]. This has been interpreted as further
evidence for deficient inhibitory control by some. How-
ever, a series of experiments have demonstrated that the
preference for immediacy is exercised only under cer-
tain conditions. Furthermore, there appears to be a
double dissociation between preference for delayed re-
wards and inhibitory control [50,48,52]. These studies
suggest that in some situations AD/HD children can
wait for rewards (to the same extent as controls) even
when this involves ongoing inhibition. In other situa-
tions they fail to wait for rewards when no inhibition is
required. But in general they will not wait for rewards
if this increases the total amount of delay experienced.
Taken together these results suggest that AD/HD chil-
dren’s decisions not to wait for rewards or events,
which appear to be the result of problems of on-going
inhibition, are often the results of an aversion to delay.
The delay aversion and the deficient inhibitory con-
trol accounts both represent attempts to develop a
unitary ‘grand’ theory of AD/HD. Not surprisingly,
and given their opposed philosophical origins, the find-
ings in support of each are difficult to account for with
reference to the other. However, there are one or two
possibilities worth exploring. First, it is possible that
the slower SSRT displayed by the AD/HD children are
an artefact related to the temporal structure of the SSP
rather than a true reflection of inhibitory problems.
Given the relative infrequency of stop signals compared
with go signals the longer SSRTs may be the result of
the different inter-stimulus-interval (ISI) durations be-
tween go and stop signals. Such ISI effects have been
found frequently with AD/HD children and have been
 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36
interpreted as either a problem with state regulation [7]
or due to the impact of delay on attention (i.e. an
expression of delay aversion; [51]). Second, it is possible
that deficient inhibitory control leads to poor perfor-
mance on tasks extended over time so that delay itself
becomes associated with negative emotions and ac-
quires an aversive quality. On an empirical level both of
these explanations of the co-existence of delay aversion
and inhibitory control problems would predict a high
level of association between performance on the SSP
and delay choice tasks.
1.2. Delay a6ersion and poor inhibitory control
‘head-to-head’
In order to clarify the relationship between these two
core characteristics of AD/HD a ‘head to head’ study
was recently performed in conjunction with the NIMH
multi-treatment study [45]. The ‘head to head’ ap-
proach employed in this study represented an extremely
potent test of the competing theories because,
1. both theoretical camps ‘signed up’ to the study and
its outcome.
2. both camps selected what was in their view the best
and most appropriate measure of ‘their’ theoretical
constructs (inhibitory control vs. delay aversion).
3. the data was collected at multiple sites indepen-
dently of either theoretical camp.
Children with a diagnosis of AD/HD (combined
type) and control children performed: (i) the standard
stop signal task [56] and (ii) a choice delay task which
was essentially the same as the task used in the first
delay aversion study [50]. In this task children chose
between small immediate (1 point after 3 s) and large
delayed reward (2 points after 30 s). Trials followed one
after the other as soon as rewards were delivered and
there was a fixed number of trials per session. This
meant that AD/HD children could reduce delay by
choosing the small reward but that in doing so they
would reduce the amount of rewards earned over a
session. The key feature of this type of task, in relation
to its current use, is that the response inhibition load in
the task is trivial and no greater for a choice of the
large delayed than the small immediate reward. This is
because, receiving the large reward does not depend on
withholding a response over the 30 s of the pre-reward
delay period. The child is active when making the
choice, but passive between the choice and the delivery
of the reward.
Three aspects of the results were particularly signifi-
cant for the current discussion. First, performance on
the two tasks as represented on the key measures
(SSRT and preference for the large delayed reward) was
not correlated. Second, there was an effect of AD/HD
on performance of both tasks (with a large effect size)
which was not altered when comorbid conduct prob-
31
lems or anxiety disorders were taken into account.
Third, using a stepwise discriminant function procedure
the two measures together proved highly diagnostic,
correctly identifying nearly 90% of cases.
While confirming that delay aversion and poor in-
hibitory control are core, but unrelated, characteristics
of AD/HD these results are clearly difficult to reconcile
within either ‘grand theory’ of AD/HD. In fact the
independence of these measures combined with their
high diagnostic value encourages the view that AD/HD
is the product of two quite distinct processes (one
underpinned by deficient inhibitory control and the
other mediated by delay aversion). The model of AD/
HD outlined below builds on this idea by specifying
these processes in terms of two pathways from neuro-
biological systems through psychological processes to
behaviour and performance.
