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Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD

Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD

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Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121(1), 65-94. doi:10.1037/0033-2909.121.1.65
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121(1), 65-94. doi:10.1037/0033-2909.121.1.65

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Psychological
Bulletin
1997, Vol. 121, No. 1.
65-94
Copyright 1997 by the American Psychological Association, Inc.
0033-29M/97/$3.00
BehavioralInhibition, Sustained Attention,
and
Executive Functions:
Constructing
a
Unifying
Theory
of
ADHD
Russell A. Barkley
Universityof Massachusetts Medical Center
Attention
deficit
hypo-activity disorder
(ADHD)
comprises
a
deficit
in behavioral inhibition. A
theoretical
model is constructed that
links
inhibition to 4 executive
neuropsychological
functionsthat appear to depend on it for their effective
execution: (a)
working memory, (b)
self-regulation
of
affect-motivation-arousal, (c)
internalization
of
speech,
and (d) reconstitution
(behavioral analy-sis
and
synthesis).
Extended
to
ADHD,
the
model
predicts
that
ADHD
should
be
associated withsecondary impairments in
these
4 executive abilities and the motor control they
afford.
The authorreviews
evidence
for
each
of
these
domains
of
functioning
and finds it to be
strongest
for
deficitsin
behavioral
inhibition, working memory, regulationofmotivation,andmotor
control
inthose withADHD. Although the
model
is promising as a potential theory of self-control and ADHD, far moreresearch is required to evaluate its merits and the many predictions it makes about ADHD.
Forover20years, attention
deficit
hyperactivity disorder(ADHD) has been viewed as comprising three primary symp-toms, these being poor sustained attention, impulsiveness,
and
hyperactivity (American Psychiatric Association [APA], 1980,1987; Barkley, 1981; Douglas, 1972,
1983).
These behavioral
deficits
arise relatively early in childhood, typically before theage of 7, and are
fairly
persistent over development (Barkley,1990;
Hinshaw,
1994; Weiss & Hechtman, 1993). The three
major
impairments now have been reduced to two,
with
hyperac-
tivity
and
impulsivity
constituting a single impairment. As aresult, three subtypes
of the
disorder
have been proposed
in the
current clinical view of ADHD
offered
in the fourth edition
of the
Diagnostic
and
Statistical Manual
of
Mental
Disorders(DSM-IV;
APA,
1994):
predominantly inattentive, predomi-
nantly
hyperactive-impulsive,andcombined types.ADHD occurs
in
approximately
3-7%
of the
childhood popu-lation (Barkley, 1990;
Szatmari,
1992), with boys being over-represented,
on
average, approximately
3:1.
The
disorder per-sists into adolescence
in
50-80%
of
cases clinically diagnosed
in
childhood
and
into adulthood
in
30-50%
or
more
of
thesesame cases (Barkley, Fischer, Edelbrock,
&
Smallish, 1990;
Russell
A. Barkley, Departments of Psychiatry and Neurology,
Univer-
sity
ofMassachusetts Medical Center.This article
was
supported
by
Grants MH45714, MH42181,
and
MH41583
from
the National Institute of Mental Health and Grant
HD28171
from the National Institute of Child Health and HumanDevelopment.I
thank
Charles Cunningham,
Eric
Mash, and Steve Hayes for theirenlightening discussions
of
this theoretical
model
and
their suggestions
for
its
improvement.
Correspondence
concerning this article should
be
addressed
to
Russell A. Barkley, Department of Psychiatry, University of Massachu-
setts
Medical Center, 55 Lake
Avenue
North, Worcester, Massachu-setts
01655.
Electronic mail may be sent via Internet to
rbarkley@
bangate
1
.ummed.edu.
Klein&
Mannuzza,
1991; Weiss & Hechtman,
1993).
