2. OUTLINE: FRONTAL LOBE
1. Evolution
2. History
3. Anatomy and connections
4. Syndromes
5. Physiology
6. Neurotransmitters
7. Dysfunction
8. Testing
9. Pathology

3. MAMMALS FRONTAL LOBE EVOLUTION
 33% of Brain area
 Most recently evolved
 Well developed only in
primates
 Human species is due to
frontal lobe
 Last to develop in ontogeny
from age 1-> 6years
 Gives our capacity to feel
empathy, sympathy,
understand humor and when
others are being ironic,
sarcastic or even deceptive.

4. HUMAN FRONTAL LOBE EVOLUTION
The high, straight forehead that characterizes modern humans,
superseding the prominent brow ridges of our ancestors, is due
to the expansion of the cortex, and especially the prefrontal
cortex, in our species.
1. Australopithecus robustus 2. Homo habilis 3. Homo erectus
4. Homo sapiens neanderthalensis 5. Homo sapiens sapiens

5. FRONTAL LOBE HISTORY 1600-1900
1. 1641 – Lateral sulcus of the brain was first defined by
Franciscus de la Boe Sylvius,
2. 1825 - Long before the time of Bouillaud the
coexistence of aphasia, with certain forms of paralysis
3. 1848 - Beginning with the tragic story of Phineas Gage
4. 1861 - The area of the brain responsible for forming
language is called Broca's area,
5. 1868 - The "prefrontal“ introduced by Richard Owen
6. 1890 - Swiss doctor working in a mental institution
decided to try a revolutionary treatment. He removed
the frontal lobe from six of his patients

6. FRONTAL LOBE
A. Lateral surface
1. Posterior - Central
sulcus
2. Inferio-Posterior –
sylvian fissure.
B. Medial sufface
C. Orbital surface

7. LATERAL SURFACE FRONTAL LOBE
 Precentral sulcus –
parallel to central
sulcus between them
precentral gyrus
 Sup and inf frontal
sulci divide sup,
middle and inf frontal
gyri

8. MEDIAL SURFACE FRONTAL LOBE
 Between cingulate
sulcus and superior
medial margin of
hemisphere
 Posterior part
vertical sulcus –
paracentral lobule

9. ORBITAL SURFACE FRONTAL LOBE
 Divided into four orbital gyri by a
well-marked H-shaped orbital
sulcus.
 The medial, anterior, lateral,
and posterior orbital gyri.
 The medial orbital gyrus
presents a well-marked antero-
posterior sulcus,
 the olfactory sulcus, for the
olfactory tract;
 the portion medial to this is
named the straight gyrus, and
is continuous with the superior
frontal gyrus on the medial
surface.

10. FUNCTIONAL FRONTAL LOBE ANATOMY
Premotor area Primary motor area
B6 B4
Central sulcus
Supplementary
motor area
(medially)
Motor cortex
1. Primary
Frontal eye field
2. Premotor
B8
3. Supplementary
Prefrontal area 4. Frontal eye
B 9, 10, 11, 12 field
Lateral sulcus/ 5. Broca’s area
Sylvian fissure
Prefrontal cortex Motor speech
1. Dorsolateral
2. Medial area of Broca
3. Orbitofrontal B 44, 45

11. PRIMARY MOTOR CORTEX
 Input: thalamus, BG,
sensory, premotor
 Output: motor fibers to
brainstem and spinal
cord
 Function: executes
design into movement
 Lesions: / tone;
power; fine motor
function on contra
lateral side

12. PRE MOTOR CORTEX
 Input: thalamus, BG,
sensory cortex
 Output: primary motor
cortex
 Function: stores motor
programs; controls
coarse postural
movements
 Lesions: moderate
weakness in proximal
muscles on
contralateral side

13. SUPPLEMENTARY MOTOR CORTEX
 Input: cingulate gyrus,
thalamus, sensory &
prefrontal cortex
 Output: premotor, primary
motor
 Function: intentional
preparation for
movement; procedural
memory
 Lesions: mutism,
akinesis; speech returns
but it is non-spontaneous

