Frontal lobe 2010


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  • Thankyou, this is one of the most helpful things I have seen while trying to live with prefrontal cortex deficits. I have printed out several of the slides to show my doctor so he can understand certain things!
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  • 1641 - This area of the brain was first defined by Franciscus de la BoeSylvius, in 1641 .(1) It is now usually referred to as the lateral sulcus or lateral fissure , and it is one of the most prominent structures of the human brain, dividing the frontal lobe and ...This area of the brain was first defined by Franciscus de la BoeSylvius, in 1641 .(1) It is now usually referred to as the lateral sulcus or lateral fissure , and it is one of the most prominent structures of the human brain, dividing the frontal lobe and parietal lobe above from the temporal lobe below. (3) In more modern times it was understood to house neural complexes vital to hearing, language skills, language comprehension, and speech. 1825 - Long before the time of Bouillaud, the coexistence of aphasia, with certain forms of paralysis, had been often observed, but he, in the year 1825, was the first to note and distinctly to proclaim its intrinsic complication with pathological conditions affecting ...Long before the time of Bouillaud, the coexistence of aphasia, with certain forms of paralysis, had been often observed, but he, in the year 1825, was the first to note and distinctly to proclaim its intrinsic complication with pathological conditions affecting circumscribed portions of the anterior lobes of the brain, and thus demonstrated the seat of articulate language. Broca, the contemporary of Bouillaud, elaborating the doctrine by subsequent experiments, was enabled to 1848 - Beginning with the tragic story of Phineas Gage in 1848, which was recounted in chapter 1, it became an intentional brain operation in the mid-twentieth century , a frontal lobotomy (-otomy means severing connections). Frontal lobotomies actually involved severing ...Beginning with the tragic story of Phineas Gage in 1848, which was recounted in chapter 1, it became an intentional brain operation in the mid-twentieth century , a frontal lobotomy (-otomy means severing connections). Frontal lobotomies actually involved severing connections within each frontal lobe (ie, left and right frontal lobes) rather than severing the connections between the two frontal lobes. Frontal lobotomies were performed (and are still performed) mostly on violent or .1861 - The area of the brain responsible for forming language is called Broca's area, identified through the work of Pierre Paul Broca in 1861. In over 95 percent of right-handed people, Broca's area is located in the left side of the frontal lobe (behind the left ...The area of the brain responsible for forming language is called Broca's area, identified through the work of Pierre Paul Broca in 1861. In over 95 percent of right-handed people, Broca's area is located in the left side of the frontal lobe (behind the left side of the forehead). In 60 percent or so of left-handed people, it is in this same location; for the rest it is located on the right side of the frontal lobe. People with purely expressive aphasia can have a broad range 1868 - The term "prefrontal" as describing a part of the brain appears to have been introduced by Richard Owen in 1868[1]. For him, the prefrontal area was restricted to the anterior-most part of the frontal lobe (approximately corresponding to the frontal pole). It has ...The term "prefrontal" as describing a part of the brain appears to have been introduced by Richard Owen in 1868[1]. For him, the prefrontal area was restricted to the anterior-most part of the frontal lobe (approximately corresponding to the frontal pole). It has been hypothesized that his choice of the term was based on the prefrontal bone present in most amphibians and reptiles[1]. Subdivisions The table below shows different ways to subdivide the prefrontal cortex starting ...1879 - "3. Casc of Tumor of Dura Mater in which the symptoms exhibited pointed to lesion in frontal lobe.—In 1879, an idiopathic case came under observation, in which the totality of the symptoms indicated a lesion in the left frontal lobe of the brain. It occurred in ..."3. Casc of Tumor of Dura Mater in which the symptoms exhibited pointed to lesion in frontal lobe.—In 1879, an idiopathic case came under observation, in which the totality of the symptoms indicated a lesion in the left frontal lobe of the brain. It occurred in a patient the subject of a small tumor above the left eyeball in the orbital cavity. A tumor had previously been removed from that position, and had now recurred. Other symptoms had however meanwhile presented themselves ...1890 - In 1890 a Swiss doctor working in a mental institution decided to try a revolutionary treatment. He removed the frontal lobe from six of his patients. One of them died immediately, one was found dead ten days later (perhaps a result of suicide), but the other four ...In 1890 a Swiss doctor working in a mental institution decided to try a revolutionary treatment. He removed the frontal lobe from six of his patients. One of them died immediately, one was found dead ten days later (perhaps a result of suicide), but the other four had undergone a radical change in their behavior. This crude experiment encouraged other researchers to investigate the possibilities of this kind of treatment on patients with severe mental disabilities: mentally
  • 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.
