Executive Functions in ADHD

Executive Functions in
Attention-Deficit/Hyperactivity Disorder
Alysa E. Doyle, Ph.D.

Objective: To examine the association between weaknesses in executive functions and attention-
deficit/hyperactivity disorder (ADHD). Method: Empirical studies examining executive functions in
ADHD samples were reviewed, with particular attention to results of recent meta-analyses. Results:
ADHD is associated with impaired performance on measures of response inhibition, working
memory, and other aspects of executive functions, yet data also suggest significant neuropsychologi-
cal variability within and across ADHD samples. Conclusion: ADHD may be best conceptualized
as a neuropsychologically heterogeneous condition. More work is needed to characterize this hetero-
geneity and its clinical and pathophysiologic implications.
(J Clin Psychiatry 2006;67[suppl 8]:21–26)

A lthough the diagnosis of attention-deficit/hyper-

activity disorder (ADHD) is made based on be-
havioral symptoms of inattention and/or hyperactivity/
and a growing recognition that certain behaviors in hyper-
active youth, including poor planning, difficulty sustain-
ing mental set, and responsiveness to external structure,
impulsivity, numerous empirical and theoretical papers resembled those of patients and animals with prefrontal le-
over the past 3 decades have highlighted neurocognitive sions.4 Together, these findings laid the groundwork for
impairments, particularly in the domain of executive func- the hypothesis that ADHD is associated with impaired
tions (EFs), that are associated with the disorder. Despite prefrontal-striatal neural networks that regulate attention,
this large body of literature, the core neuropsychological inhibition, and motor intentional behavior. Over time, this
impairments in ADHD have not been fully resolved. The hypothesis has continued to be supported by the success of
current article reviews this body of work, emphasizing stimulant medications and animal models of hyperactivity
recent meta-analytic findings as well as evidence suggest- that implicate catecholamine pathways consistent with
ing that ADHD is best conceptualized as a neuropsycho- these neuroanatomical regions5 as well as structural and
logically heterogeneous condition. functional neuroimaging studies documenting associated
abnormalities in the dorsolateral prefrontal cortex, the an-
HISTORICAL PERSPECTIVE terior cingulate cortex, the caudate nucleus, and the globus
pallidus in ADHD patients.6 Recent findings (e.g., Berquin
Although early reports of the syndrome now known as et al.7) also highlight involvement of cerebellar regions
ADHD focused on hyperactivity as the defining feature of with a high concentration of dopamine transporters and
the disorder,1 the 1970s saw a major shift in emphasis on connectivity to prefrontal regions via midbrain structures.
attentional deficits as a result of Douglas’ studies of vigi-
lance in hyperkinetic children.2 At the same time came NEUROPSYCHOLOGICAL FINDINGS
greater insights into the functions of the prefrontal cortex3
ADHD vs. Control Group Differences
Consistent with the fronto-striatal hypothesis is a large
From the Department of Psychiatry, Massachusetts General literature revealing that individuals with ADHD exhibit
Hospital, Harvard Medical School, Boston.
This article is derived from the planning teleconference relatively poor performance on clinical neuropsychologi-
“New Developments in the Treatment of Attention-Deficit/ cal tests of attention and EFs presumed to measure pre-
Hyperactivity Disorder,” which was held May 16, 2005, and
supported by an educational grant from Cephalon, Inc.
frontal dysfunction.8 The term executive functions refers
The author thanks Erik Willcutt, Ph.D.; Joel Nigg, Ph.D.; to higher-order cognitive processes that underlie self-
Larry Seidman, Ph.D.; and Bruce Pennington, Ph.D., for regulation and goal-directed behavior,9 including working
comments on a related manuscript that informed the
current article. memory, response inhibition, set shifting, abstraction,
Corresponding author and reprints: Alysa E. Doyle, Ph.D., planning, organization, fluency, and certain aspects of
Massachusetts General Hospital, Department of Child
Psychiatry, YAW 6-6A, 55 Fruit Street, Boston, MA 02114 attention.10 Although studies of EFs in ADHD have pri-
(e-mail: doylea@helix.mgh.harvard.edu). marily targeted preadolescent boys, impairments on EF

