material for neuro-psychiatric aspect of frontal lobe

1. Presenter :Dr. Divyesh Baranwal
2nd Year RESIDENT

2. CONTENTS
1. Evolution & Anatomy
2. Physiology & Bed Side Tests
3. Neuro-Psychiatric problem of Frontal lobe
• Frontal lobe Syndromes
• Traumatic Brain Injury (frontal lobe)
• Fronto temporal Lobe Dementia
• Frontal Lobe Epilepsy
• Non convulsive Status Epilepticus of Frontal lobe
• Expressive aphasia
• In Various Psychiatric conditions
4. Take Home Message

3. Mammals Frontal Lobe Evolution
• 33% of Brain area
• Most recently evolved
• Well developed only in
primates
• Human species is due to
frontal lobe(PFC)
• Gives our capacity to feel
empathy, sympathy,
understand humor and
when others are being
ironic, sarcastic or even
deceptive.

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

5. Lateral surface frontal lobe
SULCI
– Vertical
• Central
sulcus
• Precentral
sulcus
- Horizontal
• Super frontal
sulcus
• Inf frontal
sulci
•GYRI
•Precentral gyrus
•Superior frontal gyrus
•Middle frontal gyrus
•Inf erior frontal gyrus

6. Medial surface Frontal lobe
• Between cingulate sulcus and superior medial margin of hemisphere
• Posterior part vertical sulcus

7. 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.

8. Functional Frontal Lobe Anatomy
Lateral sulcus/
Sylvian fissure
Central sulcus
B6 B4
Supplementary
motor area
(medially)
B 9, 10, 11, 12
Motor speech
area of Broca
Frontal eye field
B 44, 45
B 8
Premotor area Primary motor area
Prefrontal area
Motor cortex
1. Primary
2. Premotor
3. Supplementar
y
4. Frontal eye
field
5. Broca’s area
Prefrontal cortex
1. Dorsolateral
2. Medial
3. Orbitofrontal

9. MOTOR CORTEX…

10. Primary Motor Cortex
Motor fibres cross in medulla to opp. side
• 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: weakness in proximal
muscles on contralateral side

13. Supplementary Motor Cortex
• Input:
– cingulate gyrus,
– thalamus,
– sensory cortex
– prefrontal cortex
• Output:
– Premotor cortex,
– primary motor cortex
• Function:
– intentional preparation
for movement
– procedural memory
• Lesions:
– mutism,
– akinesia

14. Bedside test
• Motor strength – hand grip
• Motor speed – finger tapping
• poor performances – local lesions,
vascular
neoplastic pathology
degenerative disease.

15. Frontal eye fields
• Input:
– Parietal cortex
– Temporal cortex
• Output:
– Caudate nucleus
– Superior colliculus
– Paramedian pontine
reticular Formation (PPRF)
• Function:
– executive: selects target and
commands movement (saccades)
• Lesion:
– eyes deviate -ipsilaterally with
destructive lesion
-contralaterally with
irritating lesions

16. Bedside test
1. follow the movement of a finger
- left to right
- up and down.
2. look from - left to right
- up and down
(with no finger to follow).
Note inability to move or jerky movement.

17. Broca’s speech area (area 44,45)
• Input: Wernicke’s area
• Output: primary motor cortex
• Function:
– speech production (dominant
hemisphere);
– emotional, melodic component
of speech (non-dominant)
• Lesions:
– motor aphasia;
– Monotonous speech

18. Functional anatomy of pre frontal cortex

19. Dorsolateral prefrontal cortex
• Connections:
– motor / sensory convergence areas,
– thalamus,
– globus pallidus,
– caudate nucleus,
– substrantia nigra
• Functions:
Subcortical structures
• motor planning, organization, and
regulation
• monitors and adjusts behavior
using ‘working memory’
• Lesions:
– executive function deficit;
– disinterest
–  attention to relevant stimuli

