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7/28/2019 4th recapitulatefrontallobe-120429144834-phpapp02

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NEUROANATOMY &

NEUROPSYCHIATRIC ASPECTS OF

FRONTAL LOBE


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CONTENTS

Anatomy of frontal lobe

Neuroanatomy

Functional anatomy

Motor cortex

Prefrontal cortex Neurotransmitters

Frontal lobe syndromes

Disease associated with frontal lobe lesions

Psychiatric illnesses

Frontal lobe epilepsy

Frontal lobe & memory


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Cerebral Features:

Sulci Small grooves dividing the gyriCentral Sulcus Divides the Frontal Lobe from the Parietal Lobe

Fissures Deep grooves, generally dividing largeregions/lobes of the brain

Longitudinal Fissure Divides the two Cerebral HemispheresTransverse Fissure Separates the Cerebrum from theCerebellum

Sylvian/Lateral Fissure Divides the Temporal Lobe from theFrontal and Parietal Lobes

Gyri Elevated ridges winding around the brain.


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Longitudinal Fissure

Transverse Fissure

Sylvian/Lateral

Fissure

Central Sulcus

Specific Sulci/Fissures:

* Note: Occasionally, the Insula is considered the fifth lobe. It is located deep to the

Temporal Lobe.


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.IT IS DIVIDED INTO TWO HEMISPHERES, EACH OF

WHICH IS DIVIDED INTO FOUR LOBES

Cerebral Cortex - The outermost layer of gray matter makingup the superficial aspect of the cerebrum


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Functional Frontal Lobe Anatomy

Phylogenetically youngest part ofbrain

Located deep to the frontal bone

of the skull Largest of all lobes

SA: ~1/3 / hemisphere

3 major areas in each lobe Dorsolateral aspect

Medial aspect

Inferior orbital aspect


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FRONTAL LOBE

Motor cortex

Primary motor

Premotor

Supplementary motor

Frontal eye field

Brocas speech area

Prefrontal cortex Dorsolateral

Medial

Orbitofrontal


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Functional Frontal Lobe Anatomy

Lateral sulcus/

Sylvian fissure

Central sulcus

Motor speech

area of Broca

Frontal eye field

BA 44, 45

BA 9, 10, 11, 12

BA 8

Primary motor areaPremotor area

Prefrontal cortex

BA 6,8 BA 4

Supplementary

motor area

(medially BA 6)


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Prefrontal area consist of paralimbic (anterior cingulate

gyrus & posterior orbitofrontal) and high order associationcortex (dorsolateral convexity & anteromedial surface)

This area was considered silent

Prefrontal

cortex


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Functional regions of the left frontal lobe (lateral

view)

functional regions of the right frontal lobe (medial

view)


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Motor Cortex

Primary motor cortex BA 4 Input: thalamus, BG, sensory,

premotor

Output: motor fibers to brainstem

and spinal cord

Function: executes design into

movement

Lesions:tone (spasticity); power; fine motor function on

contra lateral side


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Bedside test :-

Motor strength of hand grip

Motor speed on finger tapping Diagnostically, poor performances suggest local lesions

such as vascular or neoplastic pathology, or a

generalized lesion such as a degenerative disease.


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Motor Cortex

Premotor cortex BA 6

Input: thalamus, BG, sensory cortex

Output: primary motor cortex

Function: sensorimotor integration, stores motor

programs; controls coarse postural movements

Lesions: moderate weakness in proximal muscles on

contralateral side, spasticity, grasp reflex, buccofacialapraxia, inability to make use of sensory feedback in the

performance of smooth movements


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Bedside test :-

1. Sensorimotor abilities are tested by asking the

patient touch each finger to the thumb in succession as

rapidly as possible (Watch for speed and dexterity) 2. Apraxia can be tested by asking the patient to "blow

a kiss" and to demonstrate the use of a shovel.

Poor performance carries the diagnostic implications


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MOTOR CORTEX

Supplementary motor area medial aspect of BA 6

Input: cingulate gyrus, thalamus, sensory & prefrontal cortex

Output: premotor, primary motor

Function: involved in motivated behavior, initiation and goal directed behavior,intentional preparation for movement; procedural memory Lesions: transient transcortical motor aphasia (mutism), impairment in motor initiation

(akinesis); impaired rapid alternating movements, grasp reflex, alien hand syndrome


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MOTOR CORTEX

Frontal eye fields BA 8 with some area of 9 & 6 Input: parietal / temporal (what is target); posterior / parietal cortex (where is

target)

Output: caudate; superior colliculus; paramedian pontine reticular formation

Function: selects target and commands movement (saccades)

Lesion: eyes deviate ipsilaterally with destructive lesion and contralaterally withirritating lesions


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Bedside test:-

1. Ask the patient to follow the movement of a finger

from left to right and up and down.