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Alysa E. Doyle

measures have also been documented in females (e.g., ate weighted mean effect sizes for Trails B and CPT omis-
Hinshaw et al.11), adolescents (e.g., Seidman et al.12), and sions and commissions (0.55–0.59) but slightly lower
adults with ADHD (e.g., Lovejoy et al.13). Moreover, in effect sizes for the WCST (0.35) and the ROCF (0.24).
many studies, executive deficits are robust to statistical cor- In their article, nonexecutive measures yielded a smaller
rection for group differences in IQ and comorbid psychiat- overall effect size (0.39) compared with executive mea-
ric or learning disorders (e.g., Willcutt et al.14). This large sures (0.58), suggesting some specificity of an EF deficit in
number of studies has prompted several theoretical and ADHD; however, they and others also found moderate
meta-analytic papers aimed at more precisely defining the decrements in processing speed (0.40–0.65),19,28 vigilance
EF deficits in ADHD. (i.e., CPT omissions; 0.50–0.64),19,20,28 and overall intel-
The most well-known theoretical models of ADHD have lectual functioning (0.61),28 causing some researchers to
argued that specific aspects of EFs represent the “core” or question whether deficits in ADHD extend beyond the ex-
“primary” deficit in the disorder. To date, inhibitory control ecutive domain (e.g., Boonstra et al.,19 Frazier et al.28).
has been the most widely discussed core deficit in ADHD,15
with numerous studies supporting weaknesses on clinical Heterogeneity Within ADHD
and experimental measures of inhibition in individuals with Despite the well-replicated EF weaknesses in ADHD
ADHD versus non-ADHD controls.16,17 Nigg18 has argued subjects, variability between studies has been noted in con-
for specification of the construct of inhibition as a way of ceptual reviews (e.g., Pennington and Ozonoff 8) and has
clarifying the core deficits in ADHD, concluding that there been statistically supported for a variety of measures in
is stronger evidence for an inhibitory deficit when the defi- several meta-analyses,19,26,28 suggesting that it is not simply
cit refers to suppression of a prepotent motor response due to sample error. Recently, researchers have also noted
(e.g., on the stop signal test or basic go/no-go tasks), but variability within ADHD samples that is evident when
more variable evidence when inhibition refers to suppres- examining whether EF measures can be used to diagnose
sion of a conflicting response (e.g., interference control on ADHD. Data on male29 and female11 youth as well as
Stroop or flanker tests). Nigg’s argument has been sup- adults13 have indicated that many measures of EF have
ported by meta-analyses that found moderate to large effect good positive predictive power for ADHD but poor nega-
sizes for the stop signal reaction time (SSRT; 0.54– tive predictive power. That is, abnormal scores on EF mea-
0.85)16,17,19–21 and small to moderate effect sizes for the sures are generally predictive of the diagnosis; however,
Stroop Interference score (0.13–0.35).20–22 normal scores on a particular EF measure, or even a com-
Working memory represents another aspect of EF that is bination of measures,29 cannot rule ADHD out. This pat-
of significant interest to ADHD researchers23 due to neuro- tern is due to the fact that not every person with ADHD is
imaging studies showing that working memory tasks acti- impaired on every test and that some individuals with
vate fronto-striatal and cerebellar regions (e.g., Lewis et ADHD perform within the normal range on all or most
al.,24 Chen and Desmond25) and because of the face validity measures.
that trouble holding and manipulating information “on Even the well-replicated response inhibition weakness
line” contributes to ADHD symptoms. Although results is only present in a subset of individuals with ADHD. For
of individual studies are varied, meta-analyses support example, Crosbie and Schachar30 found that only 40%
working memory impairments in ADHD.19,20,26 The most of their ADHD sample fell in the impaired range on the
recent analysis by Martinussen and colleagues26 suggests SSRT. Similarly, Nigg and colleagues31 found that only
larger effect sizes for different measures of spatial working half of the ADHD Combined-Type subjects assessed at dif-
memory (0.85–1.06) versus verbal working memory (0.47– ferent ADHD research centers across the United States ex-
0.56). As these authors point out, such findings are consis- hibited SSRT scores that surpassed the 90th percentile of
tent with the neuroimaging literature that finds greater sup- controls. In this analysis, no other individual neurocogni-
port for right versus left hemispheric involvement in tive measure examined was impaired in more than 50%
ADHD.27 of ADHD subjects. Percent of subjects that surpassed the
Although response inhibition and working memory 90th percentile cutoff on other tests (including the Stroop,
are the EF weaknesses most often discussed in theories Trails B, CPT commissions, and the variability of reaction
of ADHD, meta-analyses indicate decrements of moderate time [RT] on the stop signal test) ranged from 48% to 16%
magnitude in other EF domains as well. Willcutt et al.20 at different research sites. In the Nigg et al. study31 and an-
found impairments of moderate magnitude (ds = 0.43– other recent paper,32 aggregating tests to assess a general
0.69) for measures of planning (Tower tests), organization EF deficit still only identified a subsample of ADHD cases.
(Rey-Osterreith Complex Figure [ROCF]), set shifting
(Wisconsin Card Sorting Test [WCST]), impulsivity (con- Potential Moderators of
tinuous performance test [CPT] commissions), and pro- Neuropsychological Heterogeneity
cessing speed that includes a set-shifting component Although neuropsychological heterogeneity within
(Trails B). Frazier and colleagues28 similarly found moder- ADHD has not been extensively acknowledged or studied,