  • 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
  • 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
  • The discussion so far has revolved around clinical presentations in patients with pathological lesions located in the frontal lobes.12–14,19–24 However, some cases of socalled frontal lobe syndrome occur in patients who do not have obvious damage to the frontal lobes. Some examples include episodic dyscontrol after bilateral caudate nucleus lesions,25 disinhibited behaviors after bilateral thalamic infarcts, 26 apathy and abulia with globuspallidus lesions, 27–28 or apathy and disinhibition in multiple sclerosis.29,30 Similar cases have been described with CNS Sjogren’s syndrome,31 white matter subcortical stroke,32 adrenal leukodystrophy,33 Parkinson’s disease,34 Fahr’s disease,35 and, of course, Huntington’s disease. Thus, frontal lobe syndromes can occur in patients who have brain damage in subcortical structures, in both gray and white matter.Some of these symptoms have been reported in more classical psychiatric disturbances. Some of these are major depression (apathy and mood lability), especially in old age,36 which has been associated with disturbances in the anterior cingulum; schizophrenia37 (apathy and executive disturbance), which has been associated with disruptions in the dorsolateral prefrontal cortex; attention deficit hyperactivity disorder38 and obsessive-compulsive disorder39 (repetitive, intrusive, and irresistible behaviors), which have been associated with overactivity in orbitofrontal lobe areas.
  • 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.
  • 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.
  • Frontal lobe 2010

    1. 1. OUTLINE: FRONTAL LOBE 1. Evolution 2. History 3. Anatomy and connections 4. Syndromes 5. Physiology 6. Neurotransmitters 7. Dysfunction 8. Testing 9. Pathology
    2. 2. 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.
    3. 3. HUMAN FRONTAL LOBE EVOLUTIONThe high, straight forehead that characterizes modern humans,superseding the prominent brow ridges of our ancestors, is dueto the expansion of the cortex, and especially the prefrontalcortex, in our species.1. Australopithecus robustus 2. Homo habilis 3. Homo erectus4. Homo sapiens neanderthalensis 5. Homo sapiens sapiens
    4. 4. FRONTAL LOBE HISTORY 1600-19001. 1641 – Lateral sulcus of the brain was first defined by Franciscus de la Boe Sylvius,2. 1825 - Long before the time of Bouillaud the coexistence of aphasia, with certain forms of paralysis3. 1848 - Beginning with the tragic story of Phineas Gage4. 1861 - The area of the brain responsible for forming language is called Brocas area,5. 1868 - The "prefrontal“ introduced by Richard Owen6. 1890 - Swiss doctor working in a mental institution decided to try a revolutionary treatment. He removed the frontal lobe from six of his patients
    5. 5. FRONTAL LOBE A. Lateral surface 1. Posterior - Central sulcus 2. Inferio-Posterior – sylvian fissure. B. Medial sufface C. Orbital surface
    6. 6. LATERAL SURFACE FRONTAL LOBE  Precentral sulcus – parallel to central sulcus between them precentral gyrus  Sup and inf frontal sulci divide sup, middle and inf frontal gyri
    7. 7. MEDIAL SURFACE FRONTAL LOBE  Between cingulate sulcus and superior medial margin of hemisphere  Posterior part vertical sulcus – paracentral lobule
    8. 8. ORBITAL SURFACE FRONTAL LOBE  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.
