Neuropsychology Review, VoL 4, No.

3, 1994

A Selective and Critical Review of

Neuropsychological Deficits and the Frontal Lobes

Ralph M. Reitan 1,2 and D e b o r a h Wolfson 1

Presumptions about the functions of the frontal lobes, and the sensitivity and
specificity of certain tests to measure frontal lobe functions, are having a
substantial influence on both clinical and research conclusions. In this paper
the authors examine the details of the studies that have contributed to these
presumptions, and find that the evidence to support these conclusions is weak_
A detailed evaluation of the evidence relating to the 14qsconsin Card Sorting
Test and the Thurstone Word Fluency Test is also presented. Finally, the
development of the belief that frontal lobe functions can be specifically
measured is reviewed. Th( authors of this paper conclude that the "bewildering
array" of deficits attributed to frontal lesions still seems to prevail.
KEY WORDS: frontal lobe functions; Wisconsin Card Sorting Test; Thurstone Word Fluency
Test; General vs. specific deficits.

INTRODUCTION

In the late 1930s and 1940s a great surge of interest ha t~d l~'orIta!
lobes appeared i0 the literature, only to wane in the 1950s (Hecaen and
Albert, 1978; personal observations). A resurgence of interest be~t~ is fla~
late 1970s and continues to the present time. Many factors contribut~ ro
this phasic attention to the frontal lobes, including (1) the large anatomical
area of the brain occupied by the frontal lobes (Damasio, 1991), (2) atten-
tion captured by the explosion of interest in right-brain/left-brain differen-
tiated functions (Gazzaniga et al., 1963; Sperry et al., 1969), and (3) the

1Reitan Neuropsychology Laboratory, Tucson, Arizona.

21"o whom correspondence should be addressed at Reitan Neuropsychology Laboratory, 2920
South 4th Avenue, South Tucson, Arizona 85713-4819.

161
1040-7308/94/0900-0161507.00/09 1994Plenum PublishingCorporation
 162 Reitan and Wolfson

availability of the frontal lobes to be assigned to the more general functions

of adaptive abilities not already claimed by more posterior areas of the
brain (nature abhors a vacuum).
Even a brief perusal of the recent literature reveals the current em-
phasis being placed on the frontal lobes in neuropsychological functioning.
A casual literature review identified 16 articles published within the last
few years that reached conclusions about the frontal lobes. Eight articles
reported empirical findings (Axelrod et al., 1992; Boone et al., 1990; Fiducia
and O'Leary, 1990; Gnys and Willis, 1991; Grodzinsky and Diamond, 1992;
Rybash and Colilla, 1994; Shute and Huertas, 1990; Welsh et al., 1991); in
one article the authors reported a meta-analysis of tests for diffuse brain
damage, and felt it was useful to include a category of tests intimately re-
lated to the frontal lobes (Chouinard and Braun, 1993); and seven theo-
retical review articles were devoted to explicating frontal and prefrontal
functions (Goldman-Rakic, 1993; Grafman et al., 1993; Hart and Jacobs,
1993; Lezak, 1993; Schwartz et aL, 1993; Sohlberg et al., 1993; Varney and
Menefee, 1993).
The topics of the empirical articles included the following:
1. the deterioration of frontal lobe functions among healthy older
subjects (two articles),
2. the maturation of frontal lobe functions in children (two articles),
3. establishing the test-retest reliability and construct validity of tests
of executive functioning in young children,
4. investigating the relationship of a Piagetian formal operational rea-
soning process to measures of frontal lobe dysfunction,
5. determining the role of frontal lobe functions in boys with attention
deficit-hyperactivity disorder,
,.,ft. the relationship of a special type of memory (source memory) to
a particular dimension of frontal lobe functioning.
.,,.~ .:(t3xaept for the test-retest reliability study (in which the results were
nol/.f,4.~ly supportive of the hypothesis), each of these investigations drew
conclusions about the role of the frontal lobes in neuropsychological func-
tioning. In fact, one study of normal aging effects (Axelrod et al., 1992)
"revealed the sensitivity of the MMSE (Mini-Mental State Examination)
to changes in frontal lobe functioning" (p. 70), essentially because perform-
ances on the MMSE, like the performances on three "frontal lobe" tests,
deteriorated across the age span of 50-90 years. In addition, these authors
found a correlation of 0.49 between the MMSE and a composite score
based on the three frontal lobe tests, and viewed this finding as "noteworthy
because the MMSE was intended as a measure of gross cognitive status
rather than of frontal lobe functioning" (p. 68).
Neuropsychological Deficits and Frontal Lobes 163

Although each of the studies noted above drew conclusions about the
frontal lobes (except for the study that did not fully support its hypothesis),
none of the investigations used any subjects who had documented evidence
of frontal lobe involvement. In addition, none of the subjects in any of the
studies were examined neurologically for independent evidence of frontal
lobe damage. What, then, was the basis for such conclusions? The pre-
sumption was that certain tests had previously been validated as frontal
lobe tests, and any evidence of impairment on these tests was, ipso facto,
an indication of frontal lobe impairment. (In most cases the tests used with
children had to be adapted or even changed substantially from the adult
versions, and they had never been validated by investigations of children
with frontal lobe lesions. However, this lack of validation was rarely con-
sidered to be a detriment to drawing conclusions about frontal lobe func-
tioning.)
Even more recent reports have suggested that the Category Test and
Part B of the .Trail Making Test are "frontal lobe" tests (Butters et al.,
1994; Farmer, 1994; Jarvis and Barth, 1994), a presumption also made in
two of the investigations cited above (Grodzinsky and Diamond, 1992;
Shute and Huertas, 1990). A rigorous test of this postulate, however, re-
vealed that neither the Category Test nor Part B of the Trail Making Test
was specifically sensitive to frontal damage (Reitan and Wolfson, in press).
The validity of this expanding body of knowledge about the frontal
lobes obviously depends on evidence that the tests and procedures are valid
as specific indicators of frontal, as opposed to nonfrontal, functioning. Pre-
sumptions about frontal lobe functions have clearly gotten out of hand,
unless there is strong evidence that the so-called frontal lobe tests are spe-
cifically sensitive to frontal lobe damage.
The seven theoretical and/or review articles identified in our brief
literature search describe the fundamental neuropsychological features of
the frontal lobes. Hart and Jacobs (1993) described frontal lobe functions
as those that (1) subserve selective attention; (2) provide continuity and
coherence to behavior; (3) modulate behavior so that drives are satisfied
within the constraints of the internal and external environments; and (4)
act as an overseer, based on insight and self-awareness, to monitor, adjust,
and evaluate behavior.
Goldman-Rakic (1993) referred to the literature as a basis for con-
cluding that the frontal lobes subserve (1) attention; (2) synthetic reasoning
and planning; (3) the ability to grasp the essence of a situation, utilize past
experience, or regulate behavior through verbal input; (4) initiative, spon-
taneity, and verbal and constructional fluency; (5) spatial orientation; and
(6) behavior restraint, social affect, and global features of personality.
164 Reitan and Wolfson

Lezak (1993) offered a four-part definition of frontal lobe function-

ing: (1) volition, including capabilities for awareness of one's self and sur-
r o u n d and motivational state; (2) planning, including abilities to
conceptualize change (look ahead), be objective, conceive of alternatives
and make choices, develop a plan conceptually, and sustain attention; (3)
purposive action, including productivity and self-regulation; and (4) per-
formance effectiveness, or quality control.
Varney and Menefee (1993) referred to Lezak's definition, and of-
fered a list of descriptors that characterize the individual with frontal lobe
symptoms: poor empathy, poor judgment, absentminded, indecisive, imma-
ture, poor insight, disorganized, impulsive and impolitic, poor planning,
nonreinforcing, nonspontaneous, self-centered, perplexed, low motivation,
rigid/inflexible, repeats mistakes, flat affect, disinhibited, risk seeking, and
stimulus bound. It seems that the frontal lobes are, if nothing else, versatile!
Sohlberg et al. (1993) related their conceptual framework of frontal
lobe functions with the theory proposed by Stuss (1991), and identified
frontal lobe functions as (1) sensory and perceptual, or knowledge-based
information; (2) executive control or the supervisory functions; and (3) self-
reflectiveness or self-awareness (which is dependent on the prefrontal ar-
eas).
Schwartz et al. (1993) focused on the fact that some subjects with
severe brain injury are unable to perform routine, simple activities of daily
living. These authors cited Luria's concept of frontal apraxia in this context,
but suggested that a more plausible account of frontal apraxia involves dif-
ficulties in "assembling or activating the components of the action plan or
in sustaining that activation (or both)" (p. 61).
Grafman et al. (1993) proposed that prefrontal lobe injury or dys-
function causes problems in (1) temporal coding, (2) estimation (impair-
ment in estimating lesser known facts as compared with first-order facts),
(3) sustaining attention and maintaining focus, (4) accuracy in estimating
extended time intervals, (5) forming and shifting concepts, (6) verbal func-
tions that influence working memory, (7) anticipating an expected forth-
coming motor or verbal response, (8) maintaining registered information
over time, (9) developing second-order associative responses, (10) social
conduct, and (11) mood (depression, anxiety, apathy, and disinterest). The
authors postulated that these deficits result from damage to the prefrontal
cortex, and can be subsumed under a concept of "the managerial knowl-
edge unit."
Grafman et al. noted, however, that the deficits that "have long been
associated with prefrontal lesions . . .may appear in patients with subcor-
tical degenerative disorders like Parkinson's disease, cerebellar disease, pro-
gressive supranuclear palsy, and so forth because they are part of a neural
Neuropsychological Deficits and Frontal Lobes 165

network that includes the frontal lobes" (p. 85). This statement obviously
minimizes the specific significance of the frontal lobes, and places the futic-
tion of the frontal lobes in the context of the extensive areas of connection
between the frontal lobes and the rest of the brain. If the deficits described
by these authors are attributed to impairment or interruptions within these
neural networks, the task of delineating and specifying the frontal lobe
component of the functions of these neural networks becomes even more
imposing than identifying specific deficits caused by lesions contained en-
tirely within the frontal lobes. One cannot permissively presume that certain
deficits occur because the frontal lobes are a part of the neural network.
Considering the extensive inter- and intracerebral connections within the
hemispheres, a strict application of this notion would significantly diminish
the entire concept of regional localization of function.
The theoretical/review articles cited above present an extensive range
of subjective impressions of frontal lobe functions. In fact, the list of func-
tions and deficits exceeds the entire range of behaviors included in some
theories of brain-behavior relationships (see Reitan and Wolfson, 1992a,
1993), and one would have to presume that the other areas of the brain
(the temporal, parietal, occipital, and subcortical structures) have at least
some functions. One is reminded of The Meaning of Intelligence, a book in
which Stoddard (1943) offered a broad definition of intelligence:
Intelligence is the ability fo undertake /~ctivities that are characterized by (1)
difficulty, (2) complexity, (3) abstractness, (4) economy, (5) adaptiveness to a goal,
(6) social value, (7) the emergence of originals and to maintain such activities under
conditions that demand a concentration of energy and a resistance to emotional
forces.

Interestingly, Stoddard's characteristics of intelligence seem to over-

lap extensively with the "frontal lobe" functions described previously.
As Halstead had noted, by 1947 psychological conceptualizations of
intelligence had become quite diversified, and related to a number of cri-
teria that were poorly defined and almost certainly overlapping, just as
frontal lobe functions have become today. Halstead's comment that the
essential requirement of abilities involved in intelligence was only that they
reflect "a capacity of some kind which has a Gaussian distribution in the
general population" (Halstead, 1947, p. 10) appears to apply equally to
frontal lobe functions.
Neisser (1979) felt that there is no hope of offering a definition of
intelligence (which is presumably more extensive than frontal lobe func-
tions). He concluded that "the concept of intelligence cannot be explicitly
defined, not only because of the nature of intelligence, but also because
of the nature of concepts" (p. 179). Perhaps the same conclusion applies
to frontal lobe functions.
166 Reitan a n d Woifson

Goldman-Rakic (1993) commented that such "a bewildering array of

behavioral deficits have been attributed to frontal lobe injury that a com-
mon functional denominator would appear elusive" (p. 13). Considering
the range and diversity of definitions and characterizations of frontal lobe
functions, together with their apparent importance for competent human
performance, Halstead (1947) perhaps summarized it best nearly 50 years
ago when he commented that the frontal lobes were "the organs of civili-
z a t i o n - the basis of man's despair and of his hope for the future" (p. 49).
Alternatively, in our quest to identify the neuropsychological effects of fron-
tal lobe lesions, we could perhaps follow Hebb's (1949) approach to the
definition of intelligence: he ultimately decided that intelligence was an
equivocal term that "each writer can define to suit himself, and there is
no sense in arguing over terminology" (p. 277).

