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CHAPTER
5
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It¡¦s important to assemble main clinical
findings and put them into the general picture of language as a biological
phenomenon.
I.
Clinical symptoms of speech and language disorders
(1.)
General characteristics of the patient with aphasia
A.
Reasons of disturbance in communication of adult patients
a. Cerebro-vascular accident
Symptoms:
1. One side of body doesn¡¦t move at will
2. Can¡¦t express problems successfully
3. Being stabilized around five months
4. The permanent residue of dysfunction
b. Traumatic lesions
Causation:
1. Sudden anoxic states
2. Intoxications such as carbon monoxide
c. Other disease of brain
1. Confusion
2. Perseveration
3. Memory lapse
4. Flight of associations and ideas
5. Difficulty in concentration, suppressing irrelevant thoughts and emotional lability
B.
Common syndromes of aphasic patients
a. Anosognosia
b.Glibberish
c. Can¡¦t understand anything said to him
C.
Remedies
a. Highly motivations
b. Patient¡¦s psychological conditions
c. Heightened stress
(2.)
Reception disorders
A.
Sensory aphasia is the misleading term
B.
Symptoms:
a. Inability to recognize or understand words or spoken language
b. Unable to repeat any utterance or word
c. Accompanied with other communicative problems often.
(3.)
Expressive disorders
A.
Subfluency
a. The articulation of every word apparently requires an enormous effort and concentration.
b. Utterances are reduced to telegram style
c. Their disturbed district is more central than general motor coordination of articulatory organs.
B. Superfluency
a. The flow of speech is markedly increased and can¡¦t be inhibited in accordance with the rules of either grammar or social interaction.
b. Syntax is more multilated.
c. Utterances consist of interminable phrases, clich Ás.
d. A particular word or phrase repeated again and again.
C. Semantic
disturbances
a. Inability to name color or numbers.
b. Words are substituted that are inappropriate in the context of the sentence but are semantically related.
c. Slip foreign words into utterances.
D. Difficulty in word finding
a. Anomia
b. The names of the objects patients want to search weren¡¦t really lost, they just can¡¦t find them at will.
E. Paraphasic
disturbances
a. Jargon aphasia
b. Nonsense words are produced more frequently and often exclusively.
c. Agrammatism which has the same nature of Jargon but of different scale.
F. Fixation on phrases
=> Many patients have one or two phrases which they produce fluently and correctly but which they repeat at all times.
(4.)
Disorders of manner of production
=> Patients have no problems in understanding sentences and they can produce standard sentences in terms of fluency, grammar and content. However, they might have problems as following
A. Errors of order
a. A pathological propensity for spoonrisms on the level of phonemes, words, and sometimes even whole phrases.
b. Most of the mistakes are anticipations of units yet to come.
c. Not only in speech but in writing forms.
B.
Dysarthria
a. After
a stroke or other brain injury, the muscles of the mouth, face, and respiratory
system may become weak, move slowly, or not move at all. The resulting speech
condition is called dysarthria. The type and severity of dysarthria depends on
which area of the nervous system is affected.
b. Symptoms:
1. Slurred speech
2.
speaking softly or barely able to whisper
3. slow rate of speech
4. rapid rate of speech with a "mumbling" quality
5. limited tongue, lip, and jaw movement
6. abnormal intonation (rhythm) when speaking
7. changes in vocal quality ("nasal" speech or sounding
"stuffy")
8. hoarseness
9. breathiness
10. drooling or poor control of saliva
11. chewing and swallowing difficulty Causes of Dysarthria
C. Discoordinations
a. The precise timing between the actions of the respiratory, laryngeal, and oral apparatus is out of order.
b. Symptoms:
1. Over-aspiration of sounds
2. Insufficient breath at the onset of a vowel
3. Inappropriate open or close of glottis
4. Transient interruptions of all sounds somewhat reminiscent of certain types of stuttering.
(5.)
Other language-related disorders
A. Alexia-> patients may lose the ability to read.
B. Agraphia-> patients may lose the ability to write.
II.
The underlying pathology
(1.)
Localized lesions
A.
Cerebro-vascular accidents
ê
It is what we called ¡§ stroke¡¨. A
stroke occurs when the blood supply to the brain is disturbed in some way. As a
result, brain cells are starved of oxygen causing some cells to die and leaving
other cells damaged.
Types of stroke:
1.
Thrombosis:
It
occurs when a blood clot (thrombus) forms in
an artery (blood vessel) supplying blood to the
brain. Furred-up blood vessels with fatty patches of atheroma (arteriosclerosis)
may make a thrombosis more likely. The clot interrupts the blood supply and
brain cells are starved of oxygen.
2.
Embolism: It is a blood clot that forms somewhere in the body
before travelling through the blood vessels and
lodging in the brain. This causes the brain cells to become starved of oxygen.
An irregular heartbeat or recent heart
attack may make you prone to forming emboli.
3.
Hemorrhage: It occurs when a blood vessel bursts inside the
brain and bleeds (hemorrhages). With a hemorrhage,
extra damage is done to the brain tissue by the blood that seeps into it.
4.
TIA( Transient ischaemic attack): It is a short-term stroke that
lasts for less than 24 hours. The oxygen supply to
the brain is restored quickly, and symptoms of the stroke disappear completely.