14. FRONTAL EYE FIELDS
 Input: parietal / temporal
(what is target); posterior
/ parietal cortex (where is
target)
 Output: caudate; superior
colliculus; paramedian
pontine reticular
formation
 Function: executive:
selects target and
commands movement
(saccades)
 Lesion: eyes deviate
ipsilaterally with
destructive lesion and
contralaterally with
irritating lesions

15. BROCA‟S SPEECH AREA
 Input: Wernicke‟s
 Output: primary motor
cortex
 Function: speech
production (dominant
hemisphere);
emotional, melodic
component of speech
(non-dominant)
 Lesions: motor
aphasia; monotone
speech

16. CONNECTIVITY OF PREFRONTAL REGIONS
 input from association cortex
(occipital, parietal, temporal &
olfactory areas)
 convergence of higher-order input
from all modalities.
 reciprocal connections: prefrontal
processing modulates perceptual
processing.
 LIMBIC connections
(memory/emotion)
 Input to premotor areas -
controls/programs behavior.

17. INTERACTION AMONG ASSOCIATION AREAS

18. FRONTAL LOBE SYNDROMES

19. PHINEASE GAGE (1848)
1. He becomes unreliable and fails
On 13th Sept 1848 a railroad to come to work and when
worker, hard working, present he is "lazy."
2. He has no interest in going to
diligent, reliable, church, constantly drinks alcohol,
gambles, and "whores about."
responsible, intelligent,
3. He is accused of sexually
good humored, polite god molesting young children.
fearing, family oriented 4. He ignores his wife and children
and fails to meet his financial and
foreman family obligations.
5. He has lost his sense of humour.
Following an explosion iron 6. He curses constantly and does so
bar drove into frontal lobe in inappropriate circumstances.
7. Died of status epilepticus in 1861

20. FRONTAL LOBE ABLATION IN MONKEY AND
DOGS (BIANCHI)
 "The frontal lobes are the seat of coordination and fusion of the
incoming and outgoing products of the several sensory and motor
areas of the cortex" (Bianchi, 1895)
 Loss of "perceptive power", leading to defective attention and object
recognition.
 Reduction in memory.
 Reduction in "associative power", leading to lack of coordination of the
individual steps leading towards a given goal, and thus to severe
difficulty solving anything but the most simple problem.
 Altered emotional attachments, leading to serious changes in
"sociality" [one of the main aspects of Phineas Gage's post-traumatic
behaviour].
 Disruption of focal consciousness and purposive behaviour, leading to
apathy and/or distractibility [one of the main aspects of Becky's post-
operative behaviour].
Bianchi 1922

21. FRONTAL LOBE HISTORY 1900-2010
Feuchtwanger (1923) Jacobson (1935)
200 case of frontal lobe injury  Premotor lobotomy in
 Lack of initiative primates ->
 Vacillation
 Social indifference
 Euphoria
 Tameness
 Inattentiveness
 Placidity
 Normal intellect and memory
 Forgetfulness
Egas Moniz 1935
 Difficulty in problem
 Prefrontal lobotomies in solving 
psychotics
Dandy‟s (1936)
 following bilateral frontal
lobotomy during removal of
meningioma

22. INFERIOMESIAL FRONTAL LEUKOTOMY
EGAS MONIZ 1935
Hours Weeks to months
 Drowsy  Regained memory and
 Apathetic intellect
 Incontinent
 Akinetic  With personality
 Mute changes
Days  Indifferent to the others
 Decreased initiative problem
 Lack of concern  No thought to their
 Freedom from anxiety conduct
 Apathetic  Tactless
 Distractible
 Socially inept
 Euphoria and emotional
outburst

23. FROTNAL LOBE SYNDROMES
executive function
deficit; disinterest /
apathy; emotional reactivity;
decreased drive/ attention to relevant
awareness/ stimuli
spontaneous
movements;
akinetic-abulic& Lateral
mutism
emotional lability,
Medial
disinhibition,
distractibility,
‘hyperkinesis’
Orbital