EMPIRICAL EVIDENCE

Wisconsin Card Sorting Test

The validity of the conclusions of empirical studies or the various

theoretical/review publications obviously depends on the experimental stud-
ies on which they are based. Do the scientific research findings identify
certain tests as indicators of deficits specific only to the frontal lobes? Ex-
actly this presumption is made in the research literature, with a consider-
able number of tests presumed to be specific frontal lobe indicators (for
example, the Wisconsin Card Sorting Test, the Thurstone Word Fluency
Test, the Category Test, the Stroop Test, the Design Fluency Test, the
Porteus Mazes Test, Part B of the Trail Making Test, subtests of the Wech-
sler Memory Scales, the Consonant Trigram Test, and experimental pro-
cedures involving verbal recency procedures and go-no go tasks).
The Wisconsin Card Sorting Test (WCST) and the Thurstone Word
Fluency Test (TWFT) are among the instruments identified most frequently
as frontal lobe tests. What is the evidence that these tests are specific in-
dicators of frontal lobe functions?
Milner's studies (1963, 1964) are often cited as a basis for identifying
frontal lobe functions and for using the WCST to assess frontal lobe dam-
age and normal development of frontal lobe functioning. Milner studied
patients who had undergone discrete surgical excisions for treatment of epi-
lepsy, and reported that 18 patients with frontal excisions involving dorso-
lateral areas made significantly more mistakes on the WCST than did
patients with lesions in other areas (mostly the temporal lobe).
Neuropsychological Deficits and Frontal Lobes 167

It must be noted that all of Milner's subjects had epilepsy so severe

that they had a refractory response to medication and met the criteria for
surgical intervention. Such patients are not representative even of epilepsy
generally, and certainly do not represent the full range of conditions that
produce brain damage. For example, Matthews and Kl~ve (1967) found
that patients who had complex partial seizures of unknown etiology per-
formed at significantly better levels than patients who had major motor
seizures of unknown etiology. Thus, Milner's findings may have limited gen-
eralizability to patients with other types of cerebral lesions.
Dodrill (1981) reviewed reports of patients with refractory seizures
whose neuropsychological functions deteriorated over time. He noted that
Harris (1972) and Wasterlain and Duffy (1976) demonstrated neuronal de-
generation associated with repeated seizures in animals, and that seizures
also have an inhibitory effect on brain protein synthesis, on brain growth,
and eventually on behavioral development. Citing Arieff and Yacorzynski
(1942), De Haas and Magnus (1958), and Lennox and Lennox (1960), Do-
drill commented that "with these studies as a background, it is not surpris-
ing that several investigators do implicate a gradual deterioration of
abilities" in patients who experience epileptic attacks repeatedly.
In addition to the effects on neuropsychological performances caused
by continued seizures and the long-term use of medications, and the many
social and emotional problems among epileptics "that are far in excess of
the base rate of the population" (DodriU, 1981, p. 380), the consequences
of brain impairment among epileptics during the course of development
must be considered. Gilroy and Meyer (1979) state that "about 90% of
epileptic patients have histories of epilepsy beginning in childhood" (p.
359). Although many factors obviously determine an individual's neurop-
sychological c o m p e t e n c y - - and the duration of epilepsy considered by itself
is not a strong influence - - Dodrill (1981) noted "that the earlier the age
of onset and the longer the duration, the lower the mental abilities" of the
epileptic patient (p. 371). Klcve and Matthews (1966) and Dikmen et al.
(1975) have reported similar findings.
In contrast to the Kennard principle (see Finger and Wolf, 1988),
cerebral disease or damage during the developmental years seems gen-
erally to have an adverse effect on adult neuropsychological functions in
comparison with persons who have had the advantage of normal devel-
opment of brain functions (Reitan and Wolfson, 1992b). Mahoney et al.
(1983) documented the impairment associated with severe head trauma
sustained by young children. Using the WCST, Strauss et al. (1993) also
found deficits associated with complex partial epilepsy experienced early
in life. Therefore, a number of variables may limit the generalizability of
Milner's findings.
168 Reitan and Wolfson

Immediately following Milner's (1964) presentation of her findings,

Teuber (1964a) said in his discussion,
Our cases of frontal gunshot wounds did show a deficit on the Wisconsin Card
Sorting T e s t - - a t least as a g r o u p - - a l t h o u g h there were striking exceptions in
individual c a s e s . . . O n the other hand, our posterior lobe patients also had a deficit
which seemed somewhat more severe. (p. 333)

Thus, even at the time of the original report, Milner's results were
controverted by Teuber's findings, with differences possibly relating to the
type of lesion rather than the location.
In conclusion, there are many reasons why Milner's studies should be
replicated in a study design that would relate to the effects of brain lesions
more generally and control for developmental effects among the types of
subjects she studied.
Drewe (1974) studied WCST results of patients who had types of le-
sions other than the epileptogenic foci studied by Milner, and found that
patients with frontal lesions demonstrated significantly more perseverative
errors. Robinson et al. (1980) pointed out that there was reason to believe
Drewe's frontal patients may have had greater overall impairment than her
nonfrontal groups, and raised a question about the specificity of the find-
ings on the WCST.
Robinson et al. (1980) performed a study using 123 normal subjects
and eight groups of subjects with lesions in the following locations: right
frontal, 13; right frontal plus more extensive involvement, 11; left frontal,
10; left frontal plus, 12; right nonfrontal, 9; left nonfrontal, 14, and diffuse,
38. Except for the normal subjects, each group included subjects with brain
lesions of various etiologies, but the lesions were not equivalent across eti-
ologies. The normal group made fewer perseverative responses than the
total brain-damaged sample. The frontal group performed more poorly
than the nonfrontal groups, even when perseverative scores were adjusted
for the Average Impairment Rating in an attempt to control for differences
in overall impairment. However, the frontal groups were not more impaired
than the group with diffuse involvement.
These investigators attempted to replicate clinical classifications based
on Milner's (1963) results. Whereas none of Milner's frontal cases were
able to achieve more than three categories on the WCST, 43% of the fron-
tal subjects in the Robinson et al. study achieved four or more categories,
and 39% of the nonfrontal cases achieved three or less. Using a clinically
derived cutoff score, the lack of difference between the frontal and diffuse
groups led to more than half of the diffuse cases being classified as having
frontal lesions. Thus, even though frontal cases performed somewhat more
poorly than nonfrontal cases, Robinson et al. concluded that the value of
the WCST in localizing brain lesions appears to be questionable, and stated
Neuropsychological Deficits and Frontal Lobes 169

that their findings "would n o t s u p p o r t the use o f the W C S T in a t t e m p t i n g

to discriminate focal frontal f r o m diffuse lesions" (p. 613).
A n d e r s o n et aL (1991) also published a study o f the W C S T as a meas-
ure o f frontal lobe d a m a g e with the following justification:
Research to this point has suggested that patients with frontal lobe damage may
perform worse on the WCST than do patients with focal nonfrontal damage
(Drewe, 1974; Heaton, 1981; Milner, 1963). However, one study found that subjects
with posterior lesions performed worse than subjects with anterior lesions (Teuber,
Battersby, & Bender, 1951), and most studies have found considerable variability
in WCST performances across subjects with frontal lobe damage. There have been
conflicting findings with regard to the role of dorsolateral frontal vs. orbitomesial
areas in WCST performance (Drewe, 1974; Milner, 1963). No study up to this time
has made use of modern neuroradiological techniques to investigate the locus of
damage in patients who failed the WCST, and many of the subject groups used in
prior studies have been less than ideal for purposes of the lesion method. Some
studies have combined subjects with different pathological processes, such as tumors
and strokes, into single groups, a practice which may introduce considerable error
variance (Anderson, Damasio, & Tranel, 1990). Some subjects have been studied
in the acute epoch, when neuropsychological profiles are likely to be changing and
considerable recovery may still take place. Given this situation, together with
observations of patients with extensive frontal lobe damage who performed well on
the test (Anderson, Damasio, Tranel, & Damasio, 1988; Eslinger & Damasio, 1985;
Heck & Bryer, 1986), we undertook an investigation of the sensitivity and specificity
on the WCST as an index of frontal lobe damage. (p. 910)

T h e p r e s u m p t i o n by .Anderson et al. that studies c o m b i n i n g subjects

with different pathological processes, such as t u m o r s and stroke, into single
g r o u p s are "less t h a n ideal for p u r p o s e s of the lesion m e t h o d " and " m a y
i n t r o d u c e considerable e r r o r variance" must be t e m p e r e d by a considera-
tion o f the p u r p o s e o f the study. In fact, these investigators based their
results o n 91 patients with cerebrovascular accidents (n = 71) and t u m o r s
o r seizures (n = 20), apparently including in the g r o u p patients with neo-
plasms as diverse as m e n i n g i o m a s and metastatic carcinomas. Forty-nine
patients had frontal lesions, 24 had nonfrontal lesions (affecting the tem-
poral, parietal, and occipital lobes as well as the thalamus and basal gan-
glia), and 18 patients, included in s o m e analyses, had lesions of, but n o t
limited to, the frontal lobes.
V a r i o u s analyses o f W C S T data s u p p o r t e d the following conclusions:

1. N o significant differences were f o u n d b e t w e e n the frontal and n o n -

frontal groups. In fact, the scores were quite similar.
2. O p t i m a l c u t o f f scores for frontal and n o n f r o n t a l patients correctly
classified only 6 2 % o f the subjects.
3. C o m p a r i s o n s o f left, right, and bilateral frontal d a m a g e failed to
p r o d u c e any significant differences.
4. N o reliable differences were f o u n d a m o n g patients having different
areas o f d a m a g e within the frontal lobes.
170 Reitan and Wolfson

5. The size of the lesion within the frontal lobes was not correlated
with WCST scores.
The investigators concluded that their findings failed to support a
consistent relationship between WCST scores and frontal lobe damage, and
they inveighed against using WCST performances to compose frontal and
nonfrontal groups for research purposes.
Grafman et aL (1990) compared the WCST results of 421 brain-dam-
aged subjects with 48 controls matched for age, preinjury intelligence, edu-
cation, and military service. In the brain-damaged group, 126 subjects had
lesions involving only the frontal lobes and 183 subjects had nonfrontal
lesions. The controls performed better than the brain-damaged groups, but
"patients with lesions limited to the frontal lobes performed as a group no
worse than patients with nonfrontal lesions" (p. 1120).
These authors cited Cronin-Golomb (1990) in pointing out that the
WCST "continues to be used as a measure of frontal lobe functioning in
psychiatric, focal lesion, and subcortical dementia patients" (p. 1120), and
advised using caution in the "clinical research practice of attributing poor
performance on the card-sorting test to frontal lesions" (p. 1121).
In another recent study, Van den Brock et al. (1993) used a modified
version of the WCST and found no significant differences between patients
with either frontal vs. nonfrontal lesions or left hemisphere vs. right hemi-
sphere lesions. However, the task did have high specificity and good sen-
sitivity in differentiating patients with brain lesions, regardless of the site,
from control subjects.