20. Dorsomedial prefrontal cortex
• Connections:
– temporal cortex
– parietal cortex
– thalamus, caudate, GP, substantia nigra,
– cingulate cortex
• Functions:
– motivation, initiation of activity
• Lesions:
– Paucity of spontaneous movement and
gesture,
– Sparse verbal output (repetition may be
preserved),
– Lower extremity weakness
– Incontinence

21. Orbital prefrontal cortex
• Connections:
– temporal cortex
– parietal cortex
– thalamus, globus pallidus , caudate,
– insula,
– amygdala
• Part of limbic system
• Function:
– emotional input,
– arousal,
– suppression of distracting signals
– Decision making
• Lesions:
• Disinhibited, impulsive behaviour
• Inappropriate ocular affect,
• euphoria ,emotional lability,
• Poor judgment and insight,
• Distractibility
• Orbitofrontal syndrome (BA 11,12)
•The limbic system
•Hippocampus
•Amygdalae
• anterior thalamic nuclei
•Septum
•limbic cortex
•Fornix,
•functions including
•Emotional behavior,
•motivation,
•long-term memory,
•olfaction

22. Bedside tests
 patient dress or behave in a way
-which suggests lack of
concern with the feelings of
others
-without concern to accepted
social customs.
 Go/no-go Test -asked to make a response to
one signal (the Go signal)
not to respond to another
signal (the no-go signal)
 The Stroop Test -Examines the ability to inhibit
responses

24. Bedside tests
 Make an appointment and arrive on time?
 Able to give a coherent account of current problems
 Digit span, days of the week or months of the year
backwards
 Controlled oral word association test (COWAT):
FAS verbal fluency test - as many as words in one
minute, starting with F,
then A, then S

25.  Alternating hand sequences:- one hand’s palm upwards
other place palm downwards,
asked to reverse these rapidly.
 Patient taps twice with one fist with the other, then after
the rhythm is established, the patient is asked to change
over the number of beats
 frontal lobe deficits poorly perform on these tests & unable
to follow simple instructions

26.  Commonly employed tests include Controlled Oral
Word Association Test (Benton, 1968) and the
Wisconsin Card Sorting Tests (Heaton, 1985)
Wisconsin Card Sorting Test
“Please sort the 60 cards under the 4 samples (stimulus cards).
I won’t tell you the rule, but I will announce every mistake.
The rule will change after 10 correct placements.”

27. NEUROTRANSMITTERS
Dopamine
Nor-epinephrine
Serotonin

28. Neurotransmitters: Dopaminergic tracts
• Origin: ventral tegmental
area in midbrain
• Projections:
4 1
– prefrontal cortex (mesocortical
tract
– limbic system (mesolimbic
tract)
• Function:
– reward;
– motivation;
– spontaneity;
– arousal
Mesocortical
tract
2
3

29. Neurotransmitters: Norepinephrine tracts
• Origin:
– locus ceruleus in brainstem
– lateral brainstem
tegmentum
• Projections: anterior
cortex
• Functions:
– alertness,
– arousal,
– cognitive processing of
somatosensory information

30. Neurotransmitters: Serotonin tracts
• Origin: raphe nuclei in brainstem
• Projections: number of forebrain
structures
• Function:
– minor role in prefrontal
cortex;
– sleep,
– mood, anxiety,
– feeding

31. Frontal lobe function
Motor Cognitive Behavior Arousal
Voluntary
movements
Memory Personality Attention
Planning,
Initiation
Problem
solving
Social and
sexual
Spontaneity Judgment Impulse control
Language
Expression
Abstract
thinking
Mood and affect
Eye movements

32. Left and Right
• Left
-for language related
movements
-convert thoughts
into words
• Right
-for non verbal abilities
Order and planning

33. NEUROPSYCHIATRIC DISORDER OF
FRONTAL LOBE
• Frontal lobe Syndrome
• Traumatic Brain injury (Frontal lobe)
• Frontal lobe Dementia
• Frontal lobe & Memory
• Frontal lobe & Arousal
• Frontal lobe Epilepsy
• Non-convulsive Status Epilepticus of Frontal lobe
• Expresive Aphasia
• Psychiatric illness & Frontal lobe