1.3. A dual pathway model of the de6elopment of
AD/HD
The model (schematically represented in Fig. 1) de-
scribes AD/HD as a developmental outcome of two
quite distinct psychological/developmental processes.
At a more abstract level, the model represents a recon-
ciliation of two philosophically distinct views of be-
havioural disorder— one that seeks to identify the site
of dysfunction in disorder while the other seeks to
explore the role of function. One route characterises
AD/HD as predominantly a motivational style medi-
ated by the emergence of delay aversion during child-
hood. The second sees it as predominantly a disorder of
the regulation of thought and action resulting from
inhibitory dysfunction. Each route has a number of
different components expressed at different conceptual
levels. First, there is the developmental outcome. In the
model this is separated into behavioural symptoms
(impulsiveness, inattention and overactivity) and task
engagement— the quality and quantity of task or prob-
lem focused activity. Second, are the psychological
processes that underpin these developmental outcomes.
These can be subdivided into the primary or core
characteristic and secondary process characteristics. In
this sense deficient inhibitory control is the primary
characteristic and cognitive and behavioural dysregula-
tion are its secondary manifestations. According to the
model delay aversion and inhibitory deficits exist at
different conceptual levels; delay aversion being a sec-
ondary effect of a combination of fundamental alter-
ations in reward mechanisms and characteristics of the
child’s early environment.
The dysregulation of thought and action pathway
(DTAP-solid line) is characterised by a core dysfunc-
tion in inhibitory control. In the current model, this has
two mediated effects on the developmental outcome—
it causes both behavioural symptoms and poor quality
32 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36

task engagement. The emergence of AD/HD symptoms
is mediated by behavioural dysregulation while the
effects on task engagement are mediated by cognitive
dysregulation. Such cognitive dysregulation can be seen
by the pattern of difficulties displayed by AD/HD
children on tasks requiring attentional flexibility, be-
havioural monitoring, planning and working memory.
In the model there is no direct pathway between execu-
tive functions and AD/HD symptoms. This reflects the
more modest associations between measures of these
functions and AD/HD symptoms reported in the litera-
ture [31].
In addition to the primary (though mediated) effects
on the quality of task engagement, the model makes
novel predictions of secondary behavioural effects on
task engagement. Inattentive, impulsive and overactive
behaviours inevitably reduce the amount of effective
processing time on tasks. According to the model, the
effect of primary cognitive deficits on task performance
is compounded by this secondary factor. Furthermore,
through a feedback loop from task engagement-quan-
tity to executive function we acknowledge the possibil-
ity that this reduction in the quantity of task
engagement can over time limit the opportunity for the
development of those higher order skills associated with
the provision, protection and utilisation of time. In the
model DTAP AD/HD arises out of alterations within
the higher order control circuits of the brain and there-
fore implicates the frontal and pre-frontal regions and
their associated circuitry with projections from the
basal ganglia and into the striatum being particularly
important [36].
Functions sub-served by this circuit are regulated by
dopamine activity as part of a functionally and anatom-
ically distinct meso-cortical branch of the dopamine
system [13,20].
The motivational style pathway (MSP-dashed line)
provides an alternative route to AD/HD. As mentioned
above delay aversion is not the core characteristic of
the motivational pathway in this model. Rather, it is an
acquired characteristic, which mediates the link be-
tween behavioural symptoms, task engagement and a
more fundamental biologically based alteration in re-
ward mechanisms [18]. In identifying altered reward
mechanisms as underpinning this motivational style the
model builds on evidence from animal studies showing
that AD/HD symptoms can result from a shortened
‘delay of reward gradient’ [38–40]. This means that
AD/HD children discount the value of future events at
a higher rate than other children. This leads to a

Fig. 1. A schematic representation of the dual pathway model of AD/HD. The solid line represents the pathway for AD/HD as a disorder of the
regulation of thought and action. The dashed line represents AD/HD as a motivational style.