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 Executive Functions in ADHD

the literature raises several possible factors that may be as- Hyperactive/Impulsive type (ADHD-H/I; d = –0.35).
sociated with variability of performance on EF measures. Yet, the small number of studies targeting ADHD-H/I
Family history. Two research groups have shown an as- and/or symptoms of hyperactivity/impulsivity have failed
sociation between a family history of ADHD and EF im- to show expected EF deficits.41–44 Thus, further investiga-
pairment. Crosbie and Schachar30 found that ADHD chil- tion of cognitive impairments differentially associated
dren with poor inhibition on the stop signal test had a with inattentive and hyperactive/impulsive symptom di-
significantly higher rate of familial ADHD (48%) com- mensions is warranted.
pared with a normal-inhibition ADHD group (19%) and Developmental differences. Although adolescents
controls (8%). Seidman et al.33 also found that youth with are underrepresented in the ADHD literature, studies
ADHD who had a family history of ADHD performed suggest similarities across preteen and teenage years
more poorly on subtests of the Stroop and WCST than (e.g., Seidman et al.45). Adults are less well studied than
youth with ADHD who did not have a family history of the youth but seem to show EF impairments as well19,21;
disorder.12,33 These reports raise the possibility that familial however, some differences with child samples have
and nonfamilial cases of ADHD differ neuropsycho- emerged in meta-analyses. Schoechlin and Engel46 found
logically. Further work is needed to determine whether minimal impairments on measures of planning and ab-
such differences are qualitative or quantitative. stract problem solving in adults with ADHD, possibly due
Comorbid disorders. The presence of comorbid dis- to ceiling effects of the tasks or to the most impaired
orders may exacerbate or modify the neuropsychological adults not being available for assessment.21 Lijffijt et al.17
profile of youth with ADHD. Several studies (e.g., Willcutt also found that although children and adults showed mod-
et al.,14 Seidman et al.,34 Lazar and Frank,35 Rucklidge erate to high decrements on the SSRT, adults showed
and Tannock36) have shown that individuals with ADHD greater discrepancy between baseline RT and SSRT,
with comorbid learning disorders have greater EF deficits which the authors argue is the best measure of response
than individuals with ADHD alone. However, data from inhibition. Nonetheless, given the small number of neuro-
meta-analyses are mixed. On the Stroop, van Mourik et psychological studies of adults, differences across adult
al.22 found that children with ADHD alone had better and child samples require further confirmation. Finally,
Word and Color Naming scores than individuals with read- preschool-aged children with ADHD have received mini-
ing disorders (with or without ADHD) but worse in- mal attention, with 1 such study documenting EF impair-
terference scores. Martinussen et al.26 found that comorbid ments47 and 2 failing to find them in this age group.48,49
reading and language disorders explained some of the Because most of the available data are cross-sectional,
variance among studies in spatial but not verbal working longitudinal studies are needed to better understand the
memory domains. Additionally, these authors found great- course of neuropsychological impairments within ADHD
er effect sizes for different domains of spatial working across the life span.
memory in studies that controlled for reading and
language. Normal-Range Performance
Neuropsychological studies of other comorbidities in Although the above discussion highlights factors
ADHD are fewer in number. The handful of studies of that may contribute to the neuropsychological variability
youth with ADHD and comorbid anxiety disorders suggest within ADHD samples, it does not address the fact that
that the comorbid subgroup shows less severe deficits in many individuals with ADHD do not exhibit deficits on
response inhibition than ADHD children without anxiety37 any EF measure. This section discusses possible reasons
but more severe deficits on working memory tasks.38,39 Al- for this normal-range performance.
though there have been more neuropsychological studies Executive function measures may not always capture
of ADHD plus conduct disorder, meta-analyses have not frontal system impairments. One possibility is that EF
found support for comorbid conduct disorder as a modera- measures are imperfect indicators of frontal impairment
tor of response inhibition in ADHD.16,17 or the latent construct of EF due to either (1) measure-
DSM-IV subtypes. It has been hypothesized that ment error or (2) compensatory mechanisms that allow
different patterns of EF weaknesses might distinguish some individuals to use alternative cognitive resources to
between ADHD Inattentive (ADHD-I) and Combined sub- solve “frontal” system tasks. Among the factors that may
types (ADHD-C)40; however, meta-analyses do not pro- introduce error into the measurement of EF weaknesses is
vide clear support for neuropsychological differences be- low sensitivity (for a full discussion of these factors, see
tween these subtypes. Willcutt et al.20 found no significant Doyle et al.50). Because many measures of EF were devel-
differences between ADHD-C and ADHD-I on any EF oped to assess the effects of a significant cerebral insult in
measure (mean d = 0.09 ± 0.10), and Lijffijt et al.17 found adults,8 such tests may not capture mild cognitive impair-
no effect for subtype with regard to SSRT. In contrast, van ments occurring within the context of development. Since
Mourik et al.22 found that ADHD-I showed greater individuals with EF deficits are highly responsive to ex-
deficits in interference control than ADHD-C or ADHD ternal structure,51 the structured testing situation may also