24. ORBITAL PREFRONTAL CORTEX
 Connections:
temporal,parietal, thalamus,
GP, caudate, SN, insula,
amygdala
 Part of limbic system
 Function: emotional input,
arousal, suppression of
distracting signals
 Lesions: Disinhibited,
impulsive behaviour
(pseudopsychopathic)
 Inappropriate jocular affect,
euphoria ,emotional lability,
Poor judgment and insight,
Distractibility

25. DORSOMEDIAL PREFRONTAL CORTEX
 Connections:
temporal,parietal, thalam
us, caudate, GP, substant
ia nigra, cingulate
 Functions:
motivation, initiation of
activity
 Lesions: Paucity of
spontaneous movement
and gesture, Sparse
verbal output (repetition
may be
preserved), Lower
extremity weakness and
loss of
sensation, Incontinence

26. DORSOLATERAL PREFRONTAL CORTEX
 Connections: motor /
sensory convergence
areas, thalamus, GP,
caudate, SN
 Functions: monitors
and adjusts behavior
using „working memory‟
 Lesions: executive
function deficit;
disinterest / emotional
reactivity; attention to
relevant stimuli

27. FRONTAL CONVEXITY SYNDROME (APATHETIC)
 Apathy (occasional brief  Three-step hand sequence
angry or aggressive Alternating programs
outbursts common) Reciprocal programs
Indifference Rhythm tapping
 Psychomotor retardation Multiple loops
Motor perseveration and  Poor word list generation
impersistence  Poor abstraction and
 Loss of self categorization
Stimulus-bound behaviour  Segmented approach to
 Discrepant motor and verbal visuospatial analysis
behaviour
 Motor programming deficits

28. UNILATERAL FRONTAL LOBE SYNDROME
1. Contralateral 4. Difficulty in adaptation
hemiplegia 5. Loss of initiative
2. Conjugate deviation of 6. Loss of kinetic melody
eye to side of lesion 7. Unable to solve
3. Personality change problem
(Psudopsychotic) 8. Anosmia and blindness
a. Mood elevation,
talkativeness
b. Tendency to joke, lack
of tact, silly and
childish behavior

29. DOMINANT FRONTAL LOBE
 Deficits in tests of categorization
1. Loss of motor speech and flexibility.
2. Unable to write  Problems with body schema
(autopagnosia) due to problems of
3. Sympathetic apraxia scanning, perceptual shifting and
postural mechanisms.
4. Dysphoria  Marked inactivity affects general
intellectual processes and
behavior.
 Cannot change verbal instructions
into acts, especially when the
instructions are complex or
symbolic.
 Decreased spontaneity of speech;
may result in complete loss of
voluntary speech.
 Memory deficits for verbal
material; however, deficits may be
due to defective registration.

30. RIGHT HEMIS. PREFRONTAL LESIONS
 Loss of emotional  Large lesions may exist
speech expression without obvious
symptoms; serious
 Euphoria speech disorders usually
 Constructional apraxia, not seen in right
hemisphere lesions.
associated with motor
rather than perceptual  Difficulty with drawing
tasks, though this is
difficulties; deficits may associated more with
occur as a function of right hemisphere lesions
impaired complex (3-D) in general.
spatial analysis.  Impaired visual-spatial
integration, maze
learning, non-verbal
visual memory

31. BILATERAL FRONTAL LOBE LESION
1. Pseudodepressed - 6. Active learning,
Apathy, Abulia, akinetic problem solving,
mutism, judgment
2. Impulsiveness and 7. Limitation of utilization
irritability
behavior
3. Inability to sustain
attention 8. Frontal release sign
a. Snout
4. Decomposition of gait
b. Suck
5. Sphincter disturbance
c. Palmomental
d. Grasp
e. Brow tapping

