Assessment of Frontal

Lobe Functions
Paul F. Malloy, Ph.D.
Emily D. Richardson, Ph.D.

The authors describe methods for conducting a I n this article we describe methods for conducting a
thorough assessment of functions subserved by frontal
thorough assessment of functions subserved by the
lobe systems. In all evaluations of neuropsychological
frontal lobes, employing both bedside and psycho-
functioning, the skilled practitioner must be guided by a
metric methods of assessing frontal subsystems. theoretical model of brain systems and their characteris-
Qualitative or process aspects of frontal behavior tic disturbances by various diseases. In no area is this
observable from formal testing, interview, and so- model more important than in assessment of frontal lobe
cial behavior are noted. It is argued that the skilled functions, given their highly complex nature. To set the
stage for discussion of assessment techniques, we there-
clinician must be guided by a knowledge of frontal
fore begin with a brief discussion of frontal lobe subsys-
lobe subsystems and their roles in determining spe-
tems and the effects of lesions on these subsystems. We
cific types of abnormal behavior. The clinician will then describe both bedside and psychometric methods of
then be alert to changes in incidental behaviors assessing these deficits.
that indicate frontal impairment, and bedside
maneuvers can be designed to discriminate dys-
OVERVIEW OF FRONTAL
function. Given the complexity of the behaviors
LOBE SYSTEMS
involved and the profound effects of maturation
and aging on frontal functions, neuro psycho- Historically, frontal lobe functions have been poorly un-
logical assessment can provide an invaluable tool derstood by many clinicians. Past clinical descriptions of
for testing these functions. behavior consequent to frontal lesions have been dra-
(The Journal of Neuropsychiatry and Clinical matic and evocative, but they have generally lacked the
Neurosciences 1994; 6:399-410) anatomic-clinical correlations necessary for complete un-
derstanding of these syndromes. The historical use of the
generic term frontal lobe syndrome, for example, fails to
account for the diversity of frontal lobe functions.
Situated as they are at the pinnacle of human brain-

From the Department of Psychiatry and Human Behavior, Brown Uni-

versity School of Medicine, Providence, Rhode Island; and the Depart-
ment of Medicine, Yale University Medical School, New Haven,
Connecticut. Address correspondence to Dr. Malloy, Butler Hospital,
345 Blackstone Blvd., Providence, RI 02906.
Copyright © 1994 American Psychiatric Press, Inc.

JOURNAL OF NEUROPSYCHIATRY 399

ASSESSMENT OF FRONTAL LOBE FUNCTIONS

behavior relationships, frontal functions are complex and of most healthy adults. Motor speed and dexterity can be
difficult to describe, and only recently have researchers assessed by having the patient perform rapid movements
clearly elucidated frontal subsystems. Through studies of with the hands and feet.
both animal and human subjects over the past three Neuropsychological (NP) tests of motor abilities often
decades,”2 our understanding of frontal lobe functions consist of standardization of the neurologic exam maneu-
has improved dramatically. A number of functional sub- vers. For example, the Reitan Grip Strength test3 uses a
divisions have now been identified: the primary motor dynamometer to assess the strength of each hand pre-
area, the premotor area, the frontal eye fields, the dorso- cisely. As with all standardized NP tests, the availability
lateral prefrontal area, the orbital prefrontal area, and a of norms allows the neuropsychologist to detect subtle
medial area composed of the supplementary motor area asymmetries that may elude the bedside examiner and to
and anterior cingulate gyrus. correct for handedness, gender, and age. This can be very
Each of these frontal zones has extensive connections important in that most women have significantly lower
with posterior cortical and subcortical structures (partic- grip strength than men4’5 and motor speed declines with
ularly certain thalamic nuclei and the basal ganglia). As age.6’7 Similarly, fine motor speed can be measured pre-
Mega and Cummings have illustrated in their article in cisely with the Finger Tapping Test,3 which counts the
this issue (pp. 358-370), frontal cortical zones act in con- average number of taps made with the index finger dur-
cert with these other structures to form frontal lobe sub- ing several 10-second trials.
systems. Lesions at any level of these subsystems can
disrupt the functioning of the frontal system to which it
contributes. We will describe the functions of each frontal PREMOTOR SUBSYSTEM
subsystem, the effects of lesions on complex behavior,
and both informal clinical and formal psychometric The premotor area (Brodmann area 6) is involved in
methods of assessing dysfunction in each subsystem. sensorimotor integration and in complex volitional
movement or praxis. The premotor area has connections
with secondary somatosensory areas in the parietal lobe
MOTOR SUBSYSTEM and, to a lesser extent, with primary somatosensory
areas.8 It has connections with the ventral anterior nu-
The motor area (Brodmann area 4) is critical to pyramidal cleus of the thalamus, with extrapyramidal motor struc-
motor functions, that is, control of fine motor movement. tures (especially the caudate nucleus), and with the
The motor area receives projections from posterior corti- primary motor area. Hence, it is well positioned to mod-
cal areas (especially in the primary tactile area of the ify motor plans in a dynamic way on the basis of chang-
parietal lobe) involved in somatosensory perception, as ing sensory, motor tone, and postural feedback.
well as subcortical input from the ventral lateral thalamic Lesions in the premotor area result in 1) inability to
nucleus. Primary motor output travels via the internal make use of sensory feedback to modify movements
capsule to the pyramidal tracts. smoothly and 2) apraxia. Sensorimotor abilities can be
Large lesions to the motor area result in flaccid hemi- tested at bedside by having the patient touch each finger
plegia in the contralateral side of the body, which typi- to the thumb sequentially and observing for clumsiness,
cally resolves into spastic hemiplegia. Less severe lesions slowing, or inaccuracies. The test can be made more
to the primary motor area or its connections may result sensitive by requiring the patient to close his or her eyes,
in weakness (hemiparesis) and incoordination rather emphasizing the use of somatosensory rather than visual
than frank paralysis. information to guide the movements. Luria9 has also
The clinician can test basic motor functions at bedside described a set of bedside assessment tasks that elegantly
via the familiar maneuvers of the elementary neurologic dissociate motor, sensory, and interhemispheric or callo-
exam. Of course, motor deficits may also be a result of sal aspects of sensorimotor abilities. Luria’s kinesthetic
lesions to the cerebellum, extrapyramidal system, or de- motor tasks involve the reproduction of finger positions,
scending white matter tracts, and the clinician must in- first with eyes open (to demonstrate intact unilateral
terpret results from the tests that follow in the context of motor abilities), then unilaterally with both eyes closed
the entire examination. Motor strength can be tested by (to demonstrate unilateral sensorimotor loops), and fi-
having the patient squeeze your fingers and then at- nally with both eyes closed and the patient attempting to
tempting to extricate them. This allows the comparison reproduce the passive position of one hand with the
of the relative strengths of the two hands, which should opposite hand (to demonstrate callosal transfer of sen-
be approximately equal. It should be difficult or impossi- sory information from one hemisphere to the other).
ble to remove your fingers from the grasp of either hand Apraxia, in its strictest sense, is defined as the inability

