Frontallobe dr prashant mishra


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frontal lobe ppt
svs medical college

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  • B. Mesial Syndrome - Bilateral mesial prefrontal damage involving supplementary motor and cingulate cortex (Brodmann areas 24, 25, 32, 33 and mesila 6, 8, 9) produces an amotivational, akinetic state with motor programming deficits manifesting clinically as apractic disturbances. Unilateral mesial or mild bilateral disease yields lesser degrees of difficulty in the initiation and sustaining of motor and mental activity. A common cause is anterior cerebral artery infarction due to spasm from subarachnoid hemorrhage.Medial frontal syndrome (akinetic) Paucity of spontaneous movement and gesture Sparse verbal output (repetition may be preserved) Lower extremity weakness and loss of sensation Incontinence
  • Orbitofrontal Syndrome - Damage in Brodman areas 11, 12 results in prominent affect disturbances. Emotional lability and decreased impulse control contribute to poor social integration. Problems such as loss of control of anger and inappropriate laughing, crying or sexuality are often observed. Attention capacity is usually preserved, frontal release signs (i.e. snout, suck, palmomental reflexes) are absent and the patient is typically aware of the problem but unable to control their reflexive inappropriate behavior. The most common cause of the orbital syndrome is head trauma with contra coup damage. Olfactory groove meningiomas can also present with similar complaints.Orbitofrontal syndrome (disinhibited) Disinhibited, impulsive behavior (pseudopsychopathic) Inappropriate jocular affect, euphoria Emotional labilityPoor judgment and insight Distractibility
  • Understanding the functional anatomy of the frontal lobes and their linkages with key subcortical structures is critical to putting together this picture. The discussion here will summarize the work of others and put it into clinical context.For a more extensive discussion, refer to the work of Cummings and Houk and their collaborators.40–42 There is wide acceptance that there are five brain circuits originating in the frontal lobes and linking them as functional units to subcortical structures.40–42 Two of these have primarily motor functions: one originates in the supplemental motor accessory area and is involved in the planningof movement; the other originates in the frontal eye fields and is involved in eye motion. The latter two circuits were originally described in association with Parkinson’s disease to explain the motor dysfunction of that condition.40 They appear to have little to do with the behaviors referred to as frontal lobe syndrome. Three other circuits originating in the frontal lobes appear to be the brain circuits whose dysfunction may underlie the syndromes in question. These include the dorsolateral prefrontal circuit, the lateral orbitofrontal circuit, and the anterior cingulum circuit (Figure 2).These three circuits have several common features. First, they process and integrate information from disparate brain regions. Second, each one is anatomically discrete, even though they share the same brain structures: cortical origin in the frontal lobe, the striatum, the globuspallidus, the substantianigra, and the thalamus. Third, their internal neurochemistry is similar (Figure 2). Fourth, they have progressively greater spatial constraint downward from cortex to subcortex. Fifth, they are functionally closed and parallel but communicate with other brain areas at each of the structural levels already mentioned, thus receiving external input at several points. Each circuit serves as the final step before the expression of both simple and complex behaviors.The common internal neurochemical organization of each loop is illustrated in Figure 2.40–42 Known external neurochemical modulators include dopamine, serotonin, and acetylcholine (Figure 2). The external modulators may explain the success of some of the medications used to treat these disturbances.Functionally, these circuits serve some aspect of executive function, the set of “cognitive skills responsible for the planning, initiation, sequencing, and monitoring of complex goal-directed behavior.”43 Critically, executive function is associated with both the initiation and the modulation of behavior in that both lack of initiation (motivation) and dyscontrol of behavior might be concurrent features of executive dyscontrol. Executive function is also associated with working memory,44 memory retrieval, 45 and meta-cognitive functions, such as the “theory of mind.”46 Given the anatomic segregation of function in their frontal lobe origins,47 each circuit may servedifferent aspects of executive control. For example, the anterior cingulum circuit appears to be central to the motivation of behavior.36–38 The dorsolateral prefrontal circuit serves organizational aspects of executive functioning by integrating information, focusing attention, and deciding on response.40–42 The lateral orbitofrontal circuit is critical to the integration of limbic and emotional information into contextually appropriate behavioral responses.