34. Frontal Lobe Syndromes

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

37. • FRONTAL LOBE SYNDROME cause
PREFRONTAL LESIONS
prominent personality changes
without loss of intelligence, motor, sensory
& memory functions
Frontal lobe syndrome
Features not unique to frontal
Executive syndrome
(Baddely & Wilson)
lobe pathology
Lack of one to one
correspondence b/w behavior &
location of lesion

38. • The DLPFC is concerned with planning,
strategy formation, and executive function.
• Abnorm in DLPFC
– apathy,
– personality changes,
– abulia, and
– lack of ability to plan or to sequence.
– patients have poor working memory
• The frontal operculum = expression of language.
– left frontal operculum lesion = Broca aphasia and defective verb retrieval,
– right opercular lesions = expressive aprosodia.
Aprosodia is a neurological condition characterized by the
inability of a person to properly convey or interpret emotional prosody.

39. • Personality changes include – impulsiveness
a jocular attitude
sexual disinhibition
complete lack of concern
for others.
• superior mesial lesions -develop akinetic mutism.
• inferior mesial (basal forebrain) lesions –
anterograde & retrograde
amnesia, confabulation.
•

40. • supplementary/ premotor area: transcortical motor aphasia,
impairment of rapid skilled manual
movements
• Left prefrontal injury : loss of executive & planning
function,depression,
• Right prefrontal injury : left sided extinction & neglect
blunted or labile affect,
impersistence, disinhibition,
confabulation, alien hand sign

41. •executive function
deficit;
•disinterest /
emotional reactivity;
• attention to
relevant stimuli
•emotional lability,
•disinhibition,
•distractibility,
• ‘hyperkinesis’
•apathy;
•decreased
drive/awareness
/spontaneous
movements;
•akinetic-abulic&
mutism
Medial
Lateral
Orbital
Frotnal Lobe Syndromes

42. Frontal lobe syndrome –Etiology
• Mental retardation
• Traumatic brain injury
• Brain tumors
• Degenerative dementias including
– Alzheimer disease,
– Dementia with lewy bodies,
– Parkinsonian dementias,
– Frontotemporal dementias
• Cerebrovascular disease
• Multiple sclerosis
• Schizophrenia
• Major depression
• Acute alcohol intoxication and drug abuse

43. Clinical picture
• change in personality.
• Lack of initiation and spontanity.
• Sluggish responses.
• Occasionally hyperactive and restless.
• Mood is often euphoric and out of keeping
with situation.
• Irritability and outbursts are common.
• Loss of finer senses.
• Judgements impaired.
• Fail to plan and carry through ideas.

44. Negative symptoms :
• Lack of initiative & spontaneity
• Diminution of motor activity (sluggish response)
• Task left unfinished
• New initiatives rarely undertaken
• Capacity to function independently is affected
• when vigorously urged or constrained by structural
situation pt may function quite well
(Cognition &intellect unaffected)

45. positive symptoms
• Restless
• Hyperactive lack of goal directed behavior
• Mild euphoria
• Tendency to joke/pun
• State of excitement, pressured speech
• Overfamilarity
• Outburst of irritability
• Such changes rarely sustained but if pt. left he
become inert & apathetic.

