Frontal Lobe Syndrome

Presenter: Sushma Jain

II year M.Phil. Trainee
Department of clinical psychology
DIMHANS, Dharwad
Moderator:
Vijay Kumar Hiremath
Assistant Professor
Department of clinical Psychology
DIMHANS, Dharwad
 Frontal Lobe

• The seat of the “highest” mental functions

• Center of those activities that make us characteristically
human.
• Most recent to evolve,
• Makes up around 1/3 rd of the mass of cerebral
hemispheres. (Goldman-Rakic, 1987)
• Compared with other animal species, the frontal cortex
encompasses the greatest quantity of cortical volume in
humans.
• Evolutionary perspective, the phylogenetic progression
of neural development involves increased frontal lobe
size and complexity.
• Frontal lobe function in humans reflects the
evolutionary development of speech and expressive
language and fine motor ability involving the hands.
• Control over the execution of movement and,
more broadly, behavioral responding is the
defining feature of frontal lobe function
• The organization of the frontal lobes reflects
increasing levels of functional complexity from the
motor strip to more anterior prefrontal areas.
• Frontal lobe function is among the last cognitive
functions to fully develop as people mature.
ANATOMY
area 4: motor cortex

areas 6: premotor cortex

area 8: frontal eye field

area 8A: supplementary eye field

area 44, 45: Broca’s area

area 9, 12: PFC

area 10: frontopolar prefrontal

cortex
• Lies anterior to the Central Sulcus.
• Constitutes 20% of the neocortex, is made up of
several functionally distinct regions.
• Divided into three anatomically distinct regions:
• Dorsolateral aspect
• Medial aspect
• Orbital (inferior) aspect
• General categories—motor, premotor, and
prefrontal.
• The motor cortex (including premotor) makes
up the posterior portion of both the dorsolateral
and medial aspects.
• The frontal lobe rostral to the motor area,
including the orbital cortex, is the prefrontal
cortex
• Motor areas: which occupies the pre-central gyrus(area 4)
• Premotor area which lies anterior to the motor area and
includes Brodmann’s area 6 and part of area 8.
• It can be divided into four regions:
• Lateral area 6: premotor cortex,
• medial area 6: supplementary motor cortex
• area 8: frontal eye field
• area 8A: supplementary eye field
• In humans, the lateral premotor area expanded as Broca’s
area (area 44)
•The prefrontal area (9, 10, 45, 46)
• dorsolateral prefrontal cortex (areas 9 and
46);
• inferior (ventral) prefrontal cortex (areas
11, 12, 13, and 14);
• medial frontal cortex (areas 25 and 32).
 General Functions
• The frontal lobes subserve pyramidal motor functions,
sensory-motor integration in complex volitional
movement, and executive and self-regulatory abilities.
• The motor area controls primary motor response, pre-
motor areas anterior to the motor area enable the
planning and execution of more complex motor
sequences.
• Prefrontal cortical areas are systems that facilitate pre-
motor functions, i.e. the formation of intent to respond,
planning of responses, and higher level control of
• Executive functions include the following abilities:

• Formulating goals with regard for long-term consequences,

• Generating multiple response alternatives,
• Choosing and initiating goal-directed behaviors,
• Self-monitoring the adequacy and correctness of the
behavior,
• Correcting and modifying behaviors when conditions
change, and
• Persisting in the face of distraction.
 Premotor Cortex

• The motor cortex provides a mechanism for the

execution of individual movements, the premotor
cortex selects the movements to be executed.
• Premotor region functions primarily to choose
behavior in response to external cues and the
supplementary motor region makes a greater
internal contribution when no such cues are
available.
 Prefrontal Cortex
• The prefrontal cortex is related to the ideational or
intellectual control of action.
• The dorsolateral prefrontal cortex is concerned with the
preparation and execution of action.
• Orbitofrontal cortex is related to the flexible control of
excitation and inhibition and the emotional control of
behavior.
• Medial frontal cortex mediates self initiated action and
sustains behavior at appropriate levels.
• The motor cortex is responsible for making
movements. The premotor cortex selects movements.
• The prefrontal cortex controls cognitive processes, so
that appropriate movements are selected at the
correct time and place.
• This selection may be controlled by internalized
information or external cues or it may be made in
response to context or self-knowledge.
 Asymmetry of Frontal-Lobe Function
• Results of studies of patients with frontal lesions indicate that both
frontal lobes play a role in nearly all behavior.
• Left frontal lobe has a preferential role in language-related
movements, including speech, whereas the right frontal lobe plays
a greater role in nonverbal movements such as facial expression.
• Tulving et.al (2002) proposed that the left and right frontal lobes
may play different roles in memory processing: the left prefrontal
cortex is proposed to be have a greater role in encoding
information into memory, whereas the right prefrontal cortex is
more engaged than the left in retrieval.
 Frontal Lobe -Lesion Studies