Overdevelopment, ADHDisassociated with greater risksfor lowacademic achievement, poor school performance, retention
in
grade, school suspensions and expulsions, poor peer and family
relations,
anxiety
and
depression, aggression, conduct problems
and
delinquency, early substance experimentation and abuse,driving accidents and speeding
violations,
as well as
difficulties
in adult social relationships, marriage, and employment (Bark-ley,1990; Barkley, Fischer,
et
al.,
1990; Barkley,
Guevremont,Anastopoulos,
DuPaul, & Shelton, 1993; Barkley,
Murphy,
&Kwasnik, 1996, in press; Biederman, Faraone, & Lapey, 1992;Hinshaw,1994;
Murphy
& Barkley, in press; Nadeau, 1995;Weiss&Hechtman, 1993). Mostofthese developmental risksmay
be
exacerbated
by the
presence
of
comorbid
aggression-
conduct problems (Barkley, Fischer,etal., 1990; Barkleyet
al.,
1993; Hinshaw, 1987,
1992,1994).
Treatments for ADHD
often
include parent,
family,
and teacher counseling about the disor-der; parent and teacher training in behavior management tech-niques; special education resources; and
psychoactive
medica-tions (Barkley,
1990).
The history of ADHD has been reviewed elsewhere (Barkley,1990;
Schachar,
1986;Werry,
1992),
so I only
briefly
consider
it
here. Initially, the symptoms were thought to arise out of poorvolitional inhibition and defective moral regulation of behavior(Still, 1902). Later,
problems
with hyperactivity were thoughtto be the
major
feature
of the disorder (Chess, 1960;
Laufer
&
Denhoff,
1957). Eventually, Douglas
(1972;
Douglas & Peters,1979) stressedanequalif notgreater roleforpoor sustainedattention and impulse control in the disorder. She subsequentlyamendedherviewtoinclude
four
major deficits:
(a)
poor invest-ment
and
maintenance
of
effort,
(b)
deficient
modulation
of
arousal to meet situational demands, (c) a strong inclination toseek immediate reinforcement, along
with
(d) the originallyproposed
difficulties
with impulse control (Douglas, 1980,1983). Douglas (1988) later concluded that these
four
defi-
ciencies arise
from
a more central impairment in self-regulation
in
ADHD.
65
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD.Psychological Bulletin, 121(1), 65-94. doi:10.1037/0033-2909.121.1.65Chicago/Turabian: Author-DateReference List
 
66
BARKLEY
Others have argued thatthecognitive deficitsinADHDmaybest
be
understood
as amotivational
deficit (Glow
&
Glow,1979) or as arising
from
poor
stimulus
control, a diminished
sensitivity
to reinforcement, or
deficient
rule-governed behavior
(Barkley,
1981, 1989; Haenlein
&
Caul,
1987).
Such views,however,were not widely adopted, nor did they serve as an
impetusto
much
new
research.
Zentall
(1985)
set
forth
an
optimal stimulation theory
of
ADHD, arguing that
the
hyperac-
tivity
arises
from
low levels of arousal and serves to maintain
an
optimal arousal
level;
the hyperactivity, in a sense, is a
form
ofself-stimulation.More recently,
researchers
theorizing
on
ADHDhaveemphasized poor behavioral inhibition
as the
central
im-
pairment
of the
disorder (Barkley, 1990, 1994; Quay, 1988a;Schachar, Tannock,
&
Logan, 1993;
Schachar,Tannock,
Marri-
ott,
&
Logan,
1995).
In
keeping
with
this trend, in this
article
I attempt to providea
unifying
modelofADHD thatisfoundedonprior theoriesof
the
neuropsychological
functions
of thebrain's prefrontal lobes.Poor behavioral
inhibition
is specified as the central deficiency
in
ADHD. The model then sets
forth
a linkage between response
inhibition
and
four
executive functions that depend on suchinhibition for their own
effective
performance.
These
four
func-
tionsserve
to
bring behavior under
the
control
of
internallyrepresented
information
and self-directed
actions.
By doing so,
the
four
functions permit greater goal-directed actionandtask
persistence.
The
model provides
a
more comprehensive account
of
research findings on the cognitive deficits
associated
with
ADHD than does
the
current clinical
view,
which
sees
ADHD
as
primarily an attention deficit. The model
also
predicts manyadditional deficits likely to be associated with ADHD that havereceived little
or no
testing
in
research.