46. Social awareness & behavior
• Less concerned with acts
• Loss of social graces
• Coarsening of personality
• Lack of normal tact & restraints
• Little concern about future
• Fails to plan & to carry out ideas
• Sexual disinhibition
• little insight

47. • Wisconsin card sorting test : to test cognition
• Concrete thinking or lack of abstraction
– Proverb test
– Similarity test
Bifrontal lesion
Bad judgment
Difficulty in Planning &
carrying out multistepped
behavior,
adaptation to new
situation,
understanding & reacting
social cues
Lack of awareness,
attentional deficits,
understanding,
sensitivity &
communication skills
Family,
relation,
occupation
problems

48. Unilateral Frontal lobe Syndrome
1. Contralateral
hemiplegia
2. Conjugate deviation of
eye to side of lesion
3. Personality change
(Pseudopsychotic)
a. Mood elevation,
talkativeness
b. Tendency to joke, lack of
tact, silly and childish
behavior
4. Difficulty in adaptation
5. Loss of initiative
6. Unable to solve problem
7. Anosmia and blindness

49. Dominant Frontal lobe
1. Loss of motor speech
2. Unable to write
3. Apraxia
4. Dysphoria
• Marked inactivity & affects
intellectual processes and behavior.
• Cannot change verbal instructions
into acts, especially complex or
symbolic instruction.
• Decreased spontaneity of speech
• Memory deficits for verbal
material;
due to defective registration.

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

51. TRAUMATIC BRAIN INJURY

52. Introduction
To define a traumatic brain injury is simply an injury to the brain due to
trauma to the head. A brain bleed, fractured skull, or coma as a result of
head injury are brain injuries that are easy to identify.

53. What are the causes of traumatic brain injury
 Falls
 Vehicle crashes
 Sports injuries
 Birth trauma
• Incidence- 1.7 billion/year
• Children 0 - 4 year, adolescents 15-19 years, >65 years most likely for TBI.
• A study of the role of calcium ion influx into the damaged neuron for cell
death and brain tissue swelling.
• NINDS (National Institute of Neurological Disorders and Stroke)
researchers have shown, that giving specialized chemicals can reduce cell
death caused by calcium ion influx

54. Traumatic Brain Injury Symptoms
 Physical Symptoms include
• Loss of vision
• Dizziness
• Headaches
• Blurred vision
 Cognitive symptoms
• Poor concentration
• Amnesia
• Disorientation
• Short term memory loss
 Emotional symptoms
• Depression
• Agitation
• Changes in personality
• Irritability
• Changes in appetite

55. Long-term prognosis
• Immediate post-injury complications
• Parkinson's disease and other motor problems
• Alzheimer's disease
• Dementia etc.

56. Frontotemporal Lobe Dementia
• FTLD is a neurodegenerative disease : frontal and temporal lobe
• Typical age of onset - 50 to 60 yrs.
• In contrast to Alzhiemer Disease, in which memory loss is usually the first
symptom.
• The initial symptoms of FTLD often involve changes in personality, behavior,
affective symptoms, and language function.
• The core features of FTLD as defined by the Neary criteria (Neary et al.,
1998) are
– early decline in social and personal conduct
– emotional blunting
– loss of insight.

57. Frontal lobe & memory
• Focal frontal injury may not produce a severe amnesic
disorder.
• It can cause more subtle, memory deficits as an
impairment in control of memory.
• Prefrontal cortex is crucial for monitoring and control of
memory processes, both at encoding and at time of
retrieval.

58. Frontal lobe and arousal
• Right frontal lobe damage -> bilateral inhibitory
influences on attention and arousal
• Left frontal damage -> unopposed right
cerebral inhibition -> akinesia

59. Frontal Lobe Epilepsy
• Characterized by recurrent seizures arising from the frontal lobes.
• In most centers frontal lobe epilepsy accounts for 20-30% of
operative procedures involving intractable epilepsy.
• Pt. with frontal lobe seizures present with a clear epileptic
syndrome or with unusual behavioral or motor manifestations
that are not immediately recognizable as seizures - may be
associated with facial grimacing, vocalization, or speech arrest.
• Seizures often bizarre and may be diagnosed incorrectly as
psychogenic.

