This document discusses the anatomy, functions, and clinical presentations of lesions involving the frontal lobe, including the motor cortex, prefrontal cortex, and their roles in executive function, social behavior, language, and more. Specific tests are described to evaluate functions like motor control, language, problem-solving, and emotional regulation that are mediated by the frontal lobe. A variety of clinical syndromes can result from frontal lobe lesions depending on the location and extent of the damage.

1. Neuroanatomy &
neuropsychiatric aspects of
Frontal Lobe
Presentor Guide
Dr. Anant Kumar Rathi Dr. D. K. Vijayvergia

2. 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

3. Cerebral Features:
• Gyri – Elevated ridges “winding” around the brain.
• Sulci – Small grooves dividing the gyri
– Central Sulcus – Divides the Frontal Lobe from the Parietal Lobe
• Fissures – Deep grooves, generally dividing large
regions/lobes of the brain
– Longitudinal Fissure – Divides the two Cerebral Hemispheres
– Transverse Fissure – Separates the Cerebrum from the
Cerebellum
– Sylvian/Lateral Fissure – Divides the Temporal Lobe from the
Frontal and Parietal Lobes

4. Specific Sulci/Fissures:
Central Sulcus
Longitudinal Fissure
Sylvian/Lateral
Fissure
Transverse Fissure
* Note: Occasionally, the Insula is considered the fifth lobe. It is located deep
to the Temporal Lobe.

5. Cerebrum - The largest division of the brain. It is
divided into two hemispheres, each of which is divided
into four lobes
• Cerebral Cortex - The outermost layer of gray matter
making up the superficial aspect of the cerebrum

6. Functional Frontal Lobe Anatomy
• Phylogenetically youngest
part of brain
• 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

7. Frontal lobe
• Motor cortex Prefrontal cortex
– Primary motor – Dorsolateral
– Premotor – Medial
– Supplementary motor – Orbitofrontal
– Frontal eye field
– Broca’s speech area

8. Functional Frontal Lobe Anatomy
Premotor area Primary motor area
BA 6,8 BA 4
Central sulcus
Supplementary
motor area
(medially BA 6)
Frontal eye field
BA 8
Prefrontal cortex
BA 9, 10, 11, 12
Lateral sulcus/
Sylvian fissure
Motor speech
area of Broca
BA 44, 45

9. • Prefrontal area consist of paralimbic (anterior
cingulate gyrus & posterior orbitofrontal) and high
order association cortex (dorsolateral convexity &
anteromedial surface)
• This area was considered “silent”
Prefrontal
cortex

10. Functional regions of the left frontal lobe functional regions of the right frontal lobe
(lateral view) (medial view)

11. 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

12. • 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.

13. 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,
buccofacial apraxia, inability to make use of sensory
feedback in the performance of smooth movements

14. • 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

15. 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

16. 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 with
irritating lesions

17. • 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.

18. Motor Cortex
• Broca’s speech area BA 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; 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

19. 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 of
frontal lobe injury is due to lesions in this area

20. Bedside tests:
• 1. Does the patient dress or behave in a way which
suggests lack of concern with the feelings of others
or without concern to accepted social customs.
• 2. Test sense of smell - coffee, cloves etc.
• 3. Go/no-go Test- The patient is asked to make a
response 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

21. 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

22. 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
response alternatives to environmental challenges, the
selection of the most appropriate response,
maintenance of task set, sequential ordering of data,
self-evaluation of performance and the selection of a
replacement responses if the first applied response fails
monitors and adjusts behavior using ‘working memory’
– Lesions: executive function deficit, apathy,
aspontaneity and impoverished & stereotyped
thought process

23. Bedside 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 year
backwards
• 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

24. • Alternating hand sequences :- one hand is placed palm
upwards and the other is place palm downwards, and
the patient 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

25. • Formal neuropsychological tests may be necessary
where uncertainty remains
• 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.”

26. 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

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

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

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

30. • 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

31. • 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

32. • Orbital lesions cause : Disinhibition, failure to appreciate
consequences of one’s 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,
blunted or labile affect, impersistence, disinhibition,
confabulation, alien hand sign

33. • 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

34. • 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

35. • 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

36. • 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

37. • 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 Lack of awareness, Family,
Planning & carrying out attentional deficits, relation,
multistepped behavior, understanding, occupation
adaptation to new sensitivity & problems
situation, understanding communication skills
& reacting social cues

38. • 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
be incontinent
• Tidal waves of emotional & motor behavior (brief
rage, irritability, hyperactivity) may emerge from
tranquil sea of abulia (placid, apathetic, disinterested)
• Perseveration v/s abulia :- Random A test.

39. • Classical case reports
• The Case of Phineas Gage (Harlow 1868)
 tamping iron blown through
skull: L frontal brain injury
 excellent physical recovery
 dramatic personality change:
„no longer Gage‟:stubborn,
lacked in consideration for
others, unreliable, lacking in
social skills, had profane
speech, failed to execute his
plans

40. • Utilisation behavior (Lhermitte 1986)
• Observed pt with frontal lobe lesion in complex
everyday life situation
• He noted lack of personal autonomy with an excessive
dependence on social & physical environment
(environmental dependency syndrome)
• Decisions of pts actions were not made by themselves
• Social & physical environments issue the order to use
them even the pt has neither idea or nor intend to use
them

41. 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

42. • Frontal Lobe seizures
• Tumors
• Multiple sclerosis
• Degenerative diseases
– Pick’s disease
– Huntington’s disease
• Infectious diseases
– Neurosyphilis
– Herpes simplex encephalitis

43.  Psychiatric Illness – proposed associations
– Schizophrenia
– Depression
– ADHD
– OCD
– Antisocial personality disorder

44. 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

45. 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

46. Frontal lobe & depression
• Depression is often a realistic reaction to misfortunes
• Requires the cognitive capacity to appreciate and thus feel
depressed
• In consequence :
• Area of the brain mediating the depression may become
excessively active
• Whereas yet another region of the cerebrum which is
expressing the depression may become underactive
• Right frontal lobe demonstrated increased activity in
response to negative moods
• Not only reductions in left frontal activity, but injuries to
the left frontal lobe have been consistently associated with
depression, "psycho-motor" retardation, apathy, irritability,
and blunted mental functioning

47. Frontal lobe & ADHD
• Executive functions of frontal 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 the
underlying mechanisms that cause ADHD symptoms
1. Prefrontal cortex (command center)
2. Caudate nucleus
3. Globus pallidus

48. 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
the frontal lobe and cingulate pathway
• Abnormally low levels of serotonin found in people
with OCD

49. Frontal lobe & alcoholism
• Prefrontal cortex has been linked to impulse control
because damage to this region of the brain can lead
to loss 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 and
hyperpolarize the post synaptic neuron, so ability of
the neurons in the frontal lobes to inhibit socially
unacceptable behavior is reduced

50. Frontal lobe 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

51. • Supplementary motor area : somatosensory 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 that spread to
adjacent area, 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 &
viscerosensory symptoms
• Often misdiagnosed as psychological seizures

52. • 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 : ketogenic diet, high fat & low carbohydrate

53. 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
monitoring and 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)
and even on tests of recognition (8% of studies)

54. 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
our personality
• Bilateral prefrontal cortex lesion leads to frontal lobe
sydrome

55. 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 psychogenic
seizures
• prefrontal cortex is crucial for control of memory during
encoding & recall