    9. 9. FUNCTIONAL FRONTAL LOBE ANATOMY Premotor area Primary motor area B6 B4 Central sulcus Supplementary motor area (medially) Motor cortex 1. Primary Frontal eye field 2. Premotor B8 3. Supplementary Prefrontal area 4. Frontal eye B 9, 10, 11, 12 field Lateral sulcus/ 5. Broca’s area Sylvian fissurePrefrontal cortex Motor speech 1. Dorsolateral 2. Medial area of Broca 3. Orbitofrontal B 44, 45
    10. 10. PRIMARY MOTOR CORTEX 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
    11. 11. 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
    12. 12. SUPPLEMENTARY MOTOR CORTEX Input: cingulate gyrus, thalamus, sensory & prefrontal cortex Output: premotor, primary motor Function: intentional preparation for movement; procedural memory Lesions: mutism, akinesis; speech returns but it is non-spontaneous
    13. 13. FRONTAL EYE FIELDS Input: parietal / temporal (what is target); posterior / parietal cortex (where is target) Output: caudate; superior colliculus; paramedian pontine reticular formation Function: executive: selects target and commands movement (saccades) Lesion: eyes deviate ipsilaterally with destructive lesion and contralaterally with irritating lesions
    14. 14. BROCA‟S SPEECH AREA Input: Wernicke‟s Output: primary motor cortex Function: speech production (dominant hemisphere); emotional, melodic component of speech (non-dominant) Lesions: motor aphasia; monotone speech
    15. 15. CONNECTIVITY OF PREFRONTAL REGIONS input from association cortex (occipital, parietal, temporal & olfactory areas) convergence of higher-order input from all modalities. reciprocal connections: prefrontal processing modulates perceptual processing. LIMBIC connections (memory/emotion) Input to premotor areas - controls/programs behavior.
    18. 18. 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
    19. 19. FRONTAL LOBE ABLATION IN MONKEY ANDDOGS (BIANCHI) "The frontal lobes are the seat of coordination and fusion of the incoming and outgoing products of the several sensory and motor areas of the cortex" (Bianchi, 1895) Loss of "perceptive power", leading to defective attention and object recognition. Reduction in memory. Reduction in "associative power", leading to lack of coordination of the individual steps leading towards a given goal, and thus to severe difficulty solving anything but the most simple problem. Altered emotional attachments, leading to serious changes in "sociality" [one of the main aspects of Phineas Gages post-traumatic behaviour]. Disruption of focal consciousness and purposive behaviour, leading to apathy and/or distractibility [one of the main aspects of Beckys post- operative behaviour]. Bianchi 1922
    20. 20. FRONTAL LOBE HISTORY 1900-2010Feuchtwanger (1923) Jacobson (1935) 200 case of frontal lobe injury  Premotor lobotomy in  Lack of initiative primates ->  Vacillation  Social indifference  Euphoria  Tameness  Inattentiveness  Placidity  Normal intellect and memory  ForgetfulnessEgas Moniz 1935  Difficulty in problem  Prefrontal lobotomies in solving  psychotics Dandy‟s (1936)  following bilateral frontal lobotomy during removal of meningioma
    21. 21. INFERIOMESIAL FRONTAL LEUKOTOMYEGAS MONIZ 1935Hours Weeks to months  Drowsy  Regained memory and  Apathetic intellect  Incontinent  Akinetic  With personality  Mute changesDays  Indifferent to the others  Decreased initiative problem  Lack of concern  No thought to their  Freedom from anxiety conduct  Apathetic  Tactless  Distractible  Socially inept  Euphoria and emotional outburst
    22. 22. FROTNAL LOBE SYNDROMES executive function deficit; disinterest / apathy; emotional reactivity; decreased drive/ attention to relevant awareness/ stimuli spontaneous movements; akinetic-abulic& Lateral mutism emotional lability, Medial disinhibition, distractibility, ‘hyperkinesis’ Orbital
    23. 23. ORBITAL PREFRONTAL CORTEX Connections: temporal,parietal, thalamus, GP, caudate, SN, insula, amygdala Part of limbic system Function: emotional input, arousal, suppression of distracting signals Lesions: Disinhibited, impulsive behaviour (pseudopsychopathic) Inappropriate jocular affect, euphoria ,emotional lability, Poor judgment and insight, Distractibility
