Cerebral Cortex Pathologies

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*Cerebral cortex*

The cerebral cortex is composed of gray matter and contains approximately 10 billion

neurons. The surface area of the cortex is increased by gyri. The thickness of the cortex is 1.5-4.5 mm.

It consists of nerve cells, nerve fibers, neuroglia and blood vessels.

Types of nerve cells which are present in cerebral cortex:

1) Pyramidal cells (also called Betz cells, and are found in the motor precentral gyrus of the

frontal lobe).

2) Stellate cells (also called granule cells).

3) Fusiform cells.

4) Horizontal cells ofCajal.

5) Cells ofMartinotti.

Nerve fibers of the cerebral cortex:

The nerve fibers are arranged both radially and tangentially.

The radial fibers run at right angle to the cortical surface. They include afferent projections,

commissural fibers, axons of pyramidal, stellate, and fusiform cells.

Tangential fibers run parallel to the cortical surface and are for the most part collateral and

terminal branches of afferent fibers. They include also axons of horizontal and stellate cells

and collateral branches of pyramidal and fusiform cells. They are mostly concentrated in 4-5

layers where they are called bands of Baillarger. These bands are well developed in the

sensory areas.

Layers of cerebral cortex:

1. Molecular layer (plexiform layer): Most superficial layer, it consists of dense network of tangentially oriented nerve

fibers. These fibers are derived from apical dendrites of the pyramidal cells and

fusiform cells, the axons of stellate and martinotti cells. Contains large number of

synapses.

2. External granular layer: Contains large number of stellate and pyramidal cells.

They pass to white matter of cerebral hemisphere.3. External pyramidal layer:

This composed of pyramidal cells whose body size is increases from up to down.

4. Inner granular layer: Composed of closely packed stellate cells.

In this layer external band of Baillarger is located.

5. Ganglionic layer (internal pyramidal layer):


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Contains very large and medium pyramidal cells, as well as stellate and Martinotti

cells which are arranged between them.

Internal band of Baillarger in located in this layer.

Betz cells are located in this layer.

6. Multiform layer (layerof polymorphic cells): Majority of the cells are fusiform, although there is pyramidal cells whose body is

ovoid or triangular.

Lesions of the cerebral cortex:

Motor cortex

The primary lesion of motor cortex leads to contra-lateral paralysis. Destruction of the motor

area (primary) produce more server paralysis than destruction of the premotor area

(secondary), but destruction of both area leads to total paralysis.

Lesions of the secondary motor areas produce difficulties in performance of skilled

movements with little loss of strength. Jacksonian epileptic seizures: is due to an irritative lesion of primary motor area. The

convulsions begin in the part of the body that is controlled by the primary motor area. The

convulsions may be constricted to one part of the body such as face, foot, or spread to involve

many regions.

Muscles spasticity:

Small lesions in the primary motor area that cause little changes in muscles tone. However larger

lesions in both primary and secondary motor areas results in muscular spasm.

Lesions of the frontal eye field:

A destructive lesion in the eye field of hemispheres causes the two eyes to deviates to the side of

the lesion and inability to turn the eyes to the opposite side. The involuntary tracking movement of the

eyes when following moving objects is unaffected, because the lesion doesnt involve the visual

cortex in occipital lobe.

The motor speech area of Broca(triangular part of the inferior frontal gyrus):

Destructive lesion in this area causes loss of ability to produce speech (expressive aphasia).

The patient can think of words, he can write down and understand the words meaning when they hear

it or read it.

The sensory speech area of Wernicke (Wernicke area located in the posterior part of

thesuperior temporal gyrus):

Lesions in this area causes loss the ability to understand the spoken speech and written words

(receptive aphasia).


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Since the Brocas area is not affected, speech is unimpaired and patient can produce speech,

however the patient in unaware of the meaning of the words and he uses incorrect words.

Lesions of the Brocas and Wernicke areas:

It results in a condition called (Global aphasia) in which the patient cant understand the

spoken speech or even to produce speech.

Patients who have lesions of the Insula have difficulties in pronouncing the words.

Aphasia:

Aphasia is a loss of the ability to produce and/or comprehend language, due to injury to brain areas

specialized for these functions.

y inability to comprehend language

y inability to pronounce, not due to muscle paralysis or weakness

y inability to speak spontaneously

y inability to form wordsy inability to name objectsy poor enunciationy excessive creation and use of personal neologisms

y inability to repeat a phrase

y persistent repetition of phrases

y paraphasia (substituting letters, syllables or words)

y agrammatism (inability to speak in a grammatically correct fashion)

y dysprosody (alterations in inflexion, stress, and rhythm)y uncompleted sentences

y inability to read

y inability to write.

Types of aphasia:

Type ofaphasia

Fluency Presentation

Wernicke's

aphasia

fluent

paraphasic

1. The patient speak in long sentences that have no meaning, add

unnecessary words, and even create new "words" (neologisms).

2. They have poor auditory and reading comprehension, and fluent,but nonsensical, oral and written expression.3. Great difficulty understanding the speech of both themselves and

others and are therefore often unaware of their mistakes.

4. They are also often unaware of their surroundings, and maypresent a risk to themselves and others around them.

Transcortical

sensory

aphasia

fluent Similar deficits as in Wernicke's aphasia, but repetition ability

remains intact.

Conduction

aphasia

fluent 1. Caused by damage to the arcuate fasciculus, the structure that

transmits information between Wernicke's area and Broca's area.2. Auditory comprehension is near normal, and oral expression is

fluent with occasional paraphasic errors.3. Repetition ability is poor.