 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36
preference for immediacy—i.e. behavioural impulsive-
ness. However, while clearly a key element of the
disorder, the AD/HD combined type symptom pattern
is not reducible to impulsiveness. Furthermore, as we
have demonstrated AD/HD impulsiveness (choice of
immediacy over delay) is conditional on the choice
context. In the present model, the link between AD/HD
behaviours and altered reward mechanisms is mediated
by the emergence over time of a generalised aversion to
delay. We employ a simple associative conditioning
mechanism to account for this development. The short-
ened delayed reward gradient leads the child to repeat-
edly fail to effectively respond to contextual demands
related to waiting and delay. Delay rich settings there-
fore come to acquire aversive properties through associ-
ation with the negative emotions associated with such
failure. Explicit in this mechanism is the moderating
role of cultural practices on the effect of these altered
reward mechanisms. Such effects are also likely to differ
between families. Parents who set unrealistically high
standards and are unforgiving of failures to wait are
more likely to create the context for the emergence of
delay aversion and AD/HD in impulsive children. In
keeping with previous formulations of the hypothesis,
the expression of delay aversion is context dependent.
Inattention and overactivity occurring in no choice
delay settings and impulsiveness in choice settings.
While this pathway represents a predominantly motiva-
tional route, there are secondary acquired cognitive
characteristics. The impact of AD/HD behaviour on
the quantity and quality of task engagement will be
similar to that proposed for the DTAP (disrupting the
provision, protection and utilisation of time) and there
are parallel lines for the two pathways connecting be-
haviour to engagement and through to executive dys-
function. In this case, however, this does not represent
a compounding influence on existing cognitive dysregu-
lation, but rather might be regarded as leading to a
cognitive profile that mimics elements of such dysregu-
lation. In this model MSP AD/HD is associated with
alterations in brain reward circuits especially the ven-
tral –striatal network (including the nucleus accumbens)
[33,34,37,43] associated with the meso-limbic branch of
the dopamine system [6,21].
1.4. Distincti6e features of the two pathways
While the DTAP and the MSP are potential routes to
the same AD/HD combined type diagnosis (i.e. inatten-
tive, overactive and impulsive behaviour), the model
allows a number of predictions about their distinctive
properties to be made. Some of these are outlined
below:
1. Structural and functional aspects of symptoms:
while both DTAP and MSP AD/HD will meet
criteria for combined type diagnosis their symptoms
33
are predicted to have distinct functional and struc-
tural characteristics. DTAP AD/HD arises from
dysfunction while MSP AD/HD is a functional
expression of a motivational style. Therefore, MSP
AD/HD is more likely to vary as a function of
environmental context (especially its delay structure
and stimulus quality). DTAP AD/HD should be
predominantly context independent. Furthermore,
given its dysfunctional origins, DTAP AD/HD is
more likely to ‘behave’ like a disease category with
DTAP AD/HD children appearing qualitatively dif-
ferent from children within the normal range. The
behaviour of MSP AD/HD children, on the other
hand, may be best characterised as an extreme
expression of a normally distributed trait. There has
been debate about the underlying structure of AD/
HD. Is it a category or a continuum [25,47,61]? This
model suggests, it depend on the sub-type in
question.
2. Cognitive profile: it is expected that DTAP AD/HD
will be associated with significantly more severe and
generalised cognitive impairment. This is because,
the cognitive dysregulation associated with poor
inhibitory control is compounded by the effects of
behavioural symptoms on the child’s opportunity to
develop the ability to effectively provide, protect
and utilise processing time. Impairment associated
with MSP AD/HD will be restricted to this latter
form. MSP AD/HD children should not show
deficits on those tasks and in those functions that
do not tap inter-temporal competencies. Further-
more, it is possible that given their intact control
systems children with MSP have the potential to
adapt to the constraints imposed on performance by
their condition so developing alternative informa-
tion processing strategies [48,49].
3. Genetic and non-genetic aetiology: it is possible that
the two subtypes of AD/HD can be distinguished
on the basis of activity within the meso-cortical
(DTAP) and meso-limbic (MSP) dopamine systems.
