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The Frontal lobes - Mahidol University

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19/07/54<br />

415703 Cognitive Neuropsychology<br />

Week 6:<br />

<strong>The</strong> <strong>Frontal</strong> <strong>lobes</strong><br />

Naiphinich Kotchabhakdi, Ph.D.<br />

Director, Salaya Stem Cell R & D Project,<br />

Research Center for Neuroscience,<br />

Institute of Molecular Biosciences,<br />

<strong>Mahidol</strong> <strong>University</strong> Salaya Campus,<br />

999 Phutthamonthol 4 Road, Salaya, Phutthamonthol,<br />

Nakornpathom 73170 Thailand<br />

Email: scnkc@mahidol.ac.th or naiphinich@gmail.com<br />

Web: www.neuroscience.mahidol.ac.th<br />

Main Objectives:<br />

1. <strong>The</strong> <strong>Frontal</strong> <strong>lobes</strong> and their functions<br />

2. <strong>The</strong> Motor System<br />

3. Motor Cortical Organization in the <strong>Frontal</strong> Lobe<br />

4. <strong>The</strong> Prefrontal cortex<br />

5. <strong>The</strong> <strong>Frontal</strong> <strong>lobes</strong> and higher or executive brain<br />

functions<br />

6. Deep brain structures in <strong>Frontal</strong> lobe, e.g.,<br />

Limbic brain structures and their functions<br />

7. Neuropsychology of the <strong>Frontal</strong> <strong>lobes</strong> and<br />

executive brain function disorders.<br />

<strong>The</strong> <strong>Frontal</strong> lobe is an area in the brain of humans and other<br />

mammals, located at the front of each cerebral hemisphere and positioned<br />

anterior to (in front of) the parietal <strong>lobes</strong> and superior and anterior to the<br />

temporal <strong>lobes</strong> (i.e. directly behind the forehead or "temple"). It is<br />

separated from the parietal lobe by the post‐central gyrus primary motor<br />

cortex, which controls voluntary movements of specific body parts<br />

associated with the precentral gyrus posteriorly, inferiorly by lateral<br />

sulcus[slyvian] which separates it from the temporal lobe, superiorly by the<br />

superior margin of the hemisphere and anteriorly by the frontal pole.<br />

<strong>The</strong> frontal lobe contains most of the dopamine‐sensitive neurons in the<br />

cerebral cortex. <strong>The</strong> dopamine system is associated with reward, attention,<br />

short‐term term memory tasks, planning, and drive. Dopamine tends to limit and<br />

select sensory information arriving from the thalamus to the fore‐brain. A<br />

report from the National Institute of Mental Health says a gene variant that<br />

reduces dopamine activity in the prefrontal cortex is related to poorer<br />

performance and inefficient functioning of that brain region during working<br />

memory tasks, and to slightly increased risk for schizophrenia.<br />

<strong>Frontal</strong> lobe Anatomy<br />

On the lateral surface of the human brain, the central sulcus separates the frontal lobe from<br />

the parietal lobe. <strong>The</strong> lateral sulcus separates the frontal lobe from the temporal lobe.<br />

<strong>The</strong> frontal lobe can be divided into a lateral, polar, orbital (above the orbit; also called basal<br />

or ventral), and medial part. Each of these parts consists of particular gyri:<br />

∆ Lateral part: Precentral gyrus, lateral part of the superior frontal gyrus, middle frontal<br />

gyrus, inferior frontal gyrus.<br />

∆ Polar part: Transverse frontopolar gyri, frontomarginal gyrus.<br />

∆ Orbital part: Lateral orbital gyrus, anterior orbital gyrus, posterior orbital gyrus, medial<br />

orbital gyrus, gyrus rectus.<br />

∆ Medial part: Medial part of the superior frontal gyrus, cingulate gyrus.<br />

<strong>The</strong> gyri are separated by sulci. E.g., the precentral gyrus is in front of the central sulcus, and<br />

behind the precentral sulcus. <strong>The</strong> superior and middle frontal gyri are divided by the<br />

superior frontal sulcus. <strong>The</strong> middle and inferior frontal gyri are divided by the inferior frontal<br />

sulcus.<br />

In humans, the frontal lobe reaches full maturity around only after the 20s, marking the<br />

cognitive maturity associated with adulthood.<br />

Dr. Arthur Toga, a UCLA professor of neurology, found increased myelin in the frontal lobe<br />

white matter of young adults compared to that of teens. A typical onset of schizophrenia in<br />

early adult years correlates with poorly myelinated and thus inefficient connections<br />

between cells in the fore‐brain<br />

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Functional areas in the frontal <strong>lobes</strong><br />

<strong>The</strong> motor system is the part of the central nervous system that is involved with<br />

movement. It consists of the pyramidal and extrapyramidal system.<br />

<strong>The</strong> motor pathway also called pyramidal tract or the corticospinal tract start in the motor<br />

center of the cerebral cortex.<br />

<strong>The</strong>re are upper and lower motor neurons in the corticospinal tract.<br />

<strong>The</strong> motor impulses originates in the Giant pyramidal cells or Betz cells of the motor area i.e.<br />

precentral gyrus of cerebral cortex. <strong>The</strong>se are the upper motor neurons (UMN) of the<br />

corticospinal tract. <strong>The</strong> axons of these cells pass in the depth of the cerebral cortex to the<br />

Corona radiata and then to the Internal Capsule passing through the posterior branch of<br />

internal capsule and continue to descend in the Midbrain and the Medulla Oblongata. In<br />

the lower part of Medulla oblongata 80 to 85% of these fibers decussate (pass to the<br />

opposite side) and descend in the White matter of the Lateral funiculus of the spinal cord<br />

on the opposite side. <strong>The</strong> remaining 15 to 20% pass to the same side. Fibers for the<br />

extremities (limbs) pass 100% to the opposite side. <strong>The</strong> fibers of the corticospinal tract<br />

terminate at different levels in the Anterior horn of the Grey matter of the spinal cord.<br />

Here the Lower Motor Neurons (LMN) of the corticospinal cord are located. Peripheral motor<br />

nerves carry the motor impulses from the anterior horn to the voluntary muscles.<br />

Pyramidal motor system:<br />

Corticospinal tracts<br />

tracts is a collection of<br />

axons that travel between the cerebral cortex<br />

of the brain and the spinal cord.<br />

<strong>The</strong> corticospinal tract mostly contains motor axons.<br />

It actually consists of two separate tracts in the<br />

spinal cord: the lateral corticospinal tract and the<br />

anterior corticospinal tract.<br />

An understanding of these tracts leads to an<br />

understanding of why for the most part, one side of<br />

the body is controlled by the opposite side of the<br />

brain.<br />

<strong>The</strong> corticobulbar tract is also considered to be a<br />

pyramidal tract, though it carries signals to motor<br />

neurons of the cranial nerve nuclei, rather than the<br />

spinal cord.<br />

<strong>The</strong> neurons of the corticospinal tracts are referred<br />

to as pyramidal neurons. <strong>The</strong> name comes from the<br />

shape of the corticospinal tracts, which somewhat<br />

resemble pyramids as they pass through the<br />

medulla.<br />

<strong>The</strong> corticospinal tract is concerned specifically with<br />

discrete voluntary skilled movements, especially of<br />

the distal parts of the limbs. (Sometimes called<br />

"fractionated" movements)<br />

<strong>The</strong> motor pathway<br />

<strong>The</strong> corticospinal tract originates from pyramidal cells in layer V of the<br />

cerebral cortex.<br />

About half of its fibres arise from the primary motor cortex. Other<br />

contributions come from the supplementary motor area, premotor<br />

cortex, somatosensory cortex, parietal lobe, and cingulate gyrus. <strong>The</strong><br />

average fiber diameter is in the region of 10μm; around 3% of fibres are<br />

extra‐large (20μm) and arise from Betz cells, mostly in the leg area of the<br />

primary motor cortex.<br />

Upper motor neurons<br />

Upper motor neurons<br />

<strong>The</strong> neuronal cell bodies in the motor cortex, together with their axons<br />

that travel down through the brain stem and spinal cord are commonly<br />

referred to as upper motor neurons. It should be noted however, that<br />

they do not project to muscles, and thus the term 'motor neuron' is<br />

somewhat misleading.<br />

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Betz ells<br />

Anatomy of the motor cortex<br />

<strong>The</strong> motor cortex can be divided into four main parts:<br />

∆ the primary motor cortex (or M1, Broadman area #4),<br />

responsible for generating the neural impulses controlling<br />

execution of movement<br />

and the secondary motor cortices, including<br />

∆ the posterior parietal cortex, responsible for transforming<br />

visual information into motor commands<br />

∆ the premotor cortex, (Broadman areas #6, 8, 9,10)<br />

responsible for motor guidance of movement and control of<br />

proximal and trunk muscles of the body<br />

∆ and the supplementary motor area (or SMA), responsible<br />

for planning and coordination of complex movements such<br />

as those requiring two hands.<br />

Other brain regions outside the cortex are also of great<br />

importance to motor function, most notably the cerebellum and<br />

subcortical motor nuclei.<br />

<strong>The</strong> primary motor cortex (or M1) is a brain<br />

region that in humans is located in the posterior portion<br />

of the frontal lobe. It works in association with pre‐motor<br />

areas to plan and execute movements. M1 contains large<br />

neurons known as Betz cells which send long axons down<br />

the spinal cord to synapse onto alpha motor neurons<br />

which connect to the muscles. Pre‐motor areas are<br />

involved in planning actions (in concert with the basal<br />

ganglia) and refining movements based upon sensory<br />

input (this requires the cerebellum).<br />

Location of the Primary Motor Cortex (M1)<br />

<strong>The</strong> human primary motor cortex is located in the dorsal part of the precentral gyrus and the<br />

anterior bank of the central sulcus. <strong>The</strong> precentral gyrus is anterior to the postcentral gyrus from<br />

which it is separated by the central sulcus. Its anterior border is the precentral sulcus, while inferiorly<br />

it borders to the lateral fissure (Sylvian fissure). Medially, it is contiguous with the paracentral lobule.<br />

This area can also be identified by Brodmann area number 4.<br />

Layers of the Primary Motor Cortex (M1)<br />

<strong>The</strong> internal pyramidal layer (layer V) of the precentral cortex contains giant (70‐100 micrometers)<br />

pyramidal neurons (a.k.a. Betz cells), which send long axons to the contralateral motor nuclei of the<br />

cranial nerves and to the lower motor neurons in the ventral horn of the spinal cord. <strong>The</strong>se axons<br />

form the corticospinal tract. <strong>The</strong> Betz cells' along with their long axons are referred to as the upper<br />

motor neuron (UMN).<br />

"Homunculus" " or "Little Man"<br />

<strong>The</strong>re is a broadly somatotopic representation of the different body parts in the primary motor<br />

cortex in an arrangement called a motor homunculus (Latin: little man). <strong>The</strong> leg area is located close<br />

to the midline, and the head and face area located laterally on the convex side of the cerebral<br />

hemisphere (motor homunculus). <strong>The</strong> arm and hand motor area is the largest, and occupies the part<br />

of precentral gyrus, between the leg and face area. In humans, the lateral area of the primary motor<br />

cortex is arranged from top to bottom in areas that correspond to the buttocks, torso, shoulder,<br />

elbow, wrist, fingers, thumb, eyelids, lips and jaw. Interior sections of the motor area folding into the<br />

medial longitudinal fissure correspond with the legs.<br />

<strong>The</strong>se areas are not proportional to their size in the body with the lips, face parts and hands enjoying<br />

particularly large areas. Following amputation or paralysis, motor areas can shift to adopt new parts<br />

of the body<br />

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<strong>The</strong> Modern Era: Neuropsychology Syndrome<br />

Analysis, fMRI Studies, Clinical Neuropsychology<br />

Tests & Clinical Practice<br />

Two representational areas<br />

In primates, the primary motor cortex is unusual in having in its anterior and posterior<br />

areas two representations of the digits and wrist. ] <strong>The</strong> posterior areas can be activated by<br />

attention without any sensory feedback and has been suggested to be important for<br />

initiation of movements, while the anterior areas is dependent on sensory feedback. It<br />

can also be activated by imaginary finger movements and listening to speech done<br />

without actual movements. This anterior representation area has been suggested to be<br />

important executing movements involving complex sensoriomotor interactions.<br />