32. FRONTAL LOBE SYNDROME MIMICS
 Bilateral Caudate nucleus lesion - Dyscontrol
 Globus pallidus lesion – Apathy and abulia
 Bilateral thalamic infarction
 MS – Apathy and disinhibition
 Sjogren‟s syndrome
 Subcortical stroke
 Adrenoleukodystrophy
 Parkinson‟s disease
 Fahr‟s disease
 Huntington‟s disease
 Depression
 Schizophrenia
 OCD

33. FIVE „FRONTAL SUBCORTICAL CIRCUITS‟
1. Motor
2. Oculomotor
3. Dorsolateral prefrontal
4. Lateral orbitofrontal
5. Anterior cingulate
Cummings,„93

34. 1. FRONTAL SUBCORTICAL MOTOR CIRCUIT
SMA,
Premotor,Motor
Hypo-thalamus Putamen
Thalamus Globus
VL,VA,CM Pallidus
 Supplementary Motor & Premotor : planning, initiation & storage
of motor programs; fine-tuning of movements
 Motor : final station for execution of the movement according to
the design

35. 2.FRONTAL OCULOMOTOR CIRCUIT
Frontal
Eye field
Thalamus Central
VA, MD Caudate
DM Globus
Pallidus &
Substantia Nigra
 Voluntary scanning eye movement
 Independent of visual stimuli

36. 3.DORSOLATERAL PREFRONTAL CIRCUIT
Lateral Pre-Frontal
Thalamus DL
VA, MD Caudate
DM Globus
Pallidus &
Substantia Nigra
 Executive functions: motor planning, deciding which stimuli to
attend to, shifting cognitive sets
 Attention span and working memory

37. 4. LATERAL ORBITOFRONTAL CIRCUIT
Infero-Lateral
Pre-Frontal
VM
Orbito-Frontal
Caudate
DM Globus
Thalamus
Pallidus &
VA, MD
Substantia Nigra
 Emotional life and personality structure
 Arousal, motivation, affect
 Orbitofrontal cortex: consciousness

38. 5. ANTERIOR CINGULATE CIRCUIT
Ant. Cingulate
MD
Thalamus Thalamus
Ventral Striatum
MD
RL Globus
Pallidus &
Substantia Nigra
 Abulia, akinetic mutism

39. NEUROTRANSMITTERS: DOPAMINERGIC
TRACTS
 Origin: ventral
tegmental area in
midbrain
 Projections: prefrontal
cortex (mesocortical
tract) and to limbic
system (mesolimbic
tract)
 Function: reward;
motivation;
spontaneity; arousal

40. NEUROTRANSMITTERS: NOREPINEPHRINE
TRACTS
 Origin: locus ceruleus
in brainstem and lateral
brainstem tegmentum
 Projections: anterior
cortex
 Functions: alertness,
arousal, cognitive
processing of
somatosensory info

41. NEUROTRANSMITTERS: SEROTONIN TRACTS
 Origin: raphe nuclei in
brainstem
 Projections: number of
forebrain structures
 Function: minor role in
prefrontal cortex; sleep,
mood, anxiety, feeding

42. FRONTAL LOBE FUNCTION
Motor Cognitive Behavior Arousal
Voluntary Memory Personality Attention
movements
Planning, Problem Social and
Initiation solving sexual
Spontaneity Judgment Impulse
control
Language Abstract Mood and
Expression thinking affect
Eye
movements

43. MOTOR PLANNING
1. Frontal lobe has evolved from being the main
motor planner/organizer to a higher level
behavioural/strategic planner/organizer.
2. Mental model, considering options, selecting
behaviours based on context, feedback, stored
knowledge
3. Making predictions about what will work.