Most recent attention has focused on genetic varia-
tions identifying associations between AD/HD and
polymorphisms in the D4 receptor [24,29]. The sig-
nificance of this finding with regard to the dual
pathway model is unclear. The D4 receptor is
widely distributed in the brain at relatively low
densities and may not be specifically related to
either dopamine branch [27]. Of more interest for
the current model would be abnormalities in two
other specific dopamine receptors. The D1 receptor
seems to play a central role in regulating pre-frontal
activity [2,32], while alterations in the D2 receptor
are important for reward processes [6,21] and may
be directly implicated in moderating the value of
delayed rewards [60]. The role of the dopamine
transporter (DAT), which regulates levels of extra-
34 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36
cellular dopamine also needs to be clarified with
regard to these two AD/HD pathways [62]. Non-ge-
netic factors are also likely to be important in the
aetiology of the disorder and the extent of involve-
ment of such factors may also allow us to distin-
guish between the two pathways. A recent study has
suggested no association between inhibitory control
and D4 receptor polymorphisms in a group of
AD/HD children [54]. It is possible that factors
such as birth related trauma, may make a significant
non-shared genetic contribution to DTAP AD/HD
so masking the absolute contribution of genetic
factors. There is evidence that both executive func-
tion performance and AD/HD symptoms are asso-
ciated with this factor [10,16] and that these
processes may be mediated by dopamine activity [9]
and alterations in the fronto– striatal system [59].
The central role of associative learning in the MSP
opens up the possibility that AD/HD could be
associated with environmental risks of a purely
social nature rather than those mediated by neuro-
biology. For instance, delay aversion might arise
under situations where parents or other significant
adults fail to follow through on promised rewards
leading to a distrust of future events and an unwill-
ingness to wait. AD/HD, which has developed in
this situation, should be amenable to psycho-social
interventions.
4. Environmental moderation: Taylor [57] has pro-
vided a number of developmental models for the
emergence of AD/HD through the interaction of
genetic risk and environmental factors. Although, a
discussion of these factors is beyond the scope of
the current paper, the current model also highlights
the role of social and cultural factors in moderating
the effects of biological factors. In the MSP path-
way inflexible and demanding parenting, combined
with unrealistically high expectations for self-con-
trol, is seen as a condition for the emergence of
delay aversion so providing the setting for the emer-
gence of AD/HD.
Further, although no specific predictions are made
within the model about the protective significance of
effective and positive parenting, it is likely that this
could ameliorate the negative effect of genetic and
non-genetic factors at a number of levels within the
model.
2. Concluding remarks
In the current paper, we have argued that combined
type AD/HD has two quite distinct sub-types that can
be distinguished primarily in terms of their underlying
psychological mechanisms but secondarily in terms of
the context dependant nature of symptoms, their cogni-
tive/motivational profile, their genetic and non-genetic
origins and the role of environmental factors in moder-
ating risk. The model predicts that DTAP AD/HD will
be context independent, associated with relatively
severe and generalised cognitive dysregulation, be cate-
gorical in nature and be less strongly associated with
genetic factors. MSP AD/HD will be context depen-
dent, have a more limited pattern of cognitive impair-
ment associated with the provision, protection and
utilisation of time, be a continuously distributed trait
and be more closely associated with genetic factors.
Future research should focus on exploring the coher-
ence of these two pathways, the extent to which they
act interactively or additively and their combined
power to characterise AD/HD.
References
[1] Antrop I, Roeyers H, Van Oost P, Buysse A. Stimulation
seeking and hyperactivity in AD/HD children. J Child Psychol
Psychiatry 2000;41:225 – 32.
[2] Arnsten AMT. Catecholamine regulation of the pre-frontal cor-
tex. J Psychopharmacol 1997;11:151 – 62.
[3] Barkley RA. Behavioural inhibition, sustained attention, and
executive functions: constructing a unified theory of AD/HD.
Psychol Bull 1997;121:65 – 94.
[4] Barkley RA, Grodzinsky G, DuPaul G. Frontal lobe functions
in attention deficit disorder with and without hyperactivity: a
review and research report. J Abnorm Child Psychol
1992;20:163 – 88.
[5] Bayliss DM, Roodenrys S. Executive processing and attention
deficit hyperactivity disorder: an application of the supervisory
attentional system. Dev Neuropsychol 2000;17:161 – 80.
[6] Blum K, Wood RC, Braverman ER, Chen TJH, Sheridan PJ.