Pathway<br />

As the motor axons travel down through the cerebral white matter, they move closer<br />

together and form part of the posterior limb of the internal capsule.<br />

<strong>The</strong>y continue down into the brainstem, where some of them, after crossing over to the<br />

contralateral side, distribute to the cranial nerve motor nuclei. (Note: a few motor fibers<br />

synapse with lower motor neurons on the same side of the brainstem).<br />

After crossing over to the contralateral side in the medulla oblongata (pyramidal<br />

decussation), the axons travel down the spinal cord as the lateral corticospinal tract.<br />

Fibers that do not cross over in the brainstem travel down the separate ventral<br />

corticospinal tract and most of them cross over to the contralateral side in the spinal cord,<br />

shortly before reaching the lower motor neurons.<br />

<strong>The</strong> primary motor cortex receive thalamic input from the Ventral lateral nucleus of the<br />

Thalamus.<br />

Blood supply<br />

Branches of the middle cerebral artery provide most of<br />

the arterial blood supply for the primary motor cortex.<br />

<strong>The</strong> medial aspect (leg areas) is supplied by branches of<br />

the anterior cerebral artery.<br />

Neural input from the thalamus<br />

<strong>The</strong> primary motor cortex receive thalamic input from<br />

the Ventral lateral nucleus of the Thalamus.<br />

Pathology<br />

Lesions of the precentral gyrus result in paralysis of the<br />

contralateral side of the body (facial palsy, arm‐/leg<br />

monoparesis, hemiparesis) ‐ see upper motor neuron.<br />

<strong>The</strong> premotor cortex is an area of motor<br />

cortex lying within the frontal lobe of the brain. It<br />

extends 3mm anterior to the primary motor cortex,<br />

near the Sylvian fissure, before narrowing to<br />

approximately 1mm near the medial longitudinal<br />

fissure, which serves as the posterior border for the<br />

prefrontal cortex. <strong>The</strong> premotor cortex is largely<br />

equivalent to Brodmann area 6. Activity within this<br />

region is critical to the sensory guidance of<br />

movement and control of proximal and trunk muscles<br />

of the body.<br />

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<strong>The</strong> premotor cortex is dysgranular (a transition between the agranular motor cortex and the granular<br />

eulaminate frontal cortex), which means that there is only a faint granular lamina IV. This corresponds to Brodmann<br />

area 6, with the exception that the medial surface of this area is the site of the accessory motor cortex (also known as<br />

the supplementary motor area, or SMA).<br />

Afferents<br />

Subcortical<br />

Cortical<br />

<strong>The</strong> pre‐motor cortex receives inputs originating from other areas of the cortex, including the inferior and<br />

superior parietal lobules (from which it receives multimodal sensory information) and the frontal cortex<br />

(from which it receives information related to attention and motivation) [1]<br />

Efferents<br />

Subcortical<br />

Cortico‐spinal<br />

<strong>The</strong> axons of the premotor cortex contribute to the pyramidal bundle<br />

Striatum<br />

Axons of the Vth layer contribute to the corticostriate connection ; a massive connection involving almost<br />

all parts of the cortex<br />

Thalamus<br />

<strong>The</strong> premotor cortex sends axons to the motor thalamus. This comprises a part receiving cerebellar axons<br />

( nucleus Ventralis Intermedius Vim or VL), a part receiving pallidal axons (nucleus Ventralis oralis VO) and<br />

a part receiving nigral axons (nucleus Ventralis anterio VA). <strong>The</strong> Vim is separated into two parts one<br />

ventrolateral and one mediodorsal VImM. <strong>The</strong> premotor cortex sends axons electively to VImM and VO<br />

Central complex<br />

Subthalamic nucleus<br />

Cortical<br />

Physiology<br />

Mirror neurons are cells located in the premotor cortex, the part of the brain relevant to the planning, selection and<br />

execution of actions. It is a part of the Cerebral cortex.<br />

<strong>The</strong> supplementary<br />

motor area (SMA) is a part<br />

of the sensorimotor cerebral<br />

cortex (perirolandic, i.e. on each<br />

side of the Rolando or central<br />

sulcus). It was included, on purely<br />

cytoarchitectonic arguments, in<br />

area 6 of Brodmann and the<br />

Vogts. It is located on the medial<br />

face of the hemisphere, just in<br />

front of primary motor cortex. This<br />

is an element that appeared late in<br />

evolution, in monkeys, linked to<br />

the appearance of a true medial<br />

pallidum.<br />

Supplementary Motor Area (SMA)<br />

It has been found that the SMA is likely made up of two anatomically and functionally distinct parts, and was divided into the SMA proper<br />

(or: caudal SMA) and the pre‐SMA (or: rostral SMA). In primates, the SMA proper is analogous to area F3, whereas the pre‐SMA is<br />

analogous to area F6.<br />

In monkeys it is a part of the dysgranular cortex. This means an intermediate differentiation between the more posterior agranular motor<br />

cortex and the more anterior granular eulaminate frontal cortex.<br />

Function of SMA<br />

<strong>The</strong> SMA is implicated in the planning of motor actions and bimanual control. In contrast to the premotor cortex, the SMA has been<br />

implicated in actions that are under internal control, such as the performance of a sequence of movements from memory (as opposed to<br />

movements guided by a visual cue).<br />

Pre‐SMA is involved in acquiring new sequences. <strong>The</strong>re is more activity in these neurons when the sequence is new, compared to when it<br />

has been already learned. In contrast, SMA neurons are more active when performing a sequence already learned than one still being<br />

learned. This suggests that the SMA may be more involved in retrieving the sequence. SMA neurons are more active when the task<br />

requires the arrangement of multiple movements in the correct sequence and correct temporal order. For example, some SMA neurons<br />

"prefer" a specific order of movements to be performed. Other SMA neurons fire more for the preparation of a specific rank order. For<br />

example, a neuron can fire more when a monkey is preparing to initiate the third movement, irrespective of the sequence of the three<br />

movements.<br />

SMA and Pre‐SMA can be distinguished by various physiological techniques that delineate two different areas rostrocaudally. Field and<br />

unitary responses to electrical stimulation of the primary motor cortex were distinct in the caudal part, but minimal or absent in the rostral<br />

part. Intracortical microstimulation readily evoked limb or orofacial movements in the caudal part, but only infrequently in the rostral part.<br />

Neuronal responses to visual stimuli prevailed in the rostral part, but somatosensory responses were rare. <strong>The</strong> opposite was true in the<br />

caudal part. <strong>The</strong> rostral part, roughly corresponding to area 6a beta, was operationally defined as the presupplementary motor area (pre‐<br />

SMA). <strong>The</strong> caudal part was redefined as the SMA proper. Single‐cell activity in the pre‐SMA was quantitatively compared with that in the<br />

SMA proper in relation to a trained motor task. Phasic responses to visual cue signals indicating the direction of forthcoming arm‐reaching<br />

movement were more abundant in the pre‐SMA. Activity changes during the preparatory period, which lasted until the occurrence of the<br />

trigger signal for the reaching movement, were more frequent in the pre‐SMA. Phasic, movement‐related activity was more frequent in the<br />

SMA, and its onset was often time locked to the movement onset. In the pre‐SMA, the occurrences of response time locked to the<br />

movement‐trigger signal were more frequent than in the SMA. Among neurons in both areas, directional selectivity was found in all the<br />

cue, preparatory, and movement‐related responses.<br />

Recent considerations of the diverse activities in which the SMA and pre‐SMA play a role suggest existing theories may not fully capture<br />

the fundamental functions of these regions.<br />

<strong>The</strong> SMA is the most dorsal aspect of BA6 (extending medially towards the cingulate gyrus), the ventral aspect which extends down to the<br />

sylvian fissure is the secondary motor cortex (also BA6)<br />

Decussation and synapses<br />

Some of the neuronal cell bodies in the motor cortex send long axons to the motor<br />

cranial nerve nuclei mainly of the contralateral side of the midbrain (corticomesencephalic<br />

tract), pons (Corticopontine tract), and medulla oblongata (cortico‐bulbar<br />

tract), decussating just before they reach their target nuclei.<br />

<strong>The</strong>se are called geniculate fibers. Many more motor cortex neurons, however, extend<br />

fibers all the way down to the spinal cord (corticospinal tract).<br />

► Most of the corticospinal fibers (about 80%) cross over to the contralateral side in the<br />

medulla oblongata (pyramidal decussation). Those that cross in the medulla oblongata<br />

travel in the lateral corticospinal tract.<br />

► 10% enter the lateral corticospinal tract on the same side.<br />

► <strong>The</strong> remainder of them (10%) cross over at the level that they exit the spinal cord, and<br />

these travel in the anterior corticospinal tract.<br />

Whichever of these two tracts it travels in, a corticospinal axon will synapse with another<br />

neuron in the ventral horn. This ventral horn neuron is considered a second‐order neuron<br />

in this pathway, but is not part of the corticospinal tract itself.<br />

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From cerebral to motor neurons<br />

<strong>The</strong> motor axons move closer together as they travel down through the cerebral white<br />

matter, and form part of the posterior limb of the internal capsule.<br />

<strong>The</strong> motor fibers continue down into the brainstem. <strong>The</strong> bundle of corticospinal axons is<br />

visible as two column‐like structures ("pyramids") on the ventral surface of medulla<br />

oblongata ‐ this is where the name pyramidal tract comes from.<br />

After the decussation, the axons travel down the spinal cord as the lateral corticospinal tract.<br />

Fibers that do not cross over in the medulla oblongata travel down the separate anterior<br />

corticospinal tract, and most of them cross over to the contralateral side in the spinal cord,<br />

shortly before reaching the lower motor neurons.<br />

Lower motor neurons<br />

In the spinal cord, the axons of the upper motor neuron connect (most of them via<br />

interneurons, but to a lesser extent also via direct synapses) with the lower motor neurons,<br />

located in the ventral horn of the spinal cord.<br />

In the brainstem, the lower motor neurons are located in the motor cranial nerve nuclei<br />

(oculomotor, trochlear, motor nucleus of the trigeminal nerve, abducens, facial, accessory,<br />

hypoglossal). <strong>The</strong> lower motor neuron axons leave the brain stem via motor cranial nerves<br />

and the spinal cord via anterior roots of the spinal nerves respectively, end‐up at the<br />

neuromuscular plate and provide motor innervation for voluntary muscles.<br />

<strong>The</strong> Principles of Motor Controls of Movements:<br />

1. <strong>The</strong> central nervous system (CNS) has to choose the right group<br />

of muscles by selecting specific pathways.<br />

2. <strong>The</strong> CNS must give the right amount of excitatory or inhibitory<br />

inputs (“Command”) to specific motoneuron pools<br />

3. <strong>The</strong> excitatory and inhibitory commands must be regulated<br />

“Spatially” and “Temporally”.<br />

4. <strong>The</strong> CNS must regulate the following parameters:<br />

‐ force<br />

‐displacement (distance)<br />

‐ velocity, acceleration or deceleration<br />

<strong>The</strong> extrapyramidal system is a neural network located in the<br />

brain that is part of the motor system involved in the coordination of movement.<br />

<strong>The</strong> system is called "extrapyramidal" to distinguish it from the tracts of the motor<br />

cortex that reach their targets by traveling through the "pyramids" of the medulla.<br />

<strong>The</strong> pyramidal pathways (corticospinal and some corticobulbar tracts) may directly<br />

innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn<br />

cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers<br />

around the modulation and regulation (indirect control) of anterior (ventral) horn<br />

cells.<br />

Extrapyramidal tracts are chiefly found in the reticular formation of the pons and<br />

medulla, and target neurons in the spinal cord involved in reflexes, locomotion,<br />

complex movements, and postural control. <strong>The</strong>se tracts are in turn modulated by<br />

various parts of the central nervous system, including the nigrostriatal pathway,<br />

the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory<br />

areas of the cerebral cortex. All of these regulatory components can be considered<br />

part of the extrapyramidal system, in that they modulate motor activity without<br />

directly innervating motor neurons.<br />

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Corticospinal tract damage<br />

