Download Протокол

“ЗАТВЕРДЖЕНО”
на методичній нараді кафедри
нервових хвороб, психіатрії
та медичної психології
“______” _______________ 2008 р.
Протокол № _____
Зав. кафедри нервових хвороб, психіатрії
та медичної психології
професор
В.М. Пашковський
.
.
METHODOLOGICAL INSTRUCTION № 12
THEME: LOCALIZATION OF FUNCTIONS IN BRAIN CORTEX. SYNDROMES OF
LESION. METHODS OF EXAMINATION
Modul 1. General neurology
Сontents modul 2. Pathology of the cranial nerves. The disorders of the autonomic nervous
system and brain cortex functions. Meningeal syndrome. The additional methods of
examination in neurology.
Subject:
Nervous deseases
Year 4
Medical faculty
Hours 2
Author of methodological instructions
PhD, MD Zhukovskyi O.O.
Chernivtsy 2008
1. Scientific and methodological substantiation of the theme.
The lesion of mental function make a great problem of social adaptation process of
neurological patients with mental defect after the stroke or other neurological
diseases. Also, the definition of mental defects helps to localize the level of the
nervous system lesion. If they are present, the lesions are usually in the left or right
cerebral cortex.
2. Aim: students should be able to investigate mental function, to determine
independently signs of lesion of brain hemispheres and to localize the pathological
process (focus). Students should be able to formulate and to explain the topical
diagnosis.
Students must know:
1. Anatomical structures and function of brain cortex.
2. Clinical signs of brain cortex lesion.
3. Clinical signs of lesion of consciousness level.
Students should be able to:
1.
Examine patient status.
2.
Make a conclusion about presence of pathology of brain cortex function.
3.
Put topical diagnosis and to explain it.
4. Make differential diagnosis of a pathological process level localization.
1.
2.
3.
4.
5.
Student should gain practical skills:
To gather an anamnesis and to examine patient status
In course of analysis of the complaints of the patient to find out presence of lesion
of brain cortex (defect of speech, praxis, calculation, gnosis, intellectual functions,
memory, ability to write and to read).
To carry out tests on speech, writing, reading, calculation, praxis, gnosis.
To formulate a conclusion about presence or absence of lesion signs of brain
cortex.
To examine the function of brain lobes and syndromes of their lesion.
4. Integration (basic level).
Subjects
Anatomy
Gained skills
Knowledge of anatomy of brain hemispheres and
lobes
Histology
Hystological structure of brain cortex
Physiology
Knowledge of function of brain cortex and brain
lobes.
Subject
The cerebral cortex is the mantle that covers both cerebral hemispheres and
gives them their convoluted superficial appearance. The cortex is generally viewed as
the highest functional level of the nervous system and responsible for uniquely
human characteristics, such as intricate hand movements, highly developed speech,
symbolic thought, personality, conscience, and self-awareness. These qualities are
known to depend on the cortex because, if certain areas in the cortex are damaged,
these qualities are lost or greatly impaired.
Structural Organization of the Cortex.
Structurally, the cerebral cortex contains both horizontal and vertical
organization. The horizontal organization consists of six layers made up of two types
of neurons. Cortical neurons are classified as either pyramidal or nonpyramidal
based on the shape of the cell body. Pyramidal cells have a cell body shaped like a
pyramid, with the apex pointing toward the surface of the brain. The apex gives rise
to a single apical dendrite that runs toward the surface and intersects intervening
layers at right angles. The base of the cell gives rise to several basilar dendrites that
course laterally within the layer containing the cell body. Nonpyramidal cells usually
have small, round cell bodies with dendrites arising from all aspects of the cell body.
Pyramidal and nonpyramidal cells also differ with respect to their axons. The
axon of a pyramidal cell has a main trunk that projects in the white matter to another
region of the cortex or to a more distal site within the central nervous system (CNS).