400 VOLUME 6 NUMBER

#{149} 4 FALL
#{149} 1994
 MALLOY AND RICHARDSON

to carry out a motor movement or gesture to command. Grooved Pegboard adding the visuospatial demand of
Apraxia is commonly found in association with left hemi- orienting the grooved pegs correctly in space so that they
sphere lesions,’#{176} with frontal as well as nonfrontal local- fit in the holes. The Motor Steadiness Battery16 is useful
ization.1’ Thus, the presence of apraxia should not be in patients with frontosubcortical systems disturbances
viewed as pathognomonic of frontal dysfunction, but such as Parkinson’s disease. These tests permit the quan-
praxis should be included in any comprehensive assess- tification of tremor in static postures and during inten-
ment of frontal abilities. The clinician can test praxis at tional movement by counting the number of times an
bedside by requiring the patient to perform single and electrically wired stylus touches the sides of progres-
serial limb, whole body, and facial movements. Move- sively smaller holes or grooves.
ments should include transitive (“Show me how you use
a scissors”), intransitive symbolic (“Show me how you
salute”), and nonsymbolic movements. To document the FRONTAL EYE FIELDS
presence of an apraxia, the examiner must demonstrate
that the patient has the basic motor abilities to perform The frontal eye fields (FEFs;
Brodmann area 8) are neces-
the movement. This can be done by requiring use of the sary for voluntary gaze visual search.
and The FEFs
same muscle groups in simpler movements during the permit volitional eye movements in the contralateral vi-
formal examination and by observing the incidental sual field, but, as with other frontal subsystems, this
movements of the patient on the unit (for example, the function is complex and involves integration with a num-
patient spontaneously scratches an itch in the right eye ber of other brain regions. Crowne’7 has argued that the
but cannot point to the eye on command). Evidence FEFs may play a role in directing complex attention,
suggests that the specialized motor system subserving particularly during defensive maneuvers or pursuit of a
praxis shares much cerebral territory with the language target. Fuster’8 has similarly suggested that the FEFs
system; hence, apraxias are often found in combination integrate “a running blend of current sensory input with
with aphasia. In order to demonstrate an apraxia, the prospective information by which the eye field continu-
examiner must therefore also demonstrate that the pa- ously adjusts the motor apparatus and sensory mecha-
tient understands the instruction for the movement; often nisms in order to ensure coherence in both perception
the patient will attempt a partial or distorted variant of and movement” (p. 93). Recent studies have also sug-
the required movement. Requiring the patient to imitate gested that the FEFs act in concert with dorsolateral
gestures after failure to perform to command can also be frontal zones in guiding eye movements during goal-di-
useful in this regard, although it removes many of the rected behavior, especially when memory is involved.’9
ideational aspects of praxis from the task. Lesions in the FEFs result in transient ipsilateral eye
Clinicians unfamiliar with the assessment of praxis deviation and more persistent contralateral gaze paresis.
may wish to consult the Boston Diagnostic Aphasia The patient may be capable of passively following the
Examination,12 which includes a comprehensive set of examiner’s finger throughout both right and left hemi-
maneuvers for assessing praxis among other supplemen- space (hence demonstrating there is no neglect) but can-
tary, nonlanguage tests. Although a number of other not move the eyes to the contralateral side to command
apraxia exams have been developed for experimental or when engaged in active visual search. Secondary to
and clinical purposes,’#{176}”3 none has truly psychometric these deficits in eye movement, the patient will be unable
properties or adequate norms. This is not crucial for most to efficiently pursue a target or search visual space.
clinical applications because normal persons can be ex- The clinician can also test these functions with visual
pected to perform all common movements to command search stimuli consisting of a page of randomly arranged
without error. Of course, the tasks may be failed for letters or symbols;2#{176} the patient is required to find all
multiple reasons, such as disturbed attention in the delir- occurrences of a target letter or symbol. Patients with FEF
ious patient or failure of the aphasic patient to under- lesions will be unable to actively search the side of the
stand the command. The astute clinician must be page contralateral to their lesion, although they will be
prepared to devise tasks at bedside to discriminate these capable of passive eye movements in the same visual
deficits. field. The intactness of passive gaze distinguishes such
A number of neuropsychological tests are available for patients from those with hemispatial neglect.
studying other aspects of complex movement and its A patient’s description of a complex figure such as the
disturbances. The Purdue Pegboard14 and the Grooved well-known “Cookie Theft” picture12 can be revealing in
Pegboard15 require the patient to place as many pegs into regard to ability to organize a search of an entire stimu-
holes on a board as possible within a time limit. Both tests lus. More complex search instruments with psychomet-
assess visuomotor coordination and speed, with the ric norms have also been developed. For example, in the

JOURNAL OF NEUROPSYCHIATRY 401

ASSESSMENT OF FRONTAL LOBE FUNCTIONS

Visual Search Test by Lewis and Rennick,2’ the patient is pathological range on the EXIT when compared with
required to match a checkerboard pattern presented in either Alzheimer’ s-type dementia patients or psychiatric
the center of a page with its twin from a set of patterns patients. However, these investigators suggested that
around the page. these findings may have been confounded by level of
care. In fact, Royall et al.u have shown that the EXIT is a
good predictor of level of care required, independent of
DORSOLATERAL PREFRONTAL the neuroanatomic location of the pathology. Thus, the
SUBSYSTEM specificity of the EXIT in regard to frontal lesions remains
to be demonstrated.
The dorsolateral subsystem is responsible for executive Poor integration of disparate pieces of sensory input
functions. The dorsolateral area has extensive connec- can be measured by such tests as the Hooper Visual
tions with the posterior tertiary association cortex and Organization Test (HVOT). The HVOT presents the
hence is the recipient of highly processed sensory infor- patient with pictures of common objects, such as a dog,
mation in all modalities. For example, the dorsolateral that have been cut apart and rearranged on the page like
area receives extensive input from angular and supra- a puzzle. The patient is required to put the pieces together
marginal gyri, association areas involved in multimodal mentally and determine what the object is. The frontal
processing. Executive functions include integration of patient will not be able to initiate the active processing
multimodal sensory input, generation of multiple re- necessary to identify the complete object and will erron-
sponse alternatives, maintenance of set and goal-direct- eously extrapolate from detail. Thus, one patient with a
edness, modification of behavior as conditions change, frontal convexity lesion identified the shape shown in
and self-evaluation. Figure 1 from the HVOT as “Benjamin Franklin” because
Lesions of the dorsolateral area result in 1) inability to he fixated on the part of the figure on the lower left and
integrate disparate sensory elements into a coherent failed to integrate the whole.
whole, 2) a stereotyped or limited response repertoire, 3) Similarly, Luria has described a set of incomplete pic-
easy loss of task set, 4) perseveration and inflexibility, turesV that are fragmented or out of focus, so that the
and 5) lack of self-monitoring of errors. These executive patient must “fill in the blanks” to determine the identity
functions have been the object of the most extensive of the object. Luria9 has demonstrated that dorsolateral
study of all frontal lobe functions, and consequently there frontal lesions can also result in visual search deficits of
is a large armamentarium from which the neuropsycki- quite a different sort from those resulting from frontal eye
atrist or neuropsychologist can draw for the psychomet- field lesions. By actually measuring eye movements with
ric assessment of executive abilities. a mechanical apparatus, he showed that frontal patients
Royall has developed a brief bedside test for measur-
ing a variety of frontal lobe functions, the Executive FIGURE 1. Stimulus from the Hooper Visual Organization Test.
Interview (EXIT). The EXIT includes tasks derived from Arrow indicates feature identified as “Benjamin Frank-
lin” by a frontal lobe patient.
a number of sources, including so-called frontal release
signs from the neurologic examination, abbreviated ver-
sions of neuropsychological tests such as word fluency,
and Luria’s techniques.
Many of the tasks are cleverly
arranged to elicit frontal executive dysfunction. For ex-
ample, the patient is first asked to describe a picture of a
cat climbing a tree, then asked to memorize the words
“book, tree, house.” The patient is next required to spell
“cat” as a distraction task, and finally to recall the three
words after this brief delay. The recent exposure to the
“tree-cat” picture and the interpolation of the word “cat”
during the delay makes a perseverative error of “cat” on
recall likely. Validation of the EXIT to date has been
limited largely to demonstrations that it is sensitive to
cognitive changes in dementiaZ and to the discrimina-
tion of cortical from subcortical dementias when used
with other brief screening instruments.24 Richardson et
alY provided preliminary evidence that individuals with
chronic surgical frontal lesions perform in the more