Thurstone Word Fluency Test

The nature of the task involved in the TWFT serves as a basis for
reviewing the literature about this test. The TWFT requires the subject to
write (or say) as many words as possible that begin with a certain letter
within a specified time period. Details of the procedure have varied among
investigators concerning letters and time periods, but the subject's task has
consistently been to report as many words as possible. There can be no
doubt that this test requires the subject to express verbal material of a
prescribed nature (beginning with a selected letter), and that the score de-
pends on speed of performance (the number of words expressed within a
given time period).
On one hand, this type of task is related to verbal intelligence, and
this is exactly the purpose for which the Thurstones developed the test
(Thurstone, 1938; Thurstone and Thurstone, 1949). A subject's level of in-
telligence is therefore very likely to influence the results, with more intel-
Neuropsychological Deficits and Frontal Lobes 171

ligent subjects performing better than less intelligent subjects. Because of

its significant correlation with intelligence, education would presumably be
another factor affecting performance, at least among normal subjects. More
important in a sample of brain-damaged subjects, however, would be the
presence or absence of dysphasia and, more specifically, the presence or
absence of dysnomia and an impairment of verbal fluency.
In their review of the formal dysphasia examination, Albert et al.
(1981) identified six scales to cover the range of deficits shown by dysphasic
subjects. Two of these scales related to Grammatical Form (which, accord-
ing to the authors, correlates closely with verbal fluency in aphasia), and
Word Finding, which represents an impaired ability "to find the desired
word for production in spontaneous speech and is present in every type of
dysphasia" (p. 7). Wheeler and Reitan (1962) reported word-finding deficits
in 53% of a group of subjects with heterogeneous left cerebral lesions and
in 0% of a similar group with right cerebral lesions. It appears that the
TWFT can be adversely affected by dysphasia, and might be a specific test
for certain dysphasic symptoms.
These observations suggest that an evaluation of the sensitivity of the
TWFT, either comparing groups with left vs. right cerebral lesions or fron-
tal vs. nonfrontal lesions, should consider the role of aphasia in producing
deficits. The left hemisphere's dominance for language functions (including
verbal fluency) is well known. It should also be recognized that expressive
verbal tasks are likely to be more impaired by left frontal lesions than by
left hemisphere lesions that are more posterior in location.
The TWFT appears to depend on expressive (as contrasted with re-
ceptive) verbal abilities inasmuch as it requires the production of words.
Albert et al. (1981), in discussing differential location of left hemisphere
lesions that cause expressive (nonfluent) aphasia and receptive (fluent)
aphasia, comment that "non-fluency is usually, but not always, associated
with anterior lesions; fluency with posterior lesions" (p. 9). Including
dysphasic patients in a left hemisphere group should therefore produce the
lowest TWFT scores in subjects with anterior lesions. Because of the nature
and requirements of the TWFT, any study using this test with patients hav-
ing left hemisphere lesions should describe the incidence and type of apha-
sia in the group and discuss how dysphasic deficits may have affected the
results.
In attempting to delineate the effects of dysphasia on other abilities,
Reitan (1960) studied the effects of dysphasia on a broad range of neuro-
psychological tests. Brain-damaged subjects were examined with the Rei-
tan-Indiana Aphasia Screening Test (Reitan, 1985) in order to compose
two groups: one with definite indications of dysphasia and one with n o
evidence of dysphasia. Because of the differential influence of various types
172 Reitan and Wolfson

of lesions on neuropsychological measurements (Reitan, 1964; Hom and

Reitan, 1982, 1984), the dysphasic and nondysphasic groups were matched
not only for gender, chronological age, and years of education, but also
for type of brain lesion. A non-brain-damaged comparison group, matched
with the brain-damaged groups for gender, age, and education, was also
composed. It was necessary to review the comprehensive neurological
evaluations of approximately 1500 patients in order to compose matched
triads across the three groups composed of 32 subjects each.
Each subject was given the Wechsler-Bellevue Scale (14 variables, in-
cluding Verbal IQ, Performance IQ, and Full Scale IQ), nine tests devised
by Halstead plus his Impairment Index (ten variables), and Part A and
Part B of the Trail Making Test (two variables). Both brain-damaged
groups consistently performed more poorly than the controls, except that
on the Wechsler verbal tests the scores of the nondysphasic group ap-
proached the scores of the controls. The effects of dysphasia were shown
by comparing the dysphasic and nondysphasic brain-damaged groups. These
two groups had nearly identical mean scores on all measures except the
tests that explicitly required expressive or receptive language functions. The
dysphasic group performed more poorly than the nondysphasic group on
each test that included language or language symbols. It was hypothesized
that implicit verbalization during the task, especially on complex measures
such as the Category Test and the Tactual Performance Test, might be
impaired among the dysphasic subjects and lead to lower scores; however,
on these measures the means for the two groups were nearly identical.
These findings strongly suggest that the incidence and possible effects
of dysphasia should be identified when tests that require production or
processing of verbal material are used in comparative assessment of brain-
damaged groups.
In terms of controlled comparisons, the TWFT has been less thor-
oughly researched than the WCST. The first report suggesting that the
TWFT might be a frontal lobe test came from Milner (1964), presented
in about one and one-half pages and based on seven left frontal, seven left
temporal, and four right frontal cases. All of Milner's subjects were drawn
from a limited sample of patients who had focal cortical excisions for treat-
ment of epilepsy. She found that her group of seven patients with left fron-
tal lesions p e r f o r m e d poorly on the TWFT, and her report of the
performance of this group of seven patients is frequently cited in the lit-
erature as a basis for concluding that the TWFT is a frontal lobe test.
Milner did not provide information about the incidence of dysphasia in
her subjects, 14 (77%) of whom had left hemisphere lesions. She did state
that lobectomies that spare Broca's area are not followed by any lasting
dysphasia, and that scores on most verbal tests rapidly return to normal.
Neuropsychological Deficits and Frontal Lobes 173

However, her patients were retested "about three weeks" after the first
examination, with the surgery for intractable epilepsy performed during the
interval. One could not be sure that residual dysphasia was not a factor
influencing the test results. No information was given about the age and
education of the subjects.
Benton (1968) studied three groups with frontal lesions (right, n =
8; left, n = 10; bilateral, n = 7), but made no frontal vs. nonfrontal com-
parisons. Although he did not give specific evidence of comparability of
these groups regarding the types of lesions, he noted that the subjects
mainly had intrinsic tumors, extrinsic tumors, and degenerative disease. The
means for age and education were not significantly different. Six tests were
administered: (1) FAS words to test verbal fluency; (2) assembling struc-
tures from a tray of assorted blocks; (3) learning a list of word pairs; (4)
copying designs; (5) interpreting proverbs; and (6) citing the day of the
week, the day of the month, the month, the year, and the time of day.
Benton made 18 predictions and reported that 15 predictions were
confirmed. Using six tests and three groups permitted a total of 18 com-
parisons. Three of the 18 intergroup comparisons were significant at the
.01 level, one was significant at the .025 level, four were significant at the
.05 level, five were significant at the .10 level, and the remaining five com-
parisons were not significar~t. Only 8 of the 18 comparisons were significant
at the .05 level or less, but Benton felt that "given such small groups, it is
perhaps permissible to consider differences at the 0.10 probability level (i.e.,
approaching the conventionally accepted level of 0.05) as suggestive of a
true difference" (p. 57). While one must recognize that a small n is a con-
dition that validly limits scientific conclusions, even accepting as significant
the five comparisons at the .10 level does not yield enough "significant"
results to confirm 15 of 18 hypotheses. Benton obviously "confirmed" some
hypotheses on the basis of differences attributable to chance.
The three groups were also assessed for frequency of defective per-
formances on the six tests, with a defective performance being defined as
a score "exceeded by 95-96 percent of control subjects" (p. 57). These con-
trol subjects were not described in the report; no information was given
about their age or education distributions or any other characteristics. Nev-
ertheless, the frequency of "defective" performances by the frontal lobe
patients was used to determine which deficits were characteristic of each
group. In fact, the test that required naming the day of the week, date,
month, year, and time of day was described as a bilateral test "par excel-
lence" because four of the seven bilateral patients (57%) performed defec-
tively, whereas none of the 18 patients with unilateral frontal lesions
performed defectively.
174 Reitan and Wolfson

Finally, it must be noted that because no patients with nonfrontal

lesions were used for comparisons, the specificity of the performances of
patients in this study of frontal lobe deficits was entirely undetermined.
Despite these problems, this study is frequently cited to support tests of
verbal fluency as frontal lobe measures.
Using the TWbT, Ramier and H6caen (1970) studied 76 subjects with
unilateral lesions, the majority of which were tumors (53%). Lesion types
included tumors, hematomas, traumatic injuries, angiomas, and cortical ex-
cisions. The groups were not equivalent for types of lesions; tumors were
underrepresented in the right frontal group (33%) and overrepresented in
the right nonfrontal group (71%). The lesions were in the following loca-
tions: left frontal, 17; right frontal, 12; left nonfrontal, 30; right nonfrontal,
17. Fifteen of the 47 patients with left cerebral lesions were identified as
aphasic, but no information was given about the criteria used for deter-
mining aphasia. There appeared to be age and education differences in
the groups with left vs. right cerebral lesions, but data were not reported
for frontal vs. nonfrontal lesions. Differences on these variables were not
tested statistically.
Ramier and H6caen analyzed their results with relation to lateraliza-
tion (left hemisphere vs. right hemisphere) and location of the lesion (fron-
tal vs. nonfrontal). On the TWFT, the group of subjects with left
hemisphere lesions (which included all of the aphasic subjects) performed
more poorly than the subjects with right hemisphere lesions. Since the an-
terior portion of the language area in the left hemisphere has long been
known to be principally involved in language expression, and the TWFT
obviously is an expressive verbal task, it is not surprising that the left frontal
group performed most poorly among the four groups. Although it is not
clear from this report, there is also the possibility that frontal lesions with-
out clinically obvious dysphasia produced deficits in verbal fluency.
It is apparent that, in addition to the location of the lesions, the in-
tergroup differences could have been influenced by age, education, dyspha-
sia, and type-of-lesion differences in the groups.
Perret (1974) examined 118 subjects using the TWFT and other
measures. Of these subjects, 83% had brain tumors, but the report did
not specify the types. The lesion locations were as follows: left frontal,
23; right frontal, 27; left temporal, 15; right temporal, 17; left posterior,
18; right posterior, 18. The author stated that most of the patients in the
frontal groups had large tumors. Age and education intergroup differences
were not statistically significant. Perret did not report any systematic at-
tempts to evaluate dysphasic deficits, but did presume that left hemisphere
lesions would cause impairment because of the nature and requirements
of the test.
Neuropsychologlcal Deficits and Frontal Lobes 175

In Perret's study, the left hemisphere patients performed more poorly

than the right hemisphere patients, and the left frontal group performed
more poorly than any other group. Bilateral frontal involvement did not
cause more impairment than a left frontal lesion. Perret therefore con-
cluded that "the deficits are summed in the left frontal group" (p. 329).
This study provides no assurance that expressive verbal deficits, with
or without frank aphasia, were not the basis for the results. The role of
aphasia in limiting verbal productions has been known for many years (see
Reitan, 1985), and as described previously, expressive verbal functions can
be expected to be principally impaired with left anterior lesions.
Miceli et al. (1981) measured verbal fluency using a procedure iden-
tical to Benton's to evaluate patients with cerebral lesions. Patients who
demonstrated dysphasia on their standard examination were excluded from
the investigation. Of the 149 subjects used in this study, 70% had cerebral
neoplasms, but the types of tumors were not identified. Left hemisphere
lesions were in the following locations: frontal, 15; temporal, 7; parietal,
19; and occipital, 10. Right hemisphere lesions were as follows: frontal 22;
temporal, 6; parietal, 15, and occipital, 11. Additional groups included sub-
jects who had a lesion involving more than one lobe: left hemisphere, 13;
right hemisphere, 31.
Miceli et al. presented means and standard deviations in tabular form,
but the results of inferentidl statistical analyses were reported only in the
text. Consequently, it was somewhat difficult to identify the significant find-
ings on the verbal fluency test, but it appears that these investigators found
that subjects with left hemisphere lesions performed somewhat more poorly
than subjects with right hemisphere lesions (p < .05). No significant dif-
ferences were found in comparisons of groups with lesions of individual
lobes. Including patients with lesions involving more than one lobe did not
change the results substantially, and the only significant finding (probability
level not specified) represented a difference between the right frontal and
right nonfrontal group. The results of this investigation differed from the
other studies that showed deficits particularly in the left frontal group, ap-
parently demonstrating the significance of screening out the dysphasic pa-
tients.
Pendleton et al. (1982) performed the most comprehensive study of
the TWFT published to date. They evaluated 203 subjects with cerebral
lesions (119 focal and 84 diffuse) and 134 normal paid volunteers. This
type of control group does nothing to match groups for the general illness
factor, anxiety, and other emotional stresses that may accompany hospitali-
zation. Therefore, the influence that a serious illness may have on an in-
dividual's performance cannot be evaluated, and it is difficult to determine
whether factors other than brain damage have h a d an adverse influence
176 Reitan and Wolfson

on a subject's performance. Other researchers (e.g., Reitan, 1955b) have

attempted to equate such factors by using control subjects who are ill and
hospitalized but in whom a detailed neurological examination has ruled
out past or present cerebral disease or damage.
In the Pendleton et al. study, the subjects with focal lesions were cate-
gorized according to lesion location: frontal, 47; frontal plus more extensive
involvement, 33, nonfrontal, 39. The numbers were nearly equal when sub-
divided into left and right hemisphere lesions, left and right frontal lesions,
left and right nonfrontal lesions, and total frontal and nonfrontal lesions.
A diversity of types of lesions was included, providing the advantage of
being able to generalize the results to a broad spectrum of neurological
diagnoses. However, 35% of the patients with focal lesions had intrinsic
tumors, and an additional 26% had either cerebral infarcts or hemorrhages.
These investigators used the procedure described by Milner (1964)
in which subjects were asked to produce words beginning with S and C
rather than the F, A, S words used in the Controlled Oral Word Associa-
tion Test (Benton and Hamsher, 1976).
Unfortunately, in some instances comparisons of the various sub-
groups showed significant differences on age and education. The investi-
gators performed an adjustment of TWFT scores according to age and
education, a procedure whose effect is not fully known. In fact, after a
careful evaluation of the use of analysis of covariance (ANCOVA) as a
remedy for mismatch of groups on demographic variables, Adams et al.
(1985) concluded that "ANCOVA should not be used in neuropsychologi-
cal research to equate groups unequal on variables such as age and edu-
cation or to exert statistical control whose objective is to eliminate
consideration of the co-variate as an explanation for results" (p. 445).
The major findings of the Pendleton et al. study were as follows:
1. The TWFT results were significantly different at probability levels
beyond .001 in comparisons of the normal subjects and any of the
brain-damaged groups, and differentiated brain-damaged and con-
trol subjects with about 95% accuracy. This finding may be limited
in its clinical significance, since it is rarely necessary to differentiate
persons with brain lesions from persons who are healthy and have
no complaints.
2. The TWFT showed more impairment with frontal than nonfrontal
patients (p < .05), but because of overlap of the groups, the
authors could derive no effective cutoff score to use in clinical ap-
plication. It is even entirely possible that failure to control for dys-
phasia is the basis for this relatively weak finding.
Neuropsychological Deficits and Frontal Lobes 177

. While statistical data, as contrasted with clinical application,

showed a mild difference between left and right frontal involve-
ment, a comparison of the frontal subjects with the diffuse subjects
(who had no focal lesions at all) showed no significant differences.
The authors pointed out that the frontal groups would have to per-
form more poorly than the diffuse group for the TWFT to be con-
sidered an accurate indicator of frontal lobe lesions. However,
there was no significant difference between these two groups on
the TWFT, a finding similar to the results reported by Robinson
et al. (1980) in their study of the WCST.