    24. 24. DORSOMEDIAL PREFRONTAL CORTEX Connections: temporal,parietal, thalam us, caudate, GP, substant ia nigra, cingulate 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
    25. 25. DORSOLATERAL PREFRONTAL CORTEX Connections: motor / sensory convergence areas, thalamus, GP, caudate, SN Functions: monitors and adjusts behavior using „working memory‟ Lesions: executive function deficit; disinterest / emotional reactivity; attention to relevant stimuli
    26. 26. FRONTAL CONVEXITY SYNDROME (APATHETIC) Apathy (occasional brief  Three-step hand sequence angry or aggressive Alternating programs outbursts common) Reciprocal programs Indifference Rhythm tapping Psychomotor retardation Multiple loops Motor perseveration and  Poor word list generation impersistence  Poor abstraction and Loss of self categorization Stimulus-bound behaviour  Segmented approach to Discrepant motor and verbal visuospatial analysis behaviour Motor programming deficits
    27. 27. UNILATERAL FRONTAL LOBE SYNDROME 1. Contralateral 4. Difficulty in adaptation hemiplegia 5. Loss of initiative 2. Conjugate deviation of 6. Loss of kinetic melody eye to side of lesion 7. Unable to solve 3. Personality change problem (Psudopsychotic) 8. Anosmia and blindness a. Mood elevation, talkativeness b. Tendency to joke, lack of tact, silly and childish behavior
    28. 28. DOMINANT FRONTAL LOBE  Deficits in tests of categorization1. Loss of motor speech and flexibility.2. Unable to write  Problems with body schema (autopagnosia) due to problems of3. Sympathetic apraxia scanning, perceptual shifting and postural mechanisms.4. Dysphoria  Marked inactivity affects general intellectual processes and behavior.  Cannot change verbal instructions into acts, especially when the instructions are complex or symbolic.  Decreased spontaneity of speech; may result in complete loss of voluntary speech.  Memory deficits for verbal material; however, deficits may be due to defective registration.
    29. 29. RIGHT HEMIS. PREFRONTAL LESIONS Loss of emotional  Large lesions may exist speech expression without obvious symptoms; serious Euphoria speech disorders usually Constructional apraxia, not seen in right hemisphere lesions. associated with motor rather than perceptual  Difficulty with drawing tasks, though this is difficulties; deficits may associated more with occur as a function of right hemisphere lesions impaired complex (3-D) in general. spatial analysis.  Impaired visual-spatial integration, maze learning, non-verbal visual memory
    30. 30. BILATERAL FRONTAL LOBE LESION1. Pseudodepressed - 6. Active learning, Apathy, Abulia, akinetic problem solving, mutism, judgment2. Impulsiveness and 7. Limitation of utilization irritability behavior3. Inability to sustain attention 8. Frontal release sign a. Snout4. Decomposition of gait b. Suck5. Sphincter disturbance c. Palmomental d. Grasp e. Brow tapping
    31. 31. FRONTAL LOBE SYNDROME MIMICS Bilateral Caudate nucleus lesion - Dyscontrol Globus pallidus lesion – Apathy and abulia Bilateral thalamic infarction MS – Apathy and disinhibition Sjogren‟s syndrome Subcortical stroke Adrenoleukodystrophy Parkinson‟s disease Fahr‟s disease Huntington‟s disease Depression Schizophrenia OCD
    32. 32. FIVE „FRONTAL SUBCORTICAL CIRCUITS‟1. Motor2. Oculomotor3. Dorsolateral prefrontal4. Lateral orbitofrontal5. Anterior cingulate Cummings,„93
    33. 33. 1. FRONTAL SUBCORTICAL MOTOR CIRCUIT SMA, Premotor,Motor Hypo-thalamus Putamen Thalamus Globus VL,VA,CM 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
    34. 34. 2.FRONTAL OCULOMOTOR CIRCUIT Frontal Eye field Thalamus Central VA, MD Caudate DM Globus Pallidus & Substantia Nigra  Voluntary scanning eye movement  Independent of visual stimuli
    35. 35. 3.DORSOLATERAL PREFRONTAL CIRCUIT Lateral Pre-Frontal Thalamus DL VA, MD Caudate DM Globus Pallidus & Substantia Nigra Executive functions: motor planning, deciding which stimuli to attend to, shifting cognitive sets Attention span and working memory
    36. 36. 4. LATERAL ORBITOFRONTAL CIRCUIT Infero-Lateral Pre-Frontal VM Orbito-Frontal Caudate DM Globus Thalamus Pallidus & VA, MD Substantia Nigra  Emotional life and personality structure  Arousal, motivation, affect  Orbitofrontal cortex: consciousness