In addition to the main trunk, the axon may have collateral branches that terminate
near the cell body. In contrast, the axon of the nonpyramidal cell branches profusely
and remains in the region near the cell body. Layers with high concentrations of
pyramidal cells form the output segment of the cortex while layers with
predominantly nonpyramidal cells form the receptive layers for cortical input. This
systematic arrangement of pyramidal and nonpyramidal cells produces the
horizontal layers in the cortex.
Horizontally, the cortex is divided into six cell layers on the basis of
cytoarchitecture. The layers are numbered sequentially from the surface to the
myelinated projection fibers that underlie the cortex. Layer 1 (molecular) consists
primarily of glial cells and projection fibers running parallel to the surface. Because
the projection fibers synapse on the apical dendrites of cells from deeper layers,
layer 1 functions to interconnect cortical regions. Layers 2 and 3 (external granular
and external pyramidal, respectively) contain large numbers of pyramidal cells that
project to other cortical regions. Layer 4 (internal granular) consists primarily of
nonpyramidal cells and forms the primary receptive region for cortical input. Layer 5
(internal pyramidal) contains the largest pyramidal cells and forms the primary
output region from the cortex to the rest of the nervous system. Layer 6 (multiform)
contains smaller pyramidal cells that project from the cortex to the thalamus.
While the basic six-layer structure remains constant throughout the cortex, the
thickness of individual layers varies with the function of the different cortical regions. Based on the changes in microscopic structure, cytoarchitectural maps have
been created that divide the surface of the cerebrum into distinct areas. Some areas
correspond with recognized function while others do not. The most frequently used
cytoarchitectural map was developed by Korbinian Brodmann, a German
neurophysiologist, who divided the human cerebral cortex into 52 areas.
Functionally distinct areas of the cerebral cortex are often referred to by their
Brodmann number designation.
The vertical organization of the cortex consists of columns of cells that respond
to a specific type of stimulus from a particular region of the body. The area of the
cortex that receives information from the hand contains individual columns
specialized for the sensation of touch, pressure, temperature, or pain. These
vertical columns are very important and considered to form the functional units of
the cortex. The columns of cells run perpendicular to the layers and together they
form the structural and functional organization found throughout the cortex.
The primary function of the cerebral cortex is integration. The anatomical
convergence necessary for integration occurs both within columns of cortical cells
and between cortical areas. Within individual columns, input is integrated
sequentially over time and represented by the ongoing level of activity in that
column. Integration between cortical areas occurs as the output from two or more
cortical regions converge. Such complex integration is necessary to form holistic
perceptions of the way objects feel, taste, smell, look, and relate to the surrounding
environment. Transcortical fibers, both those located in layer 1 and projection fibers
located in the white matter, provide the pathways for integration of information from
distal cortical sites. The exact location in which complex perceptions are formed
remains unknown, although association areas of the cortex are probable sites.
Neurons that project from one hemisphere to the other are called commissural
fibers (corpus callosum, anterior and posterior commissures) and provide for the
sharing of information from one hemisphere to the other.
Functional Organization of the Cortex
Functionally, the cerebral cortex contains two types of areas: one that is
dedicated to specific functional systems and one that is responsible for associating or
integrating information from other areas. Cortical regions identified with specific
functional systems are referred to as primary, secondary, and tertiary projection areas.
Cortical projection areas are often referred to by their Brodmann number designation,
for example, primary visual, 17; secondary visual, 18; tertiary visual, 19; primary
motor, 4; premotor, 6; frontal eye field, 8; primary somatosensory, 3a, 3b, 2,1;
primary olfactory, 38; primary auditory, 41 and 42; and so forth. Regions of the
cortex that are responsible for integrating information from functional systems are
referred to as association areas. The majority of the space in each lobe is occupied by
association areas. An example of cortical integration is seen when the color, taste,
shape, smell, and texture of a spherical citrus fruit are integrated to produce the
concept of "an orange."
