Frontal lobe


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neuroanatomy & neuropsychiatric aspects of frontal lobe by anant kumar rathi

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Frontal lobe

  1. 1. Neuroanatomy &neuropsychiatric aspects of Frontal LobePresentor GuideDr. Anant Kumar Rathi Dr. D. K. Vijayvergia
  2. 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. 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 largeregions/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. 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. 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. 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. 7. Frontal lobe • Motor cortex Prefrontal cortex – Primary motor – Dorsolateral – Premotor – Medial – Supplementary motor – Orbitofrontal – Frontal eye field – Broca’s speech area
  8. 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. 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. 10. Functional regions of the left frontal lobe functional regions of the right frontal lobe(lateral view) (medial view)
  11. 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. 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. 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 movementsLesions: moderate weakness in proximal muscles oncontralateral side, spasticity, grasp reflex,buccofacial apraxia, inability to make use of sensoryfeedback in the performance of smooth movements
  14. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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 lesionsBad judgment resulting from deficits affecting Lack of awareness, Family, Planning & carrying out attentional deficits, relation, multistepped behavior, understanding, occupation adaptation to new sensitivity & problemssituation, understanding communication skills & reacting social cues
  38. 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. 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. 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. 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. 42. • Frontal Lobe seizures• Tumors• Multiple sclerosis• Degenerative diseases – Pick’s disease – Huntington’s disease• Infectious diseases – Neurosyphilis – Herpes simplex encephalitis
  43. 43.  Psychiatric Illness – proposed associations – Schizophrenia – Depression – ADHD – OCD – Antisocial personality disorder
  44. 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. 45. 2. Reality distortion syndrome Positive symptoms hallucinations & delusionsIncrease rCBF in left parahippocampal gyrus & contiguous area 3. Disorganization syndrome Thought disorder & inappropriate affect Increase resting rCBF in anterior cingulate region
  46. 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. 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 symptoms1. Prefrontal cortex (command center)2. Caudate nucleus3. Globus pallidus
  48. 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. 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. 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. 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. 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. 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. 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. 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