Damage to the descending motor pathways anywhere<br />

along the trajectory from the cerebral cortex to the lower<br />

end of the spinal cord gives rise to a set of symptoms<br />

called the "upper motor neuron syndrome". A few days<br />

after the injury to the upper motor neurons a pattern of<br />

motor signs and symptoms appears, including spasticity,<br />

the decreased vigor (and increased threshold) of<br />

superficial reflexes, a loss of the ability to perform fine<br />

movements, and an extensor plantar response known as<br />

the Babinski sign. [<br />

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Basal ganglion and<br />

Extrapyramidal<br />

System<br />

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<strong>The</strong> extrapyramidal system can be affected in a number of ways,<br />

which are revealed in a range of extrapyramidal symptoms (EPS),<br />

also known as extrapyramidal side‐effects (EPSE), such as akinesia<br />

(inability to initiate movement) and akathisia (inability to remain<br />

motionless).<br />

Extrapyramidal symptoms (EPS) are various movement disorders<br />

such as acute dystonic reactions, pseudoparkinsonism, or akathisia<br />

suffered as a result of taking dopamine antagonists, usually<br />

antipsychotic (neuroleptic) drugs, which are often used to control<br />

psychosis.<br />

<strong>The</strong> Simpson‐Angus Scale (SAS) and the Barnes Akathisia Rating Scale<br />

(BARS) are used to measure extrapyramidal symptoms<br />

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<strong>The</strong> frontal eye fields (FEF) is a region located in the premotor cortex,<br />

which is part of the frontal cortex of the primate brain.<br />

Function<br />

<strong>The</strong> cortical area called frontal eye fields (FEF) plays an important role in the control of<br />

visual attention and eye movements. Electrical stimulation in the FEF elicits saccadic eye<br />

movements. <strong>The</strong> FEF have a topographic structure and represents saccade targets in<br />

retinotopic coordinates.<br />

<strong>The</strong> frontal eye field is reported to be activated during the initiation of eye movements,<br />

such as voluntary saccades and pursuit eye movements. <strong>The</strong>re is also evidence that it<br />

plays a role in purely sensory processing and that it belongs to a “fast brain” system<br />

through a superior colliculus – medial dorsal nucleus –FEF ascending pathway.In<br />

humans, its earliest activations in regard to visual stimuli occur at 45 ms with activations<br />

related to changes in visual stimuli within 45–60 ms (these are comparable with<br />

response times in the primary visual cortex). This fast brain pathway also provides<br />

auditory input at even shorter times starting at 24 ms and being affected by auditory<br />

characteristics at 30–60 ms. <strong>The</strong> FEF constitutes together with the supplementary eye<br />

fields (SEF), the intraparietal sulcus (IPS) and the superior colliculus (SC) one of the most<br />

important brain areas involved in the generation and control of eye movements,<br />

particularly in the direction contralateral to the frontal eye fields' location.<br />

Brain: <strong>Frontal</strong> eye fields<br />

<strong>Frontal</strong> eye fields is roughly located<br />

between regions #4, #6, and #8<br />

Brodmann area 8, or BA8, is part of the<br />

frontal cortex in the human brain. Situated just<br />

anterior to the premotor cortex (BA6), it includes the<br />

frontal eye fields (so‐named because they are<br />

believed to play an important role in the control of<br />

eye movements). Damage to this area, by stroke,<br />

trauma or infection, causes tonic deviation of the<br />

eyes towards the side of the injury. This finding<br />

occurs during the first few hours of an acute event<br />

such as cerebrovascular infarct (stroke) or<br />

hemorrhage (bleeding).<br />

Distinctive features (Brodmann‐1905): compared to Brodmann area 6‐<br />

1909, area 8 has a diffuse but clearly present internal granular layer (IV);<br />

sublayer 3b of the external pyramidal layer (III) has densely distributed<br />

medium sized pyramidal cells; the internal pyramidal layer (V) has larger<br />

ganglion cells densely distributed with some granule cells interspersed; the<br />

external granular layer (II) is denser and broader; cell layers are more<br />

distinct; the abundance of cells is somewhat greater.<br />

Other Functions<br />

<strong>The</strong> area is involved in the management of uncertainty. A functional<br />

magnetic resonance imaging study demonstrated that brodmann area 8<br />

activation occurs when test subjects experience uncertainty, and that with<br />

increasing uncertainty there is increasing activation.<br />

An alternative interpretation is that this activation in frontal cortex encodes<br />

hope, a higher‐order expectation positively correlated with uncertainty.<br />

Brain: Brodmann area 8<br />

Supplementary eye fields (SEF) are areas on the<br />

dorsal‐medial surface of frontal lobe of the primate brain<br />

that are involved in planning and control of saccadic eye<br />

movements. <strong>The</strong> SEF was first characterized by John Schlag<br />

and colleagues as an area where low intensity electrical<br />

stimulation can evoke saccades, similar to the more lateral<br />

frontal eye fields. More recently it was shown that SEF<br />

stimulation produces coordinated gaze movements of both<br />

the eyes and head. Neural recordings in the SEF show signals<br />

related to both vision and saccades somewhat like the<br />

frontal eye fields and superior colliculus, but currently most<br />

investigators think that the SEF has a special role in high<br />

level aspects of saccade control, like complex spatial<br />

transformations, learned transformations, and executive<br />

cognitive functions<br />

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<strong>Frontal</strong> lobe Executive Functions<br />

<strong>The</strong> executive functions of the frontal <strong>lobes</strong> involve the ability<br />

to recognize future consequences resulting from current<br />

actions, to choose between good and bad actions (or better<br />

and best), override and suppress unacceptable social<br />

responses, and determine similarities and differences<br />

between things or events. <strong>The</strong>refore, it is involved in higher<br />

mental functions.<br />

<strong>The</strong> frontal <strong>lobes</strong> also play an important part in retaining<br />

longer term memories which are not task‐based. <strong>The</strong>se are<br />

often memories associated with emotions derived from input<br />

from the brain's limbic system. <strong>The</strong> frontal lobe modifies those<br />

emotions to generally fit socially acceptable norms.<br />

Psychological tests that measure frontal lobe function include<br />

finger tapping, Wisconsin Card Sorting Task, and measures of<br />

verbal and figural fluency.<br />

Comparative Neurobiology:<br />

Evolutionary Consideration<br />

COMPARATIVE BRAIN<br />

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สมองคน<br />

<strong>Frontal</strong> lobe Evolution<br />

For many years, many scientists thought that the frontal<br />

lobe was disproportionately enlarged in humans<br />

compared to other primates. <strong>The</strong>y thought that this was<br />

an important feature of human evolution and was the<br />

primary reason why human cognition is different from<br />

that of the other primates.<br />

However, this view has been challenged by newer<br />

research. Using magnetic resonance imaging to determine<br />

the volume of the frontal cortex in humans, all extant ape<br />

species and several monkey species, Semendeferi et al.<br />

found that the human frontal cortex was not relatively<br />

larger than the cortex in the other great apes but was<br />

relatively larger than the frontal cortex in the lesser apes<br />

and the monkeys<br />

<strong>The</strong> limbic system is also tightly connected to the<br />

prefrontal cortex.<br />

Some scientists contend that this connection is<br />

related to the pleasure obtained from solving problems. To<br />

cure severe emotional disorders, this connection was<br />

sometimes surgically severed, a procedure of<br />

psychosurgery, called a prefrontal lobotomy. Patients who<br />

underwent this procedure often became passive and<br />

lacked all motivation.<br />

<strong>The</strong>re is circumstantial evidence that the limbic<br />

system also provides a custodial function for the<br />

maintenance of a healthy conscious state of mind.<br />

“Psychosurgery”<br />

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Psychosurgery<br />

In the early 20th century, a medical treatment for mental illness,<br />

first developed by Portuguese neurologist Egas Moniz, involved<br />

damaging the pathways connecting the frontal lobe to the limbic<br />

system. <strong>Frontal</strong> lobotomy (sometimes called frontal leucotomy)<br />

successfully reduced distress but at the cost of often blunting the<br />

subject's emotions, volition and personality. <strong>The</strong> indiscriminate use<br />

of this psychosurgical procedure, combined with its severe side<br />

effects and dangerous nature, gained it a bad reputation. <strong>The</strong><br />

frontal lobotomy has largely died out as a psychiatric treatment.<br />

More precise psychosurgical procedures are still used, although<br />

rarely. <strong>The</strong>y may include anterior capsulotomy (bilateral thermal<br />

lesions of the anterior limbs of the internal capsule) or the bilateral<br />

cingulotomy (involving lesions of the anterior cingulate gyri) and<br />

might be used to treat otherwise untreatable obsessional disorders<br />

or clinical depression<br />

<strong>The</strong>ories of frontal lobe functions can be differentiated into four categories:<br />

∆ Single‐process theories. Posit "that damage to a single process or system is responsible for a<br />

number of different dysexecutive symptoms” (Burgess, 2003, p. 309).<br />

∆ Multi‐process theories. Propose “that the frontal lobe executive system consists of a number of<br />

components that typically work together in everyday actions [(heterogeneity of function)]“ (Burgess,<br />

2003, p. 310).<br />

∆ Construct‐led theories. Assume “that most if not all frontal functions can be explained by one<br />

construct (homogeneity of function) such as working memory or inhibition” (Stuss, 1999, p. 348; cf.<br />

Burgess & Simons, 2005).<br />

∆ Single‐symptom theories. Suggest that a specific dysexecutive symptom (e.g., confabulation) is<br />

related to the processes and construct of the underlying structures (cf. Burgess & Simons, 2005).<br />

Stuss (1999) suggests a differentiation into two categories according to homogeneity and<br />

heterogeneity of function.<br />

Further theoretical approaches to frontal lobe function include:<br />

∆ Grafman's managerial knowledge units (MKU) / structured event complex (SEC) approach (cf. Wood<br />

& Grafman, 2003)<br />

∆ Miller & Cohen's integrative theory of prefrontal functioning (e.g. Miller & Cohen, 2001)<br />

∆ Rolls's stimulus‐reward approach and Stuss's anterior attentional functions (Burgess & Simons,<br />

2005; Burgess, 2003; Burke, 2007).<br />

It may be highlighted that the theories described above differ in their focus on certain<br />

processes/systems or construct‐lets. Stuss (1999) remarks that the question of homogeneity (single<br />

construct) or heterogeneity (multiple processes/systems) of function “may represent a problem of<br />

semantics and/or incomplete functional analysis rather than an unresolvable dichotomy” (p. 348).<br />

However, further research will show if a unified theory of frontal lobe function that fully accounts for<br />

the diversity of functions will be available.<br />

Damage to the frontal <strong>lobes</strong> can lead to a variety of results:<br />

Case Study<br />

Mr. Phineas Gage<br />

Published in<br />

New England<br />

Journal of Medicine<br />

in 1860<br />

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Brodmann’s area is a region of the cerebral cortex defined based on<br />

its cytoarchitectonics, or organization of cells<br />

Brodmann areas were originally defined and numbered by the German neurologist<br />

Korbinian Brodmann basedonthecytoarchitecture organisation of neurons he<br />

observed in the cerebral cortex using the Nissl stain. Brodmann published his maps<br />

of cortical areas in humans, monkeys, and other species in 1909, along with many<br />

other findings and observations regarding the general cell types and laminar<br />

organization of the mammalian cortex. (<strong>The</strong> same Brodmann area number in<br />

different species does not necessarily indicate homologous areas.)<br />

A more detailed and verifiable cortical map have since been published by Constantin von<br />

Economo and Georg N. Koskinas which greatly improves the quality of the cytoarchitectonic<br />

classifications.<br />

Many of the areas Brodmann defined based solely on their neuronal organization have since<br />

been correlated closely to diverse cortical functions. For example, Brodmann areas 1, 2 and<br />

3aretheprimary somatosensory cortex; area4istheprimary motor cortex; area17isthe<br />

primary visual cortex; and areas 41 and 42 correspond closely to primary auditory cortex.<br />

