Mind Ease Psychological Services and Wellness Center

FRONTAL LOBE

Symptoms of Frontal Lobe Lesions

Disturbance of Motor Functions:

Fine Movement, Speed and Strength- Damage to the primary motor cortex (area 4) is typically

associated with a chronic loss of the ability to make fine, independent finger movements,

presumably owing to a loss of direct corticospinal projections onto motor neurons. In addition,

there is a loss of speed and strength in both hand and limb movements in the contralateral limbs.

The loss of strength is not merely a symptom of damage to area 4, because lesions restricted to

the prefrontal cortex also lead to reduced hand strength.

Movement Programming:

Removal of the supplementary motor cortex results in a transient disruption of nearly all

voluntary movements (including speech, if removal is on the left). Recovery is rapid, however,

and the only permanent disability appears to be in the performance of rapidly alternating

movements with the hands or fingers. Patients with localized unilateral frontal lobectomies

(most did not include the premotor cortex) were asked to copy a series of arm or facial.

Although the patients showed mild impairment in copying the arm movements, it was small

compared with the performance of patients with left-parietal-lobe lesions. In contrast, patients

with both left- and right-frontallobe damage were dismal at copying a series of facial

movements.
Analysis of the facial-movement task showed that the groups with frontallobe lesions made more

errors of sequence than did controls or other groups of patients. In other words, patients with

frontal-lobe lesions had difficulty ordering the various components of the sequence into a chain

of movements. They recalled components correctly but in the wrong order. To be sure, these

patients made other sorts of errors as well, especially errors of memory in which items were not

recalled. Reproducing movement sequences requires temporal memory, and our impression is

that the largest deficits come from dorsolateral lesions.

The observation that frontal injury severely disrupts copying facial but not arm movements

implies that the frontal lobe may play a special role in controlling the face, perhaps even

including the tongue.

Voluntary Gaze:

Alexander Luria (1973) recorded eye movements as people examined a picture of a complex

scene. The eye-movement patterns of the patients with large frontal-lobe lesions were quite

different from those of controls or those of patients with more-posterior lesions. For example, if

a control were asked about the ages of the people in a picture, his or her eyes fixed on the heads;

if asked how they were dressed, the eyes fixed on the clothing. Patients with large frontal-lobe

lesions tended to glance over the picture more or less at random, and changing the question

about the picture failed to alter the direction or pattern of their eye movements.

Studies tried to localize the voluntary gaze deficits within the frontal lobe, but they seem likely

to stem from interrupted activity in the frontal eye fields.

Corollary Discharge
If you push on your eyeball, the world appears to move. If you move your eyes, the world

remains stable. Why? Teuber (1964) proposed that for a voluntary movement to take place, a

neural signal must produce both the movement and a signal that the movement is going to take

place. If the eyes are moved mechanically, as when you press on them, there is no such signal,

and the world moves. However, when you move your eyes, you generate a neural signal that

movement will happen, and the world stays still. This signal has been termed corollary

discharge, or reafference.

Teuber (1972) argued that a movement command through the motor system effects the

movement, and a signal (corollary discharge) from the frontal lobe to the parietal and temporal

association cortex presets the sensory system to anticipate the motor act. Thus, a person’s

sensory system can interpret changes in the external world in light of information about his or

her voluntary movement.

When you are running, for example, the external world remains stable even though your sense

organs are in motion, because the corollary discharge from the frontal lobe to the

parietotemporal cortex signals that the movements are taking place. A frontal-lobe lesion

therefore not only can disturb movement production but also can interfere with the message to

the rest of the brain that a movement is taking place. By this indirect means, perception of the

world by the posterior association cortex is altered.

Evidence that the frontal lobe participates in corollary discharge comes from the results of

studies of frontal eye field cells. Emilio Bizzi and Peter Schiller (1970), among others, found

that some cells in the frontal eye fields fire simultaneously with eye movements. These cells

cannot be causing the eyes to move: to do so, they would have to fire before the eye movements
(just as to accelerate an automobile, you must first depress the gas pedal). Rather, these frontal

eye field cells must be monitoring the ongoing movement—a process suspiciously similar to

what we would expect from a region controlling corollary discharge.