402 VOLUME 6 NUMBER

#{149} 4 FALL
#{149} 1994
 MALLOY AND RICHARDSON

failed to formulate an effective plan for scanning a narra- Test (RFF) the patient is required to draw a figure within
tive picture, adopting instead one of two maladaptive a grid of lines, enhancing the examiner’s ability to discern
strategies: 1) randomly searching all of the picture or 2) different and perseverative shapes. The RFFT has been
getting “stuck” on one salient aspect and making inap- shown to be sensitive to right versus left frontal lesions,32
propriate extrapolations. For example, one of our pa- and large-scale norms are available for adults.u
tients viewed a picture of a man in a horse-drawn sleigh Lezak hasdeveloped another task that cleverly as-
and exclaimed, “Oh, there is snow-that must be my sesses generation of multiple response alternatives. In
uncle’s farm in New Hampshire.” He failed to actively her Tinkertoy Test, the patient is presented with several
search the remainder of the picture to confirm or discon- pieces from the child’s construction toy and instructed in
firm his idea. a deliberately vague manner to make whatever he or she
Generation of multiple response alternatives can be likes from the pieces. Normal subjects or patients with
measured by word and figure fluency tasks. The most posterior lesion will typically produce a reasonably com-
widely used word fluency task is the Controlled Oral plex, representational object such as a car, whereas the
Word Fluency Test (COWA). This test requires the pa- frontal patient will be able to produce only simple, un-
tient to produce as many words as possible in one minute imaginative, and unnameable objects.
beginning with F, then A, then S. while simultaneously Luria9 has described a number of bilateral hand move-
maintaining a complex instructional set. Other categori- ments and alternating graphic sequences that theo-
cal fluency tasks (naming animals, fruits, and vegetables) retically require intact motor, premotor, and executive
have been shown to be more sensitive and specific in functions, particularly the ability to produce alternating
detecting dementia,29 but they may not tap executive response sets. Versions of these tasks are included in the
functions to the same extent as the COWA. The COWA Luria-Nebraska Neuropsychological Battery27 and a
requires not only multiple response generation, but also number of other NP instruments such as the Dementia
maintenance of a complex task set-the words must not Rating Scale and Behavioral Dyscontrol Scale.
include proper names or consist of previously used Malloy et al.37 demonstrated that these tasks are per-
words with a suffix. It also presents the opportunity to formed more poorly by patients with focal frontal lesions
observe perseverative and intrusion errors. A within-task than patients with comparably sized posterior lesions.
perseveration would consist of repeating a previous The technique that we use ensures that a response set is
word on the same letter list without awareness or self- established and then changed and that the task is sus-
correction. Between-task perseverations consist of tained long enough to observe subtle executive dysfunc-
repeating words beginning with a previous letter. Intru- tion. On the reciprocal hand movements, the patient is
sions consist of words that do not begin with any of the first required to place one hand up and one hand down,
letters, usually due to disinhibited associations (“at, after, then to reverse the hand positions, moving both hands
apple, peaches, oranges.. . In addition,
“). the letters F, simultaneously in a coordinated effort. Next, the patient
A, and S seem to “pull” for vulgar or socially inappropri- is required to place one hand in an extended position and
ate words used by frontal patients with disinhibitory the other in a clenched position, then to reverse the
deficits. We therefore routinely record not only the num- positions repeatedly. Finally, the patient must tap asym-
ber of words produced, but also the number of incorrect metrical rhythms, twice with one hand and once with the
words according to the complex rules, number of per- other. The examiner notes how quickly and smoothly the
severations, and number of socially inappropriate words. patient is able to perform the motions, as well as observ-
A nonverbal or figural fluency task was developed by ing certain pathognomonic errors: within-task persev-
Jones-Gotman and Milner,3#{176} who demonstrated that erations (such as tapping three times rather than twice),
whereas left frontal patients failed verbal fluency, right cross-task perseverations (such as thrusting the hands as
frontal patients differentially failed figural fluency. Their on the previous task rather than tapping with clenched
version of the figural fluency task involves having the fists), and oversimplifications (such as tapping twice
patient produce as many nonrepresentational drawings with each hand rather than the required asymmetrical 2-1
as possible in 5 minutes, then producing as many figures pattern).
with four parts as possible in 4 minutes. However, clini- On alternating graphic sequences, we first require the
cians have encountered some difficulty with reliable patient to copy a pattern of two crosses and a circle
scoring of this test because of uncertainty as to whether repeatedly. After the patient completes one line of this
a design is “different” or perseverative, and normative pattern, the model is removed and the patient is asked to
data have not been gathered to date. Ruff3’ therefore continue the pattern, increasing the demands of the task
developed a figural fluency task incorporating some con- in regard to maintenance of set. Next, the patient is
straints to enhance reliability. In the Ruff Figural Fluency required to copy a more difficult pattern of alternating