A transient stroke needs prompt medical attention as it is a warning of serious
risk of a major stroke.
B.
Tumor
a. Space-occupying lesions produce relatively rarely isolated aphasic symptoms.
b. In other tumors, nervous tissue is destroyed locally and replaced by an ever-increasing mass of tumor cells.
c. The veins in the immediate vicinity of the tumor are compressed by the local expansion, thus increasing the capillary pressure in this area and cause local swelling and edema.
C.
Abscess
a. It¡¦s another focal, inflammatory lesion which may cause generalized intracranial pressure.
b. It develops much more rapidly than brain tumors.
D.
Trauma
a. Fracture of the skull
b. Closed head injuries
c. Penetrating gunshot wounds.
E. Other focal lesions
(2.)
Diffuse lesions
A.
Presenile dementias
=> dementia is the loss of brain functions. It is not a single disease. Instead, dementia refers to a group of illnesses that involve memory, behavior, learning, and communicating problems.
B.
Alzheimer¡¦s Disease
a. It is a markedly premature aging of the brain.
b. It will exacerbate gradually.
c. General intellectual deterioration.
III.
Clinical syndromes
ê After introducing details of symptomatology and lesions, we have to relate the location of lesions to specific syndromes.
ê We may say that expressive disorders result more frequently from anterior lesions whereas more posterior lesions implicate receptive skills.
IV. Theoretical interpretations
(1.)
Interference vs. ¡§loss¡¨
A. Aphasic patient hasn¡¦t ¡§lost¡¨ language but still understands some statements, recognizes some words, or basically knows how language works.
B. They are only interfered with their language abilities; there are disturbances of cerebral function.
C. Neither discrete words nor discrete grammatical rules are neatly eliminated from the store of skills.
(2.)
The problem of neurological correlates
A.
Connections and associations
a. The early behaviorists thought of connections as the neurological correlate of associations.
b. End-organ cells and internuncial and central neurons and their fiber connections bear a structurally fixed and orderly relation to each other.
c. We can think associations as pairing a neutral stimulus such as a geometric pattern to a constitutionally meaningful stimulus.
d. An animal has normal pattern perception and acuity in say both the visual and auditory modality but can no longer make associations between the two.
e. Destruction of association cortex doesn¡¦t abolish a modality-specific type of behavioral associations in animals.
f. All areas of the cortex and the two hemispheres are interconnected by short and long fibers which are called commissures which are indeed the pathways for neural signals that mediate acquired behavior.
B.
Perceptions
a. Second area of interpreting the behavioral functions
b. There are correspondences between the retina and the area striata, between the distribution of touch-receptors over the skin and neurons in certain areas of the cortex.
c. It¡¦s possible to record peripherally evoked responses from the cortex.
d. Traumatic lesions of the primary visual projection area in man may lead to isomorphic scotomata.
e. We may think that neuronal activity that proceeds in a vertical direction.
f. The cerebral cortex alone can¡¦t be the exclusive locus of neurological correlates of the psychologist¡¦s behavioral categories.
g. The cortex is closely integrated with the rest of the brain and functions in coordination with other cerebral structures.
C.
Storage
a. The notion that certain aspects of behavior are stored in specific parts of the brain has received some superficial support from electrical stimulation experiments.
b. Stimulus triggers a chain of events but doesn¡¦t cause it.
c. Behavior must be the product of interaction and integration of functions of many components of the brain.
d. Effects of brain lesions upon memory
1. The patient may not be able to think of certain things at a given time to recruit memories at will.
2. He may not be able to recognize his memories with respect to his personal history.
3. He may not know when something actually happened.
e. There are no lesions that render patients permanently and irreversibly ignorant of his entire past.
f. There are lesions that prevent man from forming memories so that it
becomes very difficult to build up new remembrances.
D.
Processing
a. The central nervous system and all its tissues are always in a state of changing from a passive to an active state.
b. Any kind of pattern of engram that becomes established in the brain and that corresponds to a memory trace.
c. Peripheral stimulation evokes responses in more than single cells.
d. We can assume that a constant interchange of patterns from spatial to temporal coordinates.
(3.)
Relevance to language
A. There is no experimental evidence that any associative bonds may be disrupted by discrete cortical lesions.
B. Reasons for disputing language isn¡¦t a huge collection of paired associates
a. What is being associated during language learning isn¡¦t clear.
b. Aphasic symptoms give little support for a strict associationist hypothesis.
c. There is no evidence that any part of the brain stores anything like primitive fragments of behavior.
d. Audio-visual associations can hardly be relevant to the capacity for language.
(4.)
Time, the most significant dimension in language physiology
A. The essence of language is structure and pattern
B. Almost all of the central nervous system disorders of speech and language may be characterized as disorders of timing mechanisms. ( Exceptions are paralysis and neurogenic muscular pathology )
C. Receptive disorders are accompanied by severe productive disorders.
V.
Postscript on innate mechanisms for perception and production
=> During childhood the neutral automata are activated by appropriate input, and the machine becomes operative; the incoming signals are processed through its unique type of operation, and the emission of language responses are likewise generated by the operation of the same basic mechanism.
VI.
Conclusion