    37. 37. 5. ANTERIOR CINGULATE CIRCUIT Ant. Cingulate MD Thalamus Thalamus Ventral Striatum MD RL Globus Pallidus & Substantia Nigra Abulia, akinetic mutism
    38. 38. NEUROTRANSMITTERS: DOPAMINERGICTRACTS Origin: ventral tegmental area in midbrain Projections: prefrontal cortex (mesocortical tract) and to limbic system (mesolimbic tract) Function: reward; motivation; spontaneity; arousal
    39. 39. NEUROTRANSMITTERS: NOREPINEPHRINETRACTS Origin: locus ceruleus in brainstem and lateral brainstem tegmentum Projections: anterior cortex Functions: alertness, arousal, cognitive processing of somatosensory info
    40. 40. NEUROTRANSMITTERS: SEROTONIN TRACTS Origin: raphe nuclei in brainstem Projections: number of forebrain structures Function: minor role in prefrontal cortex; sleep, mood, anxiety, feeding
    41. 41. 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
    42. 42. MOTOR PLANNING1. Frontal lobe has evolved from being the main motor planner/organizer to a higher level behavioural/strategic planner/organizer.2. Mental model, considering options, selecting behaviours based on context, feedback, stored knowledge3. Making predictions about what will work.
    44. 44. FRONTAL LOBE AND AROUSAL Right frontal lobe -> bilateral inhibitory influences on attention and arousal Left frontal lobe unilateral excitation of arousal Left frontal damage -> unopposed right cerebral inhibition -> akinesia
    45. 45. MEMORY DEFECT Inattentiveness Defect in working memory Defect in sequencing, perseverance Can recall the details of problem, error in trying to solve Could not put them to use in the correction of further performance. Cannot categorizes series of item in group for recall
    46. 46. WORKING MEMORY
    50. 50. LEARNINGImpaired association Impaired temporal learning learning1. Reduced response 1. Impaired memory for to consequences order, recency2. Impaired on delayed 2. Could affect response tasks problem-solving,3. Impaired planning and impair responsiveness to systematic, social & contextual organized cues behaviours
    51. 51. ABSTRACTION AND JUDGMENT Cognitive functions undisturbed Concrete thinking Diminished insight Defect in planning / executive control
    52. 52. PROBLEM SOLVING Unable to think all the option and select appropriate Fails to conceptualize all the demands of the situation but thinks “concretely” – think and react directly to the stimulus
    53. 53. PROBLEM SOLVING - LURIANormal Frontal lobe lesion 1. The specification of 1. Erroneous analysis of problem and the the condition of the problem condition in which it has arisen 2. The plan of action that is selected quickly 2. A plan of action or loses its regulation strategy for the solution influence on behavior of the problem is as a whole and is formulated replaced by a perseveration of one 3. Execution, including particular link of the implementation and motor act or by the control of the plan influence of some 4. Checking of the results connection established against the original plan during the patients past experience.
    54. 54. IMPAIRED DIVERGENT THINKING1. Decreased consideration of alternative strategies/behaviors; reduced flexibility2. Decreased spontaneity, initiative, may appear lazy, unmotivated3. Knowledge/intelligence may seem intact (e.g. IQ) but its not used to generate strategies or solve problems efficiently
    55. 55. Language• Broca‟s / non-fluent aphasia• Prefrontal/ transcortical motor aphasia• Language-motor dissociation• Akinetic mutism
    56. 56. FRONTAL LOBE PERSONALITY Lack of initiative and  Organic driveness: spontaneity brief but intense Placidity: worry, meaningless activity. anxiety, self concern,  Loss of ego strength: hypochondriasis, and Witzelsucht or moria : pain reduces socially uninhibited and Psychomotor lack aunawerness of retardation: number of their abnormal movements, spoken behavior. words and thought per  Loss of regards to unit of time diminish. social conventions , Mild form abulia and only interested in severe akinetic mutism. personal gratification.