In summary, Pendleton et al. found some differences that exceeded

the .05 level, but differences at this level imply a substantial degree of over-
lap of the groups being compared, and the TWFT, considered by itself,
has limited significance in localizing frontal lobe dysfunction.

Overall Evaluation of the Wisconsin Card Sorting Test and Verbal

Fluency Measures

A careful analysis of the literature that has given rise to using the
WCST and the TWFT as frontal lobe indicators reveals that the evidence
for such applications is tenuous. In addition, a recent comparison of groups
with frontal and nonfrontal lesions, with types of lesions held comparable,
yielded no significant differences in performance between the groups on
the Category Test and Part B of the Trail Making Test (Reitan and Wolf-
son, in press).
Perhaps we should not consider these findings surprising. Several
fairly recent reviews, published after the "validational" studies reviewed
above (except for Anderson et al., 1991), have concluded that there are no
valid tests for identifying neuropsychological functions unique to the frontal
lobes. Bigler (1988) stated that "clinical neuropsychoiogy long has sought
specific tests of frontal lobe damage but to date no such tests exist that
are exclusively sensitive to frontal lobe function." He also noted that tests
purported to evaluate frontal lobe function, such as the WCST and the
Category Test, are not specific to frontal lobe damage.
Wang (1987) also reviewed neuropsychological functions supposedly
related to the frontal lobes, and concluded that there are no tests specifi-
cally sensitive to frontal lobe damage or dysfunction.
Costa (1988) concluded that although many tests are sensitive to cere-
bral dysfunction, few of them are uniquely sensitive to particular cortical
areas. Concerning frontal lobe dysfunction specifically, he wrote that "it is
178 Reitan and Wolfson

easy to find tests that are sensitive to frontal-lobe dysfunction and very
difficult to find tests that are specific for it!"
The many studies that reported significant deficits in groups of sub-
jects who did not have frontal lesions should have forewarned us that the
so-called frontal lobe tests were not specific to frontal lobe functions. For
example, Parsons (1975) and Tarter and Parsons (1971) reported that long-
term alcoholics showed various types of deficits on the WCST. Hermann
et al. (1988) used the WCST to study a group of patients with complex
partial seizures arising from either the left or right temporal lobe and a
comparison group consisting largely of patients with primary generalized
epilepsies. In apparent contrast to the "normal tendency" that Milner
(1964) reported for patients with nonfrontal lesions, these investigators
found that if the usual standards of frontal lobe involvement were applied,
57% of their subjects performed in a manner that would be considered
suggestive of frontal lobe pathology.
The pervasive tendency among many psychologists to believe so
strongly in certain tests as frontal lobe indicators has fostered a host of
reports in the literature. As noted previously, recent publications have in-
cluded studies that (1) draw specific conclusions about the deterioration
of frontal lobe function with normal aging (without considering the pos-
sibility that there might have been just as great a decline on "nonfrontal"
tests), (2) evaluate the frontal lobe influence on Piagetian concepts of cog-
nitive development, (3) devise adaptation for children of frontal lobe tests
(which have never been checked for validity despite the vast differences
in child and adult neuropsychology [Reitan and Wolfson, 1992b; Rourke
et al., 1983]), and (4) assess the role of the frontal lobes in development
of childhood abilities. Considering the findings reported in the original
studies reviewed above, this use of tests as frontal lobe indicators almost
seems to be a bizarre extension of the limited validity of these "frontal
lobe" tests.
One could postulate that this pervasive use of frontal lobe tests oc-
curs because "nature abhors a vacuum," and, as a result, there is a natural
urge to attribute functions to the frontal lobes. In a well-known and often-
cited reference, Teuber (1964b) referred to the "riddle of frontal lobe
function," and everyone loves to solve a riddle. Or perhaps frontal lobe
tests are gaining in popularity because of a cyclic variation over time
the last great surge of interest in the frontal lobes occurred in the 1930s
and 1940s, and a new generation of psychologists has rediscovered the
frontal lobes.
While any of these postulates may have some validity, the answer
probably lies in the proliferation of articles and books that promulgate the
role of the frontal lobes (e.g., Benton, 1968; Damasio, 1991; Heilman and
Neuropsychological Deficits and Frontal Lobes 179

Valenstein, 1979; Levin et al., 1991; Lezak, 1983; Luria, 1966; Milner, 1963,
1964, 1971; Stuss and Benson, 1984, 1986). With this barrage of publica-
tions, every definition and function of the frontal lobes cited above can
find a friendly home. Though the end result of controlled investigations
may be that the frontal lobes have no specific cognitive or intellectual func-
tions, it is certainly true that they play an important role in the general
higher level functions of the brain.
We noted many limitations of the studies reviewed above, including
extremely small sample sizes, limited use of appropriate and necessary com-
parison groups, selectivity of lesion types when using a brain-lesion infer-
ential model, permissive relaxation of probability levels and use of
questionable statistical adjustments of raw scores, failure to describe and
evaluate the effect of variables such as dysphasia, and emphasis on "sta-
tistical significance" even though the data did not support "clinical signifi-
cance."
Many psychologists raise questions about the influence of the frontal
lobes on the Halstead-Reitan Battery, and some of the questions specifi-
cally relate to the "frontal lobe syndrome." It is probably not surprising to
hear questions of this type, particularly since Halstead (1947) felt his tests
identified a much greater degree of deficit in patients with frontal lobe
lesions than in patients with in nonfrontal lesions.
The results of Reitan's research on the Halstead-Reitan Battery, how-
ever, have not supported the hypothesis that there is more specific and
severe impairment in persons with frontal lesions than in subjects with non-
frontal lesions (Reitan, 1964). In fact, Reitan's research indicated that the
anterior frontal areas are related to the general indicators of neuropsy-
chological impairment, whereas more posterior areas, in both the left and
right cerebral hemispheres, subserve more specific functions depending
upon which hemisphere is involved.
Nevertheless, there are some claims, particularly in the literature of
behavioral neurology (but also in clinical neuropsychology), of specific defi-
cits associated with frontal lobe impairment. How does this whole situation
add up? Do frontal lobe lesions cause any deficits specific only to the fron-
tal lobes? Do these deficits differ according to whether the left or right
frontal lobe is damaged? What is the evidence to substantiate the claim
that the frontal lobes are the seat of analytical reasoning and "executive
functions"? At this point we will briefly review the history and background
of studies of the frontal lobes in order to place the current status of the
frontal lobe question in more proper perspective.
180 Reitan and Wolfson

OVERVIEW OF THE HISTORY AND DEVELOPMENT OF

CONCLUSIONS ABOUT FRONTAL LOBE FUNCTIONS

For many years there has been a great deal of interest in the frontal
lobes. This is hardly surprising, if for no other reason than that the frontal
lobes constitute such a large anatomical percentage of the cerebral hemi-
spheres in humans. Second, although primary motor functions and coordi-
nation of motor functions are known to be controlled by the posterior
frontal cortex, a large remaining (anterior) area of the frontal lobes seems
to be involved in no specific behavioral functions, and is therefore a tempt-
ing target for placement of the elusive "highest" brain functions.
Since this is the case, and portions of the cerebral cortex posterior
to the central sulcus are devoted to primary sensory reception areas (es-
pecially involving tactile, hearing, and visual functions), there has been a
strong temptation among theorists to assign the higher level neuropsy-
chological functions such as reasoning, planning, logical analysis, and ex-
ecutive functions (involving the final output of the brain with respect to
organized and effective responses) to the anterior frontal areas.
Reitan and Wolfson (1992a) have reviewed the historical develop-
ment of brain-behavior relationships, and because of the interest in the
frontal lobes, many citations in this review were necessarily directed to the
functions subserved by the frontal lobes. (In this paper we will not present
a comprehensive review of frontal lobe functions, but the interested reader
may refer to the introductory chapter of Neuroanatomy and Neuropathology:
A Clinical Guide for Neuropsychologists by Reitan and Wolfson, 1992a, for
a more complete discussion of this topic.) However, a brief review of the
historical background is pertinent in attempting to provide answers to the
above questions.
Fulton (1943) credited the French neurologist Flourens (1824) for
conducting the first experiments involving the frontal lobes by performing
ablations of the anterior frontal lobes in dogs. Most of the early studies,
which did not localize any functions specific to the frontal lobes, supported
a holistic theory of higher level aspects of brain functions.
Loeb (1902) found that ablations of the frontal cortex in dogs had
few, if any, specific effects. He noted minimal impairment when he ampu-
tated only a single anterior frontal area, and found that both anterior fron-
tal areas had to be ablated to produce some loss of alertness. Loeb argued
that the frontal lobes had no special functions, even when bilateral frontal
resection had been performed, and claimed that for a dog there was per-
haps no operation as harmless as the removal of its frontal lobes.
Lashley's (1929) studies with rats provided no evidence of localization
of specific functions in the cerebral cortex, as stated in his principle of
Neuropsychological Deficits and Frontal Lobes 181

equipotentiality (any cortical area was equivalent to any other area). Nev-
ertheless, he did find that maze-learning ability decreased as larger total
areas of cortex were destroyed (the principle of mass action). However,
considering the much more limited range of higher level behavioral capacity
in lower animals than in humans, it might well be expected that experi-
mental studies with lower animals would fail to demonstrate any obvious
evidence of specific or regional localization of functions.
Broca (1861) attracted great attention from the scientific community
by correlating impairment of verbal communication skills with damage to
the posterior-inferior frontal area as well as adjacent cortex of the left tem-
poral lobe. Broca, believing speech was dependent on the frontal lobe cor-
tex, minimized the significance of the temporal lobe involvement. As a
result, the base of the third frontal convolution has come to be known as
Broca's area. Although this part of the cerebral cortex is still recognized
as significant in the production of expressive speech, a considerably larger
area, including a major portion of the left temporal lobe, has also been
identified as a part of the language area (Penfield and Roberts, 1959).
Only a few years after Broca published his reports, Fritsch and Hitzig
(1870) demonstrated that electrical stimulation of the posterior part of the
frontal lobes in dogs induced motor movements on the contralateral side
of the body. This discovery in.creased the impetus to pursue other locations
of function in the brain.
Franz (1907) adopted standardized testing procedures to evaluate cats
and monkeys before and after surgically imposing cerebral lesions. He con-
cluded that the frontal lobes were particularly important for the solution
of puzzlebox performances, and that unilateral lesions produced much less
of an effect than bilateral lesions. Franz deserves credit for using stand-
ardized experimental tasks that met scientific standards of replicability. He
concluded that deficits in the animals with surgical lesions would not have
been noticeable using "simple observational methods," because such ob-
servations were not made under conditions that adequately and properly
stressed the brain.
During the 1920s and 1930s, there was a continuous gradual evolution
toward identifying the frontal lobes as the seat of intellectual functions.
Gelb and Goldstein (1925) used a number of problem-solving tasks to
evaluate human subjects, and concluded that patients with anterior frontal
lesions were more impaired than subjects with lesions located elsewhere in
the cerebral cortex.
In 1935 Ackerly described in detail a patient with bilateral anterior
frontal atrophic lesions, and provided extensive information about the pa-
tient's emotional and intellectual deficits. Brickner (1936) published a book
on the frontal lobes that cited detailed individual cases to substantiate his
182 Reitan and Wolfson

