AMODEL OF ATTENTION AND ITSRELATION

TO ADHD
AllanF. Mirsky,
1
* DaisyM. Pascualvaca,
1
ConnieC. Duncan,
1,2
andLouisM. French
1
1
SectiononClinical andExperimental Neuropsychology, Laboratoryof BrainandCognition, National Instituteof Mental Health,
Bethesda, Maryland
2
Clinical PsychophysiologyandPsychopharmacologyLaboratory, Department of Psychiatry, UniformedServicesUniversityof the
HealthSciences, Bethesda, Maryland
We present a neuropsychological model of attention in nor-
mal and disordered states, including attention deficit hyperactivity
disorder (ADHD). The model is based on a factor analysis of data
derived from more than 600 children and adults. The robustness of
the model is supported by its replication in a number of studies and
its application in numerous investigations. It divides attention into a
number of elements or factors including the capacities of encoding,
focusing, and executing responses, sustaining attention, shifting
attention, as well as a measure of response stability. The factors are
assessed by measures derived from neuropsychological tests; we
have posited a system of brain structures that maintains the ele-
ments of attention, each of which may be supported by a distinct
cerebral region. We illustrate the use of the model in an investiga-
tion in progress of children referred to an inner-city family clinic for
evaluation of ADHD. The ADHD study indicates that a number of
aspects of attention are impaired in children diagnosed with ADHD,
and that the deficient attention is probably not attributable to
learning disorders. We also speculate on the possible role of immatu-
rity of brain development in ADHD. Published 1999 Wiley-Liss, Inc.

MRDD Research Reviews 1999;5:169176.

KeyWords: attention; ADHD; neuropsychology; learning disorders
T
heprevalenceof attention decit hyperactivity disorder
(ADHD) in children is estimated to be between 3 and
10%[Barkley, 1996]. The fact that millions of school
children may have this disorder has stimulated considerable
scientic, not to mention commercial, interest. An entire
industry hasbeen created, fueled by the frustrationsof parents
andteachersof childrenwiththisdiagnosis; theindustryprovides
numerous pamphlets, books, rating scales, self-help formulas,
and hardware and software devices to assess, evaluate, treat,
and/ or copewithchildren(andlately, adults) withthisdiagnosis.
Oneof themost common andmost troublesomesymptomsof
personswiththisdiagnosisistheinabilitytomaintainafocusona
task, that is, to sustain attention, for an appreciable period.
According to DSM-IV, failing to pay close attention, making
carelesserrors, andhavingdifficultysustainingattentionto tasks
or playactivitiesarethemost commonsymptomsof thedisorder
[American Psychiatric Association, 1994, p. 83]. The conse-
quencesof thisimpairment in attention on theability to learn
andtomakeprogressinschool canbedevastating.
The rst part of this article deals primarily with the
development of a model of the structure of attention, and
summarizesbrieysomeof theresearchleadinguptothemodel.
The second half of the article presents preliminary analyses of
information gathered in the course of a study of attentional
capacitiesininner-citychildrenreferredtoaclinicfor evaluation
of suspectedADHD.
DEVELOPMENT OF A MODEL OF ATTENTION
The neuropsychological approach to impaired attention,
aswithanycognitivebehavior, beginswithacareful assessment
of patients symptoms. When this has been achieved, research
may be initiated towards uncovering those parts of the brain
whose injury underlies the impairment. A further step, where
possible, istoinvestigatetheetiologyor etiologiesof thedefect.
In the research to be reviewed below, we illustrate a
heuristic example of the study of attention, based on our
research. It may be considered as representative of the
neuropsychological approach to the problem of impaired
attention. Whereasour primaryfocusof interest thusfar hasnot
been in ADHD, someof our research hasclearly impinged on
theproblem[Pascualvacaet al., 1997; Reboket al., 1997; Ricks
and Mirsky, 1974]. Moreover, some of the methods we
developedinthecourseof our researchhavebeenappliedtothe
diagnosisandinvestigationof personspresumedtohaveADHD
[e.g., Barkley, 1996; Douglas, 1980; Epstein et al., 1998;
Halperinet al., 1988, 1991, 1992].
Our particular approachtothestudyof attention(asisthe
case with many advances in neuropsychology) began with a
study of soldiers injured in war. Haldor Rosvold, one of the
pioneersinthestudyof attention, hadseenmanybrain-injured
soldierswhenheservedasapsychologist intheRoyal Canadian
ArmyinWorldWar II. Hebelievedthat manyof them, andin
particular those with injury to the frontal lobes, had attention
problems. Rosvoldwascertainthat manyof thewoundedmen
*Correspondence to: Dr. Allan F. Mirsky, Section on Clinical and Experimental
Neuropsychology, Laboratory of Brain and Cognition, NIMH, NIH, Building 15K,
Room101A, 15NorthDriveMSC 2668, Bethesda, MD20892-2668.
E-mail: Allan_Mirsky@nih.gov
MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES
RESEARCH REVIEWS 5: 169176(1999)
Publ i shed 1999 Wi l ey-Li ss, Inc.

This article is a US Government
work and, as such, is in the public domain in the United States of America.
hetestedhadbrief lapsesof attentionthat
could not be measured with standard
tests. Such interruptionsof attention, he
believed, characterized some of the
wounded soldiers. Rosvold and col-
leaguesdevisedatest tomeasurethebrief
lapsesor microsleeps. Thetest, which
was called the Continuous Performance
Test, or CPT, differed from previous
measures that were said to measure
attention. TaskssuchastheArithmeticor
Digit Span subtests of the Wechsler
Bellevue Scale, which according to the
test manuals or the literature were
measures of attention, were subject-
paced. Thatis, theindividual trialsof the
task wereadministeredif andonly if the
subject wasready. In contrast, the CPT
was experimenter-paced, i.e., a con-
tinuoussample of the subjectsbehavior
was collected during an appreciable
interval of time, duringwhichthesubject
hadtoremainvigilant andontask.