Speech

Speech entails movement selection. Passingham (1993) suggested that words are responses

generated in the context of both internal and external stimuli. If the frontal lobe has a mechanism

for selecting responses, then it must select words too. The frontal lobe contains two speech

zones: Broca’s area (area 44), which we can regard as an extension of the lateral premotor area,

and the supplementary speech area, which may be an extension of the supplementary motor area

(area 6).

Viewed in this way, Broca’s area is critical to retrieving a word on the basis of an object, word,

letter, or meaning. Like the premotor area’s role in other behaviors, Broca’s area selects words

on the basis of cues. In contrast, consistent with the general function of the supplementary motor

area, the supplementary speech area is required to retrieve words without external cues.

People with strokes in Broca’s area are impaired in using verbs and producing appropriate

grammar, a symptom known as agrammatism. People with strokes that include the

supplementary speech area and extend into the adjacent left medial frontal region are often mute.

The ability to speak usually returns after a few weeks in people with unilateral lesions but not in

those with bilateral lesions. This outcome again supports the supplementary motor areas’

bilateral participation in movement selection.

Loss of Divergent Thinking

One clear difference between the effects of parietal- and temporal-lobe lesions and the effects of

frontal-lobe lesions is performance on standard intelligence tests. Posterior lesions produce

reliable, and often dramatic, decreases in IQ scores, but frontal lesions do not. The puzzle then,

is why patients with frontal lobe damage appear to do such “stupid” things. Joy Paul Guilford

(1967) noted that traditional intelligence tests appear to measure what can be called convergent

thinking—that there is just one correct answer to each question. Definitions of words, questions

of fact, arithmetic problems, puzzles, and block designs all require single correct answers that

are easily scored. Another type of intelligence test that emphasizes the number and variety of

responses to a single question rather than a single correct answer, can measure divergent

thinking. An example is asking for a list of the possible uses for a coat hanger. Frontal-lobe

injury interferes with the intelligence required by divergent thinking rather than the convergent

type measured by standard IQ tests

Behavioral Spontaneity

Patients with frontal-lobe lesions exhibit a loss of spontaneous speech. Various investigators

have quantified this loss by using tests such as the Thurstone WordFluency Test (also called the

Chicago Word-Fluency Test). Patients are asked to first write or say as many words starting with

a given letter as they can think of in 5 min and then say as many four-letter words starting with a

given letter in 4 min.

Patients with frontal-lobe lesions have a low word output on this test. For example, when asked

to generate as many words as he could think of beginning with a specific letter, E.L., introduced

in the opening Portrait, sat for about 2 min before asking if he could use the Latin names of
plants. He was assured that he could do so but after another couple of minutes, he remarked, “I

can’t think of any!” He abandoned the plant names but even with an additional 5 min, he could

think of only six words.

Although the principal locus of this defect appears to be in the left orbitofrontal region, lesions

in the right orbitofrontal region also may produce a marked reduction in verbal fluency. Again,

we see less asymmetry in the frontal lobes. The following case exemplifies low spontaneous

verbal fluency resulting from a lesion of the right frontal lobe.

Mrs. P., a 63-year-old woman with a college degree, was suffering from a large astrocytoma of

the right frontal lobe. Given are the features of the same:

1- Low output. Mrs. P.’s only 8 words beginning with the letter s and 6 words beginning with

the letter c. (Control participants of similar age and education produce a total of about 60 words

in the same time period, as shown in Figure 16.8B.)

2. Rule breaking. This is a common characteristic of patients. We told Mrs. P. several times that

the words starting with c could contain only four letters. She replied. “Yes, yes, I know, I keep

using more each time.” Even though she understood the instructions, she could not organize her

behavior to follow them.

3. Shaky script. Her writing was rather jerky, much like that seen in a child learning to write,

implying that her tumor had invaded the motor or premotor cortex.

4. Perseveration. Mrs. P. insisted on talking throughout the test— complaining that she simply

could not think of any more words—and kept looking around the room for objects starting with

the required letter.

Marilyn Jones-Gotman and Brenda Milner (1993) devised an ingenious experiment that

broadens this deficit via a nonverbal analog. The researchers asked patients to draw as many

different designs as they could in 5 min. The drawings were supposed to be not representational

but spontaneous—much like the doodles students are prone to draw in the margins of their

textbooks. The patients were then asked to draw as many different designs as they could, but this

time using only four lines (a circle was counted as a single line).