conclusion that the highest levels of intellectual functioning were subserved

by the anterior frontal cortex. Jefferson (1937a, 1937b) also described sig-
nificant intellectual and behavioral deficits associated with Iobectomies of
both the left and right frontal areas in humans.
At about this same time two neurosurgeons, Moniz and Lima, intro-
duced the surgical procedure of prefrontal Iobotomy (prefrontal leukotomy;
Moniz, 1936, 1937). This procedure involved sectioning the white matter
pathways between the dorsomedial nucleus of the thalamus and the pre-
frontal cortex. Since the dorsomedial nucleus of the thalamus received pro-
jections from the hypothalamus, and the hypothalamus was believed very
significantly involved in emotional responses, Moniz postulated that pre-
frontal lobotomy would limit the possibility of interference with intellectual
functions served by the frontal cortex, functions that in some individuals
might otherwise be diminished by strong affective and emotional arousal.
During the 1940s and early 1950s, prefrontal lobotomy was performed
on thousands of persons who had principally psychiatric difficulties rather
than problems for which the neurological bases were more clearly under-
stood. Many clinical studies compared the pre- and postsurgical status of
the patients, but standardized methods for evaluation of brain-behavior
relationships in human beings were not generally used at this time.
Halstead et al. (1946) studied a series of patients before and after
prefrontal lobotomy, and found variable neuropsychological test results. Al-
though these investigators observed changes in their patients, it was not
possible to predict precisely what the changes would be, and Halstead de-
scribed the prefrontal lobotomy as a procedure in which "knowns" (the
patient's preoperative condition) were traded for "unknowns" (the patient's
condition after the surgery). By this time, the importance of the frontal
lobes had been widely accepted by the scientific community. In 1947 Ry-
lander, a Swedish psychiatrist, revealed his respect for the frontal lobes by
describing prefrontal lobotomy as a procedure for "ablation of the soul."
It was in this scientific environment that Halstead developed stand-
ardized neuropsychological tests to evaluate the effects of brain lesions in
human beings. In 1935, at the University of Chicago, he established the
first full-time laboratory in the world for studying the effects of cerebral
lesions on higher level brain functions. Fortunately, Halstead did not preju-
dice his selection of testing procedures; he developed standardized experi-
ments that could be p e r f o r m e d r e p e a t e d l y in the laboratory. His
experiments were initially based on his observations of routine, everyday
tasks performed by persons with cerebral lesions that varied in location
and type (Reitan, 1994).
Halstead must have felt a strong urge to identify and define the func-
tions of the frontal lobes. In his studies involving the tests that he had
Neuropsychological Deficits and Frontal Lobes 183

developed, he found that patients with frontal lesions performed much

more poorly than patients with nonfrontal lesions. The subjects with frontal
lesions also earned higher Impairment Indices. On the basis of these re-
sults, Halstead postulated a new concept of intelligence, called biological
intelligence, that was dependent principally upon the frontal lobes. The
final statement in his book, Brain and Intelligence, was that "the frontal
lobes, long regarded as silent areas, are the portion of the brain most es-
sential to biological intelligence. They are the organs of civilization- the
basis of man's despair and of his hope for the future" (Halstead, 1947).
Halstead's work, together with the great interest in prefrontal lobot-
omy, may have been influential in bringing to a zenith scientific attention
to the anterior frontal lobes. However, in the 1950s it became apparent
that prefrontal lobotomies were not a cure for the emotional problems ex-
perienced by many psychiatric patients, and other investigators, such as
Teuber (1964a), argued for the significance of impairment of nonfrontal
as well as frontal cortex. The interest in the frontal lobes eventually sub-
sided, though clinical neuropsychology had received a significant boost, and
was on its way toward eventual recognition as a discipline in its own right.
It must be noted that behavioral neurologists gradually but persist-
ently continued to investigate the relationship between the frontal lobes
and behavior, and have had a considerable influence on the current con-
ceptualization of the supposedly specific disorders associated with frontal
lobe lesions. Lezak (1983) discussed frontal lobe disorders in some detail,
devoting a section of her well-known book, Neuropsychological Assessment,
to the topic. She provided a comprehensive analysis of frontal lobe func-
tions that illustrates the difficulties implicit in this task.
Lezak began her review by noting that "the frontal lobes developed
most recently to become the largest structures of the human brain. It was
only natural for early students of brain function to conclude that the frontal
lobes must therefore be the seat of the highest cognitive functions" (p. 78).
While some early students may have reached this conclusion, even a brief
review of the history of the development of understanding the frontal lobes
tends to contest this statement, and indicates quite clearly that "early stu-
dents of brain function" (as noted above and reviewed in Reitan and Wolf-
son, 1992a) often concluded that the frontal lobes had little, if any,
significant function.
It is interesting that Lezak principally cited behavioral neurologists
to support her statements about the function and importance of the frontal
lobes. She noted that H6caen and Albert (1978) wrote that "the frontal
lobes regulate the 'active state' of the organism, control the essential ele-
ments of the subject's intentions, program complex forms of activity, and
constantly monitor all aspects of activity." (p. 79). She indicated that Nauta
184 Reitan and Wolfson

(1971), a neuroscientist trained as a neuroanatomist, characterized frontal

lobe disorders as "the derangement of behavioral programming," (p. 79),
and cited Luria (1966, 1973) and Nauta (1971) for her contention that the
"cortex and underlying white matter of the frontal lobes is the site of in-
terconnections and feedback loops between the major sensory and the ma-
jor motor systems, linking and integrating all components of behavior at
the highest level . . . . Thus, the frontal lobes are where already correlated
incoming information from all sources--external and internal, conscious
and unconscious, memory storage and visceral arousal c e n t e r s - - i s inte-
grated and enters ongoing activity." (p. 79).
Lezak cited Valenstein (1973) as differentiating between the behav-
ioral effects of dorsolateral lesions and orbitomedial lesions. Dorsolateral
lesions supposedly result in defects in the control, regulation, and integra-
tion of cognitive activities. Orbitomedial lesions, on the other hand, impair
drive and affective integration centers in the diencephalon, and are there-
fore most apt to impair emotional and social adjustment. Girgis (1971) and
Blumer and Benson (1975) have also suggested that these frontal lesions
result in different personality and psychological consequences.
Lezak cited Luria (1970) as observing that Broca's area in the pos-
terior-inferior portion of the left frontal lobe "receives information from
both the posterior language area and the temporal lobe" and serves as "the
final common path for the generation of speech impulses." A review of
Luria's publication indicates that this statement represents his theoretical
impression rather than a conclusion supported by any objective evidence.
Lezak reviewed Luria's impression that the right posterior-inferior
frontal area reflects deficits of perceptual organization and planning (as
represented by performances on the Block Design subtest of the Wechsler
Scale). She further cited Shapiro et al. (1980, 1981) as indicating that im-
paired capacity to process musical elements such as pitch, rhythm, and
phrasing tends to occur with right anterior lesions.
Reitan and Wolfson (1989) compared a group of subjects with left
hemisphere lesions to a group with right hemisphere lesion and found that
there were no differences between the groups on Seashore Rhythm Test
performances. Conflicts of this type clearly identify the problems implicit
in the area of behavioral neurology. Standardized experiments are usually
not performed, and the examination of individual subjects provides the ba-
sis for most conclusions; the investigator observes the subject, and forms
impressionistic conclusions about the individual's behavioral strengths and
weaknesses. These circumstances provide a limited opportunity to employ
one of the major hallmarks of the scientific m e t h o d - - n a m e l y , replication
by other investigators. Nevertheless, in her review of frontal lobe disorders,
Lezak principally cited behavioral neurologists who used these types of in-
Neuropsychological Deficits and Frontal Lobes 185

vestigative methods (H6caen and Albert, 1975; Luria, 1966; Nauta, 1971).
As will be noted below, the methods of behavioral neurology are concerned
principally with identifying specific deficits rather than the general, nonlo-
calized effects of cerebral lesions (Reitan and Wolfson, 1992a).
Lezak also categorized the types of behavioral difficulties associated
with prefrontal damage. She noted that these problems may also occur with
lesions involving other areas of the brain, but in such cases the patient's
difficulties "are apt to be associated with specific intellectual, sensory, or
motor disabilities." (pp. 80-81). This statement in its own right denies the
specificity of deficits that might constitute a frontal lobe syndrome.
Nevertheless, Lezak next identified the "behavioral disturbances as-
sociated with frontal lobe damage [which] can be roughly classified in five
"general groups," (p. 81), noting that the groups involve considerable over-
lap. First, Lezak noted that persons with frontal lobe damage have "prob-
lems of starting [which] appear in decreased spontaneity, decreased
productivity, decreased rate at which behavior is emitted, or decreased or
lost initiative." (p. 81). She referred to Goldstein (1944) to support this
contention, but it must be noted that this particular publication by Gold-
stein concerns his evaluation of patients with traumatic brain injury in
which neuropathological involvement has generally been recognized as dif-
fuse (even though focal lesions may also be present). Thus, even though
the frontal lobes as well as other cortical areas are often damaged in head
injuries, this study by Goldstein is hardly the most appropriate for identi-
fying specific frontal lobe deficits.
Lezak next referred to the findings of Luria (1966) and Milner (1964).
It is well known that Luria's description of deficits was based principally
on his personal observations, and as noted earlier, Milner studied patients
with chronic, focal epileptic lesions, a group of subjects that provides a
limited basis for generalization about the effects of brain damage.
Lezak's next point about frontal lobe damage concerned "difficulties
in making mental or behavioral shifts, whether they are shifts in attention,
changes in movement, or flexibility in attitude, coming under the heading
of perseveration or rigidity." (p. 81). Although she identified this type of
impairment as a frontal lobe deficit, she immediately controverted the
specificity of this conclusion by indicating that these deficits also occur with
lesions involving other areas of the brain. For example, Part B of the Trail
Making Test, one of the tests frequently identified as a measurement of
behavioral shifts in attention and flexibility, has clearly been demonstrated
to be sensitive to impaired brain functions generally, regardless of lesion
localization or lateralization (Reitan, 1955c, 1958). Specific comparisons of
performances of groups with frontal and nonfrontal lesions yield no sig-
nificant intergroup differences (Reitan and Wolfson, in press).
186 Reitan and Wolfson

According to Lezak, the third specific deficit in patients with frontal

lobe lesion relates to "problems in s t o p p i n g - - i n breaking or modulating
ongoing behavior--[and] show up in impulsivity, overreactivity, disinhibi-
tion, and difficulties in holding back a wrong or unwanted response, par-
ticularly when it may either have a strong association value or be part of
an already ongoing response chain." (p. 81). This type of behavior has been
reported in individuals with frontal lobe lesions, but no references were
given to support this "specific" deficit. In fact, the behavior is not at all
specific, is difficult to define in operational terms, and often is seen in pa-
tients with generalized brain impairment rather than only in persons with
frontal lobe lesions.
The fourth point about frontal lobe damage concerns a deficient self-
awareness. Lezak wrote that this deficit "results in an inability to perceive
performance errors, to appreciate the impact one makes on others, or to
size up a social situation appropriately." (p. 81). Again, no references are
given to support this contention. It should be noted, however, that several
investigators (Meier and French, 1966; Milner, 1954; Reitan, 1955a) have
commented that impairment in the ability "to size up a social situation
appropriately," as manifested by explicit results on instruments such as the
Wechsler Picture Arrangement subtest and the McGill Picture Anomalies
Test, is related to nonfrontal rather than frontal lesions.
Finally, Lezak noted that "a concrete attitude is also common among
patients with frontal lobe damage." (p. 82). She referred to (1) Goldstein
(1944, 1948), whose studies were based upon patients with traumatic brain
injuries, and therefore probably do not represent lesions restricted to the
frontal areas; (2) Landis (1952), whose studies were based upon chronic,
deteriorated schizophrenics who underwent cortical topectomy, and are
scarcely relevant for purposes of generalization; (3) Teuber (1964), who
also studied head-injury cases and based his inferences about localization
on the point of impact to the skull and the evidence of underlying cortical
damage; (4) Lezak (1978), who described her impressionistic observations
in an article entitled "Living with a Characterologically Altered Brain-Injured
Patient"; and (5) Milner (1971), whose sample of patients with focal, long-
standing epileptogenic lesions, subject to surgical excision, are limited in
their representation of patients with brain damage in general.
Lezak noted a number of other references that also have problems
regarding their nonspecificity for frontal as compared with nonfrontal in-
volvement. These references characterize patients with frontal lesions as
having an attitude that takes objects, experiences, and behavior "at their
most obvious face value. The patient becomes incapable of planning and
foresight or sustaining a goal-directed behavior." (p. 82). In general, frontal
patients show evidence of "apathy, carelessness, poor or unreliable judge-
Neuropsychological Deficits and Frontal Lobes 187

ment, poor adaptability to new situations, and blunted social sensibility."