• Abstraction
• Frontal lobes are involved in abstract thinking.
• Studies show that patients with frontal lesions perform
poorly on tests of abstraction. ( Fleming 1942, Kisker 1944,
Rylander 1947 )
• However such findings are controversial since a person may
fail on a test of abstract reasoning for a number of reasons
other than alteration in the ability to think abstractedly.
 Planning and Problem Solving
• People with frontal lesions or who had undergone
frontal lobotomy showed a clear loss in the area of
planning.
• Such patients also showed loss on performance in
Maze behavior ( Porteus & Kepner 1944,Porteus &
Peter 1947, Robinson & Freeman1954).
• Crown (1952) and Lewis et.al (1956) showed that the
losses in the Maze test are dependent on the location
of the lesion within the frontal lobe.
 Visuo-constructive abilities

• Patients with brain impairments have been found to

perform poorly on such tasks eg. Koh’s block design.
• Luria and Tsvetkova (1964) demonstrated that frontal
constructional difficulties arise through disruption of one
or more steps;
• Intention,
• Programming,
• Regulation or verification.
• Lhermitte et.al (1972) found that frontal patients copying
of CFT was more adequate than reproduction from
memory. When patients were given sequential training
programs their reproduction from memory improved.
However it was not generalized to other figures.
• Messerli et.al (1979) found that the spatial relationship of
many key elements in the diagram are preserved and
correctly reproduced. It is the failure to organize or
integrate the components into a whole which is at fault.
 Arithmetic problem solving
• In patients with frontal lobe lesions there does not
appear to be significant disturbances of well
established operations such as additions and
subtractions.
• Their difficulties are those of problem solving. They
seem to have forgotten how to generate and execute
even simple two-three step problems.
 Error utilization

• A major behavior change in frontal lobe cases is the apparent

lack of full awareness of deficits.
• Luria (1963, 1964) felt this is “the result of a general loss of some
feedback mechanism, a disturbance in signals of error, or an
inadequate evaluation of the patient’s own action. It’s a deficit
in matching of action carried out with the original intention.”
• Konow & Pribram (1970) described a patient who made errors,
was aware of making errors, however was not able to correct
them.
• There is error recognition, evaluation, but not error utilization
 Verbal behaviour
• The frontal lobe contains two speech zones:
• Broca’s area, which can be regarded as an extension of the lateral premotor area,
• The supplementary speech area, which may be an extension of the supplementary motor
area.
• Two major forms of aphasia occur with frontal lobe lesions. Broca’s aphasia and transcortical
motor aphasia.
• People with strokes in Broca’s area are impaired in their ability to use expressive language.
• People with strokes that include the supplementary speech area and extend into the 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.
• Patients with left frontal lesions will often appear to have intact speech, however
careful examination will often bring out evidence of perseveration, or in severe
cases echolalia.
• They also have difficulty with verbal fluency. There is an impoverishment of
spontaneous speech.
• It can be termed as verbal adynamia ( general lack or spontaneous and voluntary
action).
• This verbal adynamia is more pronounced after left frontal damage.
• Benton (1968) (FAS) examined patients with left, right and bilateral frontal lesions.
It was found that left and bilateral lesion patients performed poorer than right
lesion patients. No difference was found among left lesion patients and bilateral
lesion patients
 Perceptual Difficulties

• Teuber presented patients with an array of 48 patterns on a screen.