The D2 dopamine-receptor gene as a predictor of compulsive
disease —Bayes theorum. Funct Neurol 1995;10:37 – 44.
[7] Borger N, van der Meere J. Motor control and state regulation
in children with ADHD: a cardiac response study. Biol Psychol
2000;51:247 – 67.
[8] Bradshaw JL, Sheppard DM. The neurodevelopmental frontos-
triatal disorders: evolutionary adaptiveness and anomalous later-
alization. Brain Language 2000;73:297 – 320.
[9] Brake WG, Sullivan RM, Gratton A. Perinatal distress leads to
lateralized medial prefrontal cortical dopamine hypofunction in
adults rats. J Neurosci 2000;20:5538 – 43.
[10] Bylund B, Cervin T, Finnstrom O, Gaddlin PO, Leijon I, Mard
S, Samuelsson S, Sandstedt P, Warngard O. Very low-birth-
weight children at 9 years: school performance and behavior in
relation to risk factors. Prenatal Neonatal Med 2000;5:124 – 33.
[11] Cepeda NJ, Cepeda ML, Kramer AF. Task switching and
attention deficit hyperactivity disorder. J Abnorm Child Psychol
2000;28:213 – 26.
[12] Clark C, Prior M, Kinsella GJ. Do executive function deficits
differentiate between adolescents with AD/HD and oppositional
defiant/conduct disorder? A neuropsychological study using the
six elements test and hayling sentence completion test. J Abnorm
Child Psychol 2000;28:403 – 14.
[13] Goldman-Rakic PS. Dopamine mediated mechanisms in the
pre-frontal cortex. Semin Neurosci 1992;4:149 – 60.
[14] Gomez R, Harvey J, Quick C, Scharer I, Harris G. DSM-IV
AD/HD: confirmatory factor models, prevalence and gender and
age differences based on parent and teacher ratings of Australian
 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36
primary school children. J Child Psychol Psychiatry
1999;40:265– 74.
[15] Haenlein M, Caul W. Attention deficit disorder with hyperactiv-
ity: a specific hypothesis of reward dysfunction. J Am Acad
Child Adolesc Psychiatry 1987;26:356 –62.
[16] Harvey JM, O’Callaghan MJ, Mohey H. Executive function of
children with extremely low birth weight: a case control study.
Dev Med Child Neurol 1999;41:292 –7.
[17] Jensen PS, Hoagwood K. The book of names: DSM-IV in
context. Dev Psychopathol 1997;9:231 –49.
[18] Johansen EB, Aase H, Meyer A, Sagvolden T. Attention deficit/
hyperactivity disorder behaviour explained by dysfunctional re-
inforcement and extinction processes, Behav Brain Res
2002;130:37– 45.
[19] Karmiloff-Smith A. Development itself is the key to understand-
ing developmental disorders. Trends Cogn Sci 1998;2:389 – 98.
[20] Knable MB, Weinberger DR. Dopamine, the prefrontal cortex
and schizophrenia. J Psychopharmacol 1997;11:123 –31.
[21] Koob GF. Dopamine, addiction and reward. Semin Neurosci
1992;4:139 – 48.
[22] Kuntsi J, Stevenson J. Hyperactivity in children: a focus on
genetic research and psychological theories. Clin Child Family
Psychol Rev 2000;3:1 – 22.
[23] Kuntsi J, Oosterlaan J, Stevenson J. Psychological mechanisms
in hyperactivity I: response inhibition, deficit, working memory
impairment, delay aversion or something else. J Child Psychol
Psychiatry 2001;42:199 – 210.
[24] LaHoste GJ, Swanson JM, Wigal SB, Glabe C, Wigal T,
Kennedy JL, Dopamine DR. receptor gene polymorphism is
associated with attention deficit hyperactivity disorder. Mol Psy-
chiatry 1996;1:121 – 4.
[25] Levy F, Hay DA, McStephen M, Wood C, Waldman I. Atten-
tion-deficit hyperactivity disorder: a category or a continuum?
Genetic analysis of a large-scale twin study. J Am Acad Child
Adolesc Psychiatry 1997;36:737 –44.