Such predictions provideavenues forattemptsat
falsification
of themodelandpointtonewareasforscientific investigation.
The
goal here
is
admittedly ambitious, perhaps overly
so,
because
the
model
I
propose
may be
potentially misconstrued
as a
"theory
of
everything."
Yet its
boundaries
are
generallycircumscribed
to the
domain
of
self-regulation
in
developmentalpsychology or executive functions in neuropsychology. Albeit abroad domain,it is notunlimited.It can bereadily distinguished
from
other
major domains
of neuropsychological functioning
such
as sensation and perception, memory, language, and thespatial, sequential, emotional, and motivational domains, amongothers.
The
model
may
overlap
with
these other
domains,
how-ever, to the extent that self-regulation may
affect
them. Before
I
proceed
to
discuss
the
origins
of the
model,
its
components,
and
its
extension to ADHD, the ambitiousness of this undertak-
ing
demandsa justification for why a newmodelofADHDiseven necessary at
this
time.
The
Need
for a New
Model
of
ADHD
A newtheoryofADHDisneededfor anumberofreasons.First, current researchonADHDisnearly
atheoretical,
at
least
in
regardsto itsbasic nature. That researchis
mainly
exploratory
and
descriptive,
with
two exceptions. One is Quay's
(1988a,
1988b, 1996)
use of
Gray's (1982) neuropsychological model
of
anxiety
to
explain the origin of the
poor
inhibition seen inADHD. This Quay-Gray model states that the impulsivenessarises
from an
underfunctioning
of the
brain's behavioral
inhibi-
tionsystem. That system is said to be
sensitive
to signals ofconditioned
punishment,
and the model
predicts
that those
with
ADHD should prove
less
sensitive
to
such
signals, particularlyin passive avoidance paradigms (Milich, Hartung, Martin,
&
Haigler, 1994; Quay,
1988b).
The
second exception
is the
workof
Sergeantand van der Meere
(1988;
Sergeant,
1995a,
1995b,
1996;
van der
Meere,
in
press;
van der
Meere,
van
Baal,
&
Sergeant, 1989), who
successfully
used information-processingtheory and its associated energetic model (arousal, activation,and
effort)
forisolatingthecentraldeficit(s) inADHD withinthatparadigm (Sergeant, 1995b). However, this approach
does
not
set
forth
a
theory
of
ADHD; like
the
Quay-Gray
theory,
it
makes no
effort
at
large-scale
theory construction so as to pro-vide a
unifying
account of the
various
cognitive
deficits
associ-ated with ADHD. Apart
from
these exceptions, the current
clini-cal
view of ADHD (i.e., that of the
DSM-IV)
and the vastmajority ofcurrent research being conductedon its
nature
are
not
theory driven (Taylor, 1996).Onesignofadvancementin
a
scientific field is that its research
becomes
so driven.
This
synthesis is an attempt to
move
research
on ADHD
further
along
in
that direction.
Douglas's (1980)
earlier model
of
ADHD
is not
actually
a
theory; it is mainly descriptive and was arrived at inductively
from
a
review
of the extant
research
findings on ADHD in whichDouglas
(1980,
1983; Douglas
&
Peters,
1979) discerned
a
patternamong the findings consistently noted in this field. Thatpattern comprised the
four
deficiencies noted earlier. Althoughit was tremendously
helpful
at the time, such pattern discernmentremains
at a
descriptive level,
albeit
one
more synthetic
than
prior efforts at conceptualizing ADHD. But it is neither explana-torynor, more important, predictive of new hypotheses that aretestable. It
still
begs the question of just how the pattern itself
is to be
explained.Appealing
to the
construct
of
self-regulation(Douglas, 1988)is astepin the rightdirectionbut is ofonlymodest help unless self-regulation itselfis
defined
and theman-ner in which it leads to the
four
impairments is explained. Boththe pattern and the later use of self-regulation as an explanatoryconstruct
by
Douglas
fit
well within
the
model developed below.This theory, however, goes much
further
by providing the needed
definition
of
self-regulation, articulating
the
cognitive compo-
nents
that contributeto it,specifyingtheprimacyofbehavioral
inhibition
within
thetheory,andsetting
forth
amotor controlcomponent
to
ADHD. Most important,
the
model reveals
a
diver-sity of new, untested, yet testable predictions about cognitiveand behavioral deficits deserving of
study.
