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Similar to Frontal lobe relation to psychiatry
Frontal lobe relation to psychiatry
- 1. Presenter :Dr. SIVAANOOP MDPsychiatry Resident . Institute Of Mental Health,Hyderabad. FRONTAL LOBE- RELATION TO PSYCHIATRY
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- 3. Frontal lobe surfaces A.Lateral surface 1.Posterior - central sulcus 2.Inferio-posterior – sylvian fissure. B. Medial surface C. Orbital surface
- 4. Lateral surface frontallobe • Sulci • Vertical • Central sulcus • Precentral sulcus - Horizontal • Super frontal sulcus • Inf frontal sulci •GYRI •Precentral gyrus •Superior frontal gyrus •Middle frontal gyrus •Inferior frontal gyrus
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- 6. Orbital surface--- frontallobe • 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.
- 7. Functional frontal lobeanatomy 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 Supplementary motor area (medially) 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. Primary motor cortex Motorfibres cross in medulla to opp. side
- 10. • Primary motorcortex BA 4 – Input: thalamus, BG, sensory cortex, premotor area – Output: motor fibers to brainstem and spinal cord – Function: executes design into movement – Lesions:tone (spasticity); power; fine motor function on contra lateral side
- 11. Bedside tests •Motor strength– hand grip •Motor speed – finger tapping •Poor performances – local lesions, •Pathology - Vascular - neoplastic - Degenerative disease.
- 12. Pre motor cortex •Input: • Thalamus, • Basal ganglion • Sensory cortex • Output: primary motor cortex • Function: • Stores motor programs; • Controls coarse postural movements • Lesions: -Difficulty in performing skilled movements with little loss of strength. - Apraxia- Loss of the ability to execute or carry out learned purposeful movements
- 13. BED SIDE TESTS 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.
- 14. 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
- 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 tests 1. Followthe 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 ofpre frontal cortex
- 19. 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
- 20. Bedside tests 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 .
- 21. DEVELOPED TO ASSESSABSTRACT REASONING ABILITY AND THE ABILITY TO SHIFT COGNITIVE STRATEGIES IN RESPONSE TO CHANGING ENVIRON- MENTAL CONTINGENCIES, IS ALSO CONSIDERED A MEASURE OF THE EXECUTIVE FUNCTIONS EMPLOYED AS A CLINICAL NEUROPSYCHOLOGICAL INSTRUMENT TO SPECIFICALLY MEASURE BRAIN DYSFUNCTIONS AFFECTING THE FRONTAL LOBES. Wisconsin Card Sorting Test Drewe EA. The effect of type and area of brain lesion on Wisconsin Card Sorting Test performance. Cortex. 1974;10:159–70.
- 22. 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
- 23. Orbital prefrontal cortex•Connections: • Temporal cortex • Parietal cortex • Thalamus, globus pallidus , caudate, • Insula, • Amygdala • 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)
- 24. Bedside tests Patient dressor behaviour -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 response.
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- 26. Frontal lobe function MotorCognitive 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
- 27. Neuropsychiatric disorders of frontallobe • 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
- 28. Frontal lobe syndrome–etiology • Traumatic brain injury • Brain tumors • Degenerative dementias including • Alzheimer disease, • Dementia with lewy bodies, • Parkinsonian dementias, • Fronto temporal dementias • Cerebro vascular disease • Multiple sclerosis • Schizophrenia • Major depression • Acute alcohol intoxication and drug abuse
- 29. Clinical picture • Changein personality. • Lack of initiation and spontaneity. • 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. • Judgments impaired. • Fail to plan and carry through ideas.
- 30. 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
- 31. 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
- 32. Bilateral frontal lobelesion 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 reflex B. Rooting reflex C. Palmomental reflex D. Palmar Grasp E. Glabellar tap
- 33. Traumatic brain injury --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. 1)EDH 2)SDH 3)Contusion,Axonal Shearing lesions
- 34. Traumatic brain injurysymptoms Emotional symptoms Depression Agitation Changes in personality Irritability Changes in appetiteCognitive symptoms Poor concentration Amnesia Disorientation Short term memory loss Physical symptoms include Loss of vision Dizziness Headaches Blurred vision
- 35. Long-term complications •Immediate post-injurycomplications •Parkinson's disease and other motor problems •Alzheimer's disease •Dementia etc.
- 36. Frontotemporal lobe dementia •FTLDis a neurodegenerative disease : frontal and temporal lobe •Typical age of onset - 50 to 60 yrs. •In contrast to alzhiemers 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.
- 37. 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.
- 38. Frontal lobe andarousal •Right frontal lobe damage -> bilateral inhibitory influences on attention and arousal •Left frontal damage -> unopposed right cerebral inhibition -> akinesia
- 39. Frontal lobe epilepsy •Characterizedby recurrent seizures arising from the frontal lobes. •In most centers frontal lobe epilepsy accounts for 20-30% of operative procedures involving intractable epilepsy.