After extensive pilot work, a task
wassettledonthat requiredthesubject to
watchavisual displayfor 10minutesat a
time, and to press a response key
whenever atarget(theletter X) appeared.
A second, moredifficult versionrequired
thesubject topressthekeyonlywhenX
followed the letter A. AX tasks may be
especially sensitive to impulsive behav-
iors, becausesubjectsmayrespondtothe
A beforeverifyingthat it precedesan X.
Even more difficult is the degraded
stimulusversion; other formsof thetest
havebeendevelopedfor personswhoare
unfamiliar with English letters, and for
nonliteratepersons. Figure1 illustratesa
subject performing on acurrent version
of theCPT. Auditory versionsof theX
and AX tasks have been created also.
Visual and auditory AX taskswereused
in the ADHD study reported in the
secondhalf of thisarticle.
In theearly studies, it waslearned
that braininjurywouldleadtosignicant
impairment ontheCPT. Thiswasfound
to be the case in three separate popula-
tions, each of which comprised abrain-
injured and a non-brain-injured sub-
group: children of normal intelligence,
adultsof normal intelligence, andagroup
of mentallyretardedpersons[Rosvoldet
al., 1956]. Ineachcase, thebrain-injured
groupperformedsignicantlyworsethan
the non-brain-injured group on the
CPT. It wasassumed that thismight be
related to damageto thefrontal lobesin
these subjects. Later work, discussed
below, showed this not to be the case.
However, the 1956 publication proved
tobealandmarkintheeldof neuropsy-
chological assessmentof attention. Infact,
it wasclassied officially asalandmark
publication by the Journal of NIH
Research in 1997 [Rosvold et al., 1956/
1997]. TheCPT hasprovidedastandard
for theassessment of sustained attention,
impulsivity, and processing speed for
more than 40 years. Various commer-
cially availableversionsof theCPT have
beenpublishedandaremarketed, includ-
ing the Connors, the TOVA, the IVA,
the Vigil, and the Gordon Diagnostic
System. Inaddition, theadaptationdevel-
opedbyRutschmannandCornblatt (the
Identical Pairs CPT) [1977, 1981], and
the degraded stimulus version rst de-
scribedbyNuechterleinetal. [1983]have
addedto thearmamentariumof methods
used for the assessment of sustained
attentioninclinical populations.
Theinitial suppositionthattissuein
thefrontal lobeswascritical for sustained
attention was not supported by later
studies. Thus, patients with prefrontal
lobotomies(unpublishedobservationsby
Rosvold and Mirsky), or with epilepto-
genic foci localized in the frontal lobes
were unimpaired in performance of the
CPT [Mirskyet al., 1960]. Theeffectsof
damage to other cortical regions were
examined, as well; it was found that
epileptogenic foci or removal of signi-
cant portions of the temporal lobe (to
relieveepilepticseizures) hadnoeffecton
performance of the CPT [Fedio and
Mirsky, 1969; Lansdell andMirsky, 1964;
Mirsky&Oshima, 1973].
What, then, accounted for the
ndingthat braininjury wasassociated
with impairment on the CPT? The
information obtained fromboth human
clinical studies of epilepsy and from
animal modelssupportstheviewthat the
presence of midline subcortical brain
damageor dysfunction, rather thaninjury
to any cortical area, is responsible for
impairment in sustained attention or
vigilance.
There is a category of patients in
whomtheattentional impairmentmaybe
seen in clearest form, namely, patients
with a form of idiopathic generalized
epilepsyknownasabsenceepilepsy, or to
use an earlier designation, centrencephalic
epilepsy. The term absence refers to
the symptom that these patients show,
namely: brief interruptions of attention,
usuallyaccompaniedbyabnormal electro-
encephalogram patterns, in which the
patient is briey unresponsive [Mirsky
andVanBuren, 1965].
The designation centrencephalic re-
fers to the inference that the abnormal
tissueinthisdisorder liesdeepwithinthe
center of the brain, at the level of the
brainstem reticular formation [Peneld
and Jasper, 1954]. The centrencephalic
system, asconceptualizedbyPeneldand
Jasper [1954], is illustrated in Figure 2;
according to their view, this constitutes
thefundamental organizingsystemwithin
thebrainwiththemajor responsibilityfor
themaintenanceof consciousness, arousal,
and, in particular, attention [Lindsley,
Fig. 1. Subject taking the Continuous Performance Test (CPT) of attention. The stimuli
appear on the small screen on the right of the black box, and the subjects task is to
press the response button as soon as the target (the letter X) appears. In other versions of
the test, the target is the letter X only if it follows the letter A; auditory stimuli may be
used as well.
170 MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL.
1960; Moruzzi andMagoun, 1949; Pen-
eldandJasper, 1954].
A more recent designation for
centrencephalic or absence epilepsy is
corticoreticular, which implies that
thereissomedisturbanceof therelation-
ship between deep subcortical structures
andthecortical regionswithwhichthey
are connected [Gloor, in Myslobodsky
andMirsky, 1988].
Animal model studiesof thebrain
regions critical for sustained attention
haveprovidedsupport for thecentrence-
phalic or corticoreticular hypothesis;
moreover, the subcortical regions that
may be especially critical for sustained
attention arethemesopontinebrainstem
reticular formation, midline thalamus,
andreticular nuclei of thethalamus. The
critical role of these structures has been
foundinlesionstudies, inelectrical brain
stimulation studies, and in recordingsof
singleneuron activity duringtheperfor-
manceof attentiontasks[BakayPragayet
al., 1975; Mirsky et al., 1977; Bakay
Pragay et al., 1978; Ray et al., 1982;
Mirsky and Ray, 1988; Mirsky and
Duncan, 1990]. Therefore, the poor
CPT scoresof thebrain-injuredgroupsin
our earlier studieswereprobably caused
bythepresenceof signicant numbersof
patients, inthosegroups, withsubcortical
braindamage.