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Alysa E. Doyle

mask less severe impairments.52 These possibilities imply in conjunction with EF deficits as a neurocognitive mech-
a range of severity of EF impairments in ADHD, with anism in ADHD but are unlikely to account for all ADHD
EF measures capturing the more impaired end of the cases.
distribution. Delay aversion is a construct grounded in an animal
Compensatory mechanisms that allow some individu- model of altered reinforcement and extinction processes.61
als to recruit other cognitive resources to solve tasks that Based on this model, Sagvolden and colleagues61 posit
would normally engage frontal circuits may also explain that goal-directed behavior in youth with ADHD requires
normal-range performance. Neuroimaging studies of pa- frequent, potent reinforcers proximal to the behavior
tients with other disorders53,54 provide evidence of this being reinforced. If such reinforcers are lacking or distal,
phenomenon and suggest that such compensatory mecha- inattention and motor impulsivity occur. Consistent with
nisms are vulnerable to disruption.55 Although this possi- this model, Sonuga-Barke and colleagues62 have shown
bility has not been studied extensively in ADHD, Bush that children with ADHD exhibit aversion to delay, show-
and colleagues56 found that both ADHD adults and con- ing preferences for smaller, immediate rewards compared
trols experienced an interference effect on a counting ver- with larger, delayed rewards. Solanto et al.63 found that
sion of the Stroop test, but controls activated the anterior measures of inhibitory control and delay aversion were not
cingulate cortex when performing the task, while those correlated in ADHD subjects; however, the 2 measures to-
with ADHD activated the insula. These data require rep- gether identified the majority of ADHD cases in a dis-
lication; yet, the fact that performance was equivalent criminant function analysis. Based on these and other data,
across groups suggests alternative pathways for problem- Sonuga-Barke64 has proposed a dual pathway model of
solving. ADHD involving both EF and delay aversion. Although
Executive function deficits may not be the core deficit further data are needed to determine whether the predic-
in some or all ADHD cases. A second possibility is that tions of this model are borne out, this theory marks an im-
EF deficits may not be the core or only causal deficit un- portant contribution to the field as the first formal model
derlying ADHD. Impairments in state regulation and delay of neuropsychological heterogeneity in ADHD.
aversion are interesting candidate deficits to consider in
ADHD, because their association with the disorder is sup- SUMMARY AND IMPLICATIONS:
ported by theory and data and because they may relate NEUROPSYCHOLOGICAL HETEROGENEITY
to the neuropsychological heterogeneity within ADHD OF ADHD
samples. Due to space constraints, we describe these con-
structs briefly and refer the readers to recent reviews for The literature supports the association between ADHD
further details.57,58 and deficits in response inhibition, working memory, and
Sergeant59 has proposed the cognitive-energetic model broadly conceived domains of EF. Yet, data also reflect
of ADHD in which impairments on tasks requiring effort- neuropsychological variability within ADHD, with factors
ful control of attention and executive processes could such as family history of the disorder, comorbidity, symp-
be due, in part, to deficiencies in activation, arousal, and tom dimensions, and developmental stage potentially as-
effort that control the allocation of cognitive resources sociated with differential performance on EF measures.
rather than impaired cognitive resources per se. Consistent Moreover, the small proportion of individuals with ADHD
with this theory is evidence that the rate of presentation of who show normal-range EF performance raises questions
stimuli affects ADHD subjects differently than controls, of whether non-EF deficits, such as impairments in state
with slow rates of presentation related to poor perfor- regulation and delay aversion, underlie symptoms of
mance, potentially due to underarousal.59 Thus, it has been ADHD as well. Thus, this disorder may be best understood
suggested that the slower inhibitory process found in stud- as a neuropsychologically heterogeneous condition. While
ies of the stop signal test may reflect an arousal problem it is possible that measurement error accounts for some
rather than an inhibition problem per se.60 One potential of the observed variability, true neuropsychological het-
index of such state regulation difficulties is variability of erogeneity would be consistent with the phenotypic het-
RT, a measure of the consistency of the speed of a re- erogeneity of ADHD (e.g., symptom-based subtypes and
sponse after a stimulus. As reviewed by Castellanos and various comorbid presentations), the disorder’s likely ge-
Tannock,23 RT variability is one of the most replicated netic heterogeneity,65 and the heterogeneity found across
deficits in ADHD. Yet, RT variability may not be universal ADHD neuroimaging studies.6
within ADHD. In Nigg and colleagues’ study of heteroge- Behavioral genetic data provide further support for the
neity,31 only half of ADHD subjects from different re- notion that EF deficits are etiologically linked to ADHD
search sites fell in the impaired range on RT variability on but do not represent the single underlying deficit in the
the stop signal test, despite a relatively large effect size disorder. Because ADHD is highly heritable, if EF weak-
overall (Cohen’s d = 0.8). Thus, these data suggest that nesses were the primary deficit that gave rise to ADHD
arousal/energetic factors are clearly important to consider symptoms, family, twin, and adoption studies would be