The cerebral cortex is also somatotopically organized such that the body
surface may be represented or mapped on the cortex. The most widely described
examples of this somatotopic arrangement are found in the primary motor cortex
(area 4) and primary sensory cortex (areas 3, 1, 2). There are two important aspects
about this representation of the body or homunculus. First, the map is distorted
such that some body parts have greater representation than others. Second, the
homunculus is inverted with the lower extremity represented on the medial aspect
of the hemisphere and the head on the lateral aspect adjacent to the lateral fissure.
Both the distortion and the inversion have important functional consequences. The
body parts with the greatest cortical representation have the most precise control. In
part, the dexterity of the face and hand are due to the large amount of cortical space
dedicated to their control. The precise sensory discrimination of the mouth and hand
are due to the same disproportionate allocation of space. Inversion of the
homunculus is clinically significant because the body parts represented on the medial
aspect of the hemisphere receive their blood supply from one artery while those on
the lateral surface receive theirs from another.
Transcortical Connections.
The primary connection between the two hemispheres is provided by the
corpus callosum, the largest fiber bundle in the nervous system. The corpus
callosum forms the floor of the medial longitudinal fissure and the roof of the lateral
ventricles. In crossing the mid-line, the corpus callosum connects functionally related
areas in the two hemispheres.
Aphasia – is a disorder of language, the aphasic patient uses language
incorrectly or comprehends it imperfectly. Anatomy of aphasia. Language “ability” is
a function of the left hemisphere for almost all right-handed and for most left-handed
individuals. The anatomic components of the language are located primarily in the
region of the middle cerebral artery surrounding the Sylvian and Rolandic fissures.
Speech production involves four regions in this area, moving from posterior and
anterior. Thus, speech connections exist between Wernicke’s area on the posterior
part of the first temporal gyrus; the angular gyrus; the arcuate fascicules; and Broca’s
on the posterior third frontal gyrus. Types of aphasia. The lesion of posterior part of
lower frontal lobe (the center of Broca) causes Broca’s aphasia. Broca’s aphasia
occurs in case of motor encoding area involved and means the impairment of
spontaneous speech, repetition, reading aloud, naming (but recognizes object) and
writing, retained the comprehension of both spoken and written language function.
Testing:
1.
Speech is slow, nonfluent, produced with great effort, and poorly
articulated. There is marked reduction of total speech, which may be “telegraphic”
with the omission of small words or endings.
2.
Comprehension of written and verbal speech is good.
3.
Repetition of single words may be good, though it is done with great
effort; phrase repetition is poor, especially phrases containing small function word
(eg, “no if’s, and’s, or but’s”).
4.
The patient always writes aphasically.
5.
Object naming is usually poor although it may be better than
spontaneous speech.
6.
Hemiparesis (usually greater in the arm than in the leg) is present, as the
motor cortex is close to Broca’s area.
7.
The patient is aware of his deficit; he is frustrated and frequently
depressed.
8.
Interestingly, the patient may be able to hum a melody normally. Curses
or other ejaculatory speech may be well articulated.
According to Lurie there are three types of motor aphasia. They are:
- afferent is associated with the lesion of lower parts of gyrus postcentralis
which provide innervation of oral muscles. In this case articulation of
sounds suffers. That means the loss of automatical speech, repetition,
naming. This kind of aphasia is connected with oral apraxia.
- efferent is Broca’s aphasia. In this case articulation is preserved. But the
patient can’t spell some sounds, words and phrases. At completely aphasia
the patient doesn’t speak at all.
- dynamic is usually caused by lesion of cortical zone in front of Broca’s
centre. For this type of aphasia aspontanic speech is typical. the patient
refuses to speak in active manner. But he is able to repeat certain sentences,
words, answer the questions.
Wernicke’s aphasia occurs in case of auditory association area involved and
means the impairment of comprehension of spoken language, repetition of spoken
language, naming comprehension of written language, spontaneous speech, the
spoken language is fluent but impaired (jargon).