  • The dopamine pathways in the brainDopamine is transmitted via three major pathways. The first extends from the substantianigra to the caudate nucleus-putamen (neostriatum) and is concerned with sensory stimuli and movement. The second pathway projects from the ventral tegmentum to the mesolimbic forebrain and is thought to be associated with cognitive, reward and emotional behaviour. The third pathway, known as the tubero-infundibular system, is concerned with neuronal control of the hypothalmic-pituatory endocrine systemFigure 45-3 Dopaminergic neurons in the brain stem and hypothalamus.A. Dopaminergic neurons in the substantianigra (A9 group) and the adjacent retrorubral field (A8 group) and ventral tegmental area (A10 group) provide a major ascending pathway that terminates in the striatum, the frontotemporal cortex, and the limbic system, including the central nucleus of the amygdala and the lateral septum.B. Hypothalamic dopaminergic neurons in the A11 and A13 cell groups, in the zonaincerta, provide long descending pathways to the autonomic areas of the lower brain stem and the spinal cord. Neurons in the A12 and A14 groups, located along the wall of the third ventricle, are involved with endocrine control. Some of them release dopamine as a prolactin release inhibiting factor in the hypophysial portal circulation. . Dopaminergic Cell GroupsThe dopaminergic cell groups in the midbrain and forebrain were originally numbered as if they were a rostral continuation of the noradrenergic system because identification was based on histofluorescence, which does not distinguish dopamine from norepinephrine very well.The A8-A10 cell groups include the substantianigra pars compacta and the adjacent areas of the midbrain tegmentum (Figure 45-3). They send the major ascending dopaminergic inputs to the telencephalon, including the nigrostriatal pathway that innervates the striatum and is thought to be involved in initiating motor responses. Mesocortical and mesolimbicdopaminergic pathways arising from the A10 group innervate the frontal and temporal cortices and the limbic structures of the basal forebrain. These pathways have been implicated in emotion, thought, and memory storage. The A11 and A13 cell groups, in the dorsal hypothalamus, send major descending dopaminergic pathways to the spinal cord. These pathways are believed to regulate sympathetic preganglionic neurons. The A12 and A14 cell groups, along the wall of the third ventricle, are components of the tuberoinfundibular hypothalamic neuroendocrine system. Dopaminergic neurons are also found in the olfactory system (A15 cells in the olfactory tubercle and A16 in the olfactory bulb) and in the retina (A17 cells).Once in the brain, tyrosine can be converted to DihydrOxyPhenylAlanine (DOPA) by the tyrosine hydroxylase enzyme using oxygen, iron and TetraHydroBiopterin (THB) as co-factors. High concentrations of dopamine inhibit tyrosine hydroxylase activity through an influence on the THB co-factor. DOPA is converted to dopamine by Aromatic Amino Acid Decarboxylase (which is fairly nonspecific insofar as it will decarboxylate any aromatic amino acid) using PyridoxaLPhosphate (PLP) as a co-factor. This reaction is virtually instantaneous unless there is a Vitamin B6 deficiency. Dopamine & epinephrine are primarily inhibitory neurotransmitters that produce arousal. This may sound paradoxical, but the most likely explanation for this effect is that the postsynaptic cells for catecholamines themselves are inhibitory. There are 3-4 times more dopaminergic cells in the CNS than adrenergic cells. Dopamine in the caudate nucleus facilitates posture, whereas dopamine in the nucleus accumbens is associated with an animal's speed (and pleasure). There are two primary dopamine receptor-types: D1 (stimulatory) and D2 (inhibitory), both of which act through G-proteins. D2 receptors often occur on the dopaminergic neurons, partially for the purpose of providing negative feedback. These so-called autoreceptors can inhibit both dopamine synthesis and release. The binding of dopamine to D1-receptors stimulates the activity of AdenylylCyclase (AC), which converts ATP to cyclic AMP (cAMP), a second messenger which binds to Protein Kinase A (PKA). PKA then modulates the activity of various proteins by the addition of phosphate. There are 4 main dopaminergic tracts in the brain: (1) the nigrostriatial tract from the substantianigra to the striatum accounts for most of the brain's dopamine (2) the tuberoinfundibular tract from the arcuate nucleus of the hypothalamus to the pituitary stalk, which has a controlling effect on the release of the hormones prolactin through tonic inhibition via D2 receptors (3) the mesolimbic tract from the ventral tegmental area to many parts of the limbic system and (4) the mesocortical tract from the ventral tegmental area to the neocortex, particularly the prefrontal area. Dopamine cells project topographically to the areas they innervate.