(p. 83). Anyone who has studied persons with cerebral lesions, frontal or
nonfrontal, has seen these deficits demonstrated, regardless of the location
of the lesion. In addition, such deficits occur frequently among persons
with diffuse or generalized cerebral damage (such as Alzheimer's disease),
even when there is no specific or isolated involvement of the frontal lobes.
It must be noted that Lezak (1983), in a final section concerning the
effects of frontal lobe lesions, commented that "the uncertain relation be-
tween brain activity and human behavior obligates the clinician to exercise
care in observation and caution in prediction, and to take nothing for
granted when applying the principles of functional localization to diagnostic
problems." (p. 84). This final paragraph seems to caution the reader con-
cerning generalizations about function attributed to the frontal lobes as
well as the "limitations of its applicability of the individual case." (pp. 83-
84).
The above review of Lezak's five criteria, while presenting some of
the current generalizations about the frontal lobes, also reveals the great
difficulties inherent in postulating a theory of frontal lobe functions.
There are many other reviews of frontal lobe functions, several of
them overlapping in their content. Jouandet and Gazzaniga (1979) cited a
number of the references ngted above in our review of validation studies
in addition to reviewing the anatomy of the frontal lobes, connections with
other ares of the brain, and surgery (especially prefrontal lobotomy) for
psychiatric disorders. Citing H e b b (1939), Mettler (1949), and Teuber
(1959), Jouandet and Gazzaniga contrasted the earlier tendencies to attrib-
ute "the most stupendous of cognitive capabilities" to the frontal cortex
with a reaction contending that no specified functions could be attributed
to the prefrontal a r e a s - - t h a t there was no "indisputable evidence suggest-
ing that there existed any cognitive processes subserved exclusively by the
prefrontal regions"' (p. 26). In their analysis of the studies of Milner, Ben-
ton, and others cited above as well as various additional publications,
Jouandet and Gazzaniga concluded that "the frontal lobes have come to
contribute in their later stages of phylogenetic evolution to the limitless
analytic powers of the human psyche by superimposing on the three spatial
dimensions a profound mastery of the fourth dimension of time" (p. 54).
In the same volume, Goodglass and Kaplan (1979b) reviewed the tra-
ditional functions attributed to the frontal lobes (such as lack of drive and
spontaneous expression, socially inappropriate behavior, impairment of
flexibility, and lack of ability to plan sequential aspects of behavior), and
identified the Wisconsin Card Sorting Test, verbal fluency procedures, and
the Stroop Test as examples of frontal lobe tests.
188 Reitan and Wolfson

In an analytical review, Damasio (1985) integrated clinical and

neuropsychological deficits of patients who have frontal lesions with ana-
tomical considerations. The impact of this analysis, however, was dimin-
ished by a tendency to accept the rather weak statistical results on tests
such as the WCST and the TWFT as invariant and specific characteristics
of frontal lobe damage.
Stuss and Benson (I984) also reviewed neuropsychoIogical studies of
the frontal lobes, using headings of (1) motor functions; (2) sensory, per-
ception, and construction functions; (3) attention; (4) syndromes of abnor-
mal awareness; (5) flexibility-perseveration; (6) language, including various
types and manifestations of aphasia; (7) memory; (8) cognitive functions;
(9) frontal lobe personality; and (10) localization and hemispheric asym-
metry of frontal lobe function. These authors described many changes or
deficits supposedly resulting from frontal lobe lesions, but communicated
a mixed message when they concluded that "current explanations of ap-
parent frontal lobe malfunction remain limited and vague," and "it would
appear that a few specific prefrontal functions can be extracted. These are
broad and vague and certainly incomplete . . ." (p. 22). One must wonder
about the authors' use of the term "specific functions," described in the
next sentence as "broad and vague." Stuss and Benson provided a com-
prehensive review of the literature, couching their conclusions about frontal
lobe damage in qualified terms (which do not necessarily identify the defi-
cits as exclusively frontal), and concluded that "the neuropsychologic pic-
ture secondary to prefrontal pathology is a complex and confusing set of
behaviors" (p. 23).
A recurring observation in theoretical and review papers on the fron-
tal lobes, mentioned by Stuss and Benson, is that the cognitive deficits ex-
perienced by persons with frontal lesions are difficult to measure with
psychological tests, and that improved or more appropriate tests will likely
lead to further and clearer exposition of these subtle deficits (Hart and
Jacobs, 1993; Levin et al., 1991; Lezak, 1993; Varney and Menefee, 1993).
The vagueness with which the effects of frontal lesions are described and
the "bewildering array of behavioral deficits [that] has been attributed to
frontal lobe injury" (Goldman-Rakic, 1993, p. 13), may also be factors con-
tributing to the apparent overlap (to the point of essential identity?) with
the effects of other cerebral lesions.
When one considers the many differences among patients with cere-
bral lesions in terms of location, severity, course of recovery or deteriora-
tion, etc., it is difficult to organize, with any degree of precision, selective,
impressionistic, clinical descriptions of deficits of individual subjects. In
contrast, readily identified (specific) deficits are often prominent in persons
with nonfrontal lesions, a fact that may tend to promote a presumption of
Neuropsychological Deficits and Frontal Lobes 189

understanding of these patients. Among frontal patients, however, the spe-

cific deficits are less prominent, even though the general deficits are pro-
nounced. The critical need may therefore be to gain further insight and
understanding of the general neuropsychological deficits, over and beyond
specific deficits, that are common to persons with both frontal and non-
frontal lesions (Reitan and Wolfson, 1994). The field of behavioral neu-
rology has focused principally on the study of specific deficits, whereas
nearly all of the tests of generalized neuropsychological impairment have
their roots in clinical neuropsychology (see Reitan and Wolfson, 1992a and
1993, for a more complete discussion of general and specific neuropsy-
chological tests together with their differential origin and use in clinical
neuropsychology and behavioral neurology).
Mountain and Snow (1993) presented a detailed analytical review of
research publications and the potential for clinical applications of findings
using the Wisconsin Card Sorting Test. Their review was comprehensive
rather than selective, and included a number of studies not mentioned in
this paper. These authors concluded, as we did, that the evidence is weak
that patients with frontal lesions, when compared to patients with nonfron-
tal lesions, perform more poorly on the WCST, and that clinical findings
do not support the use of the WCST as a frontal indicator. In addition,
Mountain and Snow cautioned against using the WCST as a marker of
frontal lobe functions for research purposes--apparently, as indicated in
the introductory section of this paper, a tendency of striking prevalence.
The recent volume edited by Levin et al. (1991) provides a compre-
hensive synthesis of research on the frontal lobes, and reviews many areas
and types of deficits. Many topics of interest are addressed, but are pre-
sented in a research rather than a clinical framework. For example, the
most recent comprehensive studies comparing frontal and nonfrontal
groups on the WCST (Robinson et al., 1980) and the TWFT (Pendleton
et al., 1982) are not mentioned or referenced, even though they were pub-
lished years earlier, and were omitted probably because the focus of this
volume was directed toward experimental rather than clinical neuropsychol-
ogy.
The numerous theoretical and review papers on the frontal lobes, as
well as other secondary sources, appear to have had a significant influence
on many psychologists. This type of influence was exemplified by Knopman
et al. (1990), who reported on their examination of patients who had de-
mentia without distinctive histological features. The principal point of in-
terest of this study was that the subjects did not qualify histologically for
a diagnosis of Alzheimer's disease. Nevertheless, they had memory loss and
personality changes, in the context of an illness that lead to death, usually
within two to seven years.
190 Reitan and Wolfson

The patients in the Knopman et al. study had been examined with
"mazes, trail making, and word fluency." (p. 253). The psychometric find-
ings were interpreted as being "consistent with a 'frontal' lobe dementia"
(p. 251), a conclusion reached on the basis of the fact that these tests
measured "frontal based functions." (p. 253). Nevertheless, the authors
characterized their patients as having rather generalized cerebral involve-
ment, including "degeneration of the cerebral cortex, which was most se-
vere in the frontal and parietal cortex, less severe in the temporal cortex,
and generally absent in the occipital cortex." (p. 252). The authors con-
cluded that the findings were consistent with a "frontal" lobe dementia,
apparently because of the psychological examinations that had been per-
formed and the attribution in the literature that the tests used to examine
the patients reflect frontal damage.
It is apparent that the generalizations and conclusions communicated
by prominent neuropsychologists tend to be accepted rather uncritically by
psychologists as well as other professionals. This highlights the responsibil-
ity of researchers to be accurate in reporting their findings, particularly
when making specific statements about the behavioral correlates of patho-
logical conditions such as frontal lobe damage.
One of the tests used by Knopman et al. was the Trail Making Test,
a measure with which Reitan has probably had more clinical and research
experience than anyone. The fact is that the Trail Making Test is sensitive
to generalized cerebral damage rather than damage specific to the frontal
lobes (Reitan, 1958), but the assumptions of these investigators had been
based not on the facts, but instead on an unsupported belief that the Trail
Making Test, because of its requirements, must fit within the range of abili-
ties described theoretically as relating to frontal lobe functions. A recent
study confirms that Part B of the Trail Making Test is equally sensitive to
frontal and nonfrontal cerebral lesions (Reitan and Wolfson, in press).
Finally, we will refer specifically to Halstead-Reitan Battery results
obtained by patients with frontal and nonfrontal lesions. As noted above,
Halstead felt that the ten tests that he developed, and which provided a
basis for computing the Impairment Index, were much more adversely af-
fected by frontal than nonfrontal damage. A considerable debate ensued
after Halstead (1947) reported this conclusion, with Teuber in particular
contending that nonfrontal lesions were at least equally as impairing as
frontal lesions. In his book, Brain and Intelligence, Halstead (1947) publish-
ed neurological summaries as well as the actual test scores of the patients
used in his studies. Thus, it is possible to inspect his findings in detail with
relation to results reported by many additional investigators.
Halstead's data provides the basis for a remarkable insight. His pa-
tients with frontal lobe lesions generally performed quite poorly, document-
Neuropsychological Deficits and Frontal Lobes 191

ing the fact that frontal lobe damage is associated with significant cognitiv.e
impairment. His statistical comparisons also indicated that the patients with
frontal lobe lesions performed more poorly than the subjects with nonfron-
tal lesions. It was therefore of interest to study the results for the individual
subjects in the nonfrontal group. It was the results on his nonfrontal pa-
tients, rather than his frontal patients, that disagreed with later findings by
other investigators. Halstead's nonfrontal patients performed extremely
well on the tests compared to thousands of patients tested by Reitan and
other investigators.
Thus, the unusual aspect of Halstead's findings is not the results of
his frontal patients, but the performances of his nonfrontal patients. The
frontal patients showed evidence of impairment, just as essentially every
investigator had found. However, his nonfrontal patients usually performed
considerably better than nonfrontal subjects studied by later investigators.
In fact, Reitan's data indicate that, in an overall sense, patients with frontal
lesions perform approximately equivalently to patients with nonfrontal le-
sions, and both groups demonstrate significant impairment compared with
non-brain-damaged control groups (Reitan, 1964).
Frontal subjects differ from nonfrontal subjects in some basic re-
spects. Frontal patients routinely demonstrate generalized neuropsychologi-
cal impairment, but usually do not show any very specific higher level
deficits. Nonfrontal patients, however, often demonstrate impairment on
tests that involve auditory, tactile, and visual perception, and frequently
have dysphasic disorders (particularly with left cerebral lesions) and visual-
constructive deficits (particularly with right cerebral lesions). Therefore, pa-
tients with posterior lesions may exhibit indications of general impairment
together with more specific and lateralizing findings, whereas patients with
frontal lesions show indications of general impairment but often do not
demonstrate specific deficits. As Reitan and Wolfson have emphasized re-
peatedly, a comprehensive neuropsychological assessment must include
both general and specific indicators of neuropsychological deficits, not only
to identify localized damage, but to also provide a thorough assessment of
an individual's cognitive structure (Reitan, 1988; Reitan and Wolfson, 1986,
1988, 1993, 1994).
A historical review of frontal lobe studies suggests that the "riddle of
frontal lobe functions" may be a result of methodology rather than content.
Promising leads about specific frontal deficits essentially lost their specific-
ity when more adequate and carefully controlled studies were performed.
Persons with frontal lobe lesions may demonstrate generalized neuropsy-
chological impairment without any specific deficits (aside from dysphasic
symptoms). If this is true, the search for specific deficits, fueled by vague
theoretical descriptions, could continue forever quite fruitlessly. The meth-
192 Reitan and Wolfson

ods of behavioral neurology, with a focus on the individual person, are not
well suited to identifying general neuropsychological impairments, and will
likely lead, on a case-by-case basis, to a further elaboration of the "bewil-
dering array" of deficits that have already been described.
In attempting to gain greater understanding of the function of the
frontal lobes, it may be necessary to concentrate on general, rather than
specific, neuropsychological tests (Reitan and Wolfson, 1994), and such
general measures have been derived almost entirely from the field of clini-
cal neuropsychology rather than behavioral neurology (Reitan and Wolfson,
1993). It appears that such an approach would also lead investigators to
recognize that other cerebral areas share essentially all of the higher level
cognitive functions of the frontal lobes.