2. Ask the patient to look from left to right, up and down(with no finger to follow).

Note inability to move or jerky movement .


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MOTOR CORTEX Brocas speech area BA 44, 45

Input:wernickes area

Output: primary motor cortex

Function: speech production (dominant hemisphere); emotional melodic component of

speech (non-dominant)

Lesions: motor aphasia; dysprosody (monotonus speech)

Speech is sparse, slow, hesitant, disturbance of rhythm and articulation, difficulty in word

finding, wrong words are chosen & often mispronounced, perseveration, agrammatism

Pt recognize his mistakes & tries to correct them but becomes impatient

Phrase length is small :- telegraphic language

Writing is also affected with speech, but comprehension is preserved


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PREFRONTAL CORTEX

Orbital prefrontal cortex BA 10 & 11 Connections: temporal, parietal, thalamus, GP, caudate, SN, insula, amygdala

Part of limbic system

Function: It mediates empathic, civil and socially

appropriate behavior, emotional input, arousal,suppression of distracting signals Lesions: emotional lability, disinhibition, distractibility, hyperkinesis

Much of the personality change described in cases offrontal lobe injury is due to lesions in this area


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BEDSIDE TESTS:

1. Does the patient dress or behave in a way which

suggests lack of concern with the feelings of others orwithout concern to accepted social customs.

2. Test sense of smell - coffee, cloves etc.

3. Go/no-go Test- The patient is asked to make aresponse to one signal (the Go signal) and not to respond

to another signal (the no-go signal)

4. The Stroop Test - Examines the ability of the patient to

inhibit responses


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PREFRONTAL CORTEX

Medial prefrontal cortex

Connections: temporal, parietal, thalamus, caudate, GP, substantia nigra, cingulate

Functions: motivation, initiation of activity

Lesions: apathy; decreased drive/ awareness/ spontaneous movements; akinetic-

abulic syndrome & mutism


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PREFRONTAL CORTEX Dorsolateral prefrontal cortex BA 9 and the lateral aspect of 10 and most of

area 46 Connections: motor / sensory convergence areas,

thalamus, GP, caudate, SN

Functions: executive functioning include the integration of

sensory information, the generation of a range of responsealternatives to environmental challenges, the selection of themost appropriate response, maintenance of task set,sequential ordering of data, self-evaluation of performance

and the selection of a replacement responses if the firstapplied response fails monitors and adjusts behavior usingworkingmemory

Lesions: executive function deficit, apathy, aspontaneity

and impoverished & stereotyped thought process


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TESTS:-

1. Is the patient able to make an appointment and arrive on

time?

2. Is the patient able to give a coherent account of current

problems

Digit span, days of the week or months of the yearbackwards

Controlled oral word association test (COWAT): the patient

is asked to FAS verbal fluency test - produce as many words as

possible, in one minute, starting with F, then A, then S


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Alternating hand sequences :- one hand is placed palm

upwards and the other is place palm downwards, and thepatient is then asked to reverse these positions as rapidly

as possible or

Patient taps twice with one fist and once with the other,then after the rhythm is established, the patient is asked to

change over the number of beats

Patients with frontal lobe deficits usually perform poorly on

these tests, often unable to follow relatively simple

instructions

NECESSARY


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NECESSARY

WHERE UNCERTAINTY REMAINS

Commonly employed tests include Controlled Oral Word

Association Test (Benton, 1968) and the Wisconsin CardSorting Tests (Heaton, 1985)

Wisconsin Card Sorting Test

Please sort the 60 cards under the 4 samples (stimulus cards).

I wont tell you the rule, but I will announce every mistake.

The rule will change after 10 correct placements.