  • The noradrenaline pathways in the brainMany regions of the brain are supplied by the noradrenergic systems. The principal centres for noradrenergic neurones are the locus coeruleus and the caudal raphe nuclei. The ascending nerves of the locus coeruleus project to the frontal cortex, thalamus, hypothalamus and limbic system. Noradrenaline is also transmitted from the locus coeruleus to the cerebellum. Nerves projecting from the caudal raphe nuclei ascend to the amygdala and descend to the midbrain.Figure 45-2 Noradrenergic neurons in the pons.A. Noradrenergic neurons are spread across the pons in three more or less distinct groups: the locus ceruleus (A6 group) in the periaqueductal gray matter, the A7 group more ventrolaterally, and the A5 group along the ventrolateral margin of the pontinetegmentum.B. The A5 and A7 neurons mainly innervate the brain stem and spinal cord, whereas the locus ceruleus provides a major ascending output to the thalamus and cerebral cortex as well as descending projections to the brain stem, cerebellum, and spinal cord. A = amygdala; AO = anterior olfactory nucleus; BS = brain stem; C = cingulate bundle; CC = corpus callosum; CT = central tegmental tract; CTX = cerebral cortex; DT = dorsal tegmental bundle; EC = external capsule; F = fornix; H = hypothalamus; HF = hippocampal formation; LC = locus ceruleus; OB = olfactory bulb; PT = pretectal nuclei; RF = reticular formation; S = septum; T = tectum; Th = thalamus. The A6 cell group, the locus ceruleus, sits dorsally and laterally in the periaqueductal and periventricular gray matter (Figure 45-2). The locus ceruleus, which maintains vigilance and responsiveness to unexpected environmental stimuli, has extensive projections to the cerebral cortex and cerebellum, as well as descending projections to the brain stem and spinal cord.NOREPINEPHRINE (NORADRENALIN) Norepinephrine (along with acetylcholine) is one of the two neurotransmitters in the peripheral nervous system. Norepinephrine is synthesized from dopamine by means of the enzyme Dopamine Beta-Hydroxylase (DBH), with oxygen, copper and Vitamin C as co-factors. Dopamine is synthesized in the cytoplasm, but norepinephrine is synthesized in the neurotransmitter storage vesicles. Cells that use norepinephrine for formation of epinephrine use SAMe (S-AdenylMethionine) as a methyl group donor. Levels of epinephrine in the CNS are only about 10% of the levels of norepinephrine. The most prominent noradrenergic (ie, norepinephrine-containing) nucleus is the locus ceruleus in the pons, which account for over 40% of noradrenergic neurons in the rat brain. Most of the other noradrenergic neurons are clustered in a region described as the lateral tegmental area. The neocortex, hippocampus, and cerebellum receive noradrenergic stimulation exclusively from the locus ceruleus. Most of the dopaminergicinnervation of the hypothalamus comes from the lateral tegmental nuclei. Electrical stimulation of the locus ceruleus produces a state of heightened arousal. The noradrenergic system is most active in the awake state, and it seems to be important for focused attention, in contrast to the motor arousal of dopamine. Although the locus ceruleus has been identified as a pleasure center, it also seems to contribute to anxiety. Increased neuronal activity of the locus ceruleus is seen upon the occurrence of unexpected sensory events. Brain norepinephrine turnover is increased in conditions of stress. Benzodiazepines, the primary antianxiety drugs, decrease firing in the locus ceruleus, thus reducing distribution of noradrenalin to the forebrain and amygdala. This is part of the explanation for the use of benzodiazepines for inducing sleep. Active projection of norepinephrine from the locus coeruleus of the reticular activating system to the forebrain is a key feature of awakeness-arousal as distinguished from sleep. Norepineprhine projection to the basal nucleus of the forebrain is low in sleep -- virtually absent in REM (Rapid Eye-Movement) sleep. The basal nucleus when stimulated by norepinephrine from the locus coeruleus sends neuromodulating acetylcholine to the cerebral cortex, thereby promoting alertness. The beta-adrenergic blocking drug propranolol has also been used to treat anxiety. By blocking the adrenergic inputs to the amygdala, beta-blockers inhibit the formation of traumatic memories. Cortisol stimulation of the locus coeruleus due to chronic stress exacerbates norepinephrine stimulation of the amygdala. Beta-noradrenergic receptors also apparently inhibit feeding, whereas alpha-receptors seem to stimulate feeding. Although MAO inhibitors reduce metabolism of all catecholamines, it is believed that the anti-depressant effect is more related to norepinephrine than to dopamine. Most MAO in the brain is of type-B, but drugs selective for inhibiting MAO-A have proven to be better anti-depressants. MAO-A preferentially metabolizes norepinephrine & serotonin. MAO-A inhibiting drugs given for depression have critically elevated blood pressure in patients eating tyramine-containing foods (such as cheese) due to the failure to metabolize tyramine (which can act as a pressor agent). These drugs (eg, phenelzine & pargyline) inactivate MAO by forming irreversible covalent bonds. More modern MAO inhibitors are safer because they form reversible bonds. MAO-B inhibitors like deprenyl are also less likely to cause the "cheese effect". (Alcohol also selectively inhibits MAO-B.) Tricyclic AntidepressantsTricyclic anti-depressants derive their name from their 3-ring structure. Desipramine only inhibits norepinephrine re-uptake, with little effect on dopamine. Imipramine & amitriptyline are inhibitors of norepinephrine and serotonin re-uptake by the presynaptic terminals, but are more potent for serotonin. Cocaine is also a potent inhibitor of catecholamine re-uptake, but it does not act as an anti-depressant. Weight gain due to increased appetite is a frequent side effect of tricyclic anti-depressants, particularly of amitrip- tyline. By contrast, both cocaine & amphetamine reduce appetite. Both MAO inhibitors and tricyclic anti-depressants have immediate effects on brain monoamines, but clinically anti-depressants require several weeks of administration before they produce a therapeutic effect. It is therefore believed that it is not the immediate effects on neurotransmitters that is producing the antidepression, but the long-term effects on modification of receptors. Excessive cortisol secretion is seen in 40-60% of depressed patients, associated with diminished noradrenergic inhibition of corticotropin-releasing hormone secretion in the hypothalamus. Corticotropin-releasing hormone induces anxiety in experimental animals.