The results reveal a beautiful analog to the verbal-fluency results: lesions in the right frontal lobe

produced a large decrease in the number of different drawings produced. Controls drew about 35

drawings, left-frontal-lobe patients about 24 drawings, and right-frontal-lobe patients about 15

drawings. This deficit appears related to an impoverished output, high perseveration, and, in

some cases, representational drawings (the drawing of nameable things). As with verbal fluency,

lesions in the orbital cortex or central facial area in the frontal lobe appear to produce larger

deficits than do the more-dorsal lesions.

Frontal-lobe patients likely show reduced spontaneity not only in speech or doodling but also in

their general behavior. For example, Bryan Kolb and Laughlin Taylor (1981) recorded the

spontaneous behavior of frontal-lobe patients as they were taking a battery of

neuropsychological tests. Patients with frontal-lobe removals displayed fewer spontaneous facial

movements and expressions than did controls or patients with more-posterior lesions. In

addition, the number of words spoken by the patients in a neuropsychological interview differed

dramatically: patients with left frontal removals rarely spoke, whereas patients with right frontal

lesions talked excessively.

Strategy Formation
Patients with frontal-lobe lesions are especially impaired at developing novel cognitive plans or

strategies for solving problems. For example, when Tim Shallice and Margaret Evans (1978)

asked subjects questions that require reasoning based on general knowledge and for which no

immediate strategy is obvious, they found that frontal-lobe patients performed poorly and often

gave bizarre responses.

In a later study, Shallice and Burgess (1991) gave patients a task very much like our dinner-party

problem presented earlier. They gave subjects a list of six errands (for example, “Buy a loaf of

brown bread”) and an instruction to be at a particular place 15 min after starting. They were also

to get answers to four questions (for instance, What is the price of a pound of tomatoes?). They

were not to enter shops except to buy something and were to complete the tasks as quickly as

possible without rushing. The frontal-lobe patients found this simple task very difficult. They

were inefficient, they broke rules (for example, entered unnecessary shops), and two of the three

patients failed at least four tasks. Yet when quizzed, all the patients understood the task and had

attempted to comply. Shallice and Burgess argued that although the frontal lobe may have a

general role in planning behavior, it has a critical role in coping with novel situations. They

suggested that in contrast to routine situations, coping with a novel one— by which they mean a

novel set of external and internal states—entails activating a wide variety of processes to solve

the problem. The solution of a familiar task, by contrast, can rely on well-practiced strategies

that are more easily accessed.

ENVIRONMENTAL CONTROL OF BEHAVIOR

Perhaps frontal-lobe patients’ most commonly observed trait is difficulty in using environmental

cues (feedback) to regulate or change their behavior. This difficulty manifests itself in myriad

ways.

Response Inhibition

Patients with frontal-lobe lesions consistently perseverate on responses in a variety of test

situations, particularly those with changing demands. The best example is observed in the

Wisconsin Card-Sorting Test, a standard clinical test of frontal-lobe injury. A subject is

presented with four stimulus cards bearing designs that differ in color, form, and number of

elements.
The subject’s task is to sort the cards into piles in front of one or another of the stimulus cards.

The only help given the subject is to be told whether the choice is correct or incorrect. The test

works on the following principle: the correct solution is, first, color; when the subject has

figured out this solution, without warning the correct solution then becomes form. The subject

must now inhibit classifying the cards on the basis of color and shift to form. When the subject

has succeeded at selecting by form, the correct solution again changes unexpectedly, this time to

the number of elements. It will later become color again, and so on. Shifting response strategies

is particularly difficult for people with frontal lesions. They may continue responding to the

original stimulus (color) for as many as 100 cards until testing is terminated. Throughout this

period, they may comment that they know that color is no longer correct. They nevertheless

continue to sort on the basis of color. One person stated (correctly): “Form is probably the

correct solution now so this [sorting to color] will be wrong, and this will be wrong, and wrong

again.” Perseveration is common on any task that requires a frontal-lobe patient to shift response

strategies, thus demonstrating that the frontal lobe is necessary for behavioral flexibility. It is

important to note that on card-sorting tasks, subjects must not be given any hint that they are to

expect a change in the correct solution, because many frontal-lobe patients improve dramatically

when given this warning. The cue apparently lends them enough flexibility to solve the problem.

From the results of Milner’s (1964) work, the principal locus of this cardsorting effect appears to

be roughly around Brodmann’s area 9 in the left hemisphere dorsolateral prefrontal cortex.