We believe now that all patients
whosesymptomsincludedisturbancesin
vigilanceor sustainedattention, no mat-
ter what the diagnosis, share some
pathological involvement or disturbance
inthiscorticoreticularsystem. Thiswould
include persons with the diagnosis of
ADHD.
Furthermore, we believe that the
brainstemportion of the cerebral atten-
tion system is the primitive, but still
vitally important, platform on which
other functions of attention have been
built as the brain has developed during
evolution [MacLean, 1990]. Extensive
research conducted during the past sev-
eral decadesinfact indicatesamajor role
for limbic and neocortical structures in
the support of attention. In addition,
other studies have shown that patients
with lesions in a number of brain
structures may also have forms of im-
pairedattentionincludingneglect [Mir-
sky et al., 1991]. The structuresinclude
theinferiorparietal cortex, thehippocam-
pus, superior temporal cortex, andcorpus
striatum.
As a general principle, attentional
functions are differentiated and articu-
lated. Several yearsago, wesuggestedthat
attentive functioning results from the
coordinated action of several elements
linkedintoasystem[Mirsky, 1987, 1989;
Mirskyet al., 1991, 1995]. Thismultifac-
torial viewof attentionisinkeepingwith
information-processingstudiesthat iden-
tify a variety of functions linked to
attention such as selectivity, focusing,
sustaining concentration or vigilance,
switchingattention, distractibility, modu-
lating the intensity of attention and
attention to memorial processes such as
rehearsal, retrieval, and encoding. Based
onneuropsychological tests, weproposed
a restricted taxonomy of attentive functions.
Included within this taxonomy are the
followingfunctions: focus, execute, sustain
and stabilize, shift, and encode. This tax-
onomy wasbased, in part, on theresults
of afactor analysisof neuropsychological
test data from more than 600 subjects,
including many with disorders of atten-
tion. Thetestsselected werethought to
be especially sensitive to the effects of
poor attention.
Focus refers to the capacity to
concentrate attentional resources on a
specictask, andto beableto screenout
distracting peripheral stimuli. In our
attempts to isolate tests that tap this
capacity, we were unable to separate
focusing fromthe task demand of rapid
response. As aresult, we have used the
termfocus/ executeinanattempttocapture
theessenceof thisaspect of attention. In
our research, the tests used to measure
thisaspect of attention includetheDigit
Symbol Substitution subtest from the
Wechsler Adult Intelligence Scale-Re-
vised (WAIS-R), the Stroop Test, the
Trail MakingTest (PartsA and B) from
the Halstead-Reitan Scale, and the Tal-
land Letter Cancellation Test [Army
Individual TestBattery, 1944; Reitanand
Davidson, 1974; Stroop, 1935; Talland,
1965; Wechsler, 1981]. As reviewed in
Mirsky et al. [1991], thebrain structures
that appear tobecritical for thisattention
element comprise the superior temporal
gyrus, theinferior parietal cortex, andthe
corpusstriatum.
A second aspect of attention, sus-
tain, entailsbeingabletostayontask ina
vigilant manner for an appreciableinter-
val: not missing designated targets, re-
spondingbriskly to them, andinhibiting
responses to nontargets. Sustaining a
focusonsomeaspectof theenvironment,
as we have already discussed in some
detail, isthemajor responsibilityof rostral
midbrainstructures, includingthemeso-
pontine reticular formation and midline
andreticular thalamicnuclei. Thiscapac-
ity isassessedby scoresderivedfromthe
CPT. We assess sustained attention to
both visual and auditory stimuli, in tasks
requiringvaryingdegreesof effort. Also,
we evaluate stability of response in an
Fig. 2. The centrencephalic system may be defined as that neuron system, centering in
the higher brainstem, which has been up to the present, or may be in the future, shown to
have equal functional relationships with the two cerebral hemispheres. It forms the chief
central integrating mechanism for various areas of cortex. (From Penfield and Jasper,
Epilepsy and the functional anatomy of the human brain, 1954. Reprinted with
permission from Lippincott Williams &Wilkins, Philadelphia, PA.)
MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL. 171
attentiontaskbymeasuringthevariability
of reaction timeto target stimuli on the
CPT. Thisassessesthecapacity to main-
tainaregular, predictableresponserhythm
to task stimuli over time [Mirsky et al.,
1995].
The next element concerns the
capacity to shift attentional focus from
one aspect of astimulusto another in a
exible, efficient manner. This is mea-
suredby thevariousscoresderivedfrom
the Wisconsin Card Sorting Test, the
paradigmaticmethodof testingthiscapac-
ity [Grant and Berg, 1948]. The brain
structures that support this attention
element includethedorsolateral prefron-
tal cortexandtheanterior cingulategyrus
[Mirskyet al., 1991].
In addition, we have identied
repeatedly afourth component of atten-
tion: a mnemonic capacity to hold
information briey in mind while per-
formingsomeactionor cognitiveopera-
tion on it. This function we labeled
encode. Thisistapped by the Digit Span
andArithmetic Subtestsof theWAIS-R
[Wechsler, 1981]. The model suggests
thatthisattentionelementissupportedby
limbic system structures including the
hippocampus and the amygdala[Mirsky
et al., 1991].
Our model of attention may be
summarizedasfollows:
1. Attention is acomplex process
or set of processes. It can be
subdivided into a number of
distinct functions, including fo-
cus/ execute, sustain, stabilize, shift,
and encode. Each of thesefunc-
tions may be assessed with
measures derived from neuro-
psychological tests. Together,
thesetestscomprisean Atten-
tionBattery.