60. • IInd most common type of epilepsy
• Brief recurring seizures often while pt is sleeping
 2 forms :-
• Simple partial seizures : not affect awareness & memory.
• Complex partial seizures : affects awareness & memory.
 Symptoms :-
• Physical/emotional aura of tingling, numbness, tension
• Fear expressed on face
• Tonic posturing & clonic movements
• Often misdiagnosed as psychogenic seizures
• More specific symptoms depends on area of frontal cortex
involved

61. • Supplementary motor area - aura precedes tonic posturing
which is u/l, asymmetrical
Motor symptoms : facial grimacing, complex
automatism like kicking, pelvic
thrusting
Vocal symptoms : laughing, yelling or speech arrest
• Primary motor cortex - jacksonian seizures spread to adjacent
area.
Usually tonic, myoclonic movement with
speech arrest.
• Medial frontal, Cingulate gyrus, Orbitofrontal, Frontopolar region:
Short repetitive thrashing, pedaling, thrusting, laughing, screaming,
crying
Motor symptoms accompanied by emotional feelings &
viscerosensory symptoms
Misdiagnosed as psychological seizures

62. • Dorsolateral cortex : tonic posturing & clonic movements
c/l head turning & eye deviation
• Operculum : symptoms involve head & digestive tract as
swallowing, mastication
fearful, clonic facial movements & speech arrested
• Diagnosis : EEG, MRI
• Treatment :
• Medical : anticonvulsants as carbamazepine, phenytoin,
gabapentine, lamotrigine, topiramate etc.
• Surgical : frontal lobectomy, multiple subpial transections, gamma
knife radiosurgery, vagus nerve stimulator
• Diet : ketogenic diet, high fat & low carbohydrate

63. FRONTAL LOBE NONCONVULSIVE STATUS
EPILEPTICUS &Types
Type 1
• Mild cognitive function
impaired with mood
disturbance.
• Alertness normal , no postictal
amnesia.
• Confabulation and impaired
complex activities.
• EEG show U/L frontolateral or
frontocentral ictal activity.
Type 2
• Cyclical spatiotemporal
disorientation , behaviour
disturbances , motor and verbal
perseveration.
• Alteration of awareness with
postictal catatonic stupor and
amnesia.
• EEG show B/L Frontotemporal
and Frontocentral ictal activity,
initially started U/L then to B/l.

64. • Inclusion criteria for FLNCSE:
– Alteration of cognitive function with or without
confusion for 1 hrs.
– Focal low amplitude myoclonus or motor seizure limited
to slight head and eye daviation or both.
– Video EEG conformationof NCSE
– Ictel EEG discharges over Fp1,Fp2,lateral,medial frontal
– Ictal SPECT show clear hyperperfusion of frontal region
compare to postictal scan.
FLNCSE often occurs in pt. With no H/o of epilepsy and
indicate a frontal lesion in >1/3 cases.

65. Expressive aphasia
• Expressive aphasia(Broca's aphasia) –
by damage or developmental
issues in (area 44,45).
• Speech difficult to initiate,
non-fluent, labored,
halting
• writing is difficult as well.
• Language reduced to disjointed words & sentence
construction is poor.
• Comprehension is generally preserved.
• Patients on recovery say he knew what he wanted to
say but could not express themselves.

66.  Psychiatric Illness & Frontal lobe –
proposed associations
– Schizophrenia
– Depression
–ADHD
–OCD
– Alcohol

67. Schizophrenia
• Symptoms can be aggregated in 3 broad clusters (Liddle 1987)
1. Psychomotor poverty syndrome
Affecting speech & movement, blunting of affect
Decreased rCBF in left prefrontal & parietal cortex

68. 2. Reality distortion syndrome
Positive symptoms hallucinations & delusions
Increase rCBF in left parahippocampal gyrus & contiguous
area
3. Disorganization syndrome
Thought disorder & inappropriate affect
Increase resting rCBF in anterior cingulate region

69. Schizophrenia & frontal lobe
• Evidence
– EEG studies,
– CT scan,
– MRI,
– cerebral blood flow studies.
– Hypofrontality in PET.