• The patterns could be distinguished by shape or color or both. At a warning
signal, a duplicate of one of the 48 patterns appeared in the center of the
array, and the subject’s task was to identify the matching pattern by
pointing to it.
• Patients with frontal-lobe lesions were impaired at finding the duplicate
pattern.
• Design Fluency (Jones-Gotman and Milner)
• Lesions in the right frontal lobe produced a large decrease in the number
of different drawings produced.
• Normal controls drew about 35 drawings, left-frontal-lobe patients drew
about 24 drawings, and right-frontal-lobe patients drew about 15
drawings.
• This deficit appears to be related to an impoverished output and high
perseveration.
DYSFUNCTIONS &SYNDROMES
 General Dysfunctions

• Primary motor area lesions result in flaccid hemiplegia in the contralateral

side of the body, which typically resolves into spastic hemiplegia.
• Less severe lesions to this area or its connections result in hemi-paresis and
in coordination of the contralateral side.
• Premotor area lesions result in apraxia (difficulty programming complex
volitional movements) and the inability to make use of sensory feedback to
modify movements smoothly.
• Disruption of connections with sensory areas of the parietal lobe to this area
can also result in difficulty in integrating sensory information into ongoing
motor plans.
• Frontal eye field damage can result in the inability to control volitional eye
movements in the contralateral visual field, inability to direct complex
attention during defensive behaviors, and problems guiding eye movements
during goal directed behavior involving memory.
• Prefrontal damage impairs more complex behaviors and metacognition
 Specific Syndromes

• There are 2 types of syndromes:

• Premotor
• prefrontal syndrome (Fuster 1997)
 Premotor syndrome

• Damage to the pre-motor cortex does

not result in paralysis.
• There is disruption of fine motor
functioning and dexterity.
• With extensive damage fine motor skills
are completely lost and it gives rise to
spasticity, rigidity of movements and the
grasp reflex (Joseph, 1996).
 Prefrontal Syndrome

• Three prefrontal syndromes have

been associated with damage to
these anterior subsystems:
• (a) dorsolateral convexity,
• (b) orbital area, and
• (c) medial area.
 Dorsolateral Prefrontal Cortex (DLPFC)

• Damage to the
Dorsolateral Prefrontal
Cortex leads to
dysfunction in attention,
memory, planning,
abstract thinking,
concept formation,
mental set and language
 DYSEXECUTIVE SYNDROME

• Disorder of attention is the dysexecutive syndrome (Fuster 1997)

• Low arousal or alertness: patients appear less alert and aware of the world around
them than normal individuals ( Luria 1966/1980).
• The underlying deficit makes them less spontaneous in actions but also less aware of
the surroundings and less responsive to matters of normal concern.
• Difficulty in sustained attention: inability to concentrate on any given trend of action
or thought.
• Colour Trails
• Deficits in selective attention: Lesions of the DLPFC lead to impairment
of focused attention, making them vulnerable to interference.
• Colour Trails
• Visual Search: damage leads to loss of normal logical order in analysis of
pictorial detail.
• The examination of visual images becomes haphazard, unsystematic
and prone to unnecessary iterations.
• Search plans become sluggish particularly in the field of vision contra
lateral to the side of the lesion.
• Digit Vigilance
 Memory Dysfunction

• Patients with frontal lesions have difficulty with voluntary learning, but are able to
acquire new information when they are made to repeat material frequently
• Recent memory is found to be faulty due to high distractibility and lack of interest and
attention.
• Difficulty in intellectual organization of information to be memorized.
• It is associated with an inability to use the correct method to solve a problem in the
presence of knowledge of the necessary information (Walsh 1991,1999).
• Working memory: frontal patient exhibits an impairment of working memory (Fuster
1997).
• AVLT, Logical Memory, CFT
 Planning Dysfunction

• Planning deficit is one of the most consistently reported prefrontal

symptoms.
• The planning and execution of schemes of action guided by internal cues are
predominantly vulnerable in left DLPFC lesions.
• TOL ( Walsh 1999, Fuster 1997)
 Disorder of abstract thinking, concept
formation and mental set
• Early studies showed impairment in abstract thinking.
• Frontal patients show difficulties on conceptual task such as Wisconsin Card Sorting test
( Milner 1963) .
• They are able to express the suitable principles of categorization, but they are unable to
use this verbalization to guide action.
• Frontal patients show difficulty in changing response set, i.e. they are unable to inhibit
customary modes of responding
• WCST, Proverbs Test
 Language Dysfunction