2. Thesefunctionsarethought to
besupported by different brain
regions, which have become
specialized for thispurpose but
which are nevertheless orga-
nizedintoasystem.
3. Damage to or dysfunction in
one of these brain regions can
leadtocircumscribedor specic
decits in a particular atten-
tional function.
4. The organization of the atten-
tion system allows for shared
responsibility of functions, im-
plies that the specialization is
not absolute, and that some
structures may substitute for
othersintheevent of injury.
Figure3 isasemischematic repre-
sentationof theattentionmodel wehave
proposed, with proposed assignments of
the several elements of attention to
variouspartsof thebrain.
This model, rst articulated in
1987, hasbeenfoundtobeuseful bothin
clinical practiceand in research [Mirsky,
1987]. Thefactor structurethat gaverise
to the model has been replicated by
several other groupsof investigators; this
is reviewed more fully in Mirsky et al.
[1991]. Moreover, themodel hasformed
the basis of numerous experimental
investigations of attention in clinical
populations, as well as providing a
framework for the analysis of research
dataon such populations [e.g., Barkley,
1996; Ewing-Cobbsetal., 1998; Fletcher,
1998; Halperin, 1996; Losset al., 1998;
Taylor, 1996]. TheAttention Battery
shouldbepart of everyneuropsychologi-
cal evaluation, for theadditional informa-
tionitcanprovideontheeffectsof closed
head injuries, attention decit disorders,
seizuredisorders, andcerebral infections.
Thiswill beillustrated by reviewingthe
results to date of a study of attentional
capacitiesin inner-city children referred
to a clinic for evaluation of attention
difficulties.
APPLICATIONSOF THE
ATTENTION MODEL IN
RESEARCH ON ADHD
A number of yearsago, webegana
collaboration with the staff of a family
clinicinWashington, D.C., withtheaim
of characterizing inner-city children re-
ferredforassessmentof presumedADHD.
Our primary instrument wasthe Atten-
tion Battery, as modied for children
[Mirsky et al., 1991]. This modication
entails use of forms of the tests that are
adapted for children (i.e., the use of
WISC-R subtests vs. WAIS-R subtests,
or modication of some of the test
parametersso asto achieve more nearly
normal distributionsof scores). Thisstudy
isstill in progress, but theanalysisof the
datato thispoint issufficiently advanced
to permit preliminary descriptionsof the
neuropsychological prole of the chil-
dren.
The diagnosis of the children was
based on a structured clinical interview
withoneor bothparents, observationsof
thechildduringastructuredactivity, and
teacher andparentratingscales[Erickson,
1997]. Thesubjectscomprised 119chil-
dren (94boys) referred to theclinic and
25 controls (10 boys) from the same
socioeconomic milieu as the referred
children. The mean age in years of the
groups, respectively, was 7.9 (ADHD)
and 9.0 (Controls). Because this differ-
encein agewasstatistically signicant (P
0.003), all test scorecomparisonswere
corrected by covariance analysis. Full-
scaleIQ for thetwogroupsdidnot differ
signicantly (ADHD 91; Controls
96), although thegroupsdifferedsigni-
cantly in the expected direction in
Fig. 3. Semischematic representation of the proposed brain attention system, with
tentative attributions of functional specialization to distinct brain regions. (Adapted
from Mirsky [1987].)
172 MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL.
arithmetic, reading, and spelling, as as-
sessedby theWideRangeAchievement
Test [Jastak and Wilkinson, 1984]. Se-
lected scoresfromtheAttention Battery
arepresentedinTables1and2.
Thefollowingdiscussionshouldbe
consideredaspreliminary, asitisbasedon
partial analysisof thedata. Nevertheless,
the results of the evaluation using the
Attention Battery suggest that these
childrenwiththediagnosisof ADHDare
impaired in at least three, and possibly
four, elementsof attention, ascompared
to non-ADHD controls: thecapacity to
focus on a task in the presence of
distraction, andtoexecutebrisk, efficient
responses(Trail MakingB, StroopWord);
theability to shift attention in aexible
manner (Wisconsin Card Sorting Test);
the ability to sustain attention in the
visual andauditorymodalities(CPT); and
thecapacitytomaintainastableresponse
rhythmin theauditory modality (CPT).
Although our results suggest that
responsestendto befaster intheADHD
groupthaninthecontrols, theresponses
tend to be impulsive and poorly regu-
lated. This is seen in the trend towards
more errors of commission (#Errors in
Table2), andbythesignicant difference
in responses to partial information (re-
sponsesto theletter A intheAX task [A
not X in Table 2]). The poor response
regulation is suggested by the increased
Reaction Time (RT) Variance in the
auditoryCPT.
Wecorrectedthestatistical analyses
for differencesinagebetweenthegroups;
nevertheless, the question arises as to
whether the ADHD group is simply
delayed in comparison to the control
group from a developmental point of
view. Castellanos [1997] suggests that
ADHD may represent, at least in part, a
neurodevelopmental delay. Thisconcept
of a neurodevelopmental lag is sug-
gested by work showing that children
with ADHD progress at a relatively
constant rate but with delays in social
development andcognitivetasksrelative
totheir nonaffectedpeers[Cheluneet al.,
1986; Dykens et al., 1990]. Evoked
potential data (mismatch negativity and
contingent negative variation measures)
suggestthatthesedisturbancesof informa-
tionprocessingmayreect developmen-
tal delay, but probably not in the sense
that thebrainsof thesechildrenfunction
exactly like those of younger, healthy
children [Oades, 1998]. If thisrepresents
a developmental lag, will these chil-
dren eventually achieve parity with the
controls?Theresultsof follow-upstudies
suggest that they do not. These studies
indicate that between 70%and 80%of
children diagnosed with ADHD con-
tinueto display symptomsof inattention
andpoor impulsecontrol in adolescence
and young adulthood [Barkley et al,
1990, 1991; Fisher et al., 1990; Weissand
Hechtman, 1986]. In addition, many of
thesechildrenshowantisocial personality
traits, havehadlessformal schooling, and
exhibit ahigher prevalenceof substance
abuse by adolescence [Mannuzza et al.,
1997, 1998, 1991]. The results of these
studies also suggest that the outcome of
these children depends, to some extent,
onpsychiatriccomorbidity. For example,
childrenwithADHD andconduct prob-
lemsareat anincreasedrisk for engaging
in criminal acts, having problems in
family interactions, and show greater
emotional difficultiesthan children with
ADHD without conduct problems[Bar-
kley et al., 1991; Sattereld and Schell,
1997; Wilson and Marcotte, 1996].
