frontal lobe and its functions

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  • 1. Anatomy Circuits Physiology Normal functioning and Assesment Syndromes

2. Largest of all lobes SA: ~1/3 / hemisphere 3 major areas in each lobe Dorsolateral aspect Medial aspect Inferior orbital aspect 3. Premotor area Primary motor area B6 B4 Central sulcus Supplementary motor area (medially)Frontal eye fieldB8Prefrontal areaB 9, 10, 11, 12 Lateral sulcus/ Sylvian fissureMotor speecharea of Broca B 44, 45 4. MOTOR CORTEX PREFRONTAL CORTEX Primary Dorsolateral Area Premotor Medial Supplementary Orbitofrontal Frontal eye field Brocas speech area 5. PRIMARY MOTOR CORTEX (4) Input: thalamus, BG, sensory, premotor Output: motor fibers to brainstem and spinalcord Function: executes design into movement Lesions: / tone; power; fine motorfunction on contra lateral side 6. PREMOTOR CORTEX (6) Input: thalamus, BG, sensory cortex Output: primary motor cortex Function: stores motor programs; controls coarsepostural movements Lesions: moderate weakness in proximal muscleson contralateral side 7. SUPPLEMENTARY MOTOR (Med 6) Input: cingulate gyrus, thalamus, sensory &prefrontal cortex Output: premotor, primary motor Function: intentional preparation for movement;procedural memory Lesions: mutism, akinesis; speech returns but itis non-spontaneous 8. FRONTAL EYE FIELDS (8) Input: parietal / temporal (what is target);posterior / parietal cortex (where is target) Output: caudate; superior colliculus;paramedian pontine reticular formation Function: executive: selects target andcommands movement (saccades) Lesion: eyes deviate ipsilaterally withdestructive lesion and contralaterally withirritating lesions 9. BROCAS SPEECH AREA Input: Wernickes Output: primary motor cortex Function: speech production (dominanthemisphere); emotional, melodic component ofspeech (non-dominant) Lesions: motor aphasia; monotone speech 10. ORBITAL PREFRONTAL CORTEX (10,11) Connections: temporal,parietal, thalamus, GP,caudate, SN, insula, amygdala Part of limbic system Function: emotional input, arousal, suppressionof distracting signals Lesions: emotional lability, disinhibition,distractibility, hyperkinesis 11. DORSOMEDIAL PREFRONTAL CORTEX Connections: temporal,parietal, thalamus,caudate, GP, substantia nigra, cingulate Functions: motivation, initiation of activity Lesions: apathy; decreased drive/ awareness/spontaneous movements; akinetic-abulicsyndrome & mutism 12. DORSOLATERAL PREFRONTAL CORTEX (9,10,46) Connections: motor / sensory convergenceareas, thalamus, GP, caudate, SN Functions: monitors and adjusts behaviorusing working memory Lesions: executive function deficit; disinterest/ emotional reactivity; attention to relevantstimuli 13. DOPAMINERGIC TRACTS Origin: ventral tegmental area in midbrain Projections: prefrontal cortex (mesocortical tract)and to limbic system (mesolimbic tract) Function: reward; motivation; spontaneity; arousal 14. NOREPINEPHRINE TRACTS Origin: locus ceruleus in brainstem and lateralbrainstem tegmentum Projections: anterior cortex Functions: alertness, arousal, cognitiveprocessing of somatosensory info 15. SEROTONIN TRACTS Origin: raphe nuclei in brainstem Projections: number of forebrain structures Function: minor role in prefrontal cortex;sleep, mood, anxiety, feeding 16. Brodmann area 4 Bedside tests: Motor strength of hand grip. The patient is asked to grip the examiners fingers. Strength should be roughly equal, with greater strength on the dominant side. It should be difficult for the examiner to free her/his fingers. Diagnostically, poor performances suggest local lesions such as vascular or neoplastic pathology, or a generalized lesion such as a degenerative disease. (Peripheral nerve lesion must, of course, be excluded.) 17. Brodmann area 6 It is involved in sensorimotor integration. Lesions cause inability to make use of sensoryfeedback in the performance of smooth movementsand apraxia. Apraxia may also be a result of lesions of otherareas (parietal lobe). Bedside tests: 1. Sensorimotor abilities are tested by asking the patienttouch each finger to the thumb in succession as rapidly aspossible. Watch for speed and dexterity. 2. Apraxia can be tested by asking the patient to "blow akiss" and to demonstrate the use of an object. Poor performance carries the diagnostic implications as forthe motor cortex above. 18. Brodmann area 8, with some area 9 and 6. Voluntary eye movements are of two types. Pursuit movement occurs when the eyes to followmoving objects. Saccadic eye movements are used to followimaginary points. Bedside test: 1. Ask the patient to follow the movement of a fingerfrom 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. 