A second reason why a theory of ADHD is sorely needed isthat
the
current clinical view
of
ADHD
(i.e.,
that
of the
DSM-
IV
), being purely descriptive of two behavioral
deficits
(inatten-
tion
and
hyperactivity-impulsivity),
also
cannot readily account
for
the many cognitive and behavioral
deficits
associated withADHD that are reviewed
later
in this article. To account forsuchfindings, anymodel must
fulfill
atleastfive keyrequire-ments:
(a)
It must explain why an actual
deficit
in attention inchildren with ADHD
has not
been
found
(Schachar et al.,
1993,1995; Sergeant, 1995a,
1995b;
van der
Meere,
in
press;
van der
Meere
&
Sergeant, 1988a, 1988b,
1988c),
even though research
on
parent
and
teacher ratings
of
ADHD repeatedly
identifies
a
 
INHIBITION AND ADHD
67
factor
of
"inattention";
(b) it
must explain
the
link betweenpoor behavioral inhibition
(hyperactivity-impulsivity) and
thissister impairment of inattention, or whatever this symptom turns
out
to be;
(c)
it
also
must
link these
two
constructs
with
execu-tive or
metacognitive
functions because most, if not all, of thecognitive deficits
associated
with ADHD seem to
fall
within the
realm
of
self-regulation
or executive
functions
(Barkley,
1995;
Denckla,
1994, 1995; Douglas, 1988;
Grodzinsky
&
Diamond,1992; Pennington
&
Ozonoff,
1996;
Pennington, Grossier, &
Welsh,1993;
Seidman et
al., 1995; Torgesen, 1994; Welsh, Pen-nington,
&
Grossier, 1991; Weyandt
&
Willis,
1994);
(d) it
mustultimately connecttheliteratureonADHD
with
thelargerliteratures of developmental psychology and developmental neu-ropsychology as they pertain to self-regulation and executive
functions
if it is to argue that ADHD
arises
from
a disruption
in
developmental
processes;
and (e) it
must
be
useful
as a
scien-
tific
tool and must make explicit predictions about new phenom-enathat
will
both drive research initiativesandprovideameansof
falsifying
the theory.
A
third reason for a new model of ADHD is
that
the currentview treats the subtypes of ADHD as sharing qualitatively identi-cal
deficits
inattention while
differing
onlyin the
presence
ofhyperactive-impulsive symptoms. As noted above, it is
doubtful
thatthe problems with inattention associated with
hyperactive-
impulsive behaviorlie in therealmofattention, whereas thoseseenin thepredominantly inattentive typeofADHD appearto do so. A
digression
is necessary here. The predominantly
hyperactiveimpulsive
type actually seems to be a develop-mental precursor to the combined type. In the field trial forADHD
in the
DSM-IV,
this hyperactive-impulsive type
was
chieflyfound
among
preschool
children (Applegate et
al.,1995).
In contrast, the combined type was far more representedin
school-aged
children, as was nearly the entire sample of theinattentive type. This relationship of ADHD type to the
ages
associated with it likely arises
from
a
simple
observation made
in
prior studies. The
hyperactiveimpulsive
behavior patternseems
to
emerge
first in
development, during
the
preschoolyears, whereas the symptoms of inattention associated with itappear
to
have their onset several years later,
at
least according
to
parental
reports
(Hart, Lahey, Loeber, Applegate,
&
Frick,1995; Loeber, Green, Lahey, Christ,
&
Frick,
1992).