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 Executive Functions in ADHD

expected to reveal significant familial/genetic overlap lar genetic studies of ADHD.50 For conditions that are
between ADHD and performance on EF measures. Al- likely influenced by multiple genetic and nongenetic fac-
though the limited literature on this topic suggests that tors, biologically based phenotypes that lie in the pathway
some of the same familial and genetic influences on from genes to behavior (i.e., “endophenotypes”) may pro-
ADHD also influence impairments on EF measures, the vide a more powerful target for molecular genetic studies
magnitude of the shared familial/genetic influences is low than the disorder as a whole. Because EF impairments par-
to moderate,50 suggesting that either a significant pro- tially index the familial/genetic liability for ADHD, they
portion of these influences on ADHD differ from those may be useful for identifying at least some of the genes
on EF measures or else that some factor (e.g., measure- that confer susceptibility to ADHD or the chromosomal
ment error or heterogeneity) is limiting the detection of the regions that harbor them. In turn, expression studies may
shared influences. The fact that aggregating neuropsycho- serve to further elucidate the pathophysiology of the
logical measures often slightly increases the magnitude of disorder, including potential heterogeneous processes and
familial/genetic overlap suggests that some measurement differences and commonalities between ADHD and other
error exists but that it is unlikely to be the sole reason for neurodevelopmental disorders that also show EF im-
the modest overlap.50 pairments.8 Thus far, the use of EF measures as ADHD
Given these data, ADHD researchers should move be- endophenotypes is just beginning to be explored.
yond the search for a single, core cognitive deficit to for-
mally study the nature of the neuropsychological heteroge- CONCLUSION
neity in ADHD. What remains to be better understood, in
addition to the impact of the potential moderating vari- Although elegant theories have emphasized specific
ables discussed above, is whether there are separate and EF deficits as underlying ADHD, careful examination
unique pathways to ADHD (e.g., some individuals with EF of the empirical literature suggests neuropsychological
deficits and some with delay aversion, as hypothesized by heterogeneity within the disorder. Formal recognition and
Sonuga-Barke58) or whether there is a pool of overlapping further investigation of this heterogeneity are essential
risk factors that contribute variably to all cases of ADHD. for clinical purposes and have the potential to further
Documenting this heterogeneity is important from a our understanding of pathophysiologic processes, which,
clinical perspective. The fact that individuals with ADHD in turn, will engender novel prevention and intervention
do not show a consistent profile of EF impairments ren- strategies.
ders neuropsychological testing inappropriate as a diag-
nostic tool.29 Importantly, normal-range performance on Disclosure of off-label usage: The author has determined that,
to the best of her knowledge, no investigational information
EF measures should not be used to rule out ADHD if care- about pharmaceutical agents that is outside U.S. Food and Drug
ful diagnostic interviewing and behavioral rating scales Administration–approved labeling has been presented in this article.
support the diagnosis. Clinicians may need to educate
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