    57. 57. DECREASED INHIBITION1. Problems inhibiting incorrect/ineffective responses & switching to a new strategy2. Perseverates; not responsive to feedback or changes in environment3. Violates rules, expectancies; takes risks4. Not adaptable5. Decreased social inhibitons as well
    58. 58. DISINHIBITED SEXUALITY It is not unusual for a  Seizure activity arising hypersexual, disinhibited from the deep frontal frontal lobe injured regions have also been individual to employ force. associated with spirited physical self- increased sexual defense is probably the best behavior, including strategy of the woman. Her sexual automatisms, husband may have exhibitionism, gential regressed to the cave-man manipulation, and level, and she owes it to him masturbation to be responsive at the cave-women level. It may not be agreeable at first, but she will soon find it exhilarating if unconventional."
    59. 59. NEUROANATOMIC CORRELATION Motor  Attention  Perseveration ->  Brainstem thalamic Posteriolateral frontal system dominant lobe and  Orbitofronal syndrome connection to basal ganglia  Frontolimbic link  Posterior lesion ->  Loss of inhibition of difficulty in organizing parietal lobe  Anterior lesion ->  Echophenomenon and dissociation between environmental behavior and language dependency
    60. 60. 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
    61. 61. FRONTAL LOBE TESTS 1. Attention 2. Memory 3. Abstraction 4. Judgment 5. Planning 6. Language 7. Motor sequencing
    62. 62. 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
    63. 63. Tests of attention and memory cont‟ oDigit span orepeat 3-52; 3-52-8; 3-52-8-67..” N: >5 o Visual grasp: “look away from stimulus” o Recency test o“recall sequence of stimuli / events” o Imitation (of examiner) / utilization (of objects presented)
    64. 64. 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
    65. 65. 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” o “Methodist episcopal” o “No if‟s end‟s or but‟s” o “Around the rugged rock the ragged rascal ran”
    66. 66. MOTOR SEQUENCING: KINETIC MELODY1. Hand position test (three-step hand sequence)2. Rhythm tapping tasks3. Go no go test4. Copying tasks (multiple loops)
    67. 67. FRONTAL RELEASE SIGN Grasp reflex  Snout reflex  Forceful grapping of object on touching palm  Palmomental or sole Sucking reflex  By touching the lips  Glabellar tap Groping reflex  Involuntary following with hand/eye of moving object Stimulus capture  Utilization behavior
    68. 68. Formal Tests• Abstract thinking and set shifting; L>R • Wisconsin Card Sorting Test• Visuo-motor track, conceptualization, set shift • Trail Making• Attention, shift sets; L>R • Stroop Color & Word Test• Planning • Tower of London Test • Block design • Maze lest
    69. 69. Wisconsin Card Sorting Test“Please sort the 60 cards under the 4 samples.I won‟t tell you the rule, but I will announce every mistake.The rule will change after 10 correct placements.”