44. “PLANNING NEURONS” IN THE MONKEY
FRONTAL CORTEX

45. FRONTAL LOBE AND AROUSAL
 Right frontal lobe -> bilateral inhibitory influences
on attention and arousal
 Left frontal lobe unilateral excitation of arousal
 Left frontal damage -> unopposed right cerebral
inhibition -> akinesia

46. MEMORY DEFECT
 Inattentiveness
 Defect in working memory
 Defect in sequencing, perseverance
 Can recall the details of problem, error in trying to
solve
 Could not put them to use in the correction of
further performance.
 Cannot categorizes series of item in group for
recall

47. WORKING MEMORY

48. WORKING MEMORY IS A SHORT-TERM MEMORY REQUIRED FOR
BOTH THE ENCODING AND RECALL OF EXPLICIT KNOWLEDGE

49. NEURON FIRING IN THE PRINCIPAL SULCUS
TRACK THE WORKING MEMORY

50. IMAGING OF WORKING MEMORY

51. LEARNING
Impaired association Impaired temporal
learning learning
1. Reduced response 1. Impaired memory for
to consequences order, recency
2. Impaired on delayed 2. Could affect
response tasks problem-solving,
3. Impaired planning and impair
responsiveness to systematic,
social & contextual organized
cues behaviours

52. ABSTRACTION AND JUDGMENT
 Cognitive functions undisturbed
 Concrete thinking
 Diminished insight
 Defect in planning / executive control

53. PROBLEM SOLVING
 Unable to think all the option and select appropriate
 Fails to conceptualize all the demands of the
situation but thinks “concretely” – think and react
directly to the stimulus

54. PROBLEM SOLVING - LURIA
Normal Frontal lobe lesion
1. The specification of 1. Erroneous analysis of
problem and the the condition of the
problem
condition in which it has
arisen 2. The plan of action that
is selected quickly
2. A plan of action or loses its regulation
strategy for the solution influence on behavior
of the problem is as a whole and is
formulated replaced by a
perseveration of one
3. Execution, including particular link of the
implementation and motor act or by the
control of the plan influence of some
4. Checking of the results connection established
against the original plan during the patient's
past experience.

55. IMPAIRED DIVERGENT THINKING
1. Decreased consideration of alternative
strategies/behaviors; reduced flexibility
2. Decreased spontaneity, initiative, may appear
lazy, unmotivated
3. Knowledge/intelligence may seem intact (e.g. IQ)
but its not used to generate strategies or solve
problems efficiently

56. Language
• Broca‟s / non-fluent aphasia
• Prefrontal/ transcortical motor aphasia
• Language-motor dissociation
• Akinetic mutism

57. FRONTAL LOBE PERSONALITY
 Lack of initiative and  Organic driveness:
spontaneity brief but intense
 Placidity: worry, meaningless activity.
anxiety, self concern,  Loss of ego strength:
hypochondriasis, and Witzelsucht or moria :
pain reduces socially uninhibited and
 Psychomotor lack aunawerness of
retardation: number of their abnormal
movements, spoken behavior.
words and thought per  Loss of regards to
unit of time diminish. social conventions ,
Mild form abulia and only interested in
severe akinetic mutism. personal gratification.

58. DECREASED INHIBITION
1. Problems inhibiting incorrect/ineffective
responses & switching to a new strategy
2. Perseverates; not responsive to feedback
or changes in environment
3. Violates rules, expectancies; takes risks
4. Not adaptable
5. Decreased social inhibitons as well

59. DISINHIBITED SEXUALITY
 It is not unusual for a  Seizure activity arising
hypersexual, disinhibited from the deep frontal
frontal lobe injured regions have also been
individual to employ force. associated with
 spirited physical self- increased sexual
defense is probably the best behavior, including
strategy of the woman. Her sexual automatisms,
husband may have exhibitionism, gential
regressed to the cave-man manipulation, and
level, and she owes it to him masturbation
to be responsive at the
cave-women level. It may
not be agreeable at first, but
she will soon find it
exhilarating if
unconventional."