  • Frontal Lobe SyndromeFrontal lobe syndrome is a disorder affecting the prefrontal areas of the frontal lobe. The prefrontal lobe comprises the vast area of the frontal lobe anterior to the motor cortex and includes the undersurface of the frontal lobe, or the orbital region. The frontal lobe syndrome is said to be present when an individual who is previously capable of judgment and sustained application and organization of his life becomes aimless and improvident, and may lose tact, sensitivity, and self-control. Additionally, the individual affected by pathology in the prefrontal cortex may demonstrate impulsiveness and a failure to appreciate the consequences of his or her reckless behavior.1 Frontal lobe syndrome can be caused by head trauma or may be the consequence of brain tumor, cerebrovascular accident, infection, or a degenerative cortical disease such as Pick's disease.2 This syndrome represents an organic explanation for psychologically-based symptoms the patient may demonstrate. Due to the anterior location of the prefrontal region, lesions to this region may be missed on a standard neurological examination or on a cursory mental status examination. The mental changes produced by lesions in the prefrontal region have led to the recognition of the "frontal lobe personality," as the patient tends to demonstrate specific personality changes which are more often revealed by a qualitative analysis of the patient's attitudes and types of errors produced rather than by a crude quantitative analysis of performance.3 The behavioral changes associated with bilateral prefrontal lesions may be difficult to measure, but family, friends, and employers may tell you that the patient is "no longer the same."4 Following a head injury, personality change in the injured patient is frequently reported and is often cited by family members as the most difficult and persistant problem that they face. Spouses of patients with frontal lobe syndrome relate that "it is like living with a different person," or that the patient "is not the person I married." Post-traumatic personality changes seen with injuries to the prefrontal region may result in marital break-up, social isolation, or unemployment, as some are fired from their jobs because of inadequate performance or because of offending their co-workers.1,2,4,5,6 Compounding the problem in the identification of prefrontal involvement is the dissociation between how well a patient with a bifrontal lesion can appear during the initial office visit and how poorly they actually perform in real life.4 The consequences of damage to the prefrontal region include: alterations of attention concrete thinking perseveration reduced activity disturbed affectThe frontal lobe syndrome patient may demonstrate an attention deficit. The patient may appear slow, uninterested, may lack spontaneity, may be easily distracted by irrelevant environmental stimuli, and may be unable to sustain attention. The patient's disinterest and easy distractibility may contribute to an apparent poor memory. The frontal lobe syndrome patient's memory is normal, but absentmindedness may lead to the appearance of a memory deficit as the patient literally "forgets to remember" and has the inability to focus attention long enough to form the rudiments of memory. These patients may fill in memory gaps with confabulation, or the elaboration of imaginary facts and experiences to fill in their gaps of knowledge or memory.2,3,4,5,6 These patients may also engage in concrete thinking, which is an impairment of abstract thought. This trend may be identified during a basic mental status evaluation by the patient's inability to properly interpret proverbs.2,4 Closely linked to concrete thinking is the demonstration of "utilization behavior" in which the patient has the tendency to manually grasp and use objects presented within reach.2,3 Perseveration is common in frontal lobe syndrome patients and is the tendency to maintain a previously established motor pattern without modifying the activity according to the demands of the changing environment because of an inability to shift from one line of thinking to another.2,3,4 When faced with a series of different motor tasks, the patient may end up performing one component of the series of tasks over and over again and may demonstrate great difficulty, or an inability to change motor patterns. Perseveration is one of the reasons for poor job performance in the frontal lobe syndrome patient. These patients may demonstrate a diminution of spontaneous activity, a lack of drive, an inability to plan ahead, a lack of concern, and possible bouts of restlessness and aimless, uncoordinated behavior.1-6 These findings may also contribute to poor job performance and family relations. Lastly, the frontal lobe syndrome patient may demonstrate a disturbance of affect ranging from complete apathy to disinhibition depending upon the location of the lesion. A lesion to the dorsolateral aspect of the prefrontal region may produce apathy, emotional blunting, and an indifference to the surrounding world. Their apathy may be noted during examination and may extend toward work and family. These patients may become incontinent, not because of a lesion affecting bladder function, but because of a disregard for their surroundings and the consequences of their actions. Conversely, a patient with a lesion to the orbital region of the prefrontal lobe, or the underside, may exhibit disinhibition, a failure to appreciate the consequences of one's actions, and euphoria with a tendency to jocularity. These patients may exhibit moria (childish excitement), joking and pathological punning, sexual indiscretions, and exhibitionism.1-6 Thus, in the presence of an unremarkable neurological examination, these specific findings may be the only indication of an injury or an underlying pathology in the affected patient. Next month's column will stress simple testing procedures for frontal lobe syndrome. ReferencesWalton J. Brain Diseases of the Nervous System, 10th Edition, Oxford Medical Publishers, New York, 1993. Trimble MR. Behavior and personality disturbances, In: Bradley WG, Daroff RB, Fenichel GM, and Marsden CD, Neurology in Clinical Practice, Vol. I, Butterworth-Heinemann, Boston, 1991. Gainotti G. Frontal lobe damage and disorders of affect and personality, In: Swash M and Oxbury J, Clinical Neurology, Churchill-Livingstone, New York, 1991. Devinsky O. Behavioral Neurology, Mosby, St. Louis, 1992. Greenwood R, Barnes MP, McMillan TM, and Ward CD. Neurological Rehabilitation, Churchill-Livingstone, New York 1993. Strub RL and Black FW. The Mental Status Examination in Neurology, 3rd Ed. F.A. Davis, Philadelphia, 1991.