Higher order functions of the association cortical areas are also consistently localized to the<br />

same Brodmann areas by neurophysiological, functional imaging, and other methods (e.g.,<br />

the consistent localization of Broca's speech and language area to the left Brodmann areas<br />

44 and 45). However, functional imaging can only identify the approximate localization of<br />

brain activations in terms of Brodmann areas since their actual boundaries in any individual<br />

brain requires its histological examination.<br />

Brodmann areas for human & non‐human primates<br />

Brodmann’s areas 3D<br />

map: Lateral Surface<br />

map: Medial Surface<br />

Brodmann areas for human & non‐human primates<br />

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Paul Pierre Broca (June 28, 1824 –<br />

July 9, 1880) was a French physician,<br />

anatomist, and anthropologist. He was<br />

born in Sainte-Foy-la-Grande, France.<br />

He is best known for his research on<br />

Broca's area, a region of the frontal<br />

lobe that has been named after him.<br />

Broca's legacy<br />

<strong>The</strong> discovery of Broca's area revolutionized the<br />

understanding of speech production. New research<br />

has found that dysfunction in the area may lead to<br />

other speech disorders such as stuttering and<br />

apraxia of speech. Recent anatomical<br />

neuroimaging studies have shown that the pars<br />

opercularis of Broca's area is anatomically smaller<br />

in individuals who stutter whereas the pars<br />

triangularis appears to be normal.<br />

Speech research<br />

Broca is most famous for his discovery of the speech production center of the brain<br />

located in the ventroposterior region of the frontal <strong>lobes</strong> (now known as Broca's<br />

area). He arrived at this discovery by studying the brains of aphasic patients. His first<br />

patient in the Bicêtre Hospital was Leborgne, nicknamed "Tan" due to his inability to<br />

clearly speak any words other than "tan".<br />

In 1861, through post‐mortem autopsy, Broca determined that Tan had a lesion<br />

caused by syphilis in the left cerebral hemisphere. This lesion was determined to<br />

cover the area of the brain important for speech production. (Although history<br />

credits this discovery to Broca, it should be noted that another French neurologist,<br />

Marc acDax, made similar observations o s a generation e earlier.) e ) Today the brains ba sof many<br />

of Broca's aphasic patients are still preserved in the Musée Dupuytren, and his<br />

collection of casts in the Musée d'Anatomie Delmas‐Orfila‐Rouvière.<br />

Patients with damage to Broca's area and/or to neighboring regions of the left<br />

inferior frontal lobe are often categorized clinically as having Broca's aphasia. This<br />

type of aphasia, which often involves impairments in speech output, can be<br />

contrasted with Wernicke's aphasia, named for Karl Wernicke, which is<br />

characterized by damage to more posterior regions of the left hemisphere (in the<br />

superior temporal lobe), and by greater impairments in speech comprehension. This<br />

is an example of a double dissociation, an important tool used by<br />

neuropsychologists to investigate brain function.<br />

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Paul Broca (1824-1880)<br />

Tan’s Brain<br />

(removed in 1861)<br />

Now in the Museum of Man, Paris<br />

Expressive aphasia, known as Broca's aphasia in clinical<br />

neuropsychology and agrammatic aphasia in cognitive<br />

neuropsychology, is an aphasia caused by damage to or<br />

developmental issues in anterior regions of the brain, including (but<br />

not limited to) the left inferior frontal region known as Broca's area<br />

(Brodmann area 44 and Brodmann area 45)<br />

Presentation<br />

Sufferers of this form of aphasia exhibit the common problem of agrammatism. For them, speech is difficult to initiate,<br />

non‐fluent, labored, and halting. Similarly, writing is difficult as well. Intonation and stress patterns are deficient.<br />

Language g is reduced to disjointed words and sentence construction is poor, omitting function words and inflections<br />

(bound morphemes). A person with expressive aphasia might say "Son ... <strong>University</strong> ... Smart ... Boy ... Good ... Good ... "<br />

For example, in the following passage, a Broca's aphasic patient is trying to explain how he came to the hospital for<br />

dental surgery:<br />

Yes... ah... Monday... er... Dad and Peter H... (his own name), and Dad.... er... hospital... and ah... Wednesday...<br />

Wednesday, nine o'clock... and oh... Thursday... ten o'clock, ah doctors... two... an' doctors... and er... teeth...<br />

yah.[1]<br />

In extreme cases, patients may be only able to produce a single word. <strong>The</strong> most famous case of this was Paul Broca's<br />

patient Leborgne, nicknamed "Tan", after the only syllable he could say. Even in such cases, over-learned and rote-learned<br />

speech patterns may be retained—for instance, some patients can count from one to ten, but cannot produce the same<br />

numbers in ordinary conversation.<br />

While word comprehension is generally preserved, meaning interpretation dependent on syntax and phrase structure is<br />

substantially impaired. This can be demonstrated by using phrases with unusual structures. A typical Broca's aphasic<br />

patient will misinterpret "the dog is bitten by the man" by switching the subject and object. Patients who recover go on to<br />

say that they knew what they wanted to say but could not express themselves. Residual deficits will often be seen.<br />

Broca's area is a region of the hominid brain<br />

with functions linked to speech production.<br />

<strong>The</strong> production of language has been linked to the<br />

Broca’s area since Pierre Paul Broca reported<br />

impairments in two patients. <strong>The</strong>y had lost the<br />

ability to speak after injury to the posterior inferior<br />

frontal gyrus of the brain. Since then, the<br />

approximate region he identified has become<br />

known as Broca’s area, and the deficit in language<br />

production as Broca’s aphasia. Broca’s area is now<br />

typically defined in terms of the pars opercularis<br />

and pars triangularis of the inferior frontal gyrus,<br />

represented in Brodmann’s<br />

cytoarchitectonic map<br />

as areas 44 and 45. Studies of chronic aphasia have<br />

implicated an essential role of Broca’s area in<br />

various speech and language functions. Further,<br />

functional MRI studies have also identified<br />

activation patterns in Broca’s area associated with<br />

various language tasks. However, slow destruction<br />

of the Broca's area by brain tumors can leave<br />

speech relatively intact suggesting its functions can<br />

shift to nearby areas in the brain.<br />

Brodmann area 44, , or BA44<br />

44, is part of the frontal<br />

cortex in the human brain. Situated just anterior to premotor<br />

cortex (BA6) and on the lateral surface, inferior to BA9.<br />

This area is also known as pars opercularis (of the inferior<br />

frontal gyrus), and it refers to a subdivision of the<br />

cytoarchitecturally defined frontal region of cerebral cortex. In<br />

the human it corresponds approximately to the opercular part<br />

of inferior frontal gyrus (H). Thus, it is bounded caudally by the<br />

inferior precentral sulcus (H) and rostrally by the anterior<br />

ascending limb of lateral sulcus (H). It surrounds the diagonal<br />

sulcus (H). In the depth of the lateral sulcus it borders on the<br />

insula. Cytoarchitectonically it is bounded caudally and dorsally<br />

by the agranular frontal area 6, dorsally by the granular frontal<br />

area 9 and rostrally by the triangular area 45 (Brodmann‐1909).<br />

Together with left‐hemisphere BA 45, the left hemisphere . BA<br />

44 comprises Broca's area a region involved in semantic tasks.<br />

Some data suggest that BA44 is more involved in phonological<br />

and syntactic processing. Some recent findings also suggest the<br />

implication of this region in music perception. In 95.5% of righthanders<br />

and 61.4% of left‐handers, therefore about 90% of the<br />

clinical population, speech is lateralised in the left hemisphere.<br />

Brain: Brodmann area 44<br />

7/19/2011 NEUROPSYCHIATRY 143<br />

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Brodmann area 45 (BA45),<br />

is part of the frontal<br />

cortex in the human brain. Situated on the lateral surface,<br />

inferior to BA9 and adjacent to BA46. This area is also known as<br />

pars triangular (of the inferior frontal gyrus). In the human, it<br />

occupies the triangular part of inferior frontal gyrus (H) and, surrounding<br />

the anterior horizontal limb of lateral sulcus (H), a portion of the orbital<br />

part of inferior frontal gyrus (H). Bounded caudally by the anterior<br />

ascending limb of lateral sulcus (H), it borders on the insula in the depth<br />

of the lateral sulcus. Cytoarchitectonically it is bounded caudally by the<br />

opercular area 44 (BA44), rostrodorsally by the middle frontal area 46<br />

(BA46) and ventrally by the orbital area 47 (BA47) (Brodmann‐1909).<br />

Together with BA 44 it comprises Broca's area, a region which is active in<br />

semantic tasks, such as semantic decision tasks (determining whether a<br />

word represents an abstract or a concrete entity) and generation tasks<br />

(generating a verb associated with a noun).<br />

<strong>The</strong> precise role of BA45 in semantic tasks remains controversial. For<br />

some researchers, its role would be to subserve semantic retrieval or<br />

semantic working memory processes. Under this view, BA44 and BA45<br />

would together guide recovery of semantic information and evaluate the<br />

recovered information with regards to the criterion appropriate to a<br />

given context. A slightly modified account of this view is that activation<br />

of BA45 is needed only under controlled semantic retrieval, when strong<br />

stimulus‐stimulus associations are absent. For other researchers, BA45's<br />

role is not restricted to semantics per se, but to all activities which<br />

require task‐relevant representations from among competing<br />

representations.<br />

Brain: Brodmann area 45<br />

Brodmann area 47, , or BA47<br />

47, is part of<br />

the frontal cortex in the human brain. Curving from the<br />

lateral surface of the frontal lobe into the ventral<br />

(orbital) frontal cortex. It is below areas BA10 and BA45,<br />

and beside BA11.<br />

This area is also known as orbital area 47. In the human,<br />

on the orbital surface it surrounds the caudal portion of<br />

the orbital sulcus (H) from which it extends laterally into<br />

the orbital part of inferior frontal gyrus (H).<br />

Cytoarchitectonically yoac eco cayit is bounded caudally by the<br />

triangular area 45, medially by the prefrontal area 11 of<br />

Brodmann‐1909, and rostrally by the frontopolar area 10<br />

(Brodmann‐1909).<br />

It incorporates the region that Brodmann identified as<br />

"Area 12" in the monkey, and therefore, following the<br />

suggestion of Michael Petrides, some contemporary<br />

neuroscientists refer to the region as "BA47/12."<br />

BA47 has been implicated in the processing of syntax<br />

in spoken and signed languages, and more recently in<br />

musical syntax.<br />

Brain: Brodmann area 47<br />

<strong>The</strong> Wernicke's area is classically located as<br />

the posterior section of the superior temporal gyrus<br />

(STG) in the left (or dominant) cerebral hemisphere.<br />

This area encircles the auditory cortex on the Sylvian<br />

fissure (part of the brain where the temporal lobe<br />

and parietal lobe meet). This area is<br />

neuroanatomically described as the posterior part of<br />

Brodmann area 22.<br />

However, there is an absence of consistent<br />

definitions as to its location. Some identify it with<br />

the unimodal auditory association in the superior<br />

temporal gyrus anterior to the primary auditory<br />

cortex. Others include also adjacent parts of the<br />

heteromodal cortex in BA 39 and BA40 in the<br />

parietal lobe.<br />

While previously thought to connect Wernicke's area<br />

and Broca's area, new research demonstrates that<br />

the arcuate fasciculus instead connects to posterior<br />

receptive areas with premotor/motor areas, and not<br />

to Broca's area<br />

Wernicke and aphasia<br />

Wernicke's area is named after Carl Wernicke, a German neurologist and psychiatrist who, in<br />

1874, hypothesized a link between the left posterior section of the superior temporal gyrus<br />

and the reflexive mimicking of words and their syllables that associated the sensory and motor<br />

images of spoken words. He did this on the basis of the location of brain injuries that caused<br />

aphasia. Receptive aphasia in which such abilities are preserved is now sometimes called<br />

Wernicke's aphasia. In this condition there is a major impairment of language comprehension,<br />

while speech retains a natural‐sounding rhythm and a relatively normal syntax. Language as a<br />

result is largely meaningless (a condition sometimes called fluent or jargon aphasia).<br />

While neuroimaging and lesion evidence generally support the idea that malfunction of or damage to<br />