71. Frontal lobe & depression
• Area mediating depression become excessively active
another region not may become underactive
• Rt. frontal lobe increased activity indicate negative
moods
• Requires the cognitive capacity to appreciate and thus
feel depressed
• Reductions in left frontal activity & injuries to left
frontal lobe associated with depression, "psycho-motor“
retardation, apathy, irritability, and blunted
mental functioning.

72. Frontal lobe & ADHD
• Executive functions of frontal cortex include:
– Problem solving
– Attention
– Reasoning
– Planning
• ADHD - deficits in frontal lobe functions
• Right frontal lobe -smaller in children with ADHD
• 3 regions that cause ADHD symptoms:
1. Prefrontal cortex (command center)
2. Caudate nucleus
3. Globus pallidus

73. Frontal lobe & OCD
• OCD due to abnormalities of frontal lobe,
basal ganglia,
cingulum.
• OCD is caused by communication disturbance between
frontal lobe and basal ganglia.
• On PET Scan, OCD pt burned energy more quickly in the
frontal lobe and cingulate pathway.
• low levels of serotonin in OCD.

74. Frontal lobe & alcoholism
• Prefrontal cortex linked to impulse control,
so damage to this region lead to loss of inhibitions.
• Two neurotransmitters- gamma-amino butyric acid (GABA)
& dopamine responsible for loss of
impulse control.
• Increases dopamine release & enhances pleasure feeling.
• Alcohol co binds with GABA to GABA receptor and
hyperpolarize the post synaptic neuron, so ability of the
neurons in the frontal lobes to inhibit socially unacceptable
behavior is reduced.

75. Take Home Message
• Frontal lobe forms about 1/3 part of each cerebral
hemisphere
• Phylogenetically newest part
• 2 major parts
• (a) precentral/motor cortex :- planning, execution &
control of c/l body movements
• (b) prefrontal cortex :- emotion control center & home of
our personality
• Bilateral prefrontal cortex lesion leads to frontal lobe
sydrome
• Features of FTLD as defined by the Neary criteria

76. • Rt. frontal lobe damage -> b/l inhibitory influences on
attention and arousal
• Lt. frontal damage -> akinesia
• Frontal lobe epilepsy IInd most common type of epilepsy
symptoms depends on area of frontal cortex involved
• FLNCSE is of two types.
• Schizophrenic symptoms arise bcoz of variable rCBF in cortex.
• Area mediating depression become excessively active
• OCD is caused by problems in communication between the
frontal lobe and basal ganglia.
• Prefrontal cortex linked to impulse control & damage to this
region lead to loss of inhibitions.

77. Q. A 65 years old attend his physician because he noticed from
past 3 weeks he had dragging his rt. Foot when walking. On
physical examination there is increase tone of flexor muscle of
rt. Arm, and when he walks, tend to hold his rt. Arm adducted
and flexed . he also had his rt. Fist tightly clenched. He also have
difficulty in flexing his rt. Knee and hip . their is weakness and
increased tone of rt. Leg muscle. he was noted to move his rt.
Leg in a semicircle and place forefoot on the ground before the
heel. Pt. had a cerebrovascular lesion involving cerebral cortex.
.
which area of cortex involve to cause these symptoms?
• Ans: cerebrovascular lesion involving the left precentral gyrus

78. Q : A 53 years professor received a severe head injury while rock
climbing . During the ascent his companions ice axe fall from his
belt & struck the professor’s head, causing a depressed # of frontal
bone. After convalescing from his accident , professor returned to his
work. it become obvious to faculty that the professor’s social
behaviour had changed dramatically. Previously a smartly dressed
man, now had an unkempt appearance. the organisation of
department started to deteriorate rapidly. Finally he was removed from
college after being found one morning urinating into the trashbasket
in one of the classroom.
Tell for the condition which explain the professors’s altered behaviour.
• Ans: lesion involving both frontal lobe of cerebrum specially pre frontal cortex
(frontal lobe syndrome)

79. Thank You