JOURNAL OF NEUROPSYCHIATRY 403

ASSESSMENT OF FRONTAL LOBE FUNCTIONS

peaks and plateaus. Typical frontal errors include within- and normal subjects display increased dorsolateral fron-
task perseverations (repeating too many crosses), cross- tal metabolism during WCST performance. However,
task perseverations (inserting crosses into the peaks and negative findings have also been reported regarding the
plateaus), oversimplifications (simply drawing a series of frontal specificity of the test.40
peaks rather than the alternating pattern), and intrusions In his seminal book Brain and Intelligence: A Quantitative
of habitual responses (writing letters rather than the re- Study of the Frontal Lobes, Halstead developed many of
quired pattern of shapes). the tests that would come to comprise the Halstead-
Figure 2 presents examples of typical errors by a patient Reitan Neuropsychological Battery (HRNB). As the title
with dementia of the frontal type on these tasks. Note of Halstead’s book indicates, the frontal lobes were
that the patient understands the task demands, and she thought to provide the essential biological basis for intel-
is initially able to reproduce the figure correctly. Hence, lectual activity. Although this would now be considered
her eventual failure is not due to language or basic con- an oversimplification, many of the tests in the HRNB
struction deficits. After moving beyond the first model, continue to be used as putative tests of frontal lobe func-
however, she begins to oversimplify the figure from the tioning. The Category Test and Trail Making Test have
asymmetrical ++0++0 to the simpler +0+0. Similarly, she generally been considered measures of abstraction, set
begins to copy the second model correctly, but she then maintenance, and cognitive flexibility. Hence, clinicians
displays within-task perseverative errors (multiple peaks frequently employ these tests as measures of dorsolateral
rather than alternating peaks and plateaus) as well as frontal functions. However, research has indicated that
cross-task perseverations (crosses from the first task). patients with nonfrontal as well as frontal lesions fail
Note also that her pattern is stimulus bound, gradually these tests.4
moving up to overlap the model.
The Wisconsin Card Sorting Testy (WCST) has been
considered the premiere test of executive functions for ORBITAL PREFRONTAL SUBSYSTEM
many years. It taps a variety of executive abilities, includ-
ing maintenance of task set, flexibility in response to Few measures of orbitofrontal functions in humans are
feedback or changing circumstances, and perseverative available. Clinicians may therefore have difficulty detect-
teridencies. The WCST requires the patient to sort cards ing common behavioral sequelae of orbitofrontal dam-
into piles under four sample cards that differ in color, age. However, review of the literature suggests anosmia,
form (shapes on the card), and number of shapes. The disinhibited personality change, and failure on neuro-
patient is not provided with these categories but must psychological tests of inhibition are reliable signs of or-
discern them on the basis of feedback from the examiner. bitofrontal dysfunction. Although these signs can occur
The “correct” category varies throughout the test, and with lesions of other brain areas, their occurrence to-
measures are derived of ability to stick with the currently gether is highly suggestive of orbitofrontal damage.49
correct category and shift to the new category when Smell discrimination is often omitted from the routine
appropriate. The WCST has been shown to be sensitive neurologic exam, but the presence of anosmia in a variety
to effects of frontal lobe lesions in a number of studies,40’4’ of disorders with neuropsychiatric effects make this a
cardinal error. For example, anosmia, often an early sign
FIGURE 2. Perfonnance of a patient with demen tia of the frontal of degenerative dementia, is common in Korsakoff’s syn-
type on Luria’s Alternating Figures. drome,5#{176}and is seen in nearly 90% of patients who have
undergone repair of anterior cerebral aneurysms.5’ Right
Model ++O++O orbitofrontal damage in particular appears to affect smell
abilities.52 Assessment of smell by clinicians is also im-
++O++040+e4-O +O#{248} portant in that orbitofrontal dysfunction has dire prog-
nostic implications. For example, head-injured patients
frequently display anosmia, and those with anosmia
have poorer social and vocational outcomes than patients
without this evidence of orbital damage.
Model j-7 Anosmia can be assessed clinically by having the pa-
tient identify common aromatic substances such as cof-
fee, tobacco, or cocoa. Volatile or irritating substances
should be avoided so that the anosmic patient will not be
able to identify them by way of trigeminal stimulation.
Psychometric assessment of smell discrimination is pos-

404 VOLUME 6 NUMBER

#{149} 4 FALL
#{149} 1994
 MALLOY AND RICHARDSON

sible by use of the University of Pennsylvania Smell printed word is more salient than the color, the patient
Identification Test, which provides 40 “scratch and has to inhibit the tendency to say the word. Recent re-
sniff” items with age-corrected norms. Norms are essen- search has demonstrated that both orbital and anterior
tial in smell assessment when the patient is not com- cingulate frontal zones are activated in normal subjects
pletely anosmic, because major declines in smell during the Stroop task.62 Patients with orbitofrontal le-
thresholds are seen with normal aging.55 The examiner sions would be expected to have particular difficulty
must also keep in mind the myriad medical causes of with the inhibitory portion of this task.
reduced smell discrimination, such as infections of the
nasal passages, smoking, and medication use?
Disinhibited or socially inappropriate behavior can be SUPPLEMENTARY MOTOR AND
observed informally on the treatment unit, and family ANTERIOR CINGULATE
reports should always be sought. Orbital frontal patients
may display such behaviors as facetious humor, inappro- Goldberg and Bloom40 have argued that the supplemen-
priate sexual behavior (open masturbation, sexual over- tary motor area (SMA) and anterior cingulate gyms form
tures to strangers), and labile emotionality. Disinhibited a reciprocal system responsible for environmental search
and socially problematic behaviors may reach propor- and inhibition of exploratory behavior. The cingulate
tions resembling antisocial personality disorder in some gyrus appears to supply the drive for this environmental
patients with orbital lesions.57 We are currently develop- exploration, and the SMA appears to supply the inhibi-
ing a psychometric instrument for assessing such chang- tory component. Hence, lesions to the anterior cingulate
es, known as the Frontal Lobe Personality Scale (FLOPS), gyrus can result in akinetic mutism, in which the patient
which is undergoing validation trials through the Na- fails to respond to environmental stimuli and remains
tional Academy of Neuropsychology. Patient, staff, and inert. Unilateral lesions usually result in transient akine-
family versions of the instrument have been developed, sia, whereas bilateral lesions result in more permanent
with the expectation that frontal patients will be unaware deficits.M Conversely, lesions to the SMA and corpus
of deficits that are readily apparent to their caregivers. callosum result in the fascinating disorder known as
Rosenkilde has reviewed animal research on frontal “alien hand syndrome.”40 The patient with “alien hand”
lobe function and concluded that animals with orbito- may grab objects, throw things, and otherwise explore
frontal lesions perform more poorly than animals with the environment in a disinhibited way. The patient feels
other lesions on go/no-go tasks. Go/no-go tasks require as though he or she has no control over these movements,
the patient to make a response to a go signal and withhold whereas in reality they are probably attributable to the
or inhibit the response to the no-go signal. The task can be actions of the right hemisphere in initiating actions while
made more difficult by changing the habitual meaning of disconnected from the verbal left hemisphere. The dra-
the signals (go to a red light, no-go to a green light). A matic syndromes of akinetic mutism and alien hand ob-
bedside example of this task can involve asking the pa- viously require no special assessment techniques beyond
tient to tap his fist when the examiner says “stop” and the ability of the examiner to make the appropriate ana-
not tap when the examiner says “go.” We have demon- tomic-clinical correlations.
strated that normal subjects display activation of the
orbital cortex on topographic EEG during the inhibitory
portion of a go/no-go task.59 In that same study, patients “FRONTAL” ERRORS ON TESTS OF
with obsessive-compulsive disorder failed to show the OTHER COGNITIVE FUNCTIONS
same orbital activation, a finding that is consistent with
PET studies showing orbital dysfunction in OCD.6#{176} As Kaplan40 has eloquently argued, how a patient ap-
The Stroop TestM is another task that places demands proaches a task is frequently more informative than
on inhibitory abilities. The published version of this test whether he or she fails the task. Hence, a process ap-
consists of three stimulus arrays. On the first page, the proach to test analysis can reveal patterns of deficits not
patient is required to read the words red, green, and blue apparent in total scores. This is nowhere more true than
printed in black ink in random-ordered columns. On the in deficits due to frontal dysfunction, which impair
second page, the patient must state the color of X’s higher order mental processes or “metacognition.”
printed in red, green, or blue ink. The third page provides On memory testing, for example, the frontal patient
the critical interference trial: the patient is required to will often display impoverished learning strategies, in-
state the color of the ink, ignoring the word printed in trusions and perseverations,40 poor retrieval strategies,67
that color. For example, the patient sees the word red and difficulty with temporal tagging of learned informa-
printed in blue ink and must say “blue.” Because the tion.40 The California Verbal Learning Test (CVLT) pro-