• The nature and severity of the dysfunction depends on the location and
magnitude of the lesion.
• The ability to construct original, improvised and extended speech is
impaired in prefrontal injury (Fuster 1997).
• Broca’s Aphasia: Injury to the left inferior frontal gyrus ( Area 44 & 45) leads
to this type of aphasia
• Speech delivery is slow and effortful. It lacks normal fluidity and continuity.
• The articulation of some words may be disturbed.
• Typically patients omits articles and small liaison words and expresses most
verbs in the infinitive form
• This distortion of normal speech with its telegraphic style has been
characterized as agrammatism.
 Frontal Dynamic Aphasia

• Lesions in the more anterior portions of frontal lobes can produce

alterations of speech.
• It is more subtle and less incapacitating than Broca’s aphasia.
• There is reduction in spontaneous speech, curtailment of the amount and
range of narrative expression and loss of verbal fluency.
• It can result from right as well a left lesions.
 ORBITOFRONTAL SYNDROME
• Anosmia, disinhibited personality change, amnesia with confabulation, and failure
on neuropsychological tests of inhibition are signs of orbitofrontal damage (Malloy,
Bihrle, Duffy,& Cimino, 1993).
• Patients with orbitofrontal damage find it difficult to suppress contemporary modes
of responding .
• Perseveration in ideational, verbal and motor domains can occur due to this deficit.
• Related cognitive problems include difficulties with attention, most commonly,
increased distractibility by irrelevant stimuli and diminished sustained and divided
attention.
• Imitation of others and utilization behavior is also another symptom of damage to
the orbitofrontal cortex.
• Personality changes also occur to this damage in this
area due to loss of inhibition and insight.
•It is characterized by disturbances in affect: euphoria,
irritability, destructivity, hyperphagia and hyper reactivity.
•There is loosening of moral restraints and loss of
capacity to gauge the effects of one’s behavior on the
social interactions with others (Fuster 1997)
 MEDIAL PREFRONTAL SYNDROME

APATHETIC-AKINETIC SYNDROME
• Lesions in the medial aspects of area 6 and 8 lead to difficulties in
the initiation and performance of limb, eye or speech movements.
• It can result in "alien hand syndrome," in which the patient may
grab objects, throw things, and otherwise explore the environment
in a disinhibited way (Goldberg & Bloom, 1990).
• Lesions to the anterior cingulate gyrus can result in akinetic
mutism.
• The patient fails to respond to environmental stimuli and remains
inert.
• When the lesion is unilateral, akinesia is typically transient,
whereas persistent akinesia usually results from bilateral lesions.
• Adynamia is the predominant disorder of affect resulting
from medial frontal damage.
•There is anergia or passivity, in which patients are unable
to voluntarily initiate and sustain activity.
• The problem is one of arousal or motivation, as patients
may respond appropriately to external stimulation if it is
repeated but lapse back to inactivity when the external
source is removed.
• It is accompanied by disorders of attention and motility,
this condition is known as pseudo-depression (Walsh
1999, Fuster 1997)
 Frontal lobe personality changes
• Personality may be manifested as more activation and excitability than before the injury, or
markedly reduced activation.
Excitability can be manifested as
(a) impulsivity,
(b) emotional lability or mood swings,
(c) socially inappropriate behaviors, o
(d) immature behavior.
Symptoms of reduced activation include
(a) apathy,
(b) decreased spontaneity or abulia,
(c) lack of interest,
(d) emotional blunting.
e) Impaired social behavior
f) Altered sexual behavior
g) Behaviour spontaneity
h) Strategy formation
i) Response inhibition and inflexible behavior
j) Response inhibition
k) Risk taking and rule breaking
l) Self regulation
m) Associative learning Poor temporal memory
n) Working memory
o) Delayed response
Phineas Gage
 Imaging studies