19. Brodmann area 9 and the lateral aspect of 10 and most ofarea 46. The executive functions include the integration of sensory information, the generation of a range of response alternatives toenvironmental challenges, the selection of the most appropriate response, maintenance of task set, sequential ordering of data, self-evaluation of performance the selection of a replacement responses if the first appliedresponse fails. The executive functions largely determine the ability of theindividual to cope with the continuous, but ever changingchallenges of the environment. Thus, the patients ability to make an appointment and toarrive on time is valuable information. So too, is the ability of the patient to give a comprehensiveaccount of her/himself and the reasons for theconsultation. 20. Bedside tests: 1. Is the patient able to make an appointment andarrive on time? 2. Is the patient able to give a coherent account ofcurrent problems and the reason for the interview? Is there evidence of thought disorder? 3. Digit span, days of the week or months of the yearbackwards. 4. Controlled oral word association test (COWAT): the patient is asked to produce as many words as possible,in one minute, starting with F, then A, then S. Proper nouns and be previously used words with a differentsuffix are prohibited (Benton, 1968). Other categorical fluency tests include naming animals,fruits and vegetables (Monsch et al, 1992) 21. Normal provide more than ten items for each of thesecategories, while a patient score less than eight. Common errors include perseveration (repeatingwords which have already been given either duringthe task at hand or an earlier task). There may also be inappropriate utterances. (Thesealso suggest disinhibition which is discussed underorbitofrontal cortex, below.) 5. Alternating hand sequences. One example is that one hand is placed palm upwards andthe other is place palm downwards, and the patient is thenasked to reverse these positions as rapidly as possible. Another example is that the backs of the hands are bothplaced downwards, but one hand is clenched and the otheris open, then the patients is asked to close the open handand open the closed hand, and keep reversing the postureof the hands as rapidly as possible 22. A final example is that the patient taps twice with one fist and once withthe other, then after the rhythm is established, the patient is asked tochange over the number of beats (the fist which first tapped twice nowtaps only once). Patients with frontal lobe deficits usually perform poorly on these tests,often being unable to follow the relatively simple instructions. 6. Formal neuropsychological may be necessary where uncertaintyremains. Commonly employed tests include Controlled Oral Word Association Test (Benton,1968) and the Wisconsin Card Sorting Tests (Heaton, 1985). Head injury and dementing illnesses may result in severe impairment ofthe executive functions.Schizophrenia often has thought disorder as a major feature and theexecutive functions tests are usually also at least mildly affected.Depressive disorder may be associated with poor performance on verbalfluency tests during the acute phase, which normalizes with remission(Trichard, et al., 1995). 23. Brodmann areas 10 and 11 It mediates empathic, civil and socially appropriate behavior(Mega and Cummings, 1994).Much of the personality change described in cases of frontallobe injury (Phineas Gage being the most famous) is due tolesions in this area.Patients may become irritable, labile, disinhibited and fail torespond to the conventions of acceptable social behavior.Similar changes may occur with lesions of subcortical element ofthe frontal-subcortical circuit, as with caudate damage inHuntingtons disease. Increased concern about social behavior and contamination hasbeen associated with increased orbitofrontal and caudatemetabolism. This has been reported with lesions of the globus pallidus and inobsessive compulsive disorder. 24. Bedside tests: 1. Does the patient dress or behave in a way whichsuggests lack of concern with the feelings of othersor 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 (theGo signal) and not to respond to another signal (the no-gosignal). The most basic is to ask the patient to tap theirknee when the examiner says, Go and to make noresponse when the examiner says, Stop. The task may be made more demanding by reversing thecustomary meaning of signals. An example is to ask the patient to tap the knee when theexaminer says "Stop" and not to tap when the examinersays "Go" (Malloy and Richardson, 1994). 25. 4. The Stroop Test (Stroop, 1935) Failure of inhibition may complicate headinjury, other destructive lesions (including dementingprocesses) and schizophrenia.Failure of inhibition is found in impulse control andpersonality disorder (particularly of the antisocialtype).Depressive disorder may manifest irritability, and hasbeen associated with poor performance on the StroopTest (Trichard et al, 1995). Obsessive compu