  • Verbal fluency: FAS test. Judges ability to generate categorical lists Ask the patient to lists words beginning with letter F in one minute. Same with letter A and S. Normal adult should be able to list 15 words/letter in one minute. Total FAS words > 30. For elderly 10 words/letter/minute is acceptable.
  • Luria’s three-step test. Tell the patient that you are going to show them a series of hand movements. Demonstrate fist, edge and palm five times on your leg without verbal prompts. Ask the patient to repeat the sequence. A succession of hand positions (with the hand first placed flat, then on one side, and then as a fist, on a flat surface) or Tapping a complex rhythm (for example two loud and three soft beats) is impairedGo no go test: Ask the patient to place a hand on the table. Tap under the tale. Tell the patient to raise one finger when you tap once and not to raise the finger when you tap twice. Show the patient how it’s done and then do the test.
  • DETECTION OF FRONTAL LOBE DAMAGE Detection of frontal lobe damage can be difficult, especially if only traditional methods of neurologic testing are carried out. Indeed, this point cannot be overemphasized, since it reflects one of the main differences between traditional neurologic syndromes, which affect only elements of a person's behavior - for example, paralysis following destruction of the contralateral motor cortex -and limbic system disorders generally. In the latter it is the whole of the patient's motoric and psychic life that is influenced, and the behavior disturbance itself reflects the pathologic state. Often, changes can be discerned only with reference to the previous personality and behavior of that patient, and not with regard to standardized and validated behavioral norms based on population studies. A further complication is that these abnormal behaviors may fluctuate from one testing occasion to another. Therefore the standard neurologic examination will often be normal, as may the results of psychological tests such as the Wechsler Adult Intelligence Scale. Special techniques are required to examine frontal lobe function, and care finding out how the patient now behaves and how this compares with his premorbid performance. Orbitofrontal lesions may be associated with anosmia, and the more the lesions extend posteriorly, the more neurologic signs such as aphasia (with dominant lesions), paralysis, grasp reflexes, and oculomotor abnormalities become apparent. Of the various tasks that can be used clinically to detect frontal pathologic conditions, those given in Table 4 are of value. However, not all patients with frontal damage show abnormalities on testing, and not all tests are found to be abnormal in frontal lobe pathologic states exclusively. Table 4. Some Useful Tests at Frontal Lobe Function Word fluency Abstract thinking (if I have 18 books and two bookshelves, and I want twice as many books on one shelf as the other. how many books on each shelf?) Proverb and metaphor interpretation Wisconsin Card Sorting Test Other sorting tasks Block design Maze lest Hand position test (three-step hand sequence) Copying tasks (multiple loops) Rhythm tapping tasks Cognitive tasks include the word fluency test, in which a patient is asked to generate, in 1 minute, as many words as possible beginning with a given letter. (The normal is around 15.) Proverb or metaphor interpretation can be remarkably concrete. Problem-solving, for example carry-over additions and subtractions, can be tested by a simple question (see Table 4). Patients with frontal lobe abnormalities often find serial sevens difficult to perform. Laboratory-based tests of abstract reasoning include the Wisconsin Card Sort Test (WCST) and other object-sorting tasks. The subject must arrange a variety of objects into groups depending on one common abstract property, for example color. In the WCST, the patient is given a pack of cards with symbols on them that differ in form, color, and number. Four stimulus cards are available, and the patient has to place each response card in front of one of the four stimulus cards. The tester tells the patient if he is right or wrong, and the patient has to use that information to place the next card in front of the next stimulus card. The sorting is done arbitrarily into color, form, or number, and the patient's task is to shift the set from one type of stimulus response to another based on the information provided. Frontal patients cannot overcome previously established responses, and show a high frequency of preseverative errors. These deficits are more likely with lateral lesions of the dominant hemisphere. Patients with frontal lobe lesions also do badly on maze learning tasks, the Stroop test, and block design; they show perseveration of motor tasks and difficulty carrying out sequences of motor actions. Skilled movements are no longer performed smoothly, and previously automated actions such as writing or playing a musical instrument are often impaired. Performance on tests such as following a succession of hand positions (with the hand first placed flat, then on one side, and then as a fist, on a flat surface) or tapping a complex rhythm (for example two loud and three soft beats) is impaired. Following nondominant hemisphere lesions, singing is poor, as is recognition of melody and emotional tone, the patient being aprosodic. Perseveration (especially prominent with deeper lesions in which the modulating function of the premotor cortex on the motor structures of the basal ganglia is lost (9)) may be tested by asking the patient to draw, for example, a circle or to copy a complex diagram with recurring shapes in it that alternate one with another. The patient may continue to draw circle after circle, not stopping after one revolution, or miss the pattern of recurring shapes (Fig. 2). Imitation and utilization behavior can also be tested for. In many of these tests there is a clear discrepancy between the patient's knowing what to do and being able to verbalize the instructions, and his failure to undertake the motor tasks. In everyday life this can be extremely deceptive and lead the unwary observer to consider the patient to be either unhelpful and obstructive or (for example, in a medicolegal setting) to be a malingerer. Some of these tasks, for example the word-fluency task, or inability to make melodic patterns, are more likely to be related to lateralized dysfunction, and the inhibition of motoric tasks relates to the dorsolateral syndrome.