Moreover,the types of problems with inattention seen in the predominantlyinattentive type appear to have their onset even later than those
that
would eventually
be
associated with hyperactive-impulsivebehavior (Applegate
et
al., 1995).Returning,then,
to the
start
of
this digression,
it
appears thatthepredominantly inattentive typemaynot,in
fact,
haveitsimpairment in thesame
form
ofattentionasthat
found
in theother
two
types (see Barkley, 1990; Barkley, Grodzinsky,
&
DuPaul, 1992; Goodyear & Hynd, 1992; Hinshaw, 1994; andLahey & Carlson, 1992, for reviews). Research on the
inatten-
tive subtype suggests that symptoms of daydreaming,
"spacing
out,''
being
"in a
fog," being easily
confused,
staring
frequently,
and
being lethargic, hypoactive,
and
passive
are
more common(Barkley, DuPaul, & McMurray, 1990; Lahey & Carlson,
1992).
This type of ADHD has a
deficit
in speed of informationprocessing, generally, and in focused or selective attention, spe-
cifically
(Goodyear & Hynd, 1992; Lahey & Carlson, 1992).The deficit in the combined type of ADHD has been character-ized
as
being
in the
realm
of
sustained attention
(persistence)
and
distractibility. If this distinction is valid, the present clinicalviewof ADHD may be clustering into a single set of disorders
what
are,inreality,twoqualitatively
different
disorders.
Suchadistinction would also argue that children with ADHD combinedtype
who may
develop
theinattentive
type
as
they
get
older
(because of reductions in hyperactive behavior) are not actuallychangingtypes of ADHD at all. The type of inattention that
they continue
to
manifest
(lackofpersistenceand
distractibility)
is
still qualitatively
different
from
theinattention manifestedbychildren classifiedas theinattentive type.Any newtheoryofADHD needs
to
address this emerging distinction.
The
model
presented
here provides
a
means
of
testing this dissociationbetween types of inattention by using
functional
neuroimagingmethods along with measures of the executive functions whose
deficiencies
are
linked
inthis modelto thehyperactive-impul-sive typesofADHD.
Clarification of Terms and
Assumptions
The term
ADHD
is used here to refer
only
to that subgroup
of
this population previously
identified
ashyperactive (Chess,
1960),
hyperkinetic
(APA,
1968),
attention
deficit
disorder
with
hyperactivity
(APA, 1980), ADHD (APA,
1987),
or, more re-cently,
ADHD-combined
type
and
hyperactive-impulsive
type
(APA,
1994).
In this article, ADHD and the model of it devel-oped here do not refer to that subgroup whose chief problem isinattention alone
(predominantly
inattentive
type).
The
model
set
forth below presumes that
the
essential
impair-ment in ADHD is a
deficit involving
response inhibition.
This
deficit
leads to secondary impairments in the
four
neuropsycho-
logical
abilities that are partially dependent on inhibition fortheir
effective
execution. These secondary impairments then
lead
to
decreased
control of motor behavior by internally representedinformation andself-directed action.Oneconsequenceofthishierarchical relationship
is
that improvement
or
amelioration
of
the inhibitory
deficit
should result in improvement or normaliza-tion in the
four
executive
functions
that depend on it and alsoin improved motor control. Another consequence is that thissuccessive chain of impairments creates the appearance of poorsustainedattentioninthose with ADHD. However, this inatten-tionactually represents a reduction in the control of behavior
by
theinternally represented information contributedbythese
four
executive
functions.
That
information
permitsthetrackingof the adherence of behavior to it (i.e., rules, plans, intentions,goals, time,
etc.),
thus
creating goal-directed persistence.
Behavioral
inhibition
refers
to three interrelated processes:(a) inhibition of the initial prepotent response to an event; (b)stopping
of an
ongoing response, which thereby permits
a
delay
in
the
decision
to
respond;
and (c) the
protection
of
this period
of
delayand theself-directed responses that occur
within
it
from
disruption by competing events and responses (interfer-ence
control). It is not
just
the
delay
and the
self-directed actions
within
it that are protected but also the eventual execution ofthegoal-directed
responses
generated
from
those self-directedactions(Bronowski,1977;Fuster,1989).The
prepotentre-
sponse
is
defined
as that
response
for which immediate rein-

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