Children with ADHD who also have
markedimpairmentsinsocial functioning
present a signicantly higher rate of
mood, anxiety, and substance abuse
problems in adolescence compared to
ADHD children without such history
[Greeneet al., 1997]. Ingeneral, it seems
that childrenwithADHD onlyshowthe
most strikinglong-termproblemswithin
theacademic domain, but do not neces-
sarily present an increased risk for sub-
stanceabuseor criminality [Fergusson et
al., 1997; Mannuzzaet al., 1988].
Inadditiontotheimpactof psychi-
atric comorbidity, it is likely that the
developmental course and outcome of
children with ADHD depend on the
specic nature of their decits. The
diagnosis of ADHD is given to a
heterogeneous group of children who
show marked variability in their clinical
presentation and response to treatment.
There have been many attempts at
subgrouping such children on the basis,
for example, of thepresenceor absenceof
hyperactivity. Thesestudieshaveshown
that these groups of children differ in
clinical presentation, family history, and
associated symptoms. They also seemto
present a different type of attentional
disturbance [e.g., Barkley et al., 1990].
Our owndataindicatethat childrenwith
ADHD and learning problems show
different attentional proles from those
with ADHD alone [Erickson, 1997].
Littleisknown, however, about possible
differences in developmental trajectory
Table1. Performanceof ADHDandControl GroupsonTests
MeasuringEncode, Focus/ Execute, andShiftAttentionElements*
Element Test Score ADHD Control P Value
Encode Dig. span #Corr. 9.1 9.3 0.07
Encode Arith. #Corr. 8.0 9.3 0.80
Focus/ Ex. Cancel. Time(s) 83.5 65.1 0.03
Focus/ Ex. Coding #Corr. 9.0 11.0 0.02
Focus/ Ex. Stroop #Corr. (word) 45.4 50.4 0.001
Focus/ Ex. TrailsB Time(s) 95.7 71.8 0.06
Shift WCST #Categories 3.7 5.2 0.0001
Shift WCST Persev. errors 31.1 19.0 0.03
*WCST, WisconsinCardSortingTest.
Table2. Performanceof ADHDandControl GroupsonTests
MeasuringSustainandStabilizeAttentionElements*
Element Test Score ADHD Control P Value
Sustain CPT AX Vis. #Omissions 19.3 13.1 0.05
Sustain CPT AX Vis. #Errors 31.3 17.2 0.06
Sustain CPT AX Vis. A not X 6.2 2.9 0.01
Sustain CPT AX Vis. RT 0.48 0.51 0.28
Sustain CPT AX Aud. #Omissions 25.3 15.4 0.01
Sustain CPT AX Aud. #Errors 30.4 15.1 0.07
Sustain CPT AX Aud. A not X 3.3 1.6 0.03
Sustain CPT AX Aud. RT 0.71 0.73 0.46
Stabilize CPT AX Vis. Variance 218 190 0.14
Stabilize CPT AX Aud. Variance 321 273 0.03
*Themaximum#Omissionsis76. #Errorsrefersto responsesto nontargets, whereasA not X refersto responsesmadeto theletter A not
precedinganX.
RT, reactiontimeinseconds. Variance, reactiontimevariance. CPT, ContinuousPerformanceTest.
MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL. 173
and outcome between subgroups of
childrenwithADHD.
To understand the qualitatively
different disorders that fall under the
umbrellaof ADHD andtheprognosisof
theseconditions, it wouldbenecessaryto
evaluate a large group of children with
thediagnosisof ADHD. Thisevaluation
should comprise a comprehensive and
objective assessment of the different
elements of attention, as well as other
cognitive processes. By administering
periodic objective assessments to these
children, one could ascertain differences
in outcome, developmental trajectories,
and response to treatment. We faced a
similar dilemma 50 years ago in the
investigation of schizophrenia. An im-
provement in diagnostic procedures not
only led to a greater understanding of
schizophrenia spectrum disorders, but
alsototheearlyidenticationof children
who areat very high risk of developing
thedisorder. Thebenetsof conducting
thistypeof study on children diagnosed
with ADHD are particularly promising
because approximately 30% of these
children no longer show any symptoms
in adolescence. Furthermore, we know
that thesystemsthat support attentionare
by no means mature in childhood and,
therefore, arelikelytobemoremalleable
tospecicinterventions. Itiswell known,
for example, that full myelinizationof the
frontal cortical areas (which support the
Wisconsin Card Sorting Test) is not
complete until the later teens [Yalovlev
andLecours, 1967]. Moreover, full matu-
ration of other cortical and brainstem
cortical systems that support the focus/
executeandsustainelementsof attention,
respectively, alsomaynot occur until late
adolescence[YalovlevandLecours, 1967].