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Anomic

aphasia

fluent 1. The patient may have difficulties naming certain words, linked by

their grammatical type (e.g. difficulty naming verbs and not nouns2. Patients tend to produce grammatic, yet empty, speech. Auditorycomprehension tends to be preserved.

Broca's

aphasia

non-fluent,

effortful,

slow

1. Patient speaks short, meaningful phrases that are produced with

great effort. 2. Characterized as a nonfluent aphasia.

3. Individuals with Broca's aphasia are able to understand the speechof others.

Transcortical

motor

aphasia

non-fluent 1. Similar deficits as Broca's aphasia, except repetition ability

remains intact. 2. Auditory comprehension is generally fine for

simple conversations, but declines rapidly for more complexconversations.

Global

aphasia

non-fluent They may be totally nonverbal, and/or only use facial expressions

and gestures to communicate.

Transcorticalmixed

aphasia

non-fluent Similar deficits as in global aphasia, but repetition ability remainsintact.

Subcortical

aphasias

Characteristics and symptoms depend upon the site and size of

subcortical lesion. Possible sites of lesions include the thalamus,

internal capsule, and basal ganglia.

Lesion in the dominant angular gyrus:

The patient cant read (alexia) or write (agraphia)

Dysgraphia:

Dysgraphia (oragraphia) is a deficiency in the ability to write, regardless of the ability to read,

not due to intellectual impairment. |

Types of dysgraphia

1. Dyslexic dysgraphia:

Spontaneously written work is illegible, copied work is fairly good, and bad spelling.

2. Motor dysgraphia:

Motor dysgraphia is due to deficient fine motor skills, poor dexterity, poor muscle tone,and/or unspecified motor clumsiness.

Generally, written work is poor to illegible, even if copied by sight from another document.

Spelling skills are not impaired. Finger tapping speed results are below normal.

3. Spatial dysgraphia: Dysgraphia due to a defect in the understanding of space has illegible spontaneously written

work, illegible copied work, but normal spelling and normal tapping speed.

Symptoms of dysgraphia A mixture of upper/lower case letters, irregular letter sizes and shapes, unfinished letters. Many spelling mistakes.

Pain when writing.


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Decreased or increased speed of writing and copying, talks to self while writing, muscle

spasms in the arm and shoulder (sometimes in the rest of the body), inability to flex(sometimes move) the arm (creating an L like shape).

lesions of prefrontal cortex:

Destruction of the prefrontal cortex doesnt produce any marked loss of intelligence, but it

causes emotional changes such as euphoria and changes in patient behaviour. sensory cortex:

This cortex is located in the thalamus.

Lesions of the primary somesthetic area (post-central gyrus):

It results in contra-lateral sensory disturbances, which is most severe in the distal part of the

limbs. Painful, tactile, and thermal stimuli are often felt. The patient cant judge degree of

warmth, unable to localized tactile stimuli accurately, and unable to judge weight of objects.

Loss of muscles tone.

Lesions of the secondary somethetic area do not cause any disorders.

Lesions of the superior parietal lobule:

It interferers with patients ability to combine touch, pressure, and proprioceptive impulses.

Astereognosis: loss of integration of sensory impulses, for example patient cant recognize

that he is carrying a key in his hand when his eyes are closed.

It will interfere with recognizing the body image on the opposite side of affection. The patient

may fail to recognize that the opposite side is his own.

Lesions of primary visual area (posterior part of one clcarine sulcus):

This lesion cause loss of sight sensation in the opposite visual field (crossed homonymous

hemianopia). Lesion of upper half of one primary visual area (above calcarine sulcus) results in

inferior quadrantic hemianopia. When the lesion is below calcarine sulcus results in superiorquadrantic hemianopia.

Lesions secondary visual area (above the primary visual area):

Results in loss of ability to recognize objects seen in the opposite field of vision.

Hemianopic:

A hemianopsia is a loss of half of their visual field in both eyes.

A hemianopsia can occur after a stroke, head injury or the result of a brain tumor.

Symptoms:

1. Running into objects to the side.

2. Difficulty moving about in crowded areas.3. Difficulty finding things.

4. Often startled by moving objects or people.

5. People and objects appear and disappear.6. Losing place in reading or words come and go.

7. Struggling to find start or end of a line of print.8. Spilling drinks when eating.


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9. Unst

l

nce in wal

ing.

10. Fear of wal

ing aboutin stores or public areas

Lesi

s oft

e pri

ry auditory area (middle partoft

e superiortemporalgyrus):

Slight bilateralloss of hearing, butthe loss will be greaterin the opposite ear. Inabilit

to locate the

source of sound.

Bilaterallesion causes complete deafness.

Lesions oft e secondary auditory area (behindthe primary auditory area):

Results in inabilit

to recogni

e and to interpret sounds (acoustic verbal agnosia)

Auditory agnosia

Auditory agnosics failto ascribe values to verbal or non-verbal sounds. Individuals with pure

word deafness have intact hearing, but are unable to understand the spoken word, typically the result

of bilateraltrauma to the temporal cortico-subcortical regions ofthe brain. Nonverbal auditory

agnosics failto associate sounds with specific objects or events, such as a dog's bark orthe slamming

of a door. In these patients, the lesions tend to locate to the right hemisphere.

Cortical areas


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Cerebral Cortex Pathologies

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