Wernicke's area is common in people with receptive aphasia, this is not always so. Some people may use<br />

the right hemisphere for language, and isolated damage of Wernicke's area cortex (sparing white matter<br />

and other areas) may not cause severe receptive aphasia. Even when patients with Wernicke's area lesions<br />

have comprehension deficits, these are usually not restricted to language processing alone. For example,<br />

one study found that patients with posterior lesions also had trouble understanding nonverbal sounds like<br />

animal and machine noises. In fact, for Wernicke's area, the impairments in nonverbal sounds were<br />

statistically stronger than for verbal sounds.<br />

Right homologous area<br />

Research using Transcranial magnetic stimulation suggests that the area corresponding to the Wernicke’s<br />

area in the non‐dominant cerebral hemisphere has a role in processing and resolution of subordinate<br />

meanings of ambiguous words—such as (‘‘river’’) when given the ambiguous word (‘‘bank’’). In contrast,<br />

the Wernicke's area in the dominant hemisphere processes dominant word meanings (‘‘teller’’ given<br />

‘‘bank’’).<br />

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<strong>The</strong> Wernicke-Geschwind model of<br />

language<br />

Wernicke created an early neurological model<br />

of language, that later was revived by Norman<br />

Geschwind. <strong>The</strong> model is known as the<br />

Wernicke‐Geschwind model.<br />

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Prefrontal<br />

cortex<br />

Brodmann area 9, , or BA9, is part of the<br />

frontal cortex in the human brain. It<br />

contributes to the dorsolateral prefrontal<br />

cortex.<br />

Brodmann area 9 refers to a cytoarchitecturally defined<br />

portion of the frontal lobe of the guenon (Old world<br />

monkeys). Brodmann‐1909 regarded it on the whole as<br />

topographically and cytoarchitecturally homologous to the<br />

granular frontal area 9 and frontopolar area 10 in the<br />

human. Distinctive features (Brodmann‐1905): unlike<br />

Brodmann area 6‐1909, area 9 has a distinct internal<br />

granular layer (IV); unlike Brodmann area 6 or Brodmann<br />

area 8‐1909 its internal pyramdal layer (V) is divisible into<br />

two sublayers, an outer layer 5a of densely distributed<br />

medium sized ganglion cells that partially merges with<br />

layer IV, and an inner, clearer, cell‐poor layer 5b; the<br />

pyramidal cells of sublayer 3b of the external pyramidal<br />

layer (III) are smaller and sparser in distribution; the<br />

external granular layer (II) is narrow, with small numbers<br />

of sparsely distributed granule cells.<br />

Brain: Brodmann area 9<br />

<strong>The</strong> dorsolateral prefrontal cortex (DL‐PFC or DLPFC),<br />

according to a more restricted definition, is roughly equivalent to Brodmann areas 9 and 46.<br />

According to a broader definition DL‐PFC consists of the lateral portions of Brodmann areas<br />

9 – 12, of areas 45, 46, and the superior part of area 47.<strong>The</strong>se regions mainly receive their<br />

blood supply from the middle cerebral artery. With respect to neurotransmitter systems,<br />

there is evidence that dopamine plays a particularly important role in DL‐PFC.<br />

DL‐PFC is connected to the orbitofrontal cortex, and to a variety of brain areas, which<br />

include the thalamus, parts of the basal ganglia (the dorsal caudate nucleus), the<br />

hippocampus, and primary and secondary association areas of neocortex, including<br />

posterior temporal, parietal, and occipital areas.<br />

DL‐PFC is the last area, 45th, to develop myelinate in the human cerebrum<br />

DL‐PFC serves as the highest h cortical area responsible for motor planning, organization, i and<br />

regulation. It plays an important role in the integration of sensory and mnemonic<br />

information and the regulation of intellectual function and action. It is also involved in<br />

working memory. However, DL‐PFC is not exclusively responsible for the executive<br />

functions. All complex mental activity requires the additional cortical and subcortical<br />

circuits with which the DL‐PFC is connected.<br />

Damage to the DL‐PFC can result in the dysexecutive syndrome, [4] which leads to problems<br />

with affect, social judgement, executive memory, abstract thinking and intentionality. [<br />

Lucid dream states<br />

More recent research has found a connection between the DL‐PFC and lucid dream states<br />

in which executive function is retained<br />

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Brodmann area 10, or BA10<br />

is the<br />

frontopolar part of the frontal cortex in the human brain.<br />

BA10 was originally defined in terms of microscopic<br />

cytoarchitecturic traits in autopsy brains; modern functional<br />

imaging research cannot directly identify these boundaries<br />

and the terms anterior prefrontal, rostral prefrontal cortex<br />

and frontopolar prefrontal cortex are used to refer to the<br />

area in the most anterior part of the frontal cortex that<br />

approximates to or principally covers BA10.<br />

BA10 is the largest cytoarchitectonic area in the human<br />

brain. It has been described as "one of the least well<br />

understood dregions of the human brain". Present research<br />

suggests that it is involved in strategic processes in memory<br />

retrieval and executive function. During human evolution,<br />

the functions in this area resulted in its expansion relative to<br />

the rest of the brain.<br />

Although this region is extensive in humans, its function is poorly understood.<br />

Koechlin & Hyafil have proposed that processing of 'cognitive branching' is the<br />

core function of the frontopolar cortex. Cognitive branching enables a<br />

previously running task to be maintained in a pending state for subsequent<br />

retrieval and execution upon completion of the ongoing one. Many of our<br />

complex behaviors and mental activities require simultaneous engagement of<br />

multiple tasks, and they suggest the anterior prefrontal cortex may perform a<br />

domain‐general function in these scheduling operations. However, other<br />

hypotheses have also been proffered, such as those by Burgess et al.<br />

Brain: Brodmann area 10<br />

Brodmann area 11 is one of Brodmann's<br />

cytologically defined regions of the brain. It is<br />

involved in planning, reasoning, and decision<br />

making.<br />

Brodmann area 11, or BA11, is part of the frontal cortex in the<br />

human brain. BA11 covers the medial part of the ventral surface of<br />

the frontal lobe.<br />

Prefrontal area 11 of Brodmann‐1909 is a subdivision of the frontal<br />

lobe in the human defined on the basis of cytoarchitecture. Defined<br />

and illustrated in Brodmann‐1909, it included the areas<br />

subsequently illustrated in Brodmann‐10 as prefrontal area 11 and<br />

rostral area 12.<br />

prefrontal area 11 is a subdivision of the cytoarchitecturally defined<br />

frontal region of cerebral cortex of the human. As illustrated in<br />

Brodmann‐10, It constitutes most of the orbital gyri, gyrus rectus<br />

and the most rostral portion of the superior frontal gyrus. It is<br />

bounded medially by the inferior rostral sulcus (H) and laterally<br />

approximately by the frontomarginal sulcus (H). Cytoarchitecturally<br />

it is bounded on the rostral and lateral aspects of the hemisphere<br />

by the frontopolar area 10, the orbital area 47, and the triangular<br />

area 45; on the medial surface it is bounded dorsally by the rostral<br />

area 12 and caudally by the subgenual area 25. In an earlier map,<br />

the area labeled 11, i.e., prefrontal area 11 of Brodmann‐1909, was<br />

larger; it included the area now designated rostral area 12.<br />

Brain: Brodmann area 11<br />

Brodmann area 46, or BA46<br />

46, is part of the frontal cortex<br />

in the human brain. It is between BA10 and BA45.<br />

BA46 is known as middle frontal area 46. In the human brain it<br />

occupies approximately the middle third of the middle frontal<br />

gyrus and the most rostral portion of the inferior frontal gyrus.<br />

Brodmann area 46 roughly corresponds with the dorsolateral<br />

prefrontal cortex (DLPFC), although the borders of area 46 are<br />

based on cytoarchitecture rather than function. <strong>The</strong> DLPFC also<br />

encompasses part of granular frontal area 9, directly adjacent on<br />

the dorsal surface of the cortex.<br />

Cytoarchitecturally, BA46 is bounded dorsally by the granular frontal area<br />

9, rostroventrally by the frontopolar area 10 and caudally by the<br />

triangular area 45 (Brodmann‐1909). <strong>The</strong>re is some discrepancy between<br />

the extent of BA8 (Brodmann‐1905) and the same area as described by<br />

Walker (1940)<br />

<strong>The</strong> DLPFC plays a role in sustaining attention and working<br />

memory. Lesions to the DLPFC impair short‐term memory and<br />

cause difficulty inhibiting responses. Lesions may also eliminate<br />

much of the ability to make judgements about what's relevant<br />

and what's not as well as causing problems in organization.<br />

<strong>The</strong> DLPFC has recently been found to be involved in exhibiting<br />

self‐control. <strong>The</strong> dorsolateral prefrontal cortex, which is one of the few<br />

areas deactivated during REM sleep. Neuroscientist J. Allan Hobson has<br />

hypothesized that activation of the dorsolateral prefrontal cortex produce<br />

lucid dreams.<br />

Brain: Brodmann area 46<br />

<strong>The</strong> limbic system is also tightly connected to the<br />

prefrontal cortex.<br />

Some scientists contend that this connection is<br />

related to the pleasure obtained from solving problems. To<br />

cure severe emotional disorders, this connection was<br />

sometimes surgically severed, a procedure of<br />

psychosurgery, called a prefrontal lobotomy. Patients who<br />

underwent this procedure often became passive and<br />

lacked all motivation.<br />

<strong>The</strong>re is circumstantial evidence that the limbic<br />

system also provides a custodial function for the<br />

maintenance of a healthy conscious state of mind.<br />

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19/07/54<br />

<strong>The</strong> Brodmann area 32<br />

32, also known in the<br />

human brain as the dorsal anterior cingulate area<br />

32, refers to a subdivision of the cytoarchitecturally<br />

defined cingulate region of cerebral cortex. In the<br />

human it forms an outer arc around the anterior<br />

cingulate gyrus. <strong>The</strong> cingulate sulcus defines<br />

approximately its inner boundary and the superior<br />

rostral sulcus (H) its ventral boundary; rostrally it<br />

extends almost to the margin of the frontal lobe.<br />

Cytoarchitecturally it is bounded internally by the<br />

ventral anterior cingulate area 24, externally by<br />

medial margins of the agranular frontal area 6,<br />

intermediate frontal area 8, granular frontal area 9,<br />

frontopolar area 10, and prefrontal area 11‐1909.<br />

(Brodmann19‐09).<br />

Dorsal region of anterior cingulate gyrus is<br />

associated with rational thought processes, most<br />

notably active during the Stroop task.<br />

Brain: Brodmann area 32<br />

Stroop effect is a<br />

demonstration of the reaction time of a<br />

task. When the name of a color (e.g.,<br />

"blue," "green," or "red") is printed in a<br />

color not denoted by the name (e.g., the<br />

word "red" printed in blue ink instead of<br />

red ink), naming the color of the word<br />

takes longer and is more prone to errors<br />

than when the color of the ink matches the<br />

name of the color. <strong>The</strong> effect is named<br />

after John Ridley Stroop who first<br />

published the effect in English in 1935. <strong>The</strong><br />

effect had previously been published in<br />

Germany in 1929. <strong>The</strong> original paper has<br />

been one of the most cited papers in the<br />

history of experimental psychology, leading<br />

to more than 700 replications. <strong>The</strong> effect<br />

has been used to create a psychological<br />

test (Stroop<br />

Test) that is widely used in<br />

clinical practice and investigation.<br />

This test is considered to measure selective<br />

attention, cognitive flexibility and processing<br />

speed, and it is used as a tool in the<br />

evaluation of executive functions. An<br />

increased interference effect is found in<br />

disorders such as brain damage, dementias<br />

and other neurodegenerative diseases,<br />

attention‐deficit hyperactivity disorder, or a<br />

variety of mental disorders such as<br />

schizophrenia, addictions, and depression<br />

<strong>The</strong> anterior cingulate cortex has been related<br />

to the processing of the Stroop effect<br />

Figure 1 from Experiment 2 of the original description of the Stroop<br />

Effect (1935). 1 is the time that it takes to name the color of the dots<br />

while 2 is the time that it takes to say the color when there is a conflict<br />