We know that performance on tests of
visual sustained attention may not reach
adult levelsof accuracy until age11, and
that performance on tests of auditory
sustainedattention still havenot reached
an asymptote at age 14 [Rebok et al.,
1997]. Thesedatawereobtainedfroman
inner-city population (i.e., public school
childreninBaltimore, Maryland) compa-
rable to that reported here. The good
newsisthat somechildren with ADHD
mayeventuallycatchup. Thebadnewsis
thatthenon-ADHDchildrenarecontinu-
ing to mature as well, and are likely to
leave the children with ADHD even
furtherbehindacademically. Thediscrep-
ancybetweenthegroupsiscompounded
further by the missed years of academic
experience and training of the group
with ADHD, because of their defective
attentional skills. In most inner-city
environments, the discrepancy will
probably never be corrected. (In fact,
several studieshaveshown that children
from lower SES environments have
higher degrees of ADHD at follow-
up; this is similar to the result seen in
children who growupin nonsupportive
families with a high degree of con-
ict among family members [Weiss
and Hechtman, 1986; Barkley et al.,
1991].
Another question that arisesin the
consideration of our inner-city ADHD
population concernsthepossiblecontri-
bution of learning disabilities to the
attentional decits that we have docu-
mented in Tables 1 and 2. We do not
have, at thistime, adenitiveanswer to
that question. However, someadditional
analysesweredoneonasmaller sampleof
children derived from the total sample.
Threegroupsof childrenwerecompared:
those diagnosed as ADHD (n 24)
(using the criteriadened earlier); those
diagnosed as both ADHD and learning
disabled(LD) (n20); andcontrols(n
20). LD wasdenedasscoring15points
or morebelow Full ScaleIQ on oneor
more of the subtests (Reading, Arith-
metic, or Spelling) of the Wide Range
Achievement Test, andwith an absolute
scorebelow85. Thethreegroupsdidnot
differ signicantlyinage(overall mean
8.8years) or Verbal, Performance, or Full
Scale IQ measures (mean scores ranged
from92to100).
The only task on which the
ADHDLD groups performance dif-
feredsignicantlyfromtheother twowas
in theWord and Color naming subtests
of theStroopTest. Thisisconsistent with
their generallypoor readingabilities(i.e.,
their averageWRAT Readingscorewas
76, as compared to 92 for the ADHD
groupand99for thecontrols). Ingeneral,
however, the ADHD and ADHDLD
groups performed similarly. The excep-
tion was in performance on the CPT,
whereit wasfound that theCPT scores
differentiated the pure ADHD group
fromthe ADHDLD and the controls.
RepresentativeCPT scoresarepresented
inTable3.
Theseresultsindicatethat children
with the diagnosis of ADHD alone are
more impaired on sustained attention
than those with the dual diagnosis of
ADHD and LD; this is a somewhat
counterintuitivendingthatbearsfurther
study. However, theimpairedattentional
elements in the ADHD population are
not generally attributable to learning
difficulties per se. A more complete
descriptionof theresultsof thisanalysisis
containedinErickson[1997].
SUMMARY AND
CONCLUSIONS
Wehavepresentedaneuropsycho-
logical model of attention in normal and
disorderedstates; wehavealso illustrated
theuseof themodel in thedesign of an
investigation of children referred to an
inner-city family clinic for evaluation of
ADHD. Themodel positsdistinct aspects
or elements of attention, which are
assessed by different neuropsychological
tests; thereisevidencethat eachelement
may be supported by adistinct cerebral
region. The robustness of the model is
attestedby itsreplication in anumber of
studiesanditsapplicationinanumber of
investigations. The ADHD study in
progress indicates that a number of
aspects of attention are impaired in
children diagnosed as ADHD, and that
the decient attention is probably not
attributabletolearningdisorders. Wealso
speculateonthepossibleroleof immatu-
rityof braindevelopment inADHD.
REFERENCES
AmericanPsychiatricAssociation. 1994. Diagnostic
andstatistical manual for mental disorders. 4th
ed. Washington, DC: Author.
Army Individual Test Battery. 1944. Manual of
directionsandscoring. Washington, DC: War
Department, Adjutant GeneralsOffice.
Bakay Pragay E, Mirsky AF, Fullerton BC, et al.
1975. Effect of electrical stimulation of the
brainonvisuallycontrolled(attentive) behav-
ior in the Macaca mulatta. Exp Neurol 49:
203220.
Bakay Pragay E, Mirsky AF, Ray CL, et al. 1978.
Neuronal activity in the brain stemreticular
formation during performance of a gono
go visual attention task in themonkey. Exp
Neurol 60: 8395.
Barkley RA. 1996. Critical issues in research on
attention. In: Lyon GR, Krasnegor NA,
editors. Attention, memory and executive
Table3. MeanCPT ScoresontheCPT Visual AX Task,
SelectedGroups
CPT Score ADHD ADHD LD Control P Value
#Correct 51.5 61.1 67.0 0.001
#Omissions 20.3 13.7 8.9 0.015
#Commissions 24.3 15.9 5.2 0.003
#Correct refers to correct responses to targets where the maximum #Correct is 76; similarly, the maximum #Omissions is 76.
#Commissionsreferstoresponsestonontargets, i.e., commissionerrors. LD, learningdisabled.
174 MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL.
function. Baltimore: Paul H. Brookes. p
4556.
Barkley RA, Fischer M, Edelbrock C, Smallish L.
1990. Theadolescent outcomeof hyperactive
childrendiagnosedbyresearchcriteria: I. An8
year prospectivefollow-upstudy. Amer Acad
ChildAdolescPsychiatry29:546557
Barkley RA, Fischer M, Edelbrock C, Smallish L.
1991. Theadolescent outcomeof hyperactive
children diagnosed by research criteria III.
Mother-child interactions, family conicts
and maternal psychopathology. J Child Psy-
chol Psychiatry32:233255.
BarkleyRA, GrodzinskyG, DuPaul G, et al. 1992.