REFERENCES

Ackerly, S. S. (1935). Instinctive, emotional and medical changes following prefrontal lobe
extirpation. American Journal of Psychiatry 92: 717-729.
Adams, K. M., Brown, G. G., and Grant, I. (1985). Analysis of covariance as a remedy for
demographic mismatch of research subject groups: Some sobering simulations. Journal of
Clinical and Experimental Neuropsychology 7: 445-462.
Albert, M. L., Goodglass, H., Helm, N. A., Rubens, A. B., and Alexander, M. P. (1981).
Clinical Aspects of Dysphasia, Springer-Verlag, New York.
Anderson, S. W., Damasio, H., Jones, R. D., and Tranel, D. (1991). Wisconsin Card Sorting
Test performance as a measure of frontal lobe damage. Journal of Clinical and
Experimental Neuropsychology 13: 909-922.
Anderson, S. W., Damasio, H., and Tranel, D. (1990). Neuropsychological impairments
associated with lesions caused by tumor or stroke. Archives of Neurology 47: 397-405.
Anderson, S. W., Damasio, H., Tranel, D., and Damasio, A. R. (1988). Neuropsychological
correlates of bilateral frontal lobe lesions in humans. Soc&ty for Neuroscience 14: 1288.
Arieff, A. J., and Yacorzynski, G. K. (1942). Deterioration of patients with organic epilepsy.
Journal of Nervous and Mental Disease 96: 49-55.
Axelrod, B. N., Goldman, R. S., and Henry, R. R. (1992). Sensitivity of the Mini-Mental State
Examination to frontal lobe dysfunction in normal aging. Journal of Clinical Psychology
48: 68-71.
Benton, A. L. (1968). Differential behavioral effects in frontal lobe disease. Neuropsychologia
6: 53-60.
Benton, A. L., and Hamsher, K. deS. (1976). Multilingual Aphasia Examination, University of
Iowa, Iowa City.
Bigler, E. D. (1988). Frontal lobe damage and neuropsychological assessment. Archives of
Clinical Neuropsychology 3: 279-297.
Blumer, D., and Benson, D. F. (1975). Personality changes with frontal and temporal lobe
lesions. In Benson, D. F., and Blumer, D. (eds.), Psychiatric Aspects of Neurologic Disease,
Grune & Stratton, New York, pp. 151-169.
Boone, K. B., Miller, B. L., Lesser, I. M., Hill, E., and D'Elia, L. (1990). Performance on
frontal lobe tests in healthy, older individuals. Developmental Neuropsychology 6: 215-233.
Brickner, R. M. (1936). Bilateral frontal lobectomy: Follow-up report of a case. Archives of
Neurology and Psychiatry 41: 580-585.
Broca, P. (1861). Remarques sur le siege de la facult6 du language articule, suivies d'une
observation d'aphemie (perte de la parole). Bulletin de la Socidt~Anatomique 36: 330-357.
Neuropsychological Deficits and Frontal Lobes 193

Butters, M. A., Kaszniak, A. W., Glisky, E. L., Eslinger, P. J., and Schacter, D. L. (1994).
Recency discrimination deficits in frontal lobe patients. Neuropsychology 8: 343-353.
Chouinard, M. J., and Braun, C. M. J. (1993). A meta-analysis of the relative sensitivity of
neuropsychological screening tests. Journal of Clinical and Experimental Neuropsychology
15: 591-607.
Costa, L. (1988). Clinical neuropsychology: Prospects and problems. The Clinical
Neuropsychologist 2: 3-11.
Cronin-Golomb, A. (1990). Abstract thought in aging and age-related neurological disease.
In Boiler, F. and Grafman, J. (eds.), Handbook of Neuropsychology (Vol. 4), Elsevier
Science, Amsterdam, pp. 279-310.
Damasio, A. R. (1985). The frontal lobes. In Heilman, K. M., and Valenstein, E. (eds.),
Clinical Neuropsychology, Oxford University Press, New York, pp. 339-375.
Damasio, H. C. (1991). Neuroanatomy of frontal lobe in vivo: A comment on methodology.
In Levin, H. S., Eisenberg, H. M., and Benton, A. L. (eds.), Frontal Lobe Function and
Dysfunction, Oxford University Press, New York, pp. 92-121.
De Haas, A., and Magnus, O. (1958). In De Haas, A. (ed.), Lectures on Epilepsy, Elsevier,
New York.
Dikmen, S., Matthews, C. G., and Harley, J. P. (1975). The effect of early versus late onset
of major motor epilepsy upon cognitive-intellectual performance. Epilepsia 16: 73-81.
Dodrill, C. B. (1981). Neuropsychology of epilepsy. In Filskov, S. B., and Boll, T. J. (eds.),
Handbook of Clinical Neuropsychology, John Wiley, New York, pp. 366-395.
Drewe, E. A. (1974). The effect of type and area of brain lesion on Wisconsin Card Sort
Test performance. Cortex 10: 159-170.
Drewe, E. A. (1975). An experimental investigation of Luria's theory on the effects of frontal
lobe lesions in man. Neuropsychologia 13: 421-429.
Eslinger, P. J., and Damasio, A. R. (1985). Severe disturbance of higher cognition after
bilateral frontal lobe ablation. Neurology 35: 1731-1741.
Farmer, M. E. (1994). Cognitive deficits related to major organ failure. The potential role of
neuropsychological testing. Nehropsychology Review 2:117-160.
Fiducia, D., and O'Leary, D. S. (1990). Development of a behavior attributed to the frontal
lobes and the relationship to other cognitive functions. Developmental Neuropsychology 6:
85-94.
Finger, S., and Wolf, C. (1988). The "Kennard Effect" before Kennard. Archives of Neurology
45: 1136-1142.
Flou rens, P. (1824). Recherces exp~rimentales sur les propridtds et les fonctions du systdme nerveux
dans les animaux vertebras. Pairs: Crevot.
Franz, S. I. (1907). On the functions of the cerebrum: The frontal lobes.Archives of Psychology
(Monograph No. 2). Science Press, New York.
Fritsch, G., and Hitzig, E. (1870). Ueber die electrische Erregbarkeit des Grosshirn. Archiv
fur Anatom& und Physiologie 37: 300-332.
Fulton, J. F. (1943). Physiology of the Nervous System (2nd ed.). Oxford University Press,
London.
Fuster, J. M. (1988). The Prefrontal Cortex: Anatomy, Physiology, and Neuropsychology of the
Frontal Lobe, Raven Press, New York.
Gazzaniga, M. S., Bogen, J. E., and Sperry, R. W. (1963). Laterality effects in somesthesis
following cerebral commissurotomy in man. Neuropsychologia 1: 209-221.
Gelb, A., and Goldstein, K. (1925). Ueber Farbennamenamnesie. Psychologie Forschrift 6:
127-186.
Gilroy, J., and Meyer, J. S. (1979). Medical Neurology, Macmillan, New York.
Girgis, M. (1971). The orbital surface of the frontal lobe of the brain. Acta Psychiatrica
Scandinavica Supplementum 222: 1-58.
Gnys, J. A., and Willis, W. G. (1991). Validation of executive function tasks with young
children. Developmental Neuropsychology 7: 487-501.
Goldman-Rakic, P. S. (1993). Specification of higher cortical functions. Journal of Head
Trauma Rehabilitation 8: 13-23.
194 Reitan and Wolfson

Goldstein, K. (1944). The mental changes due to frontal lobe damage. Journal of Psychology
17: 187-208.
Goldstein, K. (1948). Language and Language Disturbances, Grune & Stratton, New York.
Goodglass, H., and Kaplan, E. (1979). Assessment of cognitive deficit in the brain-injured
patient. In Gazzaniga, M. S. (ed.), Handbook of Behavioral Neurology. Vol. 2.
Neuropsychology, Plenum, New York, pp. 3-22.
Grafman, J., Jonas, B., and Salazar, A. (1990). Wisconsin Card Sorting Test performance
based on location and size of nenroanatomical lesion in Vietnam veterans with
penetrating head injury. Perceptual and Motor Skills 71: 1120-1122.
Grafman, J., Sirigu, A., Spector, L., and Hendler, J. (1993). Damage to the prefrontal cortex
leads to decomposition of structured event complexes. Journal of Head Trauma
Rehabilitation g: 73-87.
Grodzinsky, G. M., and Diamond, R. (1992). Frontal lobe functioning in boys with
attention-deficit hyperactivity disorder. Developmental Neuropsychology 8: 427-445.
Halstead, W. C. (1947). Brain and lnteUigence: A Quantitative Study of the Frontal Lobes,
University of Chicago Press, Chicago.
Halstead, W. C., Carmichael, H. T., and Buoy, P. C. (1946). Pre-frontai lobotomy: A
preliminary appraisal of the behavioral results. American Journal of Psychiatry 103:
217-228.
Harris, A. B. (1972). Degeneration in experimental epileptic foci. Archives of Neurology 26:
434-449.
Hart, T., and Jacobs, H. E. (1993) Rehabilitation and management of behavioral disturbances
following frontal lobe injury. Journal of Head Trauma Rehabilitation g: 1-12.
Heaton, R. K. (1981). Wisconsin Card Sorting Test Manual Psychological Assessment
Resources, Odessa, FL.
Hebb, D. O. (1939). Intelligence in man after large removals of cerebral tissue: Report of
four left frontal lobe cases. Journal of General Psychology 21: 73-78.
Hebb, D. O. (1949). The Organization of Behavior: A Neuropsychological Theory. John Wiley,
New York.
H6caen, H., and Albert, M. (1975). Disorders of mental functioning related to frontal lobe
pathology. In Benson, D. F., and Blamer, D. (eds.), Psychiatric Aspects of Neurologic
Disease, Grune & Stratton, New York, pp. 137-149.
H6caen, H., and Albert, M. (1978). Human Neuropsychology, John Wiley & Sons, New York.
Heck, E. T., and Bryer, J. B. (1986). Superior sorting and categorizing ability in a case of
bilateral frontal lobe atrophy: An exception to the rule. Journal of Clinical and
Experimental Neuropsychology 8: 313-316.
Heilman, K. M., and Valenstein, E. (eds.). (1979). Clinical Neuropsychology, Oxford University
Press, New York.
Hermann, B. P., Wyler, A. R., and Richey, E. T. (1988). Wisconsin Card Sorting Test
performance in patients with complex partial seizures of temporal lobe origin. Journal of
Clinical and Experimental Psychology 10: 467-476.
Horn, J., and Reitan, R. M. (1982). Effect of lateralized cerebral damage upon contralateral
and ipsilateral sensorimotor performances. Journal of Clinical Neuropsychology 4: 249-268.
Horn, J., and Reitan, R. M. (1984). Neuropsychological correlates of rapidly vs. slowly growing
intrinsic neoplasms. Journal of Clinical Neuropsychology 6: 309-324.
Jarvis, P. E., and Barth, J. T. (1994). The Halstead-Reitan Neuropsychological Battery: A Guide
to Interpretation and Clinical Applications, Psychological Assessment Resources, Odessa,
FL.
Jefferson, G. (1937a). Left frontal lobectomy. Proceedings of the Royal Society of Medicine 30:
851-853.
Jefferson, G. (1937b). Removal of right or left frontal lobes in man. Medical Journal 2:
199-206.
Jouandet, M., and Gazzaniga, M. S. (1979). The frontal lobes. In Gazzaniga, M. S. (ed.),
Handbook of Behavioral Neurology. VoL 2. Neuropsychology, Plenum, New York, pp. 25-59.
Klr H., and Matthews, C. G. (1966). Neuropsychological evaluation of the epileptic patient.
Wisconsin Medical Journal 68: 296-301.
Neuropsychological Deficits and Frontal Lobes 195