Lesions elsewhere in the left frontal lobe, and often in the right frontal lobe, also will produce a

deficit, although attenuated, on this task.

The Stroop Test further demonstrates loss of response inhibition subsequent to frontal-lobe

damage. Subjects are presented with a list of color names. Each name is printed in colored ink
but never in the color denoted by the word (for example, the word yellow is printed in blue,

green, or red ink). The subject’s task is to name the color each word is printed in as quickly as

possible. Correct response requires inhibiting reading the color name—difficult even for many

controls. Patients with left frontal lesions are unable to inhibit reading the words and thus are

impaired in this task (e.g., Perret, 1974).

Risk Taking and Rule Breaking

Frontal-lobe patients are distinguished from other neurological patients in their common failure

to comply with instructions. Milner found it especially common on tests of stylus–maze learning

in which a buzzer indicates that the patient has made an error and is to stop and start again at the

beginning of the maze. Subjects with frontal-lobe lesions tend to disregard the signal, continuing

on the incorrect path and making more errors. This behavior is reminiscent of the inability to

modify their responses in the card-sorting task.

Lori Miller (1985) gave subjects a task to guess words on the basis of partial information. With

each additional clue, a subject was assigned a successively lower point value for a correct

answer, but points could be collected only if the answer was correct. An incorrect answer

forfeited all the points for an item. Frontal-lobe patients took more risks (and made more

mistakes) than did other patients, and the risk taking was greatest in frontal-lobe patients who

also had temporal-lobe damage.

Antoine Bechera and colleagues (2000) designed a gambling task to explore the role of the OFC

in risk taking. Subjects gradually learn how to play a unique card game. They are presented with

four decks of cards and asked to turn over the first card in any deck. Some cards are associated

with a payoff ($50 or $100); others result in a $50 or $100 penalty. Each subject is given $2000

in play money, and the goal is to make as much money in the game as possible.

The trick is that the reward and penalty contingencies of each deck differ. For example, one deck

may have high payoffs but also high penalties; another may have lower payoffs but also low

penalties. The game is set so that playing two of the four decks results in a net loss, whereas

playing the other two yields a net gain.

The results from the Bechera studies are clear: controls and patients without frontal damage

sample from all the decks for a while but quickly learn which have the best payoff. In contrast,

patients with orbitofrontal injuries do not learn this strategy and play predominantly from the

bad decks, thus losing all their money.

An important aspect of the task is that no one is allowed to keep a running tally of how they are

doing; rather they must “sense” which decks are risky and which are profitable. This ability is

clearly a function of the prefrontal cortex, and its loss makes it difficult for orbitofrontal patients
to make wise decisions, especially in social or personal matters—that is, situations in which an

exact calculation of future outcomes is not possible.

The brain-injury data are consistent with a finding by Ming Hsu and colleagues (2005), who

looked at brain activation (fMRI) in subjects engaged in a gambling task in which risk was

ambiguous. For example, subjects were asked to bet on whether a card was red or blue without

any knowledge of the probability that a card was red or blue. Brain activity was compared to a

condition in which they knew that the probability was 50:50.

Patients with orbitofrontal lesions did not find the ambiguous task aversive, but controls found it

much more aversive than the known-risk task. The subjective difference was demonstrated by

higher activation in the controls’ OFC and amygdala during the ambiguous-risk task. Taken

together, the imaging and lesion studies suggest that the OFC is part of a neural decision making

circuit that evaluates degrees of uncertainty in the world.

Self-Regulation

Patient M.L. as typical of people with ventral frontal injuries, who have deficits in regulating

their behavior in unstructured situations, in part because of a loss of autonoetic awareness. M.L.

had been a salesman, and he knew what his job had been and that he had traveled a great deal.

When pressed, however, he was unable to provide a single personal anecdote about this job.

For example, when asked if he traveled to conferences, M.L. said that, yes, he traveled to

conferences often; it was a major part of his job. Yet he could not name a single experience he

had had at a conference. His autobiographic knowledge was lost.

You can imagine what this impairment would be like if you think about high school. We are all

aware of having gone to high school and can describe what high school was like. Presumably, so

could patients like M.L. The difference, however, is that we can describe personal events that

happened in high school, whereas M.L. would not be able to do so. We can immediately see why

M.L. had difficulty relating to his wife: he simply could not recall instances that would explain

why they were married. Loss of autobiographic knowledge clearly makes it difficult to put

ongoing life events in context and leads to difficulties in regulating behavioral flexibility.