Testing:
1. Speech is fluent with normal rhythm and articulation, but it conveys
information poorly because of circumlocutions, use of empty words and
incorrect words (paraphasic errors).
2. The patient uses wrong and sounds -ie, makes paraphasic errors (“treen” for
train; “here is my clover” for here is my hand).
3. The patient is unable to comprehend written or verbal speech.
4. The content of writing is abnormal, as is speech, though the penmanship may
be good.
5. Repetition is poor.
6. Object naming is poor.
7. Hemiparesis is mild or absent, since the lesion is far from the motor cortex. A
hemianopsia or quadrantopsia may be present.
8. Patients may not realize the nature of their deficit and often are not depressed
in the acute stage.
2. Anomic (nominal) aphasia is impairment of naming objects and spontaneous
speech. Spoken language fluent but rambling and vague. Retained the repetition,
comprehension of both spoken and written language.
1.
This type of aphasia may be seen at small lesions in the angular gyrus, toxic or
metabolic encephalopathy, or with focal space-occupying lesions far the speech area,
but which exert pressure effects.
2.
Speech is fluent but conveys information poorly because of paraphasic errors
and circumlocutions (written language is impaired in the same way). Even though
this aphasia is termed anomic aphasia (difficulty in naming objects), anomia is not
unique to this type of aphasia.
3.
The patient can understand both written and spoken speech.
4.
There is no hemiplegia.
5.
Comprehension and repetition are normal.
3. Semantic aphasia occurs at lesion of temporal-parieto-occipital border of left
hemisphere. The patients cannot realize the difference between “The brother of the
father” and “the father of the brother”.
Examination of the aphasic patient.
It must first be established whether the patient is in fact aphasic; then
determine the nature of the aphasia.
1.
Listen to speech output. Is it fluent or nonfluent? If fluent the lesion is
posterior; if nonfluent it usually is anterior.
2.
Can the patient read and write with no errors? If so, he is not aphasic.
3.
Is there hemiparesis? If so, the lesion must be anterior, involving the motor
area.
4.
To delineate the various types of fluent aphasias, check to see if the patient can
repeat, comprehend, and name:
- Wernicke’s: cannot repeat or comprehend; names poorly;
- Conduction: cannot repeat but can comprehend; names poorly;
- Anomic: can both repeat and comprehend but has trouble with naming.
Apraxia is a disturbance of purposeful movement which is not accounted for
by elementary motor or sensory impairments. It occurs commonly is association with
aphasic syndromes. Apraxia is deviated in:
1. motor or kinetic
2. ideational
3. constructional and dressing
Ideational Apraxia. In ideational apraxia there is inability or failure to
comprehend, develop, or retain the concept of what is desired. It is usually due to
general suppression or less of cerebral function and resembles extreme absentmindedness. Such a patient will have difficulty in understanding what is desired and
will fail to complete the desired act. This becomes apparent when he is asked to carry
out a series of simple acts such as “Put the pencil in the cup and hand me the
matches.” After requiring that the request be repeated, he may then pick up the pencil
and fail to do anything more. The patient with ideational apraxia has lost the idea.
Ideokinetic Apraxia. Another common form of apraxia is known as
“ideokinetic” or “ideomotor” apraxia. This occurs when there is a break in
transmitting or converting the idea into the appropriate motor act. This form of
apraxia occurs most commonly with lesions of the major hemisphere at the junction
of the temporal, parietal and occipital lobes or its connections with the frontal lobes.
Despite knowing what is desired, the patient is unable to carry out a desired complex
performance. He may, for example, hesitantly touch his forehead when asked to
touch his nose. He may recognize a comb but he unable to use one to comb his hair
when asked. Then, surprisingly, he may carry out the same acts automatically that he
is unable to perform volitionally on request.
Kinetic Apraxia. Failure of the third step produces kinetic apraxia. This
phenomenon is considered to be due to a lesion of the premotor frontal cortex, and
the disability is limited to one extremity or a part of it. There is no actual weakness,
and the patient is able to use the extremity for gross movements and automatically.