Knopman, D. S., Mastri, A. R., Frey, W. H., Sung, J. H., and Rustan, T. (1990). Dementia
lacking distinctive histologic features: A common non-AIzheimer degenerative dementia:
Neurology 40: 251-256.
Landis, C. (1952). Remarks on the psychological findings attendant on psychosurgery. In The
Biology of Mental Health and Disease, Paul B. Hoeber, New York.
Lashley, K. S. (1929). Brain Mechanisms and Intelligence, University of Chicago Press, Chicago.
Lennox, W. G., and Lennox, M. A. (1960). Epilepsy and Related Disorders. Little, Brown,
Boston.
Levin, H. S., Eisenberg, H. M., and Benton, A. L. (1991). Frontal Lobe Function and
Dysfunction. New York: Oxford University Press.
Lezak, M. D. (1978). Living with the characterologically altered brain-injured patient. Journal
of Clinical Psychiatry 39: 592-598.
Lezak, M. D. (1983). Neuropsychological Assessment, Oxford University Press, New York.
Lezak, M. D. (1993). Newer contributions to the neuropsychological assessment of executive
functions. Journal of Head Trauma Rehabilitation 8: 24-31.
Loeb, J. (1902). Comparative Physiology of the Brain and Comparative Psychology, G. P. Putnam
and Sons, New York.
Luria, A. R. (1966). Higher Cortical Functions in Man. (B. Haigh, trans.). Basic Books, New
York.
Luria, A. R. (1970). The functional organization of the brain. Scientific American 222: 2-9.
Luria, A. R. (1973). The frontal lobes and the regulation of behavior. In Pribram, K. H., and
Luria, A. R. (eds.), Psychophysiology of the Frontal Lobes, Academic Press, New York,
pp. 3-26.
Mahoney, W. J., D'Souza, B. J., Hailer, J. A., Rogers, M. C., Epstein, M. H., and Freeman,
J. M. (1983). Long-term outcome of children with severe head trauma and prolonged
coma. Pediatrics 71: 756-762.
Matthews, C. G., & Kleve, H. (1967). Differential psychological performances in major motor,
psychomotor, and mixed seizure classifications of known and unknown etiology. Epilepsia
8: 117-128.
Meier, M. J., and French, L. A. (1966). Longitudinal assessment of intellectual functioning
following unilateral temporal lobectomy. Journal of Clinical Psychology 22: 23-27.
Mettler, F. A. (ed.). (1949). Columbia-Greystone Associates: Selective Partial Ablation of the
Frontal Cortex: A Correlative Study of Its Effects on Human Psychotic Subjects, Hoeber,
New York.
Miceli, G., Caltagirone, C., Gainotti, G., Masullo, C., and Silveri, M. C. (1981).
Neuropsychological correlates of localized cerebral lesions in non-aphasic brain-damaged
patients. Journal of Clinical Neuropsychology 3: 53-63.
Milner, B. (1954). Intellectual function of the temporal lobes. Psychological Bulletin 51: 42-62.
Milner, B. (1963). Effects of different brain lesions on card sorting. Archives of Neurology 9:
100-110.
Milner, B. (1964). Some effects of frontal Iobectomy in man. In Warren, J. M., and Akert,
K. (eds.), The Frontal Granular Cortex and Behavior, McGraw-Hill, New York, pp.
313-334.
Milner, B. (1971). Interhemispheric differences in the localization of psychological processes
in man. British Medical Bulletin 27: 272-277.
Moniz, E. (1936). The first attempt at operative treatment of certain psychosis. Ancephale 31:
1-29.
Moniz, E. (1937). Prefrontal leukotomy in treatment of mental disorders. American Journal
of Psychiatry 93: 1379-1385.
Mountain, M. A., and Snow, W. G. (1993). Wisconsin Card Sorting Test as a measure of
frontal pathology: A review. The Clinical Neuropsychologist 7: 108-118.
Nauta, W. J. H. (1971). The problem of the frontal lobe. Journal of Psychiatric Research 8:
167-187.
Neisser, U. (1979). The concept of intelligence. In Sternberg, R. J., and Delterman, D. K.
(eds.), Human Intelligence: Perspectives on Its Theory and Measurement, Norwood, N J,
Ablex, pp. 179-189.
196 Reitan and Wolfson

Parsons, O. A. (1975). Brain damage in alcoholics: Altered states of consciousness. In Gross,

M. M. (eds.), Alcohol Intoxication and Withdrawa~ E.rperimental Studies (No. 2), Plenum
Press, New York.
Pendleton, M. G., Heaton, R. K., Lehman, R. A., and Hulihan, D. (1982). Diagnostic utility
of the Thurstone Word Fluency Test in neuropsychological evaluations. Journal of Clinical
Neuropsychoiogy 4: 307-317.
Penfieid, W., and Roberts, L. (1959). Speech and Brain Mechanisms, Princeton University
Press, Princeton, NJ.
Perret, E. (1974). The left frontal lobe of man and the suppression of habitual responses in
verbal categorical behavior. Neuropsychologia 12: 323-330.
Rainier, A. M., and H6eaen, H. (1970). R61e respectif des atteintes frontales et de la
lat~ralization 16sionnelle dans les d~fieits de la "fluence verbale." Revue Neurologique 123:
17-22.
Reitan, R. M. (1955a). Discussion: Symposium on the temporal lobe. Archives of Neurology
and Psychiatry 74: 569-570.
Reitan R. M. (1955b). An investigation of the validity of Halstead's measures of biological
intelligence. Archives of Neurology and Psychiatry 73: 28-35.
Reitan R. M. (1955c). The relation of the Trail Making Test to organic brain damage. Journal
of Consulting Psychology 19: 393-394.
Reitan R. M. (1958). The validity of the Trail Making Test as an indicator of organic brain
damage. Perceptual and Motor Skills 8: 271-276.
Reitan R. M. (1960). The significance of dysphasia for intelligence and adaptive abilities.
Journal of Psychology 50: 355-376.
Reitan R. M. (1964). Psychological deficits resulting from cerebral lesions in man. In Warren,
J. M., and Akert, K. A. (eds.), The Frontal Granular Cortex and Behavior, McGraw-Hill,
New York.
Reitan, R. M. (1985). Aphasia and Sensory-Perceptual Deficits in Children, Neuropsychology
Press, Tucson, AZ.
Reitan, R. M. (1988). Integration of neuropsychological theory, assessment, and application.
The Clinical Neuropsychologist 2: 331-349.
Reitan, R. M. (1994). Ward Halstead's contributions to neuropsychology and the
Halstead-Reitan Neuropsychological Test Battery. Journal of Clinical Psychology 50: 47-70.
Reitan, R. M., and Wolfson, D. (1986). Traumatic Brain Injury. Vol. I. Pathophysioiogy and
Neuropsychological Evaluation, Neuropsychology Press, Tucson, AZ.
Reitan, R. M., and Wolfson, D. (1988). Traumatic Brain Injury. Vol. 11. Recovery and
Rehabilitation, Neuropsychoiogy Press, Tucson, AZ.
Reitan, R. M., and Wolfson, D. (1989). The Seashore Rhythm Test and brain functions. The
Clinical Neuropsychologist 3: 70-77.
Reitan, R. M., and Wolfson, D. (1992a). Neuroanatomy and Neuropathoiogy: A Clinical Guide
for Neuropsychoiogists (2nd ed.), Neuropsychology Press, Tucson, AZ.
Reitan, R. M., and Wolfson, D. (1992b). Neuropsychological Evaluation of Older Children.
Neuropsychology Press, Tucson, AZ.
Reitan, R. M., and Woifson, D. (1993). The Halstead-Reitan Neuropsychological Test Battery:
Theory and Clinical Interpretation (2nd ed.), Neuropsychology Press, Tucson, AZ.
Reitan, R. M., and Wolfson, D. (in press). Relationships between specific and general tests
of cerebral functioning, The Clinical Neuropsychologlst.
Reitan, R. M., and Woifson, D. (in press). The Category Test and the Trail Making Test as
measures of frontal lobe functions. The Clinical Neuropsychoiogist.
Robinson, A. L., Heaton, R. K., Lehman, R. A. W., and Stiison, D. W. (1980). The utility
of the Wisconsin Card Sorting Test in detecting and localizing frontal lobe lesions. Journal
of Consulting and Clinical Psychology 48: 605-641.
Rourke, B. P., Bakker, D. J., Fisk, J. L., and Strang, J. B. (1983). Child Neuropsychology,
Guilford, New York.
Rybash, J. M., and Colilla, J. L. (1994). Source memory deficits and frontal lobe functioning
in children. Developmental Neuropsychology 10: 67-73.
Neuropsychological Deficits and Frontal Lobes 197

Rylander, G. (1947). Discussion of W. C. Halstead's paper: Specialization of behavioral

functions and the frontal lobes. Assocation for Research in Nervous and Mental Diseases
27: 64.
Schwartz, M. F., Mayer, N. H., FitzpatrickDeSalme, E. J., and Montgomery, "M. W. (1993).
Cognitive theory and the study of everyday action disorders after brain damage. Journal
of Head Trauma Rehabilitation 8: 59-72.
Shapiro, B. E., Grossman, M., and Gardner, H. (1980). Selective deficits in processing music
after brain damage. Paper presented at the eighth annual meeting of the International
Neuropsychological Society, San Francisco.
Shapiro, B. E., Grossman, M., and Gardner, H. (1981). Selective musical processing deficits
in brain-damaged populations. Neuropsychologia 19: 161-169.
Shute, G. E., and Huertas, V. (1990). Developmental variability in frontal lobe function.
Developmental Neuropsychology 6: 1-11.
Sohlberg, M. M., Mateer, C. A., and Stuss, D. T. (1993). Contemporary approaches to the
management of executive control dysfunction. Journal of Head Trauma Rehabilitation 8:
45-58.
Sperry, R. W., Gazzaniga, M. S., and Bogen, J. E. (1969). Interhemispheric relationships: The
neocortical commissures, syndromes of hemisphere deconnection. In Vinken, P. J., and
Gruyn, G. W. (eds.), Handbook of Clinical Neurology (Vol. 4), North Holland,
Amsterdam, pp. 273-290.
Stoddard, G. (1943). The Meaning of Intelligence, Macmillan, New York.
Strauss, E., Hunter, M., and Wada, J. (1993). Wisconsin Card Sorting Performance: Effects
of age of onset of damage and laterality of dysfunction. Journal of Clinical and
Experimental Neuropsychology 15: 896-902.
Stuss, D. T. (1991). Self, awareness, and the frontal lobes: A neuropsychological perspective.
In Goethaals, G. R., and Strauss, J. (eds.), The Self" An Interdisciplinary Approach,
Springer-Verlag, New York.
Stuss, D. T., and Benson, D. F. (1984). Neuropsychological studies of the frontal lobes.
Psychological Bulletin 1: 3-28.
Stuss, D. T., and Benson, D. F. (1986). The Frontal Lobes. Raven, New York.
Tarter, R. E., and Parsons, O. A. (1971). Conceptual shifting in chronic alcoholics. Journal
of Abnormal Psychology 77: 71-75.
Teuber, H.-L. (1959). Some alterations in behavior after cerebral lesions in man. In Bass, A.
D. (ed.), Evaluation of Nervous Control from Primitive Organisms to Man, American
Assocation for the Advancement of Science, Washington, DC, pp. 157-194.
Teuber, H.-L. (1964a). Discussion. In Warren, J. M. and Akert, K. (eds.), The Frontal Granular
Cortex and Behavior, McGraw-Hill, New York, pp. 332-333.
Teuber, H.-L. (1964b). The riddle of frontal lobe function in man. In Warren, J. M., and
Akert, K. (eds.), The Frontal Granular Cortex and Behavior. McGraw-Hill, New York, pp.
410-441.
Teuber, H.-L., Battersby, W. S., and Bender, M. B. (1951). Performance of complex visual
tasks after cerebral lesions. Journal of Nervous and Mental Disease 114: 413-429.
Thurstone, L. L. (1938). Primary Mental Abilities, University of Chicago Press, Chicago.
Thurstone, L. L., and Thurstone, T. (1949). Examiner Manual for the SRA Primary Mental
Abilities Test, Science Research Associates, Chicago.
Valenstein, E. 8. (1973). Brain Control, Wiley, New York.
Van den Brock, M. D., Bradshaw, C. M., and Szabadi, E. (1993). Utility of the Modified
Wisconsin Card Sorting Test in neuropsychological assessment. British Journal of Clinical
Psychology 32: 333-343.
Varney, N. R., and Menefee, L. (1993). Psychosocial and executive deficits following closed
injury: Implications for orbital frontal cortex. Journal of Head Trauma Rehabilitation 8:
32-44.
Wang, P. L. (1987). Concept formation and frontal lobe function: The search for a clinical
frontal lobe test. In E. Perecman (ed.), The Frontal Lobes Revisited, IRBN, New York,
pp. 410-441.
198 Reitan and Wolfson

Wasterlain, C. G., and Duffy, I. E. (1976). Status epilepticus in immature rats. Archives of
Neurology 33: 821-827.
Welsh, M. C., Pennington, B. F., and Groisser, D. B. (1991). A normative-developmental
study of executive function: A window on prefrontal function in children. Developmental
Neuropsychology 7: 131-149.
Wheeler, L., and Reitan, R. M. (1962). The presence and laterality of brain damage predicted
from responses to a short Aphasia Screening Test. Perceptual and Motor Skills 15: 783-799.