[26] McBurnett K, Pffifner LJ, Willcutt E, Tamm L, Lerner M,
Ottolini YL, Furman MB. Experimental cross validation of
DSM-IV types of attention deficit/hyperactivity disorder. J Am
Acad Child Adolesc Psychiatry 1999;38:17 –24.
[27] Muglia P, Jain U, Macciardi F, Kennedy JL. Adult attention
deficit hyperactivity disorder and the dopamine D4 receptor
gene. Am J Med Genet 2000;96:273 –7.
[28] Nigg J. The AD/HD response-inhibition deficit as measured by
the stop task: replication with DSM-IV combined type-extension
and qualification. J Abnorm Child Psychol 1999;27:393 – 402.
[29] Oak JN, Oldenhof J, Van Tol HHM. The dopamine D-4 recep-
tor: one decade of research. Eur J Pharmacol 2000;405:303 – 27.
[30] Oosterlaan J, Logan GD, Sergeant JA. Response inhibition in
AD/HD, CD, co-morbid AD/HD+CD, anxious, and control
children; a meta-analysis of studies with the stop task. J Child
Psychol Psychiatry 1998;39:411 –25.
[31] Pennington BF, Ozonoff S. Executive functions and develop-
mental psychopathology. J Child Psychol Psychiatry
1996;37:51– 87.
[32] Robbins TW. Chemical neuromodulation of frontal-executive
functions in humans and other animals. Exp Brain Res
2000;133:130 – 8.
[33] Robbins TW, Everitt BJ. Functions of dopamine in the dorsal
and ventral striatum. Semin Neurosci 1992;4:119 –28.
[34] Robbins TW, Everitt BJ. Neurobehavioural mechanisms of re-
ward and motivation. Curr Opin Neurobiol 1996;6:228 –36.
[35] Ross RG, Harris JG, Olincy A, Radant A. Eye movement task
measures inhibition and spatial working memory in adults with
schizophrenia, AD/HD and a normal comparison group. Psychi-
atry Res 2000;95:35 – 42.
[36] Rubia K, Overmeyer S, Taylor E, Brammer M, Williams SCR,
Simmons A, Bullmore ET. Hypofrontality in attention deficit
35
hyperactivity disorder during higher-order motor control: a
study with functional MRI. Am J Psychiatry 1999;156:891 –6.
[37] Sagvolden T. The attention deficit disorder might be a reinforce-
ment deficit disorder. In: Georgas J, Manthouli M, Besevegis E,
Kokkevi A, editors. Contemporary Psychology in Europe: The-
ory, Research and Application. Gottengin: Hogrefe and Huber,
1991:131 – 43.
[38] Sagvolden T, Sergeant JA. attention deficit/hyperactivity disor-
der-From brain dysfunction to behaviour. Behav Brain Res
1998;94:1 – 10.
[39] Sagvolden T. Behavioral validation of the spontaneously hyper-
tensive rat (SHR) as an animal model of attention-deficit/hyper-
activity disorder (AD/HD). Neurosci Biobehav Rev
2000;24:31 – 9.
[40] Sagvolden T, Aase H, Zeiner P, Berger D. Altered reinforcement
mechanisms in attention-deficit/hyperactivity disorder. Behav
Brain Res 1998;94:61 – 71.
[41] Schachar R, Mota VL, Logan GD, Tannock R, Klim P. Confir-
mation of an inhibitory control deficit in attention deficit/hyper-
activity disorder. J Abnorm Child Psychology 2000;28:227 –35.
[42] Schachar R, Logan GD. Impulsivity and inhibitory control in
normal development and childhood psychopathology. Dev Psy-
chology 1990;26:710 – 20.
[43] Shultz W. Predictive reward signal of dopamine neurons. J
Neurophysiol 1998;80:1 – 27.
[44] Simonoff E. Extracting meaning from comorbidity: genetic
analyses that make sense. J Child Psychol Psychiatry
2000;41:667 – 74.
[45] Solanto MV, Abikoff H, Sonuga-Barke E, Schachar R, Logan
GD, Wigal T, Hechtman L, Hinshaw S, Turkel E. The ecological
validity of delay aversion and response inhibition as measures of
impulsivity in AD/HD a supplement to the NIMH multi-modal
treatment study of AD/HD. J Abnorm Child Psychol
2001;29:215 – 28.