Frontal lobe functions in attention-decit
disorder with and without hyperactivity: a
reviewandresearchreport. AbChildPsychol
20:163188.
CastellanosFX. 1997. Towardapathophysiologyof
attention-decit/ hyperactivity disorder. Clin
Pediatr 36: 383393.
Chelune GJ, Ferguson W, Koon R, et al. 1986.
Frontal lobedisinhibition in attention decit
disorder. ChildPsychiatryHumDev16:221
234.
Douglas VI. 1980. Attentional and cognitive
problems. In: Rutter M, editor. Developmen-
tal neuropsychiatry. New York: Guilford. p
280329.
DykensE, Leckman JF, RiddleM. 1990. Intellec-
tual, academic and adaptive functioning of
Tourettesyndromechildrenwithandwithout
attention decit disorder. J Abnorm Child
Psychol 18:607615.
EpsteinJN, ConnersCK, SitareniosG, Erhardt D.
1998. Continuousperformancetest resultsof
adults with attention decit hyperactivity
disorder. Clin Neuropsychologist 12:155
168.
Erickson K. 1997. Attentional performance in
children with attention-decit/ hyperactivity
disorder with or without comorbid learning
disabilities on neuropsychological tests. Un-
published Masters thesis. Washington, DC:
TheAmericanUniversity.
Ewing-CobbsL, PrasadM, Fletcher JM, LevinHS,
Miner ME, Eisenberg HM. 1998. Attention
after pediatric traumatic brain injury: a
multidimensional assessment. ChildNeuropsy-
chol 4:8186.
Fedio P, Mirsky AF. 1969. Selective intellectual
decits in children with temporal lobe or
centrencephalic epilepsy. Neuropsychologia
7:287300.
Fergusson DM, Lynskey MT, Horwood LJ. 1997.
Attentional difficulties in middle childhood
and psychosocial outcomes in young adult-
hood. J ChildPsychol Psychiatry38:633644.
Fisher M, BarkleyRA, EdelbrockCS, et al. 1990. J
Consult ClinPsychol 58:580588.
Fletcher JM. 1998. Attention in children: concep-
tual andmethodological issues. ChildNeuro-
psychol 4: 8186.
Gloor P. 1988. Neurophysiological mechanismof
generalized spike and wave discharge and its
implication for understanding absence sei-
zures. In: Myslobodsky MS, Mirsky AF,
editors. Elementsof petit mal epilepsy. New
York: Peter Lang. p159209.
Grant DA, BergEA. 1948. A behavioral analysisof
degree of reinforcement and ease of shifting
two new responses in a Weigl-type card
sortingproblem. J ExpPsychol 38: 404411.
GreeneRW, BiedermanJ, FaraoneSV, et al. 1997.
Adolescent outcomeof boyswith attention-
decit/ hyperactivitydisorderandsocial disabil-
ity: results from a 4-year longitudinal fol-
low-upstudy. J Consult ClinPsychol 65:758
767.
Halperin JM. 1996. Conceptualizing, describing
and measuring components of attention: a
summary. In: Lyon GR, Krasnegor NA,
editors. Attention, memory and executive
function. Baltimore: Paul H. Brookes. p
4556.
Halperin JM, Matier K, Bedi G, et al. 1992.
Specicity of inattention, impulsivity, and
hyperactivity to the diagnosis of attention-
decit hyperactivity disorder. J Am Acad
ChildAdolescPsychiatry31: 190192.
Halperin JM, SharmaV, Greenblatt E, et al. 1991.
Assessment of the continuous performance
test: reliability and validity in a nonreferred
sample. Psychol AssessJ Consult ClinPsychol
3: 603608.
Halperin JM, Wolf LE, Pascualvaca DM, et al.
1988. Differential assessment of attentionand
impulsivity in children. J Am Acad Child
AdolescPsychiatry27:326329.
Jastak S, Wilkinson GS. 1984. WRAFR: Wide
Range Achievement Test administration
manual. LosAngeles: Western Psychological
Services.
KinsbourneM. 1973. Minimal braindysfunctionas
aneurodevelopmental lag. AnnNY AcadSci
205:268273.
Lansdell H, MirskyAF. 1964. Attentioninfocal and
centrencephalic epilepsy. Exp Neurol 9:
463469.
LindsleyDB. 1960. Attention, consciousness, sleep
and wakefulness. In: Field J, Magoun HW,
Hall VE, editors. Handbook of physiology.
Washington, DC: American Physiological
Society. p15531593.
LossN, YeatesKO, EnrileBG. 1998. Attentionin
childrenwithmyelomeningocele. ChildNeu-
ropsychol 4:720.
MacLeanPD. 1990. Thetriunebraininevolution:
role in paleocerebral functions. New York:
PlenumPress.
Mannuzza S, Klein RG, Bessler A, et al. 1997.
Educational and occupational outcome of
hyperactiveboysgrownup. J AmAcadChild
AdolescPsychiatry36:12221227.
Mannuzza S, Klein RG, Bessler A, et al. 1998.
Adult psychiatric status of hyperactive boys
grownup. AmJ Psychiatry155:493498.
MannuzzaS, Klein RG, BonaguraN, et al. 1988.
Hyperactiveboysalmost grownup. II. Status
of subjects without a mental disorder. Arch
GenPsychiatry45:1318.
MannuzzaS, Klein RG, BonaguraN, et al. 1991.
Hyperactive boys almost grown up. V.
Replication of psychiatric status. Arch Gen
Psychiatry48:7783.
MirskyAF. 1987. Behavioral andpsychophysiologi-
cal markers of disordered attention. Environ
HealthPerspect 74: 191199.
Mirsky AF. 1989. The neuropsychology of atten-
tion. Elements of a complex behavior. In:
Perecman E, editor. Integrating theory and
practiceinclinical neuropsychology. Hillsdale,
NJ: Erlbaum. p7591.
