Presenter :Dr. Divyesh Baranwal 2nd Year RESIDENT

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

CONTENTS

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.

FRONTAL LOBE SURFACES

A. Lateral surface1. Posterior - Central sulcus2. Inferio-Posterior – sylvian

fissure.

B. Medial surfaceC. Orbital surface

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

Medial surface Frontal lobe

• Between cingulate sulcus and superior medial margin of hemisphere• Posterior part vertical sulcus

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.

Functional Frontal Lobe Anatomy

Lateral sulcus/Sylvian fissure

Central sulcus

Motor speech area of Broca

Frontal eye field

B 44, 45

B 9, 10, 11, 12

B 8

Primary motor areaPremotor area

Prefrontal area

B6 B4

Supplementarymotor area(medially)

Motor cortex1. Primary 2. Premotor3. Supplementar

y 4. Frontal eye

field5. Broca’s area

Prefrontal cortex1. Dorsolateral 2. Medial 3. Orbitofrontal

MOTOR CORTEX…

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

Motor fibres cross in medulla to opp. side

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

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

Bedside test

• Motor strength – hand grip

• Motor speed – finger tapping

• poor performances – local lesions,

vascular

neoplastic pathology

degenerative disease.

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

Bedside test1. 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.

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

Functional anatomy of pre frontal cortex

Dorsolateral prefrontal cortex• Connections:

– motor / sensory convergence areas,– thalamus, – globus pallidus, – caudate nucleus, – substrantia nigra

• Functions: • motor planning, organization, and

regulation• monitors and adjusts behavior using

‘working memory’

• Lesions: – executive function deficit; – disinterest– attention to relevant stimuli

Subcortical structures

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

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

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

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

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

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.”

NEUROTRANSMITTERS

Dopamine

Nor-epinephrine

Serotonin

Neurotransmitters: Dopaminergic tracts

• Origin: ventral tegmental area in midbrain

• Projections: – prefrontal cortex (mesocortical

tract– limbic system (mesolimbic

tract)

• Function: – reward; – motivation; – spontaneity; – arousal

Mesocortical tract

2

3

4 1

Neurotransmitters: Norepinephrine tracts

• Origin: – locus ceruleus in brainstem – lateral brainstem

tegmentum

• Projections: anterior cortex

• Functions: – alertness, – arousal, – cognitive processing of

somatosensory information

Neurotransmitters: Serotonin tracts

• Origin: raphe nuclei in brainstem

• Projections: number of forebrain structures

• Function:

– minor role in prefrontal cortex;

– sleep, – mood, anxiety, – feeding

Frontal lobe functionMotor 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

Left and Right

• Left-for language related movements

-convert thoughts into words

• Right-for non verbal abilities Order and planning

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

Frontal Lobe Syndromes

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

• FRONTAL LOBE SYNDROME cause PREFRONTAL LESIONS prominent personality changes without loss of intelligence, motor,

sensory & memory functions

Frontal lobe syndrome

Executive syndrome(Baddely & Wilson)

Features not unique to frontal lobe pathology

Lack of one to one correspondence b/w behavior &

location of lesion

• 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.

• 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.

•

• 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

•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

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

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.

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)

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.

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

• Wisconsin card sorting test : to test cognition• Concrete thinking or lack of abstraction

– Proverb test– Similarity test

Bifrontal lesionBad 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

Unilateral Frontal lobe Syndrome1. Contralateral

hemiplegia

2. Conjugate deviation of eye to side of lesion

3. Personality change (Pseudopsychotic)a. Mood elevation,

talkativenessb. 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

Dominant Frontal lobe1. 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.

Bilateral Frontal lobe lesion1. Pseudodepressed -

Apathy, Abulia, akinetic mutism

2. Impulsiveness and

irritability3. Inability to sustain

attention4. Decomposition of gait

5. Sphincter disturbance

6. Active learning & solving problem , judgment

7. Excessiveness of utilization behavior

8. Frontal release signa. Snoutb. Suckc. Palmomentald. Graspe. Brow tapping

TRAUMATIC BRAIN INJURY

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.

Introduction

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

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

Long-term prognosis

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

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.

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.

Frontal lobe and arousal

• Right frontal lobe damage -> bilateral inhibitory influences on attention and arousal

• Left frontal damage -> unopposed right cerebral inhibition -> akinesia

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.

• 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

• 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, cryingMotor symptoms accompanied by emotional feelings & viscerosensory symptomsMisdiagnosed as psychological seizures

• 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

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.

• 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.

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.

Psychiatric Illness & Frontal lobe – proposed associations

–Schizophrenia–Depression–ADHD–OCD–Alcohol

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

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

Schizophrenia & frontal lobe

• Evidence – EEG studies,– CT scan, – MRI, – cerebral blood flow studies. – Hypofrontality in PET.

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.

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 nucleus3. Globus pallidus

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.

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.

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

• 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.

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

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)

Thank You