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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


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NEUROTRANSMITTERS

Norepinephrine tracts

Origin: locus ceruleus in brainstem and lateral brainstem tegmentum

Projections: anterior cortex

Functions: alertness, arousal, cognitive processing of somatosensory information


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NEUROTRANSMITTERS

Serotonergic tracts

Origin: raphe nuclei in brainstem

Projections: number of forebrain structures

Function: minor role in prefrontal cortex; sleep, mood, anxiety, feeding


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A 45 year old man with b/l prefrontal strokes was found to

have

Normal neurological examination

Slightly flattened affect

Lack of spontaneity, mental slowness

Increased left sided motor tone

Neuropsychological testing normal intelligence & memory

Demoted at his managerial jobs d/t ineffective work habits

Unable to adequately supervise children Often lost his temper

Inattention

Bad judgment


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CLINICAL PICTURE : varies among pts.

Individual features depends on Nature & time course of pathological process

Lateralization

Localization Extent of involvement among subcortical & callosal

fibers

Secondary effect of raised ICT

Kliest first suggested that components of frontal lobe

syndrome may be related to specific regional involvement


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Orbital lesions cause : Disinhibition, failure to appreciate

consequences of ones action, euphoria (effect on personality

& social behavior) Lesions of dorsolateral convexity cause :Apathy,

aspontaneity, impoverished & stereotyped thought process

Left prefrontal injury : loss of executive & planning function,

depression,

When supplementary/ premotor area affected : transcortical

motor aphasia, impairment of rapid skilled manual movements

Right prefrontal injury : left sided extinction & neglect, bluntedor labile affect, impersistence, disinhibition, confabulation,

alien hand sign


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Patients with classical frontal lobe syndrome usually have b/l

lesions encompassing both orbital & lateral cortex

Negative symptoms :

Lack of initiative & spontaneity

General diminution of motor activity (sluggish response)

Task are left unfinished

New initiatives are rarely undertaken

Capacity to function independently in life is affected

Cognition & intellect may remain unaffected

Yet when vigorously urged or constrained by structural

situation pt may function quite well


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Other pts may show positive symptoms

Restless Hyperactive yet lack of goal directed behavior

Mild euphoria

Tendency to joke/pun

State of excitement, pressured speech

Overfamilarity

Outburst of irritability

Such changes are rarely sustained and when left to

themselves these pts become inert & apathetic


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Social awareness & behavior

Less concerned with consequences of his acts Loss of social graces

Coarsening of personality

Lack of normal adult tact & restraints

Little concern about his future

Fails to plan ahead, to carry out ideas

Sexual disinhibition

Pt usually has little insight into the changes


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Inability to plan & execute multistepped behavior is

hallmark of prefrontal lesions

Can manage simple one or two step command Evaluated by asking the pt & spouse, do things get

started but not completed?

Ask pt about planning a vacation, changing a tyre. Test of sequential motor & visual patterns

Reciprocal coordination test

Sequential motor test Visual pattern completion task


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Wisconsin card sorting test : shift cognition sets

Perseveration is another symptom of frontal lobe disorder

but not pathognomic Concrete thinking or lack of abstraction

Proverb test

Similarity test

Bifrontal lesions

Bad judgment resulting

from deficits affecting

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

Abulia : Poverty of thought action & emotion is common


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Abulia : Poverty of thought action & emotion is common

with large midline and b/l dorsofrontal lesion

Abulia is characterized by loss of spontaneity & will power

They comprehend the question, hesitate, delay respond,

seem to ignore or give yes no answer

Severely abulic pt do not speak unless spoken, do not

move unless they are hungry or ready to void & may beincontinent

Tidal waves of emotional & motor behavior (brief rage,

irritability, hyperactivity) may emerge from tranquil sea ofabulia (placid, apathetic, disinterested)

Perseveration v/s abulia :- Random A test.


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DISEASES COMMONLY ASSOCIATED WITH

FRONTAL LOBE LESIONS

Traumatic brain injury Gunshot wound

Closed head injury

Contusions and intracerebral hematomas

Vascular disease Common cause especially in elderly

ACA territory infarction

Damage to medial frontal area

MCA territory

Dorsolateral frontal lobe

ACom aneurysm rupture

Personality change, emotional disturbance


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Frontal Lobe seizures

Tumors

Multiple sclerosis Degenerative diseases

Picks disease

Huntingtons disease

Infectious diseases Neurosyphilis

Herpes simplex encephalitis


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Psychiatric Illness proposed associations Schizophrenia

Depression

ADHD

OCD

Antisocial personality disorder

O


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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

2. Reality distortion syndrome


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2. Reality distortion syndrome