with the written word<br />

Brodmann area 24 is part of the anterior<br />

cingulate in the human brain.<br />

In the human this area is known as ventral anterior<br />

cingulate area 24, and it refers to a subdivision of the<br />

cytoarchitecturally defined cingulate cortex region of<br />

cerebral cortex (area cingularis anterior ventralis). It<br />

occupies most of the anterior cingulate gyrus in an arc<br />

around the genu of corpus callosum. Its outer border<br />

corresponds approximately to the cingulate sulcus.<br />

Cytoarchitecturally it is bounded internally by the<br />

pregenual area 33, externally by the dorsal anterior<br />

cingulate area 32, and caudally by the ventral<br />

posterior cingulate area 23 and the dorsal posterior<br />

cingulate area 31.<br />

Francis Crick, one of the discoverers of DNA, listed<br />

area 24 as the seat of free will because of its<br />

centrality in abulia and amotivational syndromes.<br />

Brain: Brodmann area 24<br />

Aboulia or Abulia (from the Greek "αβουλία", meaning<br />

"non‐will"), in neurology, refers to a lack of will or initiative<br />

and is one of the Disorders of Diminished Motivation or<br />

DDM. Aboulia falls in the middle of the spectrum of<br />

diminished motivation, with apathy being less extreme and<br />

akinetic mutism being more extreme than aboulia. A<br />

patient with aboulia is unable to act or make decisions<br />

independently. d It may range in severity from subtle bl to<br />

overwhelming. It is also known as Blocq's disease (which<br />

also refers to abasia and astasia‐abasia). Abulia was<br />

originally considered to be a disorder of the will. [<br />

29


19/07/54<br />

Aboulia has been known to clinicians since 1838. However, in the time since its<br />

inception, the definition of aboulia has been subjected to many different forms, some<br />

even contradictory with previous ones. Aboulia has been described as a loss of drive,<br />

expression, loss of behavior and speech output, slowing and prolonged speech latency,<br />

and reduction of spontaneous thought content and initiative. <strong>The</strong> clinical features most<br />

commonly associated with aboulia are:<br />

1. Difficulty in initiating and sustaining purposeful movements<br />

2. Lack of spontaneous movement<br />

3. Reduced spontaneous movement<br />

4. Increased response‐time to queries<br />

5. Passivity<br />

6. Reduced emotional responsiveness and spontaneity<br />

7. Reduced social interactions<br />

8. Reduced interest in usual pastimes<br />

Especially in patients with progressive dementia, it may affect feeding. Patients may<br />

continue to chew or hold food in their mouths for hours without swallowing it. <strong>The</strong><br />

behavior may be most evident after these patients have eaten part of their meals<br />

and no longer have strong appetites.<br />

Amotivational syndrome is a psychological condition associated<br />

with diminished inspiration to participate in social situations and activities,<br />

with lapses in apathy caused by an external event, situation, substance (or<br />

lack of), relationship, or other cause.<br />

While some have claimed that chronic use of cannabis causes amotivational<br />

syndrome in some users, empirical studies suggest that there is no such thing<br />

as "amotivational syndrome", per se, but that chronic cannabis intoxication<br />

can lead to apathy and amotivation. From a World Health Organization report:<br />

<strong>The</strong> evidence for an "amotivational syndrome" among adults consists largely<br />

of case histories i and observational reports (e.g. Kl Kolanskyand Moore, 1971;<br />

Millman and Sbriglio, 1986). <strong>The</strong> small number of controlled field and<br />

laboratory studies have not found compelling evidence for such a syndrome<br />

(Dornbush, 1974; Negrete, 1983; Hollister, 1986)... (I)t is doubtful that<br />

cannabis use produces a well defined amotivational syndrome. It may be more<br />

parsimonious to regard the symptoms of impaired motivation as symptoms of<br />

chronic cannabis intoxication rather than inventing a new psychiatric<br />

syndrome.<br />

Apathy (also called impassivity or<br />

perfunctoriness) is a state of<br />

indifference, or the suppression of emotions<br />

such as concern, excitement, motivation and<br />

passion. An apathetic individual has an<br />

absence of interest in or concern about<br />

emotional, social, spiritual, philosophical or<br />

physical life.<br />

<strong>The</strong>y may lack a sense of purpose or<br />

meaning in their life. He or she may also<br />

exhibit hb insensibility bl or sluggishness. <strong>The</strong><br />

opposite of apathy is flow. In positive<br />

psychology, apathy is described as a result of<br />

the individual feeling they have much more<br />

than the level of skill required to confront a<br />

challenge. It may also be a result of<br />

perceiving no challenge at all (e.g. the<br />

challenge is irrelevant to them, or conversely,<br />

they have learned helplessness).<br />

Brodmann area 25 (BA25) is an area in the<br />

cerebral cortex of the brain and delineated based on<br />

its cytoarchitectonic characteristics, also called the<br />

subgenual area, area subgenualis or subgenual<br />

cingulate. It is the 25th "Brodmann area" defined by<br />

Korbinian Brodmann (thus its name). BA25 is located in the<br />

cingulate region as a narrow band in the caudal portion of<br />

the subcallosal area adjacent to the paraterminal gyrus. <strong>The</strong><br />

posterior parolfactory sulcus separates the paraterminal<br />

gyrus from BA25. Rostrally it is bound by the prefrontal area<br />

11 of Brodmann. This region is extremely rich in serotonin<br />

transporters and is considered as a governor for a vast<br />

network involving areas like hypothalamus and brain stem,<br />

which influences changes in appetite and sleep; the<br />

amygdala and insula, which affect the mood and anxiety; the<br />

hippocampus, which plays an important role in memory<br />

formation; and some parts of the frontal cortex responsible<br />

for self‐esteem.<br />

One study has noted that BA25 is metabolically overactive in treatmentresistant<br />

depression and has found that chronic deep brain stimulation in the<br />

white matter adjacent to the area is a successful treatment for some patients.<br />

A different study found that metabolic hyperactivity in this area is associated<br />

with poor therapeutic response of persons with Major Depressive Disorder to<br />

cognitive‐behavioral therapy and venlafaxine<br />

Brain: Brodmann area 25<br />

Brodmann area 33, , also known as<br />

pregenual area 33, is a subdivision<br />

of the cytoarchitecturally defined<br />

cingulate region of cerebral cortex. It<br />

is a narrow band located in the<br />

anterior cingulate gyrus adjacent to<br />

the supracallosal gyrus in the depth<br />

of the callosal sulcus.<br />

Cytoarchitecturally it is bounded by<br />

the ventral anterior cingulate area<br />

24 and the supracallosal gyrus<br />

(Brodmann‐1909).<br />

Brain: Brodmann area 33<br />

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19/07/54<br />

Impairment of social and moral behavior<br />

related to early damage in human prefrontal<br />

cortex<br />

Steven W. Anderson, Antoine Bechara, Hanna Damasio, Daniel Tranel &<br />

Antonio R. Damasio<br />

Department of Neurology, Division of Behavioral Neurology and Cognitive<br />

Neuroscience, <strong>The</strong> <strong>University</strong> of Iowa College of Medicine, Iowa City, Iowa 52242,<br />

USA<br />

<strong>The</strong> long-term consequences of early prefrontal cortex lesions<br />

occurring before 16 months were investigated in two adults. As is the<br />

case when such damage occurs in adulthood, the two early-onset<br />

patients had severely impaired social behavior despite normal basic<br />

cognitive abilities, and showed insensitivity to future consequences of<br />

decisions, defective autonomic responses to punishment contingencies<br />

and failure to respond to behavioral interventions. Unlike adult-onset<br />

patients, however, the two patients had defective social and moral<br />

reasoning, suggesting that the acquisition of complex social<br />

conventions and moral rules had been impaired. Thus early-onset<br />

prefrontal damage resulted in a syndrome resembling psychopathy.<br />

เด็กสมาธิสั้น ซน พฤติกรรมไม่เหมาะสมกับกาลเทศะ<br />

(Attention Deficit/Hyperactivity: AD/HD)<br />

ระบบประสาทสมองใน<br />

เด็กสมาธิสั้น ซน<br />

พฤติกรรมไม่เหมาะสม<br />

กับกาลเทศะ<br />

มีความผิดปกติของ<br />

สารเคมสอประสาทใน<br />

ีสื<br />

่ ส<br />

สมองโดปามีน<br />

(Dopamine)<br />

Prefrontal lobe syndrome<br />

• Personality changes<br />

• Deficits in strategic planning<br />

• Perseveration<br />

• Release of primitive reflexes<br />

• Abulia = general slowing of the intellectual<br />

faculties i.e. apathetic, slow speech etc.<br />

<strong>The</strong> Moral Brain and<br />

decision making<br />

31


19/07/54<br />

Fig. 2. Brain areas exhibiting differences in activity between conditions shown in<br />

three axial slices of a standard brain (28). Slice location is indicated by Talairach (28)<br />

z coordinate. Data are for the main effect of condition in Experiment 1. Colored areas<br />

reflect the thresholded F scores. Images are reversed left to right to follow radiologic convention.<br />

Fig. 1. Effect of condition on activity in brain areas identified in Experiment 1. R,<br />

right; L, left; B, bilateral. Results for the middle frontal gyrus were not replicated in<br />

Experiment 2. <strong>The</strong> moral‐personal condition was significantly different from the<br />

other two conditions in all other areas in both Experiments 1 and 2. In Experiment<br />

1 the medial frontal and posterior cingulate gyri showed significant differences<br />

between the moral‐impersonal and non‐moral conditions. In Experiment 2 only the posterior cingulate gyrus was<br />

significantly different in this comparison. Brodmann's Areas and Talairach (28) coordinates (x, y, z) for each area are as<br />

follows (left to right in graph): 9/10 (1, 52, 17); 31 (-4, -54, 35); 46 (45, 36, 24); 7/40 (-48, -65, 26); 7/40 (50, -57, 20).<br />

Jorge Moll, Roland Zahn, Frank Krueger and Jordan Grafman are at <strong>The</strong> Cognitive<br />

Neuroscience Section, National Institute<br />

of Neurological Disorders and Stroke, Building 10; Room 5C205; MSC 1440, NIH,<br />

Bethesda, Maryland 20892‐1440, USA.<br />

Ricardo de Oliveira‐Souza is at the Cognitive and Behavioral Neuroscience Unit,<br />

LABS‐D’Or Hospital Network, R. Pinheiro Guimaraes 22, 3rd floor, Rio de Janeiro<br />