- 40. Fronto lobe epilepsy •2nd most common type of epilepsy • Brief recurring seizures often while pt is sleeping 2 types :- • 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
- 41. Frontal lobe nonconvulsivestatus epilepticus •Two main types of frontal lobe NCSE •-Absence status- •-Complex partial status epilepticus-
- 42. Frontal lobe nonconvulsivestatus epilepticus &types Type 1 • Mild cognitive function impaired with mood disturbance. • Alertness normal , no postictal amnesia. • Confabulation and impaired complex activities. • EEG shows 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 shows b/l frontotemporal and frontocentral ictal activity, initially started u/l then to b/l.
- 43. Expressive aphasia • Expressiveaphasia(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.
- 44. Psychiatric illness &frontal lobe – proposed associations –Schizophrenia –Depression –Adhd –Ocd –Alcohol
- 45. Schizophrenia 1. Psychomotor povertysyndrome Affects speech & movement, blunting of affect Decreased regional central blood flow in left prefrontal &parietal cortex
- 46. Schizophrenia & frontal lobe •Evidence • Eeg studies, • Ct scan, • Mri, • Cerebral blood flow studies. • Hypofrontality in pet.
- 48. Schizophrenia • Mri hasbeen useful in revealing subtle structural brain abnormalities in schizophrenia patients, including ventricular enlargement, volume reduction in the frontal and parietal lobes, and gray matter reduction of medial temporal lobe structures • It is unknown whether the brain abnormalities observed with mri in schizophrenia are confounded by chronicity or whether there is a continual degenerative process. • Chronic schizophrenia patients may demonstrate pathology secondary to chronic neuroleptic medication and long-term institutionalization. Heschl's gyrus and planum temporale regions drawn on a coronal MR slice (left), and a 3D rendering shown overlayed on an axial MR slice. Shenton, ME et al. A review of MRI findings in schizophrenia Schizophrenia Research 49 (2001) 1-52.
- 49. Frontal lobe &depression • Rt. Frontal lobe increased activity negative moods • Reductions in left frontal activity & injuries to left frontal lobe depression, "psycho-motor“ retardation, apathy, irritability, and blunted mental functioning. • In brain-imaging studies using PET scans, depressed people abnormally low activity in the prefrontal cortex, and more specifically in its lateral, orbitofrontal, and ventromedial regions. • Bilateral hypo metabolism of orbital-inferior prefrontal cortex and anterior temporal cortex seen in depressed subjects.
- 50. Frontal lobe &ADHD •ADHD - deficits in frontal lobe functions. • structural and chemical alterations in the prefrontal cortex. • pre frontal cortex is smaller in size than that of individuals who do not have the disorder. •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
- 51. 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. • OCD patients were hypermetabolic in the left orbital frontal gyri and in both sides of the caudate nuclei •On pet scan, OCD pt burned energy more quickly in the frontal lobe and cingulate pathway. •Low levels of serotonin in OCD.
- 52. Frontal lobe &alcoholism •Prefrontal cortex linked to impulse control, So damage to this region leads 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.
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- 54. • Frontal lobeforms 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 syndrome • Features of FTLD is defined by the neary criteria
- 55. • Rt. Frontallobe 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 • Schizophrenic symptoms arise bcoz of variable rcbf in cortex. • Depressed people display abnormally low activity in the prefrontal cortex • 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.
- 56. References •Netter’s atlas ofHuman Anatomy •Snells Clinical neuro anatomy-7th edition •Synopsis of psychiartry- Kaplan and sadocks-11th edition •Lishman’s –textbook of Neuropsychiatry-4th edition • FRONTAL LOBES, BASAL GANGLIA, TEMPORAL LOBES--THREE SITES FOR SCHIZOPHRENIA? BUCHSBAUM MS PMID 2287928 • REGIONAL CEREBRAL BLOOD FLOW IN MONOZYGOTIC TWINS DISCORDANT AND CONCORDANT FOR SCHIZOPHRENIA. BERMAN KF1, TORREY EF, DANIEL DG, WEINBERGER DR PMID 1360197 • FRONTAL LOBE DYSFUNCTION IN SECONDARY DEPRESSION
- 57. REFERENCES • DREWE EA.THE EFFECT OF TYPE AND AREA OF BRAIN LESION ON WISCONSIN CARD SORTING TEST PERFORMANCE. CORTEX. 1974;10:159–70 • FRONTAL LOBE DYSFUNCTION IN OBSESSIVE- COMPULSIVE DISORDER AND MAJOR DEPRESSION: A CLINICAL-NEUROPSYCHOLOGICAL STUDY PAOLO CAVEDINI, STEFANO FERRI ET.AL