60. NEUROANATOMIC CORRELATION
 Motor  Attention
 Perseveration ->  Brainstem thalamic
Posteriolateral frontal system
dominant lobe and  Orbitofronal syndrome
connection to basal
ganglia  Frontolimbic link
 Posterior lesion ->  Loss of inhibition of
difficulty in organizing parietal lobe
 Anterior lesion ->  Echophenomenon and
dissociation between environmental
behavior and language dependency

61. FRONTAL LOBE HISTORY TAKING
 Personality changes (over familiar, tactless and
sexual indiscretions)
 Hyperorality
 Distractibility
 Poor motivation
 Inability to adapt to new situations
 Poor problem solving skills

62. FRONTAL LOBE TESTS
1. Attention
2. Memory
3. Abstraction
4. Judgment
5. Planning
6. Language
7. Motor sequencing

63. Tests of attention and memory
o Alternative sequence (e.g. copying MNMN)
o Luria‟s „fist-edge-palm‟ test (show 3X)
o Go/no-go:
o”tap once if I tap twice, don‟t tap if I tap
once”
o“tap for A”
oread 60 letters at 1/sec; N: < 2 errors

64. Tests of attention and memory cont‟
oDigit span
orepeat 3-52; 3-52-8; 3-52-8-67..” N: >5
o Visual grasp: “look away from stimulus”
o Recency test
o“recall sequence of stimuli / events”
o Imitation (of examiner) / utilization (of
objects presented)

65. Tests of abstraction and judgment
o Interpret proverbs (e.g.“the golden hammer
opens iron doors”)
o Explain why conceptually linked words are the
same (e.g. coat & skirt)
o Plan & structure a sequential set of activities
(“how would you bake a cake?”)
o Insight / reaction to own illness

66. Language tests
o Thurstone / word fluency test (“recite as many
words beginning with „F‟ in 1 min as you can,
then with „A‟, „S‟”); N: >15
o Repetition (Broca‟s vs transcortical)
o “Ball”
o “Methodist”
o “Methodist episcopal”
o “No if‟s end‟s or but‟s”
o “Around the rugged rock the ragged rascal ran”

67. MOTOR SEQUENCING: KINETIC MELODY
1. Hand position test (three-step hand sequence)
2. Rhythm tapping tasks
3. Go no go test
4. Copying tasks (multiple loops)

68. FRONTAL RELEASE SIGN
 Grasp reflex  Snout reflex
 Forceful grapping of
object on touching palm
 Palmomental
or sole
 Sucking reflex
 By touching the lips
 Glabellar tap
 Groping reflex
 Involuntary following with
hand/eye of moving
object
 Stimulus capture
 Utilization behavior

69. Formal Tests
• Abstract thinking and set shifting; L>R
• Wisconsin Card Sorting Test
• Visuo-motor track, conceptualization, set shift
• Trail Making
• Attention, shift sets; L>R
• Stroop Color & Word Test
• Planning
• Tower of London Test
• Block design
• Maze lest

70. Wisconsin Card Sorting Test
“Please sort the 60 cards under the 4 samples.
I won‟t tell you the rule, but I will announce every mistake.
The rule will change after 10 correct placements.”

71. Trail Making Test
5 B
A 4
6
1 C
2
3 D
7
Various levels of difficulty:
1. “Please connect the letters in alphabetical order as fast as you can.”
2. “Repeat, as in „1‟ but alternate with numbers in increasing order”

72. Stroop Color and Word Tests
RED BLUE ORANGE YELLOW
GREEN RED PURPLE RED
GREEN YELLOW BLUE RED
YELLOW ORANGE RED GREEN
BLUE GREEN PURPLE RED
“Please read this as fast as you can”

73. Tower of London Tests
Various levels of difficulty:
e.g. “Please rearrange the balls on the pegs, so that each peg has
one ball only. Use as few movements as possible”

74. FRONTAL PATHOLOGY
 Injury
 Tumor
 Abscess, infection
 Dementia
 Epilepsy
 Stroke
 Developmental

75. TRAUMATIC BRAIN INJURY
o Gunshot wound
o Closed head injury
o Widespread stretching and shearing of fibers
throughout
o Frontal lobe more vulnerable
o Contusions and intracerebral hematomas

76. FRONTAL LOBE INJURY
Attention disorder – Language
• Distractibility 1. Dynamic aphasia
Memory 2. Normal motor speech
• Poor “forgetting to 3. Normal repetition
remember” 4. Difficulty in
Thinking prepositioning
 Concrete 5. Difficulty in structuring
 Perseveration and sentence
stereotypy, 6. Lack of coherence
 unable to switch task 7. Socially inappropriate
and disinhibited