22281‐080, Brazil.<br />

Correspondence to J.G. e‐mail: grafmanj@ninds.nih.gov<br />

Cognitive Neuroscience Section, NINDS, NIH:<br />

http://intra.ninds.nih.gov/Lab.asp?Org_ID=83<br />

Cognitive and Behavioural Neuroscience Unit,<br />

LABS‐D’Or Hospital Network:<br />

http://www.rededor.com.br/cbnu/<br />

32


19/07/54<br />

<strong>Frontal</strong> lobe and Executive Function<br />

Disorder<br />

33


19/07/54<br />

<strong>The</strong> <strong>Frontal</strong> Lobes Are Considered<br />

Our Emotional Control Center and<br />

Home to Our Personality<br />

<strong>The</strong>re Is No Other Part of the Brain Where<br />

Lesions Can Cause Such a Wide Variety of<br />

Symptoms.<br />

‐ involved in motor function, problem<br />

solving, spontaneity, memory, language,<br />

initiation, judgement, impulse control,<br />

and social iland sexual behavior. bh ‐ extremely vulnerable to injury due to<br />

their location at the front of the cranium,<br />

proximity to the sphenoid wing and their<br />

large size.<br />

<strong>The</strong>re Are Important Asymmetrical Differences<br />

in the <strong>Frontal</strong> Lobes.<br />

<strong>The</strong> left frontal lobe is involved in controlling<br />

language related movement, whereas the<br />

right frontal lobe plays a role in non‐verbal<br />

abilities.<br />

Some researchers emphasize that this rule is<br />

not absolute and that with many people,<br />

both <strong>lobes</strong> are involved in nearly all<br />

behavior.<br />

Disturbance of motor function is typically<br />

characterized by loss of fine movements<br />

and strength of the arms, hands and fingers.<br />

Complex chains of motor movement also seem<br />

to be controlled by the frontal <strong>lobes</strong>.<br />

Patients with frontal lobe damage exhibit little<br />

spontaneous facial expression, which points<br />

to the role of the frontal <strong>lobes</strong> in facial<br />

expression.<br />

Broca's Aphasia, or difficulty in speaking, has<br />

been associated with frontal damage.<br />

34


19/07/54<br />

An interesting phenomenon of frontal lobe<br />

damage is the insignificant effect it can have<br />

on traditional IQ testing.<br />

<strong>Frontal</strong> lobe damage seems to have an<br />

impact on divergent thinking, or flexibility<br />

and problem solving ability.<br />

<strong>The</strong>re is also evidence showing lingering<br />

interference with attention and memory<br />

even after good recovery from a TBI.<br />

One Characteristics of <strong>Frontal</strong> Lobe Damage<br />

Is Difficulty in Interpreting Feedback From the<br />

Environment<br />

Perseverating on a response, risk taking and<br />

non‐compliance with rules, and impaired<br />

associated learning (using external cues<br />

to help guide behavior) are a few<br />

examples of this type of deficit.<br />

<strong>The</strong> frontal <strong>lobes</strong> are also thought to play a<br />

part in our spatial orientation, including<br />

our bodies orientation in space.<br />

One of the Most Common Effects of <strong>Frontal</strong><br />

Damage Can Be a Dramatic Change in Social<br />

Behavior.<br />

A person's personality can undergo<br />

significant changes after an injury to the<br />

frontal <strong>lobes</strong>, especially when both <strong>lobes</strong><br />

are involved.<br />

<strong>The</strong>re are some differences in the left versus<br />

right frontal <strong>lobes</strong> in this area.<br />

Left frontal damage usually manifests as<br />

pseudodepression and right frontal<br />

damage as pseudopsychopathic.<br />

One of the most common effects of frontal<br />

damage can be a dramatic change in social<br />

behavior.<br />

Sexual behavior can also be effected by<br />

frontal lesions.<br />

Orbital frontal damage can introduce<br />

abnormal sexual behavior, while<br />

dorsolateral lesions may reduce sexual<br />

interest.<br />

Some Common Tests for <strong>Frontal</strong> Lobe<br />

Function Are:<br />

Wisconsin Card Sorting (response<br />

inhibition);<br />

Finger Tapping (motor skills);<br />

Token Test (language skills).<br />

<strong>The</strong> Wisconsin Card Sorting Test<br />

(WCST) is a neuropsychological test of "setshifting",<br />

i.e. the ability to display flexibility in the<br />

face of changing schedules of reinforcement.<br />

<strong>The</strong> WCST was written by David A. Grant and Esta A. Berg.<br />

<strong>The</strong> Professional Manual for the WCST was written by Robert<br />

K. Heaton, Gordon J. Chelune, Jack L. Talley, Gary G. Kay, and<br />

Glenn Curtiss.<br />

Clinically, the test is widely used by neuropsychologists,<br />

clinical psychologists, neurologists and psychiatrists in<br />

patients with acquired brain injury, neurodegenerative<br />

disease, or mental tlillness such as schizophrenia. h i It has been In particular, patients with ihlesions<br />

considered a measure of executive function because of its of the dorsolateral frontal lobe<br />

reported sensitivity to frontal lobe dysfunction. As such, the<br />

make a higher number of<br />

WCST allows the clinician to assess the following "frontal"<br />

lobe functions: strategic planning, organized searching,<br />

perseverative errors than control<br />

utilizing environmental feedback to shift cognitive sets, participants.<br />

directing behavior toward achieving a goal, and modulating A recent factor analysis of the WCST<br />

impulsive responding. <strong>The</strong> test can be administered to those has shown these perseverative errors<br />

6.5 years to 89 years of age.<br />

to be the most useful outcome<br />

Although successful completion of the test relies upon a measure in assessing cases. A more<br />

number of intact cognitive functions including attention, sophisticated description of deficits of<br />

working memory, and visual processing, it is loosely termed a this type is "executive dysfunction".<br />

"frontal lobe" test on the basis that patients with any sort of<br />

frontal lobe lesion generally do poorly at the test.<br />

35


19/07/54<br />

Current News:<br />

‐ Multi-Tasking Pinpointed to <strong>Frontal</strong> Lobes.<br />

‐ Two Brain Areas Involved in Doing Math.<br />

‐ Brain Can Compensate for Damage to Language<br />

Systems After Injury.<br />

‐ Injury to <strong>Frontal</strong> Lobes May Affect Appreciation<br />

of Humor.<br />

Finger Tapping (motor skills)<br />

Executive Function Disorder<br />

<strong>The</strong> frontal <strong>lobes</strong> represent a large area<br />

of the brain and brain centers within<br />

the frontal lobe have numerous<br />

interconnections with other parts of<br />

the brain.<br />

<strong>The</strong>se include connections with emotion<br />

and mood centers as well as cognitive<br />

centers.<br />

Executive Function Disorder<br />

This high degree of complexity results in<br />

a number of syndromes that are<br />

associated with lesions of this area.<br />

<strong>The</strong>re are three general anatomical<br />

divisions of the frontal cortex: the<br />

limbic, the precentral and the<br />

prefrontal cortices.<br />

<strong>The</strong> <strong>Frontal</strong> Lobes<br />

<strong>The</strong> precentral cortex consists of areas<br />

that lie immediately before the<br />

central sulcus.<br />

<strong>The</strong>se consist of the primary and<br />

secondary motor control areas.<br />

<strong>The</strong> <strong>Frontal</strong> Lobes<br />

<strong>The</strong> limbic component consists of<br />

the inferior and medial parts of the<br />

cingulate gyrus and the posterior<br />

parts of the orbital frontal areas.<br />

<strong>The</strong>se areas have inter‐ connections<br />

with the amygdala, hippocampus,<br />

thalamus and other parts of the<br />

limbic system.<br />

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19/07/54<br />

<strong>The</strong> <strong>Frontal</strong> Lobes<br />

<strong>The</strong> prefrontal cortex is anterior to the<br />

motor control areas and comprises the<br />

greater part of the frontal lobe.<br />

It is subdivided into the dorsolateral,<br />

mesial and orbital areas.<br />

<strong>The</strong>se sections are histologically distinct<br />

and probably represent functional<br />

differences.<br />

<strong>The</strong> <strong>Frontal</strong> Lobes<br />

<strong>The</strong> prefrontal cortex is the area<br />

implicated in the studies of<br />

personality and the behavioral<br />

effects of frontal lobe lesions.<br />

It has extensive interconnections<br />

with virtually every other part of<br />

the cerebrum.<br />

<strong>The</strong> <strong>Frontal</strong> Lobes<br />

<strong>The</strong>se include association areas in<br />

the temporal, occipital and parietal<br />

<strong>lobes</strong>, the limbic system, the dorsal<br />

medial nucleus of the thalamus<br />

and the basal ganglia.<br />

<strong>The</strong> <strong>Frontal</strong> Lobes<br />

Bilateral lesion of the inferior medial<br />

sections of the frontal <strong>lobes</strong> causes<br />

emotional and behavioral changes.<br />

Intellectual impairment results from<br />

lesion of the dorso‐ lateral portion of<br />

the frontal <strong>lobes</strong>.<br />

Cognitive Impairment<br />

Although patients with frontal lobe<br />

lesions may have extensive brain<br />

injury and numerous behavioral<br />

changes they will typically score<br />

within the normal range on IQ tests.<br />

Cognitive Impairment<br />

<strong>The</strong> cognitive impairment associated with<br />

frontal lobe lesions involve cognitive<br />

abilities that are not measured by<br />

conventional IQ tests.<br />

<strong>The</strong>se include impairment of hypothesis<br />

testing and abstract reasoning, memory<br />

disorder, attention deficits and difficulty<br />

in initiation of cognitive activity.<br />

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Impairment of Abstract Reasoning,<br />

Hypothesis Testing and Modulation of<br />

Cognition<br />

<strong>The</strong> overriding function of the frontal areas<br />

is to modulate and control motor function,<br />

emotion, attention and other cognitive<br />

activity.<br />

Virtually all aspects of frontal lobe impairment<br />

can be considered a specific aspect<br />

of a general deficit of control.<br />

Impairment of Abstract Reasoning, Hypothesis<br />

Testing and Modulation of Cognition<br />

In the domain of reasoning, a deficit of<br />

modulation is manifested as poor abstract<br />

reasoning and failure to maintain goal‐<br />

directed behavior.<br />

Abstract reasoning involves making complex<br />

associations between semantic elements<br />

and identifying super‐ordinate categories,<br />

reasoning by general rules and formulating<br />

hypotheses.<br />

Impairment of Abstract Reasoning,<br />

Hypothesis Testing and Modulation of<br />

Cognition<br />

If abstract reasoning is not present then the<br />

patient has difficulty formulating the<br />

super‐ordinate category that subsumes<br />

individual semantic elements.<br />

For example, the patient may not be able to reason that<br />

cars, trains, airplanes and the like, are members of the<br />

category of modes of transportation.<br />

Impairment of Abstract Reasoning,<br />

Hypothesis Testing and Modulation of<br />

Cognition<br />

Another manifestation of abstract reasoning<br />

involves the development of rules that<br />

guide future behavior.<br />

<strong>The</strong> reasoning person identifies common<br />

features and themes in the experiences of<br />

everyday life and formulates general rules<br />

that govern behavior in these situations.<br />

Impairment of Abstract Reasoning,<br />

Hypothesis Testing and Modulation of<br />

Cognition<br />

Rules may also be taught by others but reasoning<br />

people usually verify and endorse<br />

the validity of rules before using them.<br />

People who have sustained injury to the<br />

frontal <strong>lobes</strong> have difficulty formulating<br />

these rules.<br />

Impairment of Abstract Reasoning,<br />

Hypothesis Testing and Modulation<br />

of Cognition<br />

Indeed, even if a rule is given to the patient<br />

there is still great difficulty in using it to<br />

guide bh behavior.<br />

As a result of this general inability to<br />

formulate and use rules, the patient<br />

cannot conceptualize goal states and use<br />

the goals as objectives to guide thought<br />

and actions.<br />

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Impairment of Abstract Reasoning,<br />