• In general, the results of imaging studies have shown specific activation for
prefrontal functions that were identified historically in lesion studies.
• There is a striking regularity in activation for most cognitive demands, there was a
similar recruitment of the dorsolateral, ventrolateral, and anterior cingulate
regions.
• Suggests that regional specialization exists within the frontal lobe, a frontal lobe
network is consistently recruited for the solution of a diverse set of cognitive
problems
• The frontal lobes of the cerebral cortex are traditionally considered to be the seat of the
• “highest” mental functions and the center of those activities that make us
characteristically
• human. This is largely because in evolutionary terms the frontal cortex has been the most
• recent to evolve, and humans happen to possess particularly large frontal lobes.
• The four divisions, of the frontal lobes are the motor and premotor cortex; the prefrontal
• cortex (sometimes referred to as “frontal granular cortex” because of the type of cells
• predominant in this area, or as dorsolateral cortex); Broca’s area, which we assume to
exist
• in the left frontal lobe only and the orbital (or orbitofrontal) cortex.
 1) DISTURBANCES OF MOTOR FUNCTION

• Frontal lesions can impair a person’s ability to make a wide variety of

movements, to order movement sequences, and even to speak.
• Fine Movements, Speed, and Strength
• Damage to the primary motor cortex 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
 • Movement Programming

In a classic paper in 1950, Karl Lashley asked how movements are put
together in a particular order. “How is it that, in a tennis game, a player
can make very rapid movements, seemingly much too fast to have
considered each movement by itself”? Lashley presumed that this
function—serially ordering complex chains of behavior in relation to
varying stimuli—must somehow be a function of the neocortex.
Although he believed it to be a function of the entire neocortex, it
appears more likely to be a function of the frontal lobes. Removal of the
supplementary motor cortex results in a transient disruption of nearly
all voluntary movements (including speech, if the removal is on the
left).
 • Voluntary Gaze:

• A number of studies using quite different procedures have been

reported in which frontal- lobe lesions produce alterations in
voluntary eye gaze. For example, Teuber presented patients with
an array of 48 patterns on a screen. The patterns could be
distinguished by shape or color or both.
• At a warning signal, a duplicate of one of the 48 patterns appeared
in the center of the array, and the subject’s task was to identify the
matching pattern by pointing to it. Patients with frontal-lobe
lesions were impaired at finding the duplicate pattern.
 • Speech
• The frontal lobe contains two speech zones: Broca’s area,
which can be regarded as an extension of the lateral
premotor area, and the supplementary speech area, which
may be an extension of the supplementary motor area.
• People with strokes in Broca’s area are impaired in their
ability to use verbs and to produce appropriate grammar, a
symptom known as agrammatism. People with strokes that
include the supplementary speech area and extend into the
left medial frontal region are often mute.
 2) LOSS OF DIVERGENT THINKING
• Frontal-lobe injury interferes with the intelligence required by divergent thinking, rather
than the convergent type measured by standard IQ tests.
• Behavioural Spontaneity
• Patients with frontal-lobe lesions have long been recognized to exhibit a loss of
spontaneous speech. Various investigators have been able to quantify this loss by using
tests such as the Thurstone Word-Fluency Test (also referred to as the Chicago Word-
Fluency Test). Patients are asked to write or to say, first, as many words starting with a
given letter as they can think of in 5 minutes and, then, as many four-letter words starting
with a given letter in 4 minutes.
• Patients with frontal-lobe lesions have a low output of words in this test. Although the
principal locus of this defect appears to be in the left orbital frontal region, lesions in the
right orbital frontal region also may produce a marked reduction in verbal fluency.
• Strategy Formation
• Patients with frontal-lobe lesions are especially impaired at developing novel
cognitive plans or strategies for solving problems. For example, when Shallice and
Evans asked subjects questions that required reasoning based on general knowledge
for which no immediate obvious strategy was available, they found that frontal-lobe
patients did very poorly and often gave bizarre responses.
 • ENVIRONMENTAL CONTROL OF BEHAVIOR: IMPAIRED RESPONSE
INHIBITION AND INFLEXIBLE BEHAVIOR