[46] Sonuga-Barke EJS. Annotation: On dysfunction and function in
psychological theories of childhood disorder. J Child Psychol
Psychiatry 1994;35:801 – 15.
[47] Sonuga-Barke EJS. Categorical model in child psychopathology;
a conceptual and empirical analysis. J Child Psychol Psychiatry
1998;39:115 – 33.
[48] Sonuga-Barke EJS, Houlberg K, Hall M. When is impulsiveness
not impulsive?; the case of hyperactive children’s cognitive style.
J Child Psychol Psychiatry 1994;35:1247 – 53.
[49] Sonuga-Barke EJS. Internal length and time use in AD/HD; A
comparison of 4 models. J Abnormal Child Psychol, in press.
[50] Sonuga-Barke EJS, Taylor E, Sembi S, Smith J. Hyperactivity
and delay aversion I: the effect of delay on choice. J Child
Psychol Psychiatry 1992;33:387 – 98.
[51] Sonuga-Barke EJS, Taylor E. The effect of delay on hyperactive
and non-hyperactive children’s response times. J Child Psychol
Psychiatry 1992;33:1091 – 6.
[52] Sonuga-Barke EJS, Williams E, Hall M, Saxton T. Hyperactivity
& delay aversion III; the effect on cognitive style of imposing
delay after errors. J Child Psychol Psychiatry 1996;37:189 –94.
[53] Spencer T, Biederman J, Wilens T. Attention deficit disorder and
comorbidity. Pediatr Clin North Am 1999;46:915 – 27.
[54] Swanson J, Oosterlaan J, Murias M, Schuck S, Flodman P,
Spence MA, Wasdell M, Ding Y, Chi H, Smith M, Mann M,
Carlson C, Kennedy JL, Sergeant JA, Leung P, Zhang Y, Sadeh
A, Chen C, Whalen CK, Babb KA, Moyzis R, Posner MI.
Attention deficit/hyperactivity disorder children with a 7-repeat
allele of the dopamine D4 receptor gene have extreme behaviour
but normal performance on critical neuro-psychological tests of
attention. Proc Natl Acad Sci 2000;97:4754 – 9.
[55] Swanson JM, Sergeant JA, Taylor E, Sonuga-Barke EJS, Jensen
PS, Cantwell DP. Attention deficit/hyperactivity disorder and
hyperkinetic disorder. Lancet 1998;351:429 – 33.
36 E.J.S. Sonuga-Barke / Beha6ioural Brain Research 130 (2002) 29–36
[56] Tannock R, Schachar R, Logan G. Methylphenidate and cogni-
tive flexibility-dissociated dose effects in hyperactive-children. J
Abnorm Child Psychol 1995;23:235 –66.
[57] Taylor E. Developmental neuropsychology of attention deficit
and impulsiveness. Dev Psychopathol 1999;11:607 – 28.
[58] Todd RD. Genetics of attention deficit disorder: are we ready for
molecular genetic studies. Am J Med Genet 2000;96:241 – 3.
[59] Toft PB. Prenatal and perinatal striatal injury: a hypothetical
cause of attention-deficit-hyperactivity disorder. Pediatr Neurol
1999;21:602 – 10.
[60] Wade TR, de Wit H, Richards JB. Effects of dopaminergic drugs
on delayed reward as a measure of impulsive behaviour in rats.
Psychopharmacology 2000;150:90 – 101.
[61] Waldman ID, Robinson BF, Rowe DCA. logistic regression
based extension of the TDT for continuous and categorical
traits. Ann Hum Genet 1999;63:329 – 40.
[62] Waldman ID, Rowe DC, Abramowitz A, Kozel ST, Mohr JH,
Sherman SL, Cleveland HH, Sanders ML, Card JHC, Stever C.
Association and linkage of the dopamine transporter gene and
attention-deficit hyperactivity disorder in children: heterogeneity
owing to diagnostic subtype and severity. Am J Hum Genet
1998;63:1767 – 76.
[63] Zentall SS, Zentall TR. Optimal stimulation: a model of disor-
dered activity and performance in normal and deviant children.
Psychol Bull 1983;94:446 – 71.