JOURNAL OF NEUROPSYCHIATRY 405

ASSESSMENT OF FRONTAL LOBE FUNCTIONS

vides an excellent tool for examining these process di- on the COWA, whereas patients with posterior lesions or
mensions.69 The CVLT involves the presentation of a psychiatric disorders do not.
16-word list over five learning trials, with free, cued, and
recognition recall of the original list after an interpolated
interference list. Indices are provided for a number of GENERAL GUIDELINES FOR BEDSIDE
learning and memory processes disturbed by frontal dys- ASSESSMENT
function. Hence, it is possible to observe the frontal pa-
tient producing a shallow learning curve across the five Although formal neuropsychological testing remains a
trials (due to inefficient encoding strategies), mixing up valuable diagnostic resource, the clinician must also have
the first and second lists (due to problems in temporal some practical clinical tools that allow the sensitive eval-
tagging), showing inordinate gains from cued or recog- uation of frontal functions at bedside. It could be argued
nition recall in comparison to free recall (due to inability that the only truly valid assessment of executive func-
to formulate a retrieval strategy), and producing large tions can be obtained through the observation of an
numbers of perseverations and intrusions. This is a mark- individual’s behavioral response to the ambiguous and
edly different pattern from that of the patient with shifting challenges encountered in autonomous social
Alzheimer’s disease, for example, who will not typically behavior. Bearing this in mind, the clinician should seize
benefit from cueing or recognition to any significant every opportunity to observe the patient’s ability to
degree. demonstrate insight, plan ahead, and execute effective
Delis et al.7#{176}
have also developed a variation of the strategies to meet different environmental challenges.
card-sorting technique that allows the examiner to ana- For example, is the patient able to efficiently schedule an
lyze qualitative or process aspects of problem-solving appointment and arrive at your office on time? Typically,
abilities. In its initial validation trial, the test was admin- the patient with executive deficits will require a third
istered to four subject groups: patients with focal frontal party to identify the necessity for the psychiatric inter-
lobe lesions, patients with both frontal dysfunction and vention and plan a schedule. Similarly, the task of under-
amnesia (Korsakoff’s syndrome), patients with circum- standing one’s medical insurance policy represents a
scribed (non-Korsakoff) amnesia, and normal control considerable test of executive skills!
subjects. The patients with frontal lobe lesions and pa- The physical appearance of the patient may also pro-
tients with Korsakoff’s syndrome were impaired on eight vide valuable clues. In extreme cases, frontal patients
of the nine process components of the task. Qualitative neglect personal hygiene, presenting with soiled clothes,
analysis demonstrated a wide spectrum of deficits in unshaven face, and even incontinence about which they
abstract thinking, cognitive flexibility, and use of knowl- display no concern. In less severe cases, the observant
edge to regulate behavior, all of which contributed to the examiner will note inappropriate attire such as a heavy
problem-solving impairment of these patients. jacket in summer, unzipped fly, or a mismatched outfit.
Frontal patients often will perform well on simple at- The social demeanor of the patient is often revealing in
tentional tasks, such as digits forward, but display char- regard to the disinhibited personality change discussed
acteristic errors on complex attentional tasks requiring earlier in relation to the orbitofrontal subsystem. Such
active manipulation of information. This deficit is often patients may become overly familiar with the examiner,
most apparent when the patient is required to overcome asking inappropriately personal questions, making com-
overlearned or habitual behavior patterns. For example, ments about the examiner’s appearance, offering sexual
when asked to recite the days of the week backward, overtures, or engaging in rude or embarrassing behavior.
frontal patients have difficulty reorganizing the infor- Emotional overreaction is also seen and often has a rapid
mation return
and to the habitual pattern in which on/off quality.
the material is usually used: “Sunday, Saturday.. . Fri- it is particularly important that the clinician appreciate
day. . . Thursday. . Friday, . Saturday, Sunday.” his or her role shaping
in the patient’s behavior. For
This process approach can even be applied to the ef- example, the interviewer may unconsciously compens-
fects of lesions to frontal subsystems. Crowe71 has dem- ate for a patient’s apathy and cognitive disorganization,
onstrated that qualitative analysis of errors on fluency assuming a directive and paternal role and using only
tasks can be useful in discriminating orbital from other closed-ended questions. In other words, the examiner
frontal lesions. Patients with orbitofrontal lesions pro- may “act as the patient’s frontal lobes” and thereby miss
duced more disinhibited responses
on word fluency than important clues. The apparently simple task of describ-
patients with dorsolateral frontal
lesions. We commonly ing one’s presenting complaint in a cohesive and perti-
observe that patients with closed head injury and orbital nent fashion places considerable demands on such
damage produce vulgar or sexually oriented responses frontal functions as insight, judgment, social sensitivity,

406 VOLUME 6 NUMBER

#{149} 4 FALL
#{149} 1994
 MALLOY AND RICHARDSON

and self-reflection. Indeed, patients with frontal lesions (“Start with this big rectangle, and then draw these diag-
have been shown to be remarkably poor at providing onal lines.. . “) to see if performance then improves
coherent autobiographical information! A detailed his- markedly.
tory that includes work, hobbies, daily routine, and inter- From this
discussion it should be clear that the evalua-
personal relationships will provide valuable information tion of frontal lobe functions should not be limited to the
regarding the patient’s ability to orchestrate his or her formal mental status examination. Executive functions
life. But it is essential that the examiner question family influence the performance of virtually all mental pro-
or caretakers as well because a discrepancy between cesses. By the time the examiner embarks on the formal
patient and family report of problems is a hallmark of cognitive examination, he or she should have already
frontal lobe dysfunction. obtained significant indications of the patient’s capaci-
Although the examiner must refrain from providing ties. All components of the formal mental status exam
too much structure during the early stages of the exami- will then provide data regarding the patient’s ability to
nation, it can be equally useful to deliberately provide strategize, monitor, and adapt cognitive behavior to
additional structure once it is established that frontal changing circumstance and to evaluate his or her own
deficits exist. In this way, the clinician can demonstrate performance.
that the reason for failure lies in a dysexecutive syn- Table I provides a guide to informal bedside maneu-
drome rather than in more basic cognitive functions. vers the clinician may use to assess each domain of frontal
For example, if one observes that the patient fails a com- functions. This is not meant to be a comprehensive list,
plex construction task such as copying the Rey-Osterrieth but rather a set of suggested screening instruments that
figure, it is often useful to provide a strategy to the patient will provide a reasonable sampling of frontal functions.