• Perhaps the most commonly observed trait of frontal-lobe patients is their

difficulty in using information from environmental cues (feedback) to regulate
or change their behavior. This difficulty manifests itself in a number of ways.
 Tests for Eliciting Frontal Lobe Dysfunction
• Attention
– Spontaneous arousal of attention
– Distraction
– Excessive broadening/ narrowing of attention
•Tests of visual search
-Frontal lobe lesions (R>L)
-OFC>DLPFC
-Errors (Frontal>Non-frontal)
– Visual scanning of numbers (Instructions for tests 1 & 2: no's 1-20 are arranged randomly(1-50 for item 2).
Please strike off no's in serial order. Time taken & errors noted. For item 3, cancel all the repeated no's
(time: 2mins). Note errors.
– Visual scanning of pictures
– Visual exploration test
• Mental set
1. Psychomotor perseveration

- Frontal lobe lesions

a) Motor Alternation tests (fist & ring test) ( Left frontal>Right
frontal)
b) Continuous drawing tests (Once examiner ascertains the shapes
(circle, triangle, cross) can be drawn by the pt, examiner calls out
the names in random order from a prepared list and patient draws
it).Deficits seen more in orbito-frontal lesion patients.
c) BGT & BVRT
• 1. Psychomotor deficits
• Execution of motor tasks
• Test of Optic- kinesthetic organization (copy different finger positions shown by
examiner. Deficits present if subject fails to show correct finger position or mirror
reversals occur)
• Test of optic-spatial organization (transpose various hand movements by examiner)
(RF>LF)
• Kinetic melody disturbance (Rhythmical tapping with 2 hands, For example, tap twice
with left and once with right. Then change instructions. Complex instructions).
• Premotor lesions implicated. If cerebellar lesions present tapping becomes rigid, without
smoothness, or patient may fail to tap properly.
Deficits in working memory
Bilateral frontal lobe lesions
Test of mental control
Delayed response tests
Deficits of ideational and design fluency test
a) Ideational fluency (Semantic fluency is tested by asking the patients to name objects which are round and
made of wood (time: 2 mins each. Score: each correct response)
Deficits in Left temporoparietal>Right temporoparietal.
No deficits in right temporoparietal lesion patients.
b) Design Fluency
- Deficits in RF >LF
- Deficits in Left temporoparietal<Right temporoparietal. No deficits in left temporoparietal lesion
patients.Original by Gotman & Milner (1974)-was 5 mins.
- Free condition (Draw non-specific drawings (but not scribblings) of neither actual objects, designs or
derivatives of them). Time: 2 mins.
- Fixed condition (draw designs using lines, circles, or combinations, altogether not exceeding four in no.) Score
is no. of designs drawn. If exceeds four components in no. in each design it is considered an error. Time:2 mins
• Deficits in visuospatial planning tasks
• Deficits in RF>LF
• Differentiate between frontal and parietal involvement.
• Bender gestalt test
• Alexander passalong test
• Object assembly test
• Maze tests
• Frontal Amnesia (inability to spontaneously recall names, information or events when one
attempts to recall Might recall at a later stage. Inability to evoke temporo-spatial
coordinates of the info when asked). Often found in alcohol dependent subjects.
• Expressive speech disturbances (formal assessment not included)- note down errors in
speech.
• Changes in voluntary activity, personality and affect (To be noted through behavior
observation and clinical history. Might precede cognitive complaints and seek
psychiatric help first)
- Decreased familial, social and occupational activities
- Lack of self-care
- Loss of interest
- Lack of initiative
- Inability to plan out activities, difficulty in decision-making
- Apathy, Akinesia, Abulia
- Affect: labile, depressed, euphoric
- Impulsivity
- Poor social judgement
- Disinhibition
- Inappropriate sexual behavior or comments
 References

• Bryan Kolb and Ian Q. Whishaw Fundamental of Neuropsychology 5 and 7 edition

th th

• Maria A. Patestas and Leslie P. Gartner A Textbook of Neuroanatomy (Blackwell

publishing)
• Mike R. Schoenberg and James G. Scott The Little Black Book of Neuropsychology A
Syndrome-Based Approach
• Vishram Singh, Textbook of clinical neuroanatomy second edition
• John W. Burruss, MD et al (2000) article on Functional Neuroanatomy of the Frontal Lobe
Circuits
• Jessica A. Grahn et al (2008)The cognitive functions of the caudate nucleus Progress in
Neurobiology journal homepage:www.elsevier.com/locate/pneurobio