  • Frontallobe dr prashant mishra

    1. 1. Presenter :Dr. Prashant MishraModerator : Dr. V Sharbandh Raj
    2. 2. OUTLINE: FRONTAL LOBE 1. Evolution 2. Anatomy and connections 3. Physiology 4. Circuits and Neurotransmitters 5. Dysfunction  Frontal lobe Syndromes  Frontotemporal Lobe Dementia  Frontal Lobe Epilepsy  Expressive aphasia  Schizophrenia  Depression 6. Frontal lobeTesting
    3. 3. MAMMALS FRONTAL LOBE EVOLUTION  33% of Brain area  Most recently evolved  Well developed only in primates  Human species is due to frontal lobe  Last to develop in ontogeny from age 1-> 6years  Gives our capacity to feel empathy, sympathy, understand humor and when others are being ironic, sarcastic or even deceptive.
    4. 4. FRONTAL LOBE A. Lateral surface 1. Posterior - Central sulcus 2. Inferio-Posterior – sylvian fissure. B. Medial surface C. Orbital surface
    5. 5. FUNCTIONAL FRONTAL LOBE ANATOMY Premotor area Primary motor area B6 B4 Central sulcus Supplementary motor area (medially) Frontal eye field B8 Prefrontal area B 9, 10, 11, 12 Lateral sulcus/ Motor cortex Sylvian fissure 1. PrimaryPrefrontal cortex Motor speech 2. Premotor 1. Dorsolateral area of Broca 3. Supplementary 2. Medial 4. Frontal eye 3. Orbitofrontal B 44, 45 field 5. Broca’s area
    6. 6. Sub cortical structures a b 1 c d 2
    7. 7. MOTOR CORTEX
    8. 8. PRIMARY MOTOR CORTEX Motor fibres cross in medulla to opp. side 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
    9. 9. PRE MOTOR CORTEX Input:  thalamus,  BG,  sensory cortex Output: primary motor cortex Function:  stores motor programs;  controls coarse postural movements Lesions: moderate weakness in proximal muscles on contralateral side
    10. 10. 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,  akinesis
    11. 11. 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  eyes deviate contralaterally with irritating lesions
    12. 12. 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;  monotone speech
    14. 14. LATERAL SURFACE FRONTAL LOBE SULCI  Vertical  Central sulcus  Precentral sulcus •GYRI •Precentral gyrus  Horizontal •Superior frontal gyrus  Super frontal sulcus •Middle frontal gyrus  Inf frontal sulci •Inf erior frontal gyrus
    15. 15. MEDIAL SURFACE FRONTAL LOBE Between cingulate sulcus and superior medial margin of hemisphere Posterior part vertical sulcus
    16. 16. ORBITAL SURFACE FRONTAL LOBE  Divided into four orbital gyri by a well-marked H-shapedM L 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 gyrus rectus
    18. 18. DORSOLATERAL PREFRONTAL CORTEX Connections:  motor / sensory convergence areas,  thalamus,  globus pallidus,  caudate nucleus, Subcortical structures  substrantia nigra Functions:  motor planning, organization, and regulation  monitors and adjusts behavior using „working memory‟ DLPFC Lesions:  executive function deficit;  disinterest  attention to relevant stimuli
    19. 19. 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 and loss of sensation,  Incontinence
    20. 20. ORBITAL PREFRONTAL CORTEX Connections:  temporal cortex  parietal cortex  thalamus, globus pallidus, caudate,  insula,  amygdala Part of limbic system •The limbic system Function: •Hippocampus  emotional input, •Amygdalae  arousal, • anterior thalamic nuclei  suppression of distracting signals •Septum  Decision making •limbic cortex •Fornix, Lesions: •functions including Disinhibited, impulsive behaviour •Emotionbehavior, Inappropriate jocular affect, •motivation, euphoria ,emotional lability, •long-term memory, Poor judgment and insight, •olfaction Distractibility
    21. 21. FIVE „FRONTAL SUBCORTICAL CIRCUITS‟1. Motor Motor cortex2. Oculomotor3. Dorsolateral prefrontal Lateral4. Lateral orbitofrontal Inferior Prefrontal cortex5. Anterior cingulate Medial
    22. 22. 1. FRONTAL SUBCORTICAL MOTOR CIRCUIT SMA, Premotor,MotorHypo-thalamus Putamen Thalamus Globus Pallidus Supplementary Motor & Premotor : planning, initiation & storage of motor programs; fine-tuning of movements Motor : final station for execution of the movement according to the design