He has lost the ability to make fine skilled movements such as finger wiggling,
opposition, writing, or piano playing. Observations for awkwardness while carrying
out relatively complicated acts such as dressing and undressing should be made. It
should be noted whether the patient has difficulty in conceiving how to hop, how to
touch his nose, and how to wiggle his fingers or tap his toes.
Specific Test.
Observations on the motor-pattern performance of patient are made during the
various parts of the neurological examination when the patient is asked to show his
teeth, stick out his tongue, wiggle his fingers, tap his toes, hop, walk tandem, touch
his nose, and so forth. Instruct the patient by word or gesture to:
1. Touch his nose.
2. Drink from a glass or paper cup.
3. Use a folder of matches.
Get the patient to follow simple spoken directions. Say to the patient:
1. Close your eyes.
2. Point to your nose and your chin.
3. Put the pencil in the glass (or paper cup) and hand me the matches.
4. Repeat after me, “I bought a new hat, a pair of shoes, and a white shirt”.
Constructional and Dressing Apraxia. Lesion of the posterior parietal region
of the nondominant hemisphere may impair performances related to spatial concepts.
Constructional apraxia may be demonstrated by having the patient try to copy
geometric forms or draw the face of a clock. Further testing includes having the
patient try to arrange sticks in a specific pattern or to arrange Koch blocks in a
desired design. Dressing apraxia is tested simply by asking the patient to put on a
shirt or bathrobe.
Agnosias are disorders of recognition which are not accounted for by
elementary motor or perceptual disturbances.
Testing for tactile recognition (stereognosis) is considered as a part of the
general sensory examination, while the tests for recognition of various forms of
auditory and visual recognition are considered in the chapter on language and motor
speech. Defects of recognition on a somewhat different integrated level are
considered here.
Autotopagnosia – agnosia for body parts there may be lack of recognition of
hands, eyes, feet, and so forth, of the examiner, and even in pictures. With agnosia for
parts of a whole the patient is able to recognize a bicycle but is unable to recognize
and name the wheels, handlebars, seat, and other parts.
Somatotopagnosia includes disturbances in recognition of the patient’s own
body or body parts. It is due to lesions of the poster-inferior parietal lobe in the region
of the interparietal sulcus of the dominant hemisphere or to a subcortical lesion
isolating this area from the thalamus. It is often associated with acalculia, visual
verbal agnosia, or anosognosia. Autotopagnosia may be limited to one part of the
body or may be more general, involving relationship of the body as a whole. The
limited form includes lack of recognition of one half of the body or one extremity and
inability to recognize and name individual fingers (finger agnosia) or other body
parts. In mild forms the patient may have a sense of distortion of the involved parts of
the body and disturbances of laterality. This may be tested by asking the patient to
name various parts of his own body and to identify right and left.
Anosognosia is lack of awareness or denial of the existence of disease. An
obvious example is a denial by the hemiplegic patient that he is paralyzed. This
usually is associated with severe disturbance of sensation but is not due to the sensory
loss; for instance, knowledge of the paraplegic patient that the paralyzed and
anesthetic limbs belong to him. True anosognosia occurs with lesions of the inferior
parietal lobe in the region of the supramarginal gyrus.
Hemispheric Specialization.
Historically, the cerebral hemispheres were viewed as mirror images of one
another. The duplication of anatomy and physiology was justified on the basis of
the crossed organization of the nervous system such that the right hemisphere
controls the somatic and visceral functions of the left side of the body and the left
hemisphere controls the right side. It was not until the corpus callosum (the major
fiber bundle regulating communication between the two hemispheres) was sectioned
that it became evident that the two hemispheres specialized in different functions. In
the absence of the corpus callosum, each hemisphere behaves as an individual brain
with independent perception, learning, memory, thoughts, and emotional reactions,
and neither is aware of the experiences of the other; literally, the right hand does not
know what the left hand is doing.