TABLE 1. A bedside battery for assessing frontal lobe functions

Dysfunctions Means of Assessment

I.Motor functions
Reduced grip strength Patient squeezes fingers of examiner; compare bilaterally
Reduced fine motor speed Rapid hand movements
II. Premotor functions
Poor sensorimotor integration Patient touches each finger sequentially to thumb
Apraxia Single and serial limb movements
Ill. Dorsolateral/executive functions
Disturbed complex and directed attention Digit span forward much better than digits backward
Difficulty with mental manipulation of information (e.g.,on months of the year
backward returns to habitual pattern of months forward)
Disorganized search strategy on letter cancellation
Inability to generate multiple response alternatives Adequate closed-set word generation: grocery items
Poor open-set word generation: F-A-S words
Behavioral inflexibility Luria’s alternating graphic sequences
Luria’s bilateral hand movements
N. Orbital/inhibitory functions
Behavioral disinhibition Go/no-go test
Anosmia Inability to identify odor of tobacco, coffee, chocolate
V. General observations
‘Prontal” errors on other tests Poor organization and strategy (e.g., doesn’t plan number placement on dock
drawing)
Marked improvement with increased structure (e.g., much better recall with
cueing and recognition than free recall)
Perseverative and intrusion errors
Abnormal behavior during interview and testing Reduced initiative and drive
Apathy
Poor insight into deficits
Inappropriate social behavior, disinhibition
Environmental dependency
Perseveration
Poor self-monitoring of errors
Easy agitation, hypomanic-like state
Discrepancies in patient vs. caregiver report of problems

JOURNAL OF NEUROPSYCHIATRY 407

ASSESSMENT OF FRONTAL LOBE FUNCTIONS

EFFECTS OF AGE ON FRONTAL LOBE tion behavior probably represents dysfunction in multi-
FUNCTIONS ple frontal subsystems.
Second, many patients will show combinations of fron-
Clinicians should be particularly cautious in assessing tal syndromes because naturally occurring lesions dam-
frontal lobe functions in children and elderly persons. age multiple subsystems. This mixed picture is found in
There is increasing evidence that the frontal lobes do not most areas of neuropsychology, yet a theoretical schema
mature fully until adolescence,tm’74 and children perform remains essential in organizing the clinical examination.
much more poorly than adults on most frontal lobe tests75 In aphasia, for example, an understanding of the local-
(if indeed they are capable of understanding the instruc- ization and connections of the language system and
tions). Conversely, recent research has clearly shown that aphasia subtypes is crucial, even though most patients
there is greater loss of neurons in the frontal lobes than will display mixed aphasias rather than pure subtypes.
in posterior areas with normal aging76 and greater change This knowledge will ensure that the examiner makes a
in frontal lobe functioning than other abilities 77 For ex- comprehensive assessment of language abilities (fluency,
ample, there is a marked decline in performance on the comprehension, repetition, naming, reading and writ-
Wisconsin Card Sorting Test with age39: The average ing), will allow the examiner to make sense of the find-
30-year-old produces only 10 perseverative errors on this ings, and will often yield behavioral data that can be
task, whereas the average 70-year-old produces more correlated with neuroimaging.
than 20. In contrast, confrontational naming perfor- Third, some deficits may be the result of either frontal
mance, dependent mainly on the posterior left hemi- or nonfrontal lesions. For example, abstract reasoning
sphere, appears to change little with age.78 Even primitive can be viewed as a measure of ability to shift mental set
behaviors such as so-called frontal release signs (glabel- from the specific (concrete or tangible) to the general
lar, grasp, palmomental, snout, suck, root, and jaw jerk (abstract) principle. It is often measured at bedside via
reflexes) are strongly affected by aging, with 40% of proverb interpretation or similarities. However, abstract
normal individuals showing some of these signs after age reasoning is strongly dependent on innate intelligence
607 Neuropsychological assessment is therefore ex- and education. Thus, although abstraction is very suscep-
tremely useful in children and the elderly, since availabil- tible to the effects of injury involving frontal systems,
ity of norms allows age corrections. poor ability to abstract is not specific to frontal injury.
In summary, the skilled clinician must be knowledge-
able about frontal lobe subsystems and their roles in
LIMITATIONS TO LOCALIZATION OF determining specific types of abnormal behavior. The
FRONTAL FUNCTIONS clinician can then devise maneuvers to discriminate dys-
function at bedside and recognize changes in incidental
We have taken a highly localizational approach to frontal behaviors that indicate frontal impairment. Because of
systems; at minimum this approach should provide a the complexity of these behaviors and the profound ef-
useful heuristic to help clinicians organize their thinking. fects of maturation and aging on frontal function, neuro-
However, it is important to recognize the limitations of psychological assessment is an invaluable tool for testing
any localizational model. frontal lobe functions.
First, the examiner must remember that most complex
behaviors require that various frontal subsystems act in References
concert to produce adaptive functioning. Sustained and I. Goidman-Rakic PS: Circuitry of the primate prefrontal cortex and
directed attention is an example of an ability involving regulation of behavior by representational memory, in Handbook
multiple frontal zones, including dorsolateral, orbital, of Physiology: the Nervous System: Higher Functions of the Brain,
vol 5, sec I, edited by Plum F, Mountcastle V. Bethesda, MD,
and cingulate areas.62’8#{176}Utilization behavior81 is another
American Physiological Society, 1987, pp 373-417
example. In this condition, the patient automatically uti- 2. Cummings JL: Frontal-subcortical circuits and human behavior.
lizes objects in his or her environment in a habitual way, Arch Neurol 1993; 50:873-880
3. Reitan RM, Wolfson D: The Halstead-Reitan Neuropsychological
whether or not this use is appropriate at the time.
Test Battery. Tucson, AZ, Neuropsychology Press, 1985
Lhermitte described a former nurse with frontal damage
4. Kupke 1, Lewis R, Rennick P: Sex differences in the neuropsycho-
who spied a syringe in the examining room and at- logical functioning of epileptics. I Consult Clin Psychol 1979;
tempted to inject the examiner with it. This emergence of 47:1128-1130
5. Fromm-Auch D, Yeudall LI: Normative data for the Haistead-
habitual or high-probability behavior in response to en-
Reitan Neuropsychological Tests. J Clin Exp Neuropsychol 1983;
vironmental stimuli has been reported with large bilat- 5:221-238
eral frontal lesions,82 mesial frontal lesions,u caudate 6. Ernst J, Warner MH, Townes BD, et a!: Age group differences on
infarction,TM and even thalamic infarction.85 Thus, utiliza- neuropsychological battery performance in a neuropsychiatric pop-