Hypothesis Testing and Modulation of<br />

Cognition<br />

Actions are motivated by very concrete,<br />

superficial goals, such as immediate<br />

gratification of simple impulses.<br />

Hypothesis formulation and testing also involves<br />

the generalization of experiences in the form of<br />

rules or general principles. This cognitive<br />

function is likewise affected by lesions of the<br />

frontal <strong>lobes</strong>.<br />

Disturbance of Behavior and<br />

Personality<br />

Patients with lesions of the ventro‐<br />

medial portion of the frontal <strong>lobes</strong><br />

have a behavioral syndrome<br />

characterized by lack of originality and<br />

creativity, impairment of attention, and a<br />

tendency to display inappropriate<br />

emotions and behavior.<br />

Disturbance of Behavior and<br />

Personality<br />

<strong>The</strong>y have difficulty initiating behavior;<br />

when they do engage in activity, they<br />

may continue the activity it without<br />

t<br />

stopping.<br />

<strong>The</strong>y may only start activity when<br />

prompted by others.<br />

Disturbance of Behavior and<br />

Personality<br />

Although controversial, emotional<br />

disturbance most often results from<br />

lesion of the orbital frontal areas.<br />

<strong>The</strong>se areas have interconnections<br />

with the amygdala and<br />

hypothalamus.<br />

Disturbance of Behavior and<br />

Personality<br />

Emotional disturbances include laughing<br />

or crying in situations inappropriate to<br />

the emotion.<br />

<strong>The</strong> emotional response also appears<br />

superficial and variable.<br />

<strong>The</strong> patient usually has no awareness<br />

that their emotional response is<br />

incorrect or extreme.<br />

Aphasia<br />

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19/07/54<br />

Language Impairment<br />

Broca's area resides in the left frontal<br />

lobe and lesion of this area produces a<br />

well‐known impairment of language<br />

referred to as Broca's aphasia.<br />

Patients with dorsolateral frontal lobe<br />

lesions may also have additional<br />

language impairment that is distinct<br />

from Broca's aphasia.<br />

Language Impairment<br />

<strong>The</strong> first of these is a general reduction of<br />

language production although language<br />

utterances that are produced are fluent<br />

and maintain correct syntax.<br />

Patients with frontal lobe lesions have<br />

difficulty initiating speech and<br />

maintaining a complex, spontaneous<br />

conversation.<br />

Language Impairment<br />

This is referred to as a deficit in<br />

"verbal fluency", although language<br />

productions are actually fluent.<br />

Language Impairment<br />

Patients with frontal lesions in secondary<br />

motor control areas may also display<br />

mutism.<br />

In particular, lesions of the cingulum often<br />

result in essential mutism.<br />

Here, the patient comprehends language but<br />

cannot produce any vocalizations, including<br />

language.<br />

Language Impairment<br />

This is viewed as a deficit of the basic<br />

motor control of the oral apparatus to<br />

the point where there is no initiation of<br />

activity.<br />

<strong>The</strong> patient is often indifferent to<br />

communication in general and does<br />

not show the frustration characteristic<br />

of Broca's aphasia.<br />

Language Impairment<br />

A pure agraphia is also associated with<br />

lesions of supplemental motor areas of the<br />

left dorsolateral frontal lobe (Exner's<br />

area).<br />

Exner's area (Broadman area #46<br />

46) is above<br />

Broca's area (Broadman area #44,45) and<br />

anterior to the primary motor control area.<br />

In this disorder, the patient is not aphasic<br />

but has difficulty writing and reading.<br />

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19/07/54<br />

Impairment of Motor Function<br />

<strong>The</strong> highly controlled, volitional components<br />

of motor control are located in the frontal<br />

<strong>lobes</strong> on the dorso‐ lateral surface anterior<br />

to and including the primary motor control<br />

area (the motor strip).<br />

Other components of the motor control<br />

system are the Basal Ganglia and the<br />

Cerebellum.<br />

<strong>The</strong> cortical system in the frontal <strong>lobes</strong> are<br />

involved in the complex control of skeletal<br />

muscles in the execution of actions.<br />

Impairment of Motor Function<br />

Lesions of the dorsolateral frontal areas<br />

results in a number of motor<br />

impairments.<br />

<strong>The</strong>se include:<br />

‐perseveration,<br />

‐inco‐ordination,<br />

‐motor impersistence, and<br />

‐hypokinesia.<br />

Impairment of Motor Function<br />

‐Patients with left frontal lobe lesions<br />

may also have ideomotor apraxia.<br />

-Lesions within hemisphere cause<br />

worse motor impairment of the<br />

opposite extremities.<br />

Impairment of Motor Function<br />

<strong>The</strong>se deficits again involve the<br />

general modulation and control<br />

functions that are characteristic<br />

of the frontal <strong>lobes</strong>.<br />

Impairment of Motor Function<br />

<strong>The</strong>re is some evidence that control is<br />

lateralized to each frontal area.<br />

<strong>The</strong> left hemisphere is dominant for<br />

motor control and the modulation of<br />

language.<br />

<strong>The</strong> right hemisphere is more involved<br />

in the modulation of actions that are<br />

executed in a spatial context, such as<br />

three‐dimensional block construction.<br />

Impairment of Reflexes<br />

<strong>The</strong> frontal <strong>lobes</strong> play the primary role in the<br />

inhibition of fundamental reflexes that<br />

were presumably inherited as part of<br />

primitive brain structures characteristic of<br />

the primate brain.<br />

<strong>The</strong>se reflexes include the grasp reflex and<br />

the snout and sucking reflexes. <strong>The</strong> grasp<br />

reflex is elicited by stroking the skin of the<br />

palm.<br />

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19/07/54<br />

Impairment of Reflexes<br />

<strong>The</strong> patient grasps the object and has<br />

difficulty releasing the grasp even when<br />

told to attend to the hand and release<br />

the grasp.<br />

Snout and sucking reflexes are elicited i by<br />

stimulating the lips and space between<br />

the upper lip and the nose. Here, the<br />

patient extends the lips outward for the<br />

snout reflex.<br />

Impairment of Reflexes<br />

<strong>The</strong> patient is compelled to suck on<br />

an object placed in the lips when<br />

the suck reflex is present.<br />

<strong>The</strong> frontal <strong>lobes</strong> usually inhibit these<br />

reflexes during childhood and<br />

adulthood. When the frontal lobe is<br />

lesioned, this inhibition is removed<br />

and the reflexes return.<br />

Impairment of Social Behavior<br />

Since frontal lobe lesions result in a<br />

pervasive defect in planning and<br />

modulation of behavior, these patients<br />

have compelling deficits in maintining<br />

appropriate p social responses.<br />

Social perception and action are very<br />

complex. In addition, people do not<br />

have a wide tolerance for social<br />

behavior; even minor deviations in<br />

social behavior are noticeable.<br />

Impairment of Social Behavior<br />

Patients with frontal lobe lesions have great<br />

difficulty generating appropriate<br />

behavioral options in social situations and<br />

then choosing the best alternative.<br />

<strong>The</strong>y also base their behavior on concrete<br />

simple motivations and cannot formulate<br />

or comprehend more complex or abstract<br />

reasons for acting.<br />

Much social behavior requires a complex<br />

and abstract appreciation of the social<br />

setting.<br />

Confabulation and Reduplication<br />

Syndrome<br />

Patients with severe frontal lobe lesions<br />

tend to fabricate quick, impulsive<br />

answers to questions.<br />

Some responses may be quite fanciful<br />

and imaginative. <strong>The</strong> patient cannot<br />

inhibit a response in order to check its<br />

validity.<br />

Confabulation and Reduplication<br />

Syndrome<br />

This tendency to fabricate an answer<br />

is called confabulation.<br />

It is most common among patients<br />

with basal forebrain lesions and<br />

among patients with additional<br />

impairment of memory ability.<br />

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19/07/54<br />

Confabulation and Reduplication<br />

Syndrome<br />

Another syndrome that is similar to<br />

confabulation is reduplication.<br />

Here, the patient with a frontal lobe<br />

lesion confabulates that the current<br />

environment, usually the hospital, is<br />

actually another place that is similar<br />

to the current setting but has a<br />

different name and location.<br />

Confabulation and Reduplication<br />

Syndrome<br />

<strong>The</strong> patient may even claim that the current<br />

hospital is a university dormitory or an<br />

apartment building.<br />

<strong>The</strong> confabulated place is always somewhere<br />

else and it is usually familiar to the patient,<br />

such as the hospital in the patient's home<br />

town.<br />

<strong>The</strong> patient will often maintain this<br />

confabulation even when confronted with<br />

salient, contradictory information.<br />

Apraxia<br />

Callosal Disconnection<br />

Syndromes<br />

Executive Function Disorder<br />

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19/07/54<br />

Blood supply<br />

Branches of the middle cerebral artery provide most of<br />

the arterial blood supply for the primary motor cortex.<br />

<strong>The</strong> medial aspect (leg areas) is supplied by branches of<br />

the anterior cerebral artery.<br />

Neural input from the thalamus<br />

<strong>The</strong> primary motor cortex receive thalamic input from<br />

the Ventral lateral nucleus of the Thalamus.<br />

Pathology<br />

Lesions of the precentral gyrus result in paralysis of the<br />

contralateral side of the body (facial palsy, arm‐/leg<br />

monoparesis, hemiparesis) ‐ see upper motor neuron.<br />

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19/07/54<br />

Schizophrenia<br />

• Schizophrenia is a psychotic disorder involving<br />

disturbance of thought, emotion and behavior<br />

• <strong>The</strong> lifetime prevalence of schizophrenia is<br />

about 1%<br />

– Onset is usually in late adolescence<br />

– Substance abuse is a co‐morbid condition in 50% of<br />

schizophrenia patients<br />

Ch 11.1<br />

Positive Symptoms of Schizophrenia<br />

Negative Symptoms of Schizophrenia<br />

• Positive symptoms involve excesses or distortions<br />

– Disorganized speech (thought disorder)<br />

– Hallucinations are sensory experiences that occur in the<br />

absence of environmental stimulation<br />

• Hallucinations are commonly auditory<br />

– Delusions are beliefs that are contrary to reality<br />

• Persecutory delusions are common<br />

• Negative schizophrenia symptoms are characterized by<br />

behavioral deficits<br />

– Avolition refers to a lack of energy and an inability to persist<br />

in routine activities<br />

– Alogia refers to a reduction in the amount or content of<br />

speech<br />

– Anhedonia is an inability to experience pleasure<br />

– Asociality refers to a severe impairment in social<br />

relationships<br />

Ch 11.2<br />

Ch 11.3<br />

Etiology of Schizophrenia<br />

• Genetic studies using twin, family and adoption<br />

techniques reveal that a predisposition for<br />

schizophrenia is transmitted genetically<br />

Genetic Studies of Schizophrenia<br />

Relation to<br />

Proband<br />

Spouse 1.00<br />

Grandchildren 2.84<br />

Nieces/nephews 2.65<br />

Children 9.35<br />

Siblings 7.30<br />

DZ twins 12.08<br />

MZ twins 44.30<br />

Percentage<br />

Schizophrenic<br />

Ch 11.5<br />

Ch 11.6<br />

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19/07/54<br />

Biochemistry of Schizophrenia<br />

• Dopamine theory holds that the positive symptoms of<br />

schizophrenia result from excessive activity of<br />

dopamine in brain<br />

– Anti‐schizophrenia drugs block dopamine receptors<br />

• <strong>The</strong> anti‐schizophrenia h i drugs take several weeks to act clinically, i ll yet<br />

rapidly block dopamine receptors<br />

– Ingestion of amphetamine can induce psychosis;<br />

amphetamine causes the release of dopamine from neurons<br />

Ch 11.7<br />

Dopamine <strong>The</strong>ory of Schizophrenia<br />

Brain Pathology in Schizophrenia<br />

• Brains of schizophrenic patients show<br />

– Reduced volume of temporal and frontal cortex<br />

– Enlarged ventricles (reflecting loss of brain cells)<br />

• For 12 of 15 twins, the schizophrenic h i twin could be<br />

identified by enlarged ventricles<br />

– Reduced metabolic activity within prefrontal cortex<br />

(frontal hypoactivation)<br />

Ch 11.8<br />

Ch 11.9<br />

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19/07/54<br />

DSM‐IV Schizophrenia Categories<br />

• Disorganized schizophrenia involves<br />

– Disorganized speech and flat affect<br />

– A general disruption of behavior<br />

• Catatonic schizophrenia involves<br />

– Prolonged motor immobility states that alternate with<br />

periods of excitability<br />

• Paranoid schizophrenia involves the presence of<br />

prominent delusions including persecution and<br />

grandiosity<br />

Ch 11.4<br />

Early Forms of Treatment<br />

Insulin Coma <strong>The</strong>rapy<br />

Psychosurgery<br />

Electroconvulsive <strong>The</strong>rapy (ECT)<br />

Smooth Pursuit Eye Tracking<br />

Biological Interventions<br />

Neuroleptics<br />

Haldol & Clozapine<br />

Trial and Error<br />

“Extrapyramidal” Side Effects<br />

Tardive Dyskineasia<br />

Akineasia<br />

<strong>The</strong>rapies for Schizophrenia<br />

• Psychosurgery is the intentional destruction of<br />

brain tissue to alter behavior<br />

– Prefrontal lobotomy was used to treat<br />

schizophrenia<br />

• Drug therapies supplanted psychosurgery<br />

– Use of neuroleptic medications to treat positive<br />

symptoms of schizophrenia<br />

• Chlorpromazine was introduced in the US in 1954<br />

Ch 11.10<br />

Psychological Treatments for<br />

Schizophrenia<br />

• Social‐skills training involves teaching behaviors to<br />

interact successfully with others<br />

• Family therapy aims to reduced expressed emotion<br />

(hostility, overly critical)<br />

• Personal therapy aims to reduce expressed emotion,<br />

uses relaxation techniques and teaches social skills<br />

Ch 11.11`<br />

47

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