77. FRONTAL LOBE INJURY CONT.
Mood, affect, behavior
1. Reduced activity
2. Lack of drive and initiative
3. Lack of concern
4. Bouts of restlessness and uncoordinated behavior
5. Apathy, emotional blunting, indifference to the
surrounding
6. Bouts of euphoria
7. Disinhibition – irritability and aggression
8. Witzelsucht – inappropriate facetiousness and tendency
to pun

78. FRONTAL LOBE EPILEPSY
 Clinical Features  EEG
 Frequent seizure with clustering  May show no ictal or interictal
 Brief stereotyped seizure abnormality
 Nocturnal attacks  May show bilateral spike waves
 Sudden onset and cessation  May show focal changes often
 Absence of psychic aura widespread
 Absence of postictal confusion  Imaging/ pathology
 Rapid evolution with awareness  Hemartoma
lost at onset  Benign tumors
 Prominent complex bilateral motor  Gliomas
automatism involving lower limbs  Angioma
 Prominent ictal posturing and tonic  Dysplasia
spasm
 Post traumatic
 Versive head and eye turning
 Atrophy
 Bizarre automatism
 Tuberculoma
 Frequent secondary generalization
 Cysticercosis
 Status epilepticus common

79. FRONTAL LOBE AND PSYCHIATRY
 Schizophrenia :  Personality disorder:
 Involving dorsolateral
prefrontal cortex Antisocial Personality
 affective changes, disorder with
impaired motivation,
poor insight. and other impulsivity of frontal
"defect symptoms
 Evidence : lobe
Neuropathologic studies,
(23) in EEG studies, (24)  Attention deficit
in radiological studies
using CT measures, (25) syndrome with
with MRI, (26) and in
cerebral blood flow distractibility of frontal
(CBF) studies. lobe

80. FRONTAL LOBE DEMENTIA
 Trouble in maintaining normal  Language Problems
social and interpersonal  limited speech output, lack of
functioning. speech spontaneity, stereotyping of
phrases (ie., use of pat phrases
 They may violate rules of repeatedly and excessively),
politeness and may make perseveration (a meaningless
inappropriate remarks. persistence of verbal activity), a
 They may become emotionally decreased vocabulary, a
considerable amount of repetition,
aroused very easily. especially of brief words and
 Insensitivity – lack of consideration phrases.
to others.  Often there is jargon and instead of
being able to find the word to
 lack of restraint - stealing or describe an object, the person with
unsocial behaviour this disease will give a description
 Obsession – of it instead (ie., a "watch" referred
to as "something you tell the time
 Sexual misadventures,. with"). This means that the person
may not be able to name objects
 Kluver Bucy Syndrome early in the disease.
 hypersexuality, gluttony, and an  Eventually the person becomes
obsession to touch and seize any mute for periods and then
objects in the person's field of completely mute by the end of the
vision. Overeating may lead to disease.
considerable weight gain.

81. VASCULAR DISEASE
o Common cause especially in elderly
o ACA territory infarction
o Damage to medial frontal area
o MCA territory
o Dorsolateral frontal lobe
o ACom aneurysm rupture
o Personality change, emotional disturbance

82. FRONTAL LOBE DISEASE
 Degenerative diseases
– Pick‟s disease
– Huntington‟s disease
 Infectious diseases
– Neurosyphilis
– Herpes simplex encephalitis

83. FRONTAL LOBE DISEASE
 Tumors
– Gliomas, meningiomas
– subfrontal and olfactory groove meningiomas:
profound personality changes and dementia
 Multiple Sclerosis
– Frontal lobes 2nd highest number of plaques
– euphoric/depressed mood, Memory problems,
cognitive and behavioral effects

84. FRONTAL LOBE PATHOLOGY
Frontal lobe abscess
Meningioma

85. FRONTAL PATHOLOGY
Tuberous sclerosis Frontal glioblastoma