408 VOLUME 6 NUMBER

#{149} 4 FALL
#{149} 1994
 MALLOY AND RICHARDSON

ulation: international descriptive study with replications. Archives 33. Ruff RM, Light R, Evans R: The Ruff Figural Fluency Test: a norma-
of Clinical Neuropsychology 1987; 2:1-12 tive study with adults. Developmental Neuropsychology 1987;
7. Villardita C, Cultrera S, Cupone V, et al: Neuropsychological test 3:37-51
performances and normal aging. Archives of Gerontology and Ger- 34. Lezak M: Neuropsychological Assessment, 2nd edition. New York,
iatrics 1985; 4:311-319 Oxford University Press, 1983
8. Pandya DN, Barnes CL. Architecture and connections of the frontal 35. Mattis S: Dementia Rating Scale Professional Manual. Odessa, FL,
lobe, in The Frontal Lobes Revisited, edited by Perecman E. New Psychological Assessment Resources, 1973
York, IRBN Press, 1987: 41-72 36. Grigsby J, Kaye K, Robbins U: Reliabilities, norms and factor struc-
9. Luna AR: Higher Cortical Functions in Man. New York, Basic Books, ture of the Behavioral Dyscontrol Scale. Percept Mot Skills 1992;
1980 74:883-892
10. DeRenzi E, Moth F, Nicheffi P: Imitating gestures: a quantitative 37. Malloy PF, Webster JS, Russell W: Tests of Luria’s frontal lobe
approach to ideomotor apraxia. Arch Neurol 1980; 37:6-10 syndrome. International Journal of Clinical Neuropsychology 1985;
11. KoIb B, Milner B: Performance of complex arm and facial move- 7:88-94
ments after focal brain lesions. Neuropsychologia 1981; 19:491 -503 38. Neary D, Snowden JS, Northen B, et al: Dementia of frontal lobe
12. Goodglass H, Kaplan E: The Assessment of Aphasia and Related type. J Neurol Neurosurg Psychiatry 1988; 51:353-361
Disorders. Philadelphia, Lea and Febiger, 1972 39. Heaton RK, Chelune GJ, lalley JL, et al: Wisconsin Card Sorting Test
13. Kertesz A: The Western Aphasia Battery. London, Ontario, Univer- Manual: Revised and Expanded. Odessa, FL, Psychological Assess-
sity of Western Ontario, 1980 ment Resources, 1993
14. Psychological Research Foundation: Examiner’s manual for the 40. Drewe EA: The effect of type and area of brain lesion on Wisconsin
Purdue Pegboard. Chicago, Science Research Associates, 1948 Card Sorting Test performance. Cortex 1974; 10:159-1 70
15. Lafayette Instrument Company: Instructions for the Grooved Peg- 41. Milner B: Effects of different brain lesions on card sorting. Arch
board. Lafayette, IN, Lafayette Instrument Company, n.d. Neurol 1963; 9:90-100
16. Lafayette Instrument Company: Instructions for the Steadiness Tes- 42. Marenco S, Coppola R, Daniel DG, et al: Regional cerebral blood
ter. Lafayette, IN, 1977 flow during the Wisconsin Card Sorting Test in normal subjects
17. Crowne DP: The frontal eye fields and attention. Psychol Bull 1983; studied by xenon-133 dynamic SPECT: comparison of absolute val-
93:232-260 ues, percent distribution values, and covariance analysis. Psychiatry
18. FusterjM: The Prefrontal Cortex: Anatomy, Physiology, and Neuro- Res 1993; 50:177-1 92
psychology of the Frontal Lobe. New York, Raven, 1980 43. van den Broek MD, Bradshaw CM, Szabadi E: Utility of the Modified
19. Pierrot DC, Israel I, Berthoz A, et al: Role of the different frontal lobe Wisconsin Card Sorting Test in neuropsychological assessment. Br
areas in the control of the horizontal component of memory-guided J Clin Psychol 1993; 32:333-343
saccades in man. Exp Brain Res 1993; 95:166-171 44. Halstead WC: Brain and Intelligence: A Quantitative Study of the
20. McFie J, Piercy MF, Zangwffl OL: Visuo-spatial agnosia associated Frontal Lobes. Chicago, University of Chicago Press, 1947
with lesions of the right cerebral hemisphere. Brain 1950; 73:167-190 45. Reitan RM: An investigation of the validity of Halstead’s measures
21. Lewis RF, Rennick PM: Manual for the Repeatable Cognitive-Per- of biological inteffigence. Arch Neurol Psychiatry 1955; 73:28-35
ceptual-Motor Battery. Grosse Pointe Park, MI, Axon, 1979 46. Reitan RM: Impairment of abstraction ability in brain damage:
22. Royall DR, Mahurin RK, Gray KF: Bedside assessment of executive quantitative versus qualitative changes. J Psychol 1959; 9:21 1-215
cognitive impairment: the executive interview. J Am Geriatr Soc 47. Pendleton MG, Heaton RK: A comparison of the Wisconsin Card
1992; 40:1221-1226 Sorting Test and the Category lest. J Cliii Psychol 1982; 38:392-396
23. Royall DR, Mahurin RK,TrueJE, etal: Executive impairment among 48. Klove H: Validation studies in adult clinical neuropsychology, in
the functionally dependent: comparisons between schizophrenic Clinical Neuropsychology: Current Status and Applications, edited
and elderly subjects. Am J Psychiatry 1993; 150:1813-1819 by Reitan RM, Davison LA. Washington, DC, VH Winston and Sons,
24. Royall DR, Mahurin RK, Cornell J, et al: Bedside assessment of 1974, pp 21 1-227
dementia type using the Qualitative Evaluation of Dementia. Neu- 49. Mailoy PF, Bihrle A, Duffy J, et a!: The orbitomedial frontal syn-
ropsychiatry, Neuropsychology, and Behavioral Neurology 1993; drome. Arch Cliii Neuropsychol 1993; 8:185-202
6:235-244 50. Jones BP, Butters NM, Moskowitz HR. et al: Olfactory and gustatory
25. Richardson ED, Duffy J, Royall DR: Examination of a new bedside capacities of alcoholic Korsakoff patients. Neuropsychologia 1978;
measure for assessment of executive dysfunction (abstract). J Neuro- 16:323-338
psychiatry Clin Neurosci 1993; 5:452-453 51. Eriksen KD, Boge RT, Kruse LC: Anosmia following operation for
26. Hooper HE: The Hooper Visual Organization Test Manual. Beverly cerebral aneurysms in the anterior circulation. J Neurosurg 1990;
Hills, CA, Western Psychological Services, 1958 72:864-865
27. Golden CJ, Hammeke TA, Purisch AD: Manual for the Luria- 52. Zatorre RJ, Jones-Gotman M: Human olfactory discrimination after
Nebraska Neuropsychological Battery. Los Angeles, Western Psy- unilateral frontal or temporal lobectomy. Brain 1991; 114:71-84
chological Services, 1980 53. Varney N: Prognostic significance of anosmia in patients with dosed
28. Benton AL: Differential behavioral effects in frontal lobe disease. head trauma. J Clin Exp Neuropsychol 1988; 10:250-254
Neuropsychologia 1968; 6:53-60 54. Doty RL: The University of Pennsylvania Smell Identification Test
29. Monsch AU, Bondi MW, Butters N, et al: Comparisons of verbal Administration Manual. Philadelphia, Sensonics, 1983
fluency tasks in detection of dementia of the Alzheimer type. Arch 55. Cain WS, Gent JF: Olfactory sensitivity: reliability, generality, and
Neurol 1992; 49:1253-1258 association with aging. J Exp Psycho! Hum Percept Perform 1991;
30. Jones-Cotman M, Milner B: Design fluency: the invention of non- 17:382-391
sense drawings after focal cortical lesions. Neuropsychologia 1977; 56. Ship JA, Weiffenbach JM: Age, gender, medical treatment, and
15:653-674 medication effects on smell identification. J Gerontol 1993; 48:26-32
31. Ruff RM: Ruff Figural Fluency Test Administration Manual. San 57. Meyers CA, Berman SA, Scheibel RS, et al: Case report: acquired
Diego, CA, Neuropsychological Resources, 1988 antisocial personality disorder associated with unilateral left orbital
32. Ruff RM, Allen CC, Farrow CE, et al: Figural fluency: differential frontal lobe damage. J Psychiatry Neurosci 1992; 17:121-125
impairment in patients with left versus right frontal lobe lesions. 58. Rosenkilde CE: Functional heterogeneity of the prefrontal cortex in
Arch Clin Neuropsychol 1994; 9:41-55 the monkey: a review. Behav Neural Biol 1979; 25:301-345