Positive symptoms hallucinations & delusions

Increase rCBF in left parahippocampal gyrus & contiguous area

3. Disorganization syndrome

Thought disorder & inappropriate affect

FRONTAL LOBE & DEPRESSION


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FRONTAL LOBE & DEPRESSION Depression is often a realistic reaction to misfortunes

Requires the cognitive capacity to appreciate and thus feeldepressed

In consequence :

Area of the brain mediating the depression may become

excessively active

Whereas yet another region of the cerebrum which is expressingthe depression may become underactive

Right frontal lobe demonstrated increased activity in response tonegative moods

Not only reductions in left frontal activity, but injuries to the leftfrontal lobe have been consistently associated with depression,

"psycho-motor" retardation, apathy, irritability, and blunted

FRONTAL LOBE & ADHD


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FRONTAL LOBE & ADHD Executive functions offrontal cortex include:

Problem solving

Attention

Reasoning

Planning

ADHD suffers usually have deficits in these functions

Right frontal lobe is smaller in children with ADHD

Problems in the circuit between three regions are theunderlying mechanisms that cause ADHD symptoms

1. Prefrontal cortex (command center)

2. Caudate nucleus


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FRONTAL LOBE & OCD

OCD could be due to abnormalities of the frontal lobe,

basal ganglia, and cingulum

OCD is caused by problems in communication between

the frontal lobe and basal ganglia

On PET Scan, OCD pt burned energy more quickly in thefrontal lobe and cingulate pathway

Abnormally low levels of serotonin found in people with

OCD

ALCOHOLISM


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ALCOHOLISM

Prefrontal cortex has been linked to impulse control

because damage to this region of the brain can lead toloss of inhibitions

Two neurotransmitters, gamma-amino butyric acid

(GABA) and dopamine are responsible for the loss of

impulse control in those who consume alcohol

Alcohol increases the amount of dopamine release and

enhances the normal feeling of pleasure

Alcohol co binds with GABA to GABA receptor andhyperpolarize the post synaptic neuron, so ability of the

neurons in the frontal lobes to inhibit socially

unacceptable behavior is reduced


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EPILEPSY IInd most common type of epilepsy

Brief recurring seizures often while pt is sleeping 2 forms :-

Simple partial seizures : does 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

Supplementary motor area : somatosensory aura precedes tonic


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Supplementary motor area : somatosensory aura precedes tonicposturing 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 that spread to adjacentarea, often triggers to IInd round of seizures

Usually tonic, myoclonic movements with speech arrest

Medial frontal, Cingulate gyrus, Orbitofrontal, Frontopolar region :

Short repetitive thrashing, pedaling, thrusting, laughing, screaming,crying

Motor symptoms are accompanied by emotional feelings &


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Dorsolateral cortex : tonic posturing & clonic movements

c/l head turning & eye deviation

Operculum : symptoms involve head & digestive tract as swallowing,

mastication

Person is fearful, clonic facial movements & speech is often 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 : keto enic diet hi h fat & low carboh drate


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FRONTAL LOBE & MEMORY Focal frontal injury does not produce a severe amnesic

disorder It can cause more subtle, yet definable, memory deficits

in form of an impairment in the control of memory

Prefrontal cortex appears to be crucial for the monitoringand control of memory processes, both at the time of

encoding and at the time of retrieval

Significant impairment was observed on tests of free

recall (80% of studies), cued recall (50% of studies) andeven on tests of recognition (8% of studies)


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TO CONCLUDE

Frontal lobe forms about 1/3 part of each cerebral hemisphere

Phylogenetically newest part

Previously considered silent brain, but now found to produce

variety of symptoms

2 major parts

(a) precentral/motor cortex :- planning, execution & control of

c/l body movements

(b) prefrontal cortex :- emotion control center & home of ourpersonality

Bilateral prefrontal cortex lesion leads to frontal lobe sydrome


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TO CONCLUDE

Left prefrontal cortex lesion :- psuedodepressive type Right prefrontal cortex lesion :- psuedopsychotic type

Inability to plan & execute multistepped behavior is hallmark of

prefrontal lesion

Frontal lobe functions are deranged in schizophrenia,

depression, ADHD, OCD, antisocial personality disorder,

alcoholism etc.

Frontal lobe epilepsy is often misdiagnosed as psychogenicseizures

prefrontal cortex is crucial for control of memory during

encoding & recall


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