    23. 23. 2.FRONTAL OCULOMOTOR CIRCUIT Frontal Eye field Central Thalamus Caudate Globus Pallidus & Substantia Nigra  Voluntary scanning eye movement  Independent of visual stimuli
    24. 24. 3.DORSOLATERAL PREFRONTAL CIRCUIT Lateral Pre- Frontal Thalamus Caudate Globus Pallidus & Substantia Nigra Executive functions: motor planning, deciding which stimuli to attend to, shifting cognitive sets Attention span and working memory
    25. 25. 4. LATERAL ORBITOFRONTAL CIRCUIT Infero-Lateral Pre- Frontal Orbito-Frontal Caudate Globus Pallidus & Thalamus Substantia Nigra  Emotional life and personality structure  Arousal, motivation, affect
    26. 26. 5. ANTERIOR CINGULATE CIRCUIT Ant. Cingulate MD Thalamus Striatum Thalamus Globus Pallidus & Substantia Nigra Abulia –lack of initiative Akinetic mutism - neither move nor speak
    27. 27. NEUROTRANSMITTERS: DOPAMINERGICTRACTS Origin: ventral tegmental4 area in midbrain 1 Mesocortical tract Projections:  prefrontal cortex (mesocortical tract  limbic system (mesolimbic tract) 2 Function:  reward;  motivation; 3  spontaneity;  arousal
    28. 28. NEUROTRANSMITTERS: NOREPINEPHRINETRACTS Origin:  locus ceruleus in brainstem  lateral brainstem tegmentum Projections: anterior cortex Functions:  alertness,  arousal,  cognitive processing of somatosensory information
    29. 29. NEUROTRANSMITTERS: SEROTONIN TRACTS Origin: raphe nuclei in brainstem Projections: number of forebrain structures Function:  minor role in prefrontal cortex;  sleep,  mood, anxiety,  feeding
    30. 30. FRONTAL LOBE FUNCTION Motor Cognitive Behavior Arousal Voluntary Memory Personality Attention movements Planning, Problem Social and Initiation solving sexual Spontaneity Judgment Impulse control Language Abstract Mood and Expression thinking affect Eye movements
    32. 32. PHINEASE GAGE (1848) 1. He becomes unreliable and failsOn 13th Sept 1848 a railroad to come to work and when worker, hard working, present he is "lazy." 2. He has no interest in going to diligent, reliable, church, constantly drinks alcohol, gambles, and "whores about." responsible, intelligent, 3. He is accused of sexually good humored, polite god molesting young children. fearing, family oriented 4. He ignores his wife and children and fails to meet his financial and foreman family obligations. 5. He has lost his sense of humour.Following an explosion iron 6. He curses constantly and does so bar drove into frontal lobe in inappropriate circumstances. 7. Died of status epilepticus in 1861
    33. 33. FROTNAL LOBE SYNDROMES •executive function deficit; •apathy; •disinterest / emotional •decreased reactivity; drive/awareness/ • attention to relevant spontaneous stimuli movements; •akinetic- Lateral abulic& mutism •emotional lability, Medial •disinhibition, •distractibility, • ‘hyperkinesis’ Orbital
    34. 34. FRONTAL LOBE SYNDROMES 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 theinability of a person to properly convey or interpret emotional prosody.
    35. 35.  Patients with orbitofrontal lesions shows disinhibition, emotional lability, and memory disorders. Personality changes from orbital damage include impulsiveness, a jocular attitude, sexual disinhibition, and complete lack of concern for others. Patients with superior mesial lesions typically develop akinetic mutism. Patients with inferior mesial (basal forebrain) lesions tend to manifest anterograde and retrograde amnesia and confabulation.
    36. 36. FRONTAL LOBE SYNDROME -CAUSES 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
    37. 37. CLINICAL PICTURE Profound change in personality. Lack of initiation and spontanity. Response are sluggish. Occasionally patient are hyperactive and restless. Mood is often euphoric and out of keeping with patients situation. Irritability and outbursts are common. Loss of finer senses. Judgements are impaired. Fail to plan and carry through ideas.