Associative Learning

Patients with large frontal-lobe lesions, it is often claimed, are unable to regulate their behavior

in response to external stimuli—that is, to learn from experience. Alexander Luria and Evgenia

Homskaya (1964) described patients with massive frontal-lobe tumors who could not be trained

to respond consistently with the right hand to a red light and with the left hand to a green light,

even though the patients could indicate which hand was which and could repeat the instructions.

In an extensive series of studies, Michael Petrides (1997) examined the ability of both human

patients and monkeys with frontal lesions to make arbitrary stimulus–response associations. In

one study, Petrides asked frontal-lobe patients to learn arbitrary associations between colors and

hand postures. For example, patients were presented with nine colored stimuli, and their task

was to learn which posture was associated with which colored stimulus. Damage to either the

left or right hemisphere results in poor performance on this task. Again, the behavioral

impairments in frontal-lobe patients could not be attributed to a memory deficit because

temporal-lobe patients who performed poorly on other tests of memory performed at normal on
these tasks. Rather, the problem is in learning to select, from a set of competing responses, the

ones appropriate to the various stimuli.

Impaired Social and Sexual Behavior

Social and sexual behaviors require flexible responses that are highly dependent on contextual

cues. Frontal-lobe lesions interfere with both. An obvious and striking effect of frontal-lobe

damage in humans is a marked change in social behavior and personality.

The most publicized example of personality change subsequent to frontallobe lesions is that of

Phineas Gage, first reported by John Harlow in 1868. Gage was a dynamite worker who

survived an explosion that blasted an iron tamping bar through the front of his head. The bar was

about 1 m long and 3 cm wide at its widest point.

After the accident, Gage’s behavior changed completely. He had been of average intelligence

and was “energetic and persistent in executing all of his plans of operation” according to

Harlow, who described Gage’s personality after the injury as follows:

The equilibrium or balance, so to speak, between his intellectual faculties and animal

propensities seems to have been destroyed. He is fitful, irreverent, indulging at times in the

grossest profanity, manifesting but little deference to his fellows, impatient of restraint or advice

when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and

vacillating, devising many plans of operation, which are no sooner arranged than they are

abandoned in turn for others appearing more feasible. A child in his intellectual capacity and

manifestations, he has the animal passions of a strong man. (Blumer and Benson, 1975, p. 153)
Gage’s injury affected primarily the left frontal lobe from the orbital region upward into the

precentral region. Gage’s skull has been examined carefully, but the first person with extensive

frontal damage to undergo close scrutiny at autopsy was a furrier who fell 30 m from a window.

He suffered a compound fracture of the frontal bones and severe injury to the right frontal lobe.

Remarkably, he was never unconscious and was confused only briefly. Before the fall, the

furrier had been good natured and sociable; afterward he became nasty and cantankerous.

Autopsy, about a year after the accident, revealed deep scarring of the orbital part of both frontal

lobes, but more extensive on the right.

Pseudodepression and Pseudopsychopathy

From 1900 until about 1950, many excellent psychiatric studies of the effect of brain lesions on

personality (especially Kleist’s, cited in Zangwill, 1966) found consistently that damage to the

orbitofrontal regions is associated with moredramatic changes in personality than are

dorsolateral lesions, although the latter also have significant effects. Clinical descriptions of

frontal-lobe lesions’ effects on personality abound, and while few systematic studies have been

conducted, at least two types of personality change have been clinically observed in such

patients.

Dietrich Blumer and Frank Benson (1975) have termed them pseudodepression and

pseudopsychopathy. Patients classified as pseudodepressed exhibit such symptoms as outward

apathy and indifference, loss of initiative, reduced sexual interest, little overt emotion, and little

or no verbal output. Patients classified as pseudopsychopathic exhibit immature behavior, lack

of tact and restraint, coarse language, promiscuous sexual behavior, increased motor activity,
and a general lack of social graces. The following two case histories illustrate these personality

types.