    70. 70. Trail Making Test 5 B A 4 6 1 C 2 3 D 7Various levels of difficulty:1. “Please connect the letters in alphabetical order as fast as you can.”2. “Repeat, as in „1‟ but alternate with numbers in increasing order”
    72. 72. Tower of London TestsVarious levels of difficulty:e.g. “Please rearrange the balls on the pegs, so that each peg hasone ball only. Use as few movements as possible”
    73. 73. FRONTAL PATHOLOGY  Injury  Tumor  Abscess, infection  Dementia  Epilepsy  Stroke  Developmental
    74. 74. TRAUMATIC BRAIN INJURYo Gunshot woundo Closed head injury o Widespread stretching and shearing of fibers throughout o Frontal lobe more vulnerableo Contusions and intracerebral hematomas
    75. 75. FRONTAL LOBE INJURYAttention disorder – Language • Distractibility 1. Dynamic aphasiaMemory 2. Normal motor speech • Poor “forgetting to 3. Normal repetition remember” 4. Difficulty inThinking prepositioning  Concrete 5. Difficulty in structuring  Perseveration and sentence stereotypy, 6. Lack of coherence  unable to switch task 7. Socially inappropriate and disinhibited
    76. 76. FRONTAL LOBE INJURY CONT.Mood, affect, behavior 1. Reduced activity 2. Lack of drive and initiative 3. Lack of concern 4. Bouts of restlessness and uncoordinated behavior 5. Apathy, emotional blunting, indifference to the surrounding 6. Bouts of euphoria 7. Disinhibition – irritability and aggression 8. Witzelsucht – inappropriate facetiousness and tendency to pun
    77. 77. FRONTAL LOBE EPILEPSY  Clinical Features  EEG  Frequent seizure with clustering  May show no ictal or interictal  Brief stereotyped seizure abnormality  Nocturnal attacks  May show bilateral spike waves  Sudden onset and cessation  May show focal changes often  Absence of psychic aura widespread  Absence of postictal confusion  Imaging/ pathology  Rapid evolution with awareness  Hemartoma lost at onset  Benign tumors  Prominent complex bilateral motor  Gliomas automatism involving lower limbs  Angioma  Prominent ictal posturing and tonic  Dysplasia spasm  Post traumatic  Versive head and eye turning  Atrophy  Bizarre automatism  Tuberculoma  Frequent secondary generalization  Cysticercosis  Status epilepticus common
    78. 78. FRONTAL LOBE AND PSYCHIATRY Schizophrenia :  Personality disorder:  Involving dorsolateral prefrontal cortex Antisocial Personality  affective changes, disorder with impaired motivation, poor insight. and other impulsivity of frontal "defect symptoms  Evidence : lobe Neuropathologic studies, (23) in EEG studies, (24)  Attention deficit in radiological studies using CT measures, (25) syndrome with with MRI, (26) and in cerebral blood flow distractibility of frontal (CBF) studies. lobe
    79. 79. FRONTAL LOBE DEMENTIA Trouble in maintaining normal  Language Problems social and interpersonal  limited speech output, lack of functioning. speech spontaneity, stereotyping of phrases (ie., use of pat phrases They may violate rules of repeatedly and excessively), politeness and may make perseveration (a meaningless inappropriate remarks. persistence of verbal activity), a They may become emotionally decreased vocabulary, a considerable amount of repetition, aroused very easily. especially of brief words and Insensitivity – lack of consideration phrases. to others.  Often there is jargon and instead of being able to find the word to lack of restraint - stealing or describe an object, the person with unsocial behaviour this disease will give a description Obsession – of it instead (ie., a "watch" referred to as "something you tell the time Sexual misadventures,. with"). This means that the person may not be able to name objects Kluver Bucy Syndrome early in the disease.  hypersexuality, gluttony, and an  Eventually the person becomes obsession to touch and seize any mute for periods and then objects in the persons field of completely mute by the end of the vision. Overeating may lead to disease. considerable weight gain.
    80. 80. VASCULAR DISEASEo Common cause especially in elderlyo ACA territory infarction o Damage to medial frontal areao MCA territory o Dorsolateral frontal lobeo ACom aneurysm rupture o Personality change, emotional disturbance
    81. 81. FRONTAL LOBE DISEASE  Degenerative diseases – Pick‟s disease – Huntington‟s disease  Infectious diseases – Neurosyphilis – Herpes simplex encephalitis
    82. 82. FRONTAL LOBE DISEASE Tumors – Gliomas, meningiomas – subfrontal and olfactory groove meningiomas: profound personality changes and dementia Multiple Sclerosis – Frontal lobes 2nd highest number of plaques – euphoric/depressed mood, Memory problems, cognitive and behavioral effects
    83. 83. FRONTAL LOBE PATHOLOGYFrontal lobe abscess Meningioma
    84. 84. FRONTAL PATHOLOGYTuberous sclerosis Frontal glioblastoma