Table 1. Behaviors Controlled by Each Hemisphere
Behavior
Perception/cognition
Left hemisphere
Processing and producing language
Information processing
Cognitive style
Linear, sequential
Observing and analyzing details
Academic skills
Reading: word recognition, sound-symbol
relationship, reading comprehension
Performing mathematical calculations
Motor
Movement sequencing
Performing movements or gestures on
command
Expression of positive emotions
Emotions
Right hemisphere
Processing nonverbal stimuli (complex shapes,
sounds, speech inflection)
Visual-spatial perception
Drawing inferences, integrating information
Simultaneous, holistic
Grasping overall organization or gestalt, sees
patterns
Mathematical reasoning/judgment
Alignment of numbers in calculations
Sustaining a movement or posture
Expression of negative emotions
Perception of emotions.
The left hemisphere is characterized primarily by its specialization in
language (speech, reading, writing) and is therefore operationally defined as the
dominant hemisphere. Roughly 98 percent of the population has language controlled
by the left hemisphere. The plenum temporal (the area of the temporal lobe
specialized for speech) is larger in the left hemisphere by the 31st week of gestation,
suggesting that this asymmetry does not develop in response to experience, but is
innate. The left hemisphere also excels in intellectual, rational, verbal, and
analytical thinking. It assumes primary control of analytical processes such as
calculation, stereognosis (interpretation of sensory stimuli) from the right side of the
body, audition from the right ear, vision from the right visual field, and olfaction
from the left nostril.
The right hemisphere excels in perceiving and in emotional, nonverbal, and
intuitive thinking. The right hemisphere also controls spatial orientation, nonverbal
ideation, music appreciation, olfaction from the right nostril, audition from the left
ear, vision from the left visual field, and stereognosis from the left side of the body.
Because the right hemisphere usually does not control language, it is a more
difficult hemisphere to evaluate. For example, in the absence of a corpus callosum, if
a key is placed in an individual's left hand and vision is occluded, he or she can still
interpret the sensory feedback and recognize the object. However, the object is
recognized in the right hemisphere, and because the right hemisphere does not
have the ability to produce speech, the individual cannot identify the object
verbally. If asked to identify the test object by selecting from an array, the
individual experiences no difficulty in selecting the key. The right hemisphere
recognizes the object but does not have access to the left hemisphere, which would
permit the individual to identify it verbally.
In a normally functioning brain, that is, a brain with an intact corpus callosum,
each specialized region assumes primary responsibility for a particular aspect of the
overall functional task. The results of specialized analyses are then shared freely
among regions and hemispheres to enable individuals to perform a wide range of
behaviors with no difficulty. In information processing parlance, this is called a
parallel, distributed control system, that is, a task is broken down into components,
with each component sent to a specialized center for analysis. Once complete, the
results are freely shared among centers. Because each of the centers operates
independently, they can all work on their part of the larger task, at the same time
greatly speeding resolution time.
Clinical Aspects.
Cerebrovascular accidents (CVA) also provide a means for studying the function
of the cerebral cortex. Cerebrovascular accidents or strokes may occur in any vascular
territory in the brain. The behavioral dysfunction that accompanies the stroke will
depend on which areas of the brain are affected.
Because the longitudinal systems connecting the brain and body are crossed,
the symptoms and signs of CVA are seen on the side opposite the lesion. Because the
right and left hemispheres specialize in controlling different functions, right and left
CVAs produce very different clinical manifestations.
At birth the brain is already genetically predisposed to acquire language
because of the presence of Wer-nicke's area (22) in the left hemisphere. This area is
concerned with the comprehension of spoken and written language. If Wernicke's
area is damaged, a receptive aphasia, commonly referred to as word deafness, is
produced. In this type of aphasia, the auditory apparatus functions perfectly but the
sounds being sensed are not perceived as language. This aphasia may also affect
speech production because individuals are unable to understand their own spoken
words. If the angular gyms (area 39), which connects the visual cortex with
Wernicke's area, is damaged, the individual experiences a visual word deafness
(alexia) wherein the visual apparatus is functioning perfectly but written language
is not perceived. This type of aphasia may be accompanied by an inability to write
language (agraphia).