Mirsky AF, Anthony BJ, Duncan CC, et al. 1991.
Analysis of the elements of attention: a
neuropsychological approach. Neuropsychol
Rev2:109145.
MirskyAF, BakayPragayE, HarrisS. 1977. Evoked
potential correlates of stimulation-induced
impairment of attention in Macaca mulatta.
ExpNeurol 57: 242256.
Mirsky AF, Duncan CC. 1990. Behavioral and
electrophysiological studies of absence epi-
lepsy. In: Avoli N, Gloor P, KostopoulosG,
etal., editors. Generalizedepilepsy: neurobio-
logical approaches. NewYork: PlenumPress.
p254269.
Mirsky AF, Fantie BD, Tatman JE. 1995. Assess-
ment of attention across the lifespan. In:
Mapou RL, Spector J, editors. Clinical
neuropsychological assessment: a cognitive
approach. NewYork: PlenumPress. p1748.
MirskyAF, OshimaHI. 1973. Effect of subcortical
aluminumcreamlesionsonattentivebehavior
and the electroencephalogram in monkeys.
ExpNeurol 39:118.
Mirsky AF, Primac DW, AjmoneMarsan C, et al.
1960. A comparison of thepsychological test
performanceof patientswithfocal andnonfo-
cal epilepsy. ExpNeurol 2:7589.
MirskyAF, RayC. 1988. Studiesintheneuropsy-
chology of attention impairment: human
symptoms and animal models. In: Galbraith
GC, Kietzman ML, Donchin E, editors.
Neurophysiology and psychophysiology: ex-
perimental andclinical applications. Hillsdale,
NJ: Erlbaum. p114137.
MirskyAF, VanBurenJM. 1965. Onthenatureof
the absence in centrencephalic epilepsy: a
study of some behavioral, electroencephalo-
graphic and autonomic factors. Electroen-
cephalogr ClinNeurophysiol 18: 334348.
Moruzzi G, Magoun HW. 1949. Brain stem
reticular formationandactivationof theEEG.
ElectroencephalogrClinNeurophysiol 1:455
473.
Nuechterlein KH, Parasuraman R, JiangQ. 1983.
Visual sustainedattention: imagedegradation
produces rapid sensitivity decrement over
time. Science220:327329.
OadesRD. 1998. Frontal, temporal andlateralized
brain function in children with attention-
decit hyperactivity disorder: apsychophysi-
ological andneuropsychological viewpointon
development. BehavBrainRes94:8395.
PascualvacaD, AnthonyB, ArnoldLE, et al. 1997.
Attention performancein an epidemiological
sampleof urbanchildren. Theroleof gender
and verbal intelligence. Child Neuropsychol
3:1327.
Peneld W, Jasper H, editors. 1954. Epilepsy and
the functional anatomy of the human brain.
Boston: Little, Brown.
Ray C, Mirsky AF, Bakay Pragay E. 1982.
Functional analysis of attention-related unit
activity in the reticular formation of the
monkey. ExpNeurol 77: 544562.
Rebok GW, Smith CB, Pascualvaca DM, et al.
1997. Developmental changes in attentional
performancein urban children fromeight to
thirteen years. Child Neuropsychol 3:2846.
Reitan RM, Davidson LA, editors. 1974. Clinical
neuropsychology: current statusand applica-
tions. Washington, DC: V.H. Winston and
Sons.
Ricks NL, Mirsky AF. 1974. Sustained attention
and theeffectsof distraction in underachiev-
ing second-grade children. J Educ Boston
Univ156:417.
RosvoldHE, Mirsky AF, Sarason I, et al. 1956. A
continuousperformancetest of braindamage.
J Consult Psychol 20:343350. Reprintedasa
Landmark Publication in J NIH Res1997;9:
4148.
Rutschmann J, Cornblatt B, Erlenmeyer-Kimling
L. 1977. Sustainedattentioninchildrenat risk
for schizophrenia. Arch Gen Psychiatry 34:
571575.
Rutschmann J, Cornblatt B, Erlenmeyer-Kimling
L. 1981. Sustainedattentioninchildrenat risk
for schizophrenia: ndingswithtwocontinu-
ous performance tests in a new sample. J
AbnormChildPsychol 14:365385.
SattereldJH, Schell A. 1997. A prospectivestudy
of hyperactive boys with conduct problems
MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL. 175
andnormal boys: adolescent andadult crimi-
nality. J AmAcad Child Adolesc Psychiatry
36:17261735.
Stroop JR. 1935. Studies of interference in serial
verbal reactions. J ExpPsychol 18:643662.
TallandGA. 1965. Derangedmemory. NewYork:
AcademicPress.
Taylor HG. 1996. Critical issues and future
directions in the development of theories,
models, and measurements for attention,
memory, and executive function. In: Lyon
GR, Krasnegor NA, editors. Attention,
memory and executive function. Baltimore:
Paul H. Brookes. p399412.
Wechsler D. 1981. Wechsler Adult Intelligence
ScaleRevised: manual. New York: Psycho-
logical Corporation.
WeissG, HechtmanL. 1986. Hyperactivechildren
grownup. NewYork: GuilfordPress.
Wilson JM, Marcotte AC. 1996. Psychosocial
adjustmentandeducational outcomeinadoles-
centswith achildhooddiagnosisof attention
decit disorder. J Am Acad Child Adolesc
Psychiatry35:579587.
YakovlevPI, LecoursAR. 1967. Themyelogenetic
cyclesof regional maturationof thebrain. In:
Minkowski A, ed. Regional development of
the brain in early life. Oxford: Blackwell. p
370.
176 MRDD RESEARCH REVIEWS A MODEL OF ATTEN TI ON MI RSKY ET AL.