Pseudodepression

Prior to the accident, the patient had been garrulous, enjoyed people, had many friends and

talked freely. He was active in community affairs, including Little League, church activities,

men’s clubs, and so forth. It was stated by one acquaintance that the patient had a true

charisma, “whenever he entered a room, . . . everything became more animated, happy and

friendly.” Following the head injury, he was quiet and remote. He would speak when spoken to

and made sensible replies but would then lapse into silence. He made no friends on the ward,

spent most of his time sitting alone smoking. He was frequently incontinent of urine,

occasionally of stool. He remained unconcerned about either and was frequently found soaking

wet, calmly sitting and smoking. If asked, he would matter-offactly state that he had not been

able to get to the bathroom in time but that this didn’t bother him. . . . He could discuss many

subjects intelligently, but was never known to initiate either a conversation or a request. . . . He

was totally unconcerned about his wife and children. Formerly a warm and loving father, he did

not seem to care about his family. Eventually, the family ceased visiting because of his

indifference and unconcern. (Blumer and Benson, 1975, pp. 156–157)

Pseudopsychopathy

A 32-year-old white male was admitted for behavioral evaluation. History revealed that he had

sustained a gunshot wound in Vietnam 5 years previously. A high-velocity missile had entered

the left temple and emerged through the right orbit. Infection necessitated surgical removal of

most of the orbital surface of the right frontal lobe. . . .

Prior to injury he had been quiet, intelligent, proper, and compulsive. He was a West Point

graduate and spent the ensuing years as a military officer attaining the rank of captain. Both as

a cadet and later as an officer, he was known to be quiet, strict, and rigid. He was considered a

good commander, trusted by his men, but never shared camaraderie with his troops or with his

peers. Subsequent to injury, he was outspoken, facetious, brash, and disrespectful.

There was no evidence of self-pity, although he frequently made rather morbid jokes about his

condition (for example, “dummy’s head”). On admission to the hospital, he had just failed at an

extremely simple job. (Blumer and Benson, 1975, pp. 155)

Blumer and Benson assert that all elements of pseudodepression and pseudopsychopathy are

observable only after bilateral frontal-lobe damage. Nevertheless, some elements of these two

rather different syndromes can be observed in most, if not all, persons with unilateral frontal-

lobe lesions. Pseudodepression appears most likely to follow lesions of the left frontal lobe,

whereas pseudopsychopathic behavior seems likely to follow lesions of the right frontal lobe.

Deficits in Social and Sexual Behavior

Historically, changes in sexual behavior are among the most difficult symptoms of frontal-lobe

damage to document properly, largely because of social taboos against investigating people’s

sexual lives. To date, there are no such empirical studies, but anecdotal evidence suggests that

frontal lesions do alter libido and related behavior. Orbitofrontal lesions may introduce abnormal

sexual behavior (such as public masturbation) by reducing inhibitions, although the frequency of

sexual behavior is not affected. Conversely, dorsolateral lesions appear to reduce interest in

sexual behavior, although patients are still capable of the necessary motor acts and can perform

sexually if led through the activity “step by step.”

The results of several studies show that frontal-lobe lesions in monkeys significantly alter social

behavior. In one interesting study (Butter and Snyder, 1972), the dominant (alpha) male was

removed from each of several groups of monkeys, and the frontal lobes were removed from half

of the alpha monkeys. When the animals were later returned to their groups, they all resumed the

position of dominant male, but within a couple of days, all the monkeys without frontal lobes

were deposed and fell to the bottom of the group hierarchy.

Analogous studies of wild monkeys show similar results: those with frontallobe lesions fall to

the bottom of the group hierarchy and eventually die, because they are helpless alone. Exactly

how the social behavior of these animals changed is unknown, but the changes are likely as

dramatic as those in the social behavior of humans with similar deficits.

Monkeys’ social interactions are complex and include significant context dependent behavior. A

monkey’s behavior will change in accord with the configuration of the proximal social group,

and monkeys may lose this ability after frontal-lobe lesions. There are likely to be additional

components of this behavioral change, however, that relate to interpreting species-typical

sensory cues, whether they be odors, facial expressions, or sounds.

The deficit in perception of facial expression by human frontal-lobe patients may be related to

the loss of cells that code for facial expression. Certain cells in the superior temporal sulcus are

especially responsive to facial expression Edmund Rolls (1998) and his colleagues showed that a

population of cells in the orbitofrontal cortex also codes for faces. Some of these face-selective

neurons are responsive to facial expression or movement. It is thus not surprising that patients

with orbitofrontal lesions might have difficulty understanding facial expressions. We could
speculate that there are also likely to be cells in the prefrontal cortex that are responsive to tone

of voice, a verbal analog of facial expression.