    38. 38. FRONTOTEMPORAL LOBE DEMENTIA FTLD is a neurodegenerative disease : frontal and temporal lobe Typical age of onset is between 50 and 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.
    39. 39. FRONTAL LOBE EPILEPSY Frontal lobe epilepsy is 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. Patients with frontal lobe seizures may 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
    40. 40. EXPRESSIVE APHASIA Expressive aphasia, known as Brocas aphasia caused by damage or developmental issues in (area 44,45). For them, speech is difficult to initiate, non-fluent, labored, and halting. Similarly, writing is difficult as well. Intonation and stress patterns are deficient. Language is reduced to disjointed words and sentence construction is poor. Comprehension is generally preserved, meaning interpretation dependent on syntax and phrase structure is substantially impaired. Patients who recover go on to say that they knew what they wanted to say but could not express themselves.
    41. 41. SCHIZOPHRENIA & FRONTAL LOBE some schizophrenic symptoms are found in frontal lobe disorder, in particular that involving dorsolateral prefrontal cortex. Symptoms included are those of the affective changes, impaired motivation, poor insight. Evidence  EEG studies, in  CT scan,  with MRI,  cerebral blood flow studies.  Hypofrontality in PET.
    42. 42. DEPRESSION & FRONTAL LOBE Right frontal lobe demonstrated increased activity in response to negative moods whereas left frontal activity decreases. 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. In severely depressed patients demonstrate insufficient activation and a significant lower integrated amplitude of the eeg evoked response over the left vs right frontal lobe.
    43. 43. FRONTAL LOBE HISTORY TAKING Personality changes (over familiar, tactless and sexual indiscretions) Hyperorality Distractibility Poor motivation Inability to adapt to new situations Poor problem solving skills
    44. 44. FRONTAL LOBE TESTS 1. Attention 2. Memory 3. Abstraction 4. Judgment 5. Planning 6. Language 7. Motor sequencing
    45. 45. Tests of attention and memoryo Alternative sequence (e.g. copying MNMN)o Luria‟s „fist-edge-palm‟ test (show 3X)o Go/no-go: o”tap once if I tap twice, don‟t tap if I tap once” o“tap for A” oread 60 letters at 1/sec; N: < 2 errors
    46. 46. Tests of attention and memory cont‟ oDigit span orepeat 3-52; 3-52-8; 3-52-8-67..” N: >5 o Recency test o“recall sequence of stimuli / events” o Imitation (of examiner) / utilization (of objects presented)
    47. 47. Tests of abstraction and judgmento Interpret proverbs (e.g.“the golden hammer opens iron doors”)o Explain why conceptually linked words are the same (e.g. coat & skirt)o Plan & structure a sequential set of activities (“how would you bake a cake?”)o Insight / reaction to own illness
    48. 48. Language tests o Thurstone / word fluency test (“recite as many words beginning with „F‟ in 1 min as you can, then with „A‟, „S‟”); N: >15 o Repetition (Broca‟s vs transcortical) o “Ball” o “Methodist”
    49. 49. MOTOR SEQUENCING: KINETIC MELODY1. Hand position test (three-step hand sequence)2. Rhythm tapping tasks3. Go no go test4. Copying tasks
    50. 50. FRONTAL RELEASE SIGN – PRIMITIVE REFLEXES Grasp reflex  Snout reflex  Forceful grapping of object on touching palm or sole  Palmomental Sucking reflex  Glabellar tap  By touching the lips Groping reflex  Involuntary following with hand/eye of moving object
    51. 51. Formal Tests• Abstract thinking and set shifting • Wisconsin Card Sorting Test• Visuo-motor track, conceptualization, set shift • Trail Making• Attention, shift sets • Stroop Color & Word Test• Planning • Tower of London Test • Block design • Maze lest
    52. 52. Wisconsin Card Sorting Test perseverence•Used to assess the following "frontal" lobe functions: •strategic planning, •organized searching, •utilizing environmental feedback to shift cognitive sets, •directing behavior toward achieving a goal •modulating impulsive responding.
    53. 53. Trail Making Test 5 B A 4 6 1 C 2 3 D 7It provides information about •visual search speed •scanning, •speed of processing, •mental flexibility, and executive functioning.
    54. 54. Stroop Color and Word Tests “Please read this as fast as you can” RED BLUE ORANGE YELLOW GREEN RED PURPLE RED GREEN YELLOW BLUE RED YELLOW ORANGE RED GREEN BLUE GREEN PURPLE RED attention, shiftingLesion : anterior cingulate cortex and dorsolateral prefrontal cortex
    55. 55. Tower of London TestsUse:for the assessment of executive functioning specifically to detect deficits in planning
    56. 56. Reference:1. CTP2. OTP3. Snells neuroanatomy4. Internet
    57. 57. Thank You