JOURNAL OF NEUROPSYCHIATRY 409

ASSESSMENT OF FRONTAL LOBE FUNCTIONS

59. Mailoy P, Rasmussen 5, Braden W, et al: Topographic evoked po- tion and frontal damage. Neuropsychologia 1993; 31:823-839
tential mapping in obsessive-compulsive disorder: evidence of fron- 73. Yakolev P1, Lecours AR: The myelogenetic cycles of regional matu-
tal lobe dysfunction. Psychiatry Res 1989; 28:63-71 ration of the brain, in Regional Development of the Brain, edited by
60. Baxter U, Phelps ME, Mazziotta JC, et al: Local cerebral glucose Minkowski A. Philadelphia, FA Davis, 1967, pp 2-70
metabolic rates in obsessive-compulsive disorder: a comparison 74. Passler MA, Isaac W, Hynd GW: Neuropsychological development
with rates in unipolar depression and in normal controls. Arch Gen of behavior attributed to frontal lobe functioning in children. Devel-
Psychiatry 1987; 44:211-218 opmental Neuropsychology 1985; 1:349-370
61. Stroop JR: Studies of interference in serial verbal reactions. J Exp 75. Levin HS, Coihane KA, Hartmann J, eta!: Developmental changes
Psychol 1935; 18:643-662 in performance on tests of purported frontal lobe functioning. De-
62. Bench CJ, Frith CD, Grasby PM, etal: Investigations of the functional velopmental Neuropsychology 1991; 7:277-396
anatomy of attention using the Stroop test. Neuropsychologia 1993; 76. Coffey CE, Wilkinson WE, Parashos IA, eta!: Quantitative cerebral
31:907-922 anatomy of the aging human brain: a cross-sectional study using
63. Goldberg G, Bloom KK: The alien hand sign: localization, lateraliza- magnetic resonance imaging. Neurology 1992; 42:527-536
tion and recovery. Am J Phys Med Rehabil 1990; 69:228-238 77. Boone KB, Miller BU, Lesser IM: Frontal lobe cognitive functions in
64. Damasio AR, Van Hoesen GW: Emotional disturbances associated aging: methodologic considerations. Dementia 1993; 4:232-236
with focal lesions of the limbic frontal lobe, in Neuropsychology of 78. Van Gorp WG, Satz P. Kiersch ME, et al: Normative data on the
Human Emotion, edited by Heilman KM. Satz P. New York, Boston Naming lest for a group of normal older adults. J Cliii Exp
Guilford, 1983, pp 85-110 Neuropsychol 1986; 6:702-705
65. Kaplan process
E: The approach to neuropsychological assessment 79. Jacobs, U, Grossman, MD: Three primitive reflexes in normal adults.
of psychiatric patients. J Neuropsychiatry Clin Neurosci 1990; 2:72- Neurology 1980; 30:184-188
87 80. Bianchi A, Zolo P. Salmaso D: Effects of frontal lesions on a selective
66. VilkkiJ: Perseveration in memory for figures after frontal lobe lesion. attention task. Ital J Neurol Sd 1993; 14:355-359
Neuropsychologia 1989; 27:1101-1104 81. Uhermitte F, Pillon B, Serdaru M: Human autonomy and the frontal
67. Kopelman MD: Frontal dysfunction and memory deficits in the lobes, I: imitation and utilization behavior: a neuropsychological
alcoholic Korsakoff syndrome and ALzheimer-type dementia. Brain study of 75 patients. Ann Neurol 1986; 19:326-334
1991; 114:117-137 82. Hoffmann MW, Bill PU: The environmental dependency syndrome,
68. Shimamura AP, Janowsky JS, Squire LR: Memory for the temporal imitation behaviour and utilisation behaviour as presenting symp-
order of events in patients with frontal lobe lesions and amnesic toms of bilateral frontal lobe infarction due to moyamoya disease. S
patients. Neuropsychologia 1990; 28:803-813 Afr MedJ 1992; 81 :271-273
69. Delis DC, KramerJH, Kaplan E, etal: The California Verbal Learning 83. Shaffice T, Burgess PW, Schon F, et al: The origins of utilization
Test: Research Edition. New York, The Psychological Corporation, behaviour. Brain 1989; 112:1587-1598
1987 84. Degos JD, da Fonseca N, Gray F, et a!: Severe frontal syndrome
70. Delis DC, Squire LR, Bthrle A, et al: Componential analysis of associated with infarcts of the left anterior cingulate gyrus and the
problem-solving ability: performance of patients with frontal lobe head of the right caudate nucleus: a clinico-pathological case. Brain
damage and amnesic patients on a new sorting test. Neuro- 1993; 116:1541-1548
psychologia 1992; 30:683-697 85. Eslinger PJ, Warner GC, Grattan LM, eta!: “Frontal lobe” utilization
71. Crowe SF: Dissociation of two frontal lobe syndromes by a test of behavior associated with paramedian thalamic infarction. Neurol-
verbal fluency. J Clin Exp Neuropsychol 1992; 14:327-339 ogy 1991; 41:450-452
72. Della SS, Uaiacona M, Spinnier H, et al: Autobiographical recollec-

410 VOLUME 6 NUMBER

#{149} 4 FALL
#{149} 1994