Speech production is also controlled in the left hemisphere in Broca's area (44
and 45). Damage in this area results in a productive aphasia characterized by
impaired ability to produce verbal language. The motor apparatus for speech is
intact, language is heard and perceived, and organized thought processes occur, but
coherent verbal self-expression is impossible. Rhythmic speech, as in singing, seems
to be a special case: It is specifically controlled in area 45; therefore, normal speech
may be absent but singing is still possible. Mel Tillis is a male vocalist who stutters
when speaking but does not stutter when singing.
The functions controlled by the cerebral cortex are dependent on the integrated
output of columns of cells rather than the actions of any single neuron. This point is
well illustrated by a clinical example. Convulsive activity is produced by changes in
the collective properties of large numbers of cortical neurons. The
electroencephalogram (EEG) uses electrodes applied to the scalp to record the
activity of many cortical neurons simultaneously and is the best clinical tool for
examining global cortical activity. Epileptic seizures are the direct result of
abnormal, synchronized discharge of a large number of cortical neurons as seen on
EEG. Synchronization of these normally independently discharging units produces
stereotyped and involuntary changes in behavior, including transient loss of awareness, jerking movements, and possibly massive convulsions and loss of
consciousness. Normally, lateral or surround inhibition of columns of cortical
neurons prevents independently discharging units from becoming synchronized.
Lateral or surround inhibition is created when a neuron or column of neurons
facilitatethemselves and inhibit adjacent neurons. This arrangement helps to clarify
the message being transmitted by the neuron or column and prevent interference of
"crosstalk" from adjacent neurons. During an epileptic seizure, this surround
inhibition breaks down and the discharge of columns of cortical neurons becomes
synchronized at the seizure frequency, thereby losing control of their normal
function and producing the seizure behavior. Thus, epileptic seizures are disorders of
the cerebral cortex.
Abnormal discharge patterns of cortical neurons may be caused by many
factors: trauma, oxygen deprivation, tumors, infection, and toxic states. However,
only about half the individuals with epilepsy have clearly demonstrable causes.
Depending on the size of the area recruited, epileptic seizures can be either
partial or general. Both forms produce distinctive, abnormal EEG patterns called
spikes. Partial seizures begin from a focal center and spread to adjacent cortical
regions by recruiting cells to beat at the seizure frequency. The area of the cortex
involved in the abnormal discharge pattern will determine the associated behavioral
activity. If the seizure involves the motor cortex, the individual will
exhibitabnormal motor activity. Consciousness, visual, or auditory areas experiencing
an abnormal discharge pattern will produce abnormal consciousness, visual, or
auditory perceptions, respectively. Within a given cortical region, the body part with
the largest representation is the most likely to be involved in the seizure activity. For
example, the largest part of the motor ho-munculus is dedicated to the hand and face
and they are also the most common body parts involved in motor seizures. The
spread of partial seizures appears to be limited by powerful postsynaptic
hyperpolarization in the cortex. During a generalized epileptic seizure, the abnormal
discharge activity is evident over the entire brain at seizure onset and may result
from an abnormal input originating in the brain stem reticular formation.
A common strategy for the medical management of seizure disorders is the
administration of a generalized depressant such as phenytoin (Dilantin). The drug
makes it more difficult for each neuron to reach discharge threshold, thereby making
it more difficult to produce pathologically synchronized discharge of cortical cells.
1.
2.
3.
Sign of the Frontal Lobe’s Lesion
Monoparesis or paralyzes
Motor Jackson’s seizures
Cortical (frontal) ataxia with astasia (inability to standing) and abasia
(inability to walking without paresis)
4.
5.
6.
7.
Paralysis of conjugate gaze to the opposite side with deviation of the eyes
toward the side of the lesion. Irritative lesion produces a conjugate deviation of
the eyes away from the side of the lesion.
Agraphia
Apraxia of speech –Brocka’s aphasia
Emotional reactions.
3.
4.
5.
6.
Sign of the Temporal Lobe’s Lesion
Quadrantic defects which extend to the point of fixation without macular
sparing
Defects in upper quadrants of the homonymous half-fields on the side
opposite the lesion
Sensory aphasia
Auditory, smell, and testing hallucinations
Auditory, smell, and testing agnosia
Temporal ataxia
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Sign of the Parietal Lobe’s Lesion
Anesthesia
Sensory Jackson’s seizures
Performance of complex act
Agnosia
Anosognosia
Autotopagnosia
Astereognosia
Pseudomelia
Inability to do calculation
Defects of reading
1.
2.
3.
4.
5.
Sign of the Frontal Lobe’s Lesion
Congruous homonymous hemianopsia with central sparing
Bilateral homonymous hemianopsia
Visual hallucinations
Scotoma
Visual agnosia.
1.
2.
Self assessment:
Tests for self-assessment:
1. How many layers has the brain cortex?
2. Gyruses of frontal lobe.
3. Gyruses of parietal lobe.
4. Gyruses of temporal lobe.
5. Gyruses of occipital lobe.
6. Function’ centers of the left frontal cortex.
7. Function’ centers of the left parietal cortex.
8. Function’ centers of the left temporal cortex.
9. Function’ centers of the occipital cortex.
10.Clinical signs of irritation of cortex precentral gyrus.
11.Clinical signs of irritation of cortex postcentral gyrus.
12.Clinical signs of lesion of upper parts of cortex precentral gyrus.
13.Name types of aphasia.
14.Name types of agnosia.
15.Name types of apraxia.
16.When does the motor (Broca’s) aphasia occur?
17.When does the sensor (Wernicke’s) aphasia occur?
18.When does the alexia appear?
19.Patient has seizures which start from head and eyes turning left. Where is
pathological focus?
Tests
1. Lesion of what part of the cortex leads to astereognosia
a) temporal lobe;
b) frontal lobe;
c) occipital lobe;
d) parietal lobe;
e) postcentral gyrus.
2.
a)
b)
c)
d)
e)
3.
a)
b)
c)
d)
e)
What symptoms appear when Wernicke center is damaged
Anomic (nominal) aphasia;
Motor aphasia;
Sensory aphasia;
Ideational apraxia;
Constructional apraxia.
What is the thickness of brain cortex
0,5 – 1,0 mm;
1,3 – 4,5 mm;
5 – 8 mm;
10 – 12 mm;
15 – 20 mm.
Real-life situations:
1.
Describe the signs of of left frontal lobe lesion.
2.
Patient has partial seizures in left extremities which cause general attack.
Where is a pathological focus
3.
Patienthas periodic vision and olfaction hallucinations. Where is a
pathological focus
References:
1.
Basic Neurology. Second Edition. John Gilroy, M.D. Pergamon press.
McGraw Hill international editions, medical series. – 1990.
2.
Clinical examinations in neurology /Mayo clinic and Mayo foundation. – 4th
edition. –W.B.Saunders Company, Philadelphia, London, Toronto. – 1976.
3.
McKeough, D.Michael. The coloring review of neuroscience /D.Michael
McKeough/ - 2nd ed. – 1995.
4.
Neurology for the house officer. – 3th edition. – howard L.Weiner, MD and
Lawrence P. Levitt, MD, - Williams&Wilkins. – Baltimore. – London. –
1980.
5.
Neurology in lectures. Shkrobot S.I., Hara I.I. Ternopil. – 2008.
6.
Van Allen’s Pictorial Manual of Neurologic Tests. – Robert L. Rodnitzky. 3th edition. – Year Book Medical Publishers, inc.Chicago London Boca
Raton. - 1981.