Speech and Language Flashcards

1
Q

What is commnication? Speech?

A

Communication involves the exchange of thoughts, messages, or other info

Speech is the mechanical process of producing vocal sounds to communicate.

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2
Q

What is language?

A

Language employs a system of arbitrary signals, such as voice sounds, gestures, or written symbols, that permit communication. The symbols are constrained in their interrelationship by perception, production, and central processing rules.

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3
Q

Language consists of:

A

semantics (meaning of language including words, sentences, symbols, etc.),

phonology (the sound of words), and

syntax (the rules of grammar).

Note that one of the central ‘design features’ of human language is that the relationship between the sound of a word and its meaning is arbitrary; given the sound of an unknown word, it is not possible to infer its meaning. Arbitrariness is one of the characteristics of all languages.

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4
Q

Speech is the communication through vocalized sounds or phonation that form spoken words and sentences.

A

Phonation describes the distinct sounds produced by larynx.

A phoneme is a distinct sound that contrasts with other distinct sounds. For example, American English has 25 consonant and 17 vowel phonemes.

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5
Q

What is dysphonia?

A

Dysphonia is defined as a disturbance of phonation causing an alteration of volume. It can be either hypophonia or hyperphonia.

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6
Q

What is Dysarthria?

A

disturbance of articulation caused by impaired motor control resulting in a slurring of speech.

Mutism is just an absence of phonation.

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7
Q

This slide presents the anatomic substrate for speech. Below is the familiar view of neocortex with the sensory homuculis in blue and the motor homunculis in purple.

A

Below is a sagittal section through the lower face and neck to emphasize the muscles used in normal phonation. These muscles include the tongue, and muscles controlling the lips, pharynx, vocal cords, etc.

Any disruption to these motor pathways or to the muscles themselves can cause slurring of words denoted as dysarthria.

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8
Q

What are the different types of dysarthria?

A

flaccid

spastic

ataxic

hypo- or hyperkinetic

mixed

Each is caused by a different lesion of the nervous system.

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9
Q

Describe flaccid dysarthria?

A

Flaccid dysarthria is characterized by hypernasality, imprecise consonant production and breathiness. It is associated with weakness and decreased muscle tone.

The lesion typically involves muscle, the neuromuscular junction or the lower motor neuron.

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10
Q

Diseases that produce flaccid paralysis include:

A

some muscular dystrophies, inflammatory myopathies and myasthenia gravis.

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11
Q

Describe spastic dysarthria

A

Spastic dysarthria is characterized by imprecise consonants and a harsh, strained, strangled quality of the voice. It is associated with weakness, spastic muscle tone and hyperreflexia.

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12
Q

Spastic dysarthria implicates what?

A

an upper motor neuron lesion as might be caused by stroke or multiple sclerosis.

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13
Q

Describe ataxic dysarthria

A

Ataxic dysarthria is characterized by slow rate, prolonged phonemes, irregular articulatory pauses and imprecise consonants. It is associated with limb dysmetria and other components of ataxia.

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14
Q

The site of lesion for ataxic dysarthria involves what areas?

A

the cerebellum and/or cerebellar efferent pathways. Diseases that can do this are multiple and include the spinocerebellar atrophies, stroke and multiple sclerosis.

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15
Q

Describe hypokinetic dysarthria

A

Hypokinetic dysarthria is characterized by a reduced range of articulation. The vocal output is bradykinetic, that is, significantly slowed down, and the disturbance may range from mildly imprecise to totally unintelligible.

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16
Q

Hypokinetic dyakinesia is associated with what?

A

It is associated with other Parkinsonian features including generalized bradykinesia, rigidity, resting tremor and postural instability.

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17
Q

The site of lesion producing hypokinetic dysarthria involves what?

A

the basal ganglia and/or the striatonigral-thalamo-cortical pathways. The classic example is Parkinson’s disease.

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18
Q

Describe hyperkinetic dysarthria

A

Hyperkinetic dysarthria is characterized by alterations in pitch and loudness, phonatory arrest, sounding strained, with alterations in the precision of vowels and consonants. Associated clinical findings include combinations of spasticity, ataxia and abnormal involuntary movements such as chorea and dystonia.

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19
Q

The lesion that produces hyperkinetic dysarthria involves what area?

A

the basal ganglia and subcortical motor pathways. Diseases that produce hyperkinetic dysarthria include Huntington’s disease, some spino-cerebellar atrophies and Tourette syndrome.

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20
Q

Describe mixed dysarthria

A

Mixed dysarthrias are characterized by slow rate, short phrases, imprecise consonants, hypernasality and harshness in the vocalization. Associated clinical features are weakness and spasticity.

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21
Q

The lesion producing mixed dysarthria involves what areas?

A

both upper and lower motor neuron dysfunction. This is typically due to motor neuron disease such as amyotrophic lateral sclerosis.

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22
Q

To examine speech, you begin by listening carefully while your patient is providing the history. If you suspect dysarthria from the history interview, you should pursue this further by having the patient read text and repeat selected tongue twister phrases. You should listen for speech volume, rate of speech, and for the correctness of articulation.

A
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23
Q

Language is a system of arbitrary symbols (sounds, written symbols, gestures) that communicate thoughts, ideas, emotions, etc. What is Aphasia?

A

loss of ability for spoken and written language.

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24
Q

What is alexia?

A

Alexia refers to the loss of the ability to read when no visual impairment exists.

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25
Q

What is agraphia?

A

Agraphia is the loss of the ability to write when no motor impairment exists.

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26
Q

What is paraphasia?

A

Paraphasia refers to language errors due to word or sound substitution.

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27
Q

What is a semantic paraphasia?

A

involves the substitution of one word for another, for example, fork for spoon.

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28
Q

What is a phonemic paraphasia?

A

The substitution of one sound for another, for example moon for spoon.

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29
Q

What is a neologism?

A

is the creation of meaningless words, for example, woon for spoon.

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30
Q

This slide presents a language board made up of various symbols on the left that have specific meaning presented in the boxes with written words on the right. Language scientists have used language boards of this type to test the ability of primates to communicate through symbols, that is test their language abilities. The more accomplished of these animals are described as having vocabularies of several thousand symbols involving words or phrases, equivalent to a 3 to 4 year old child.

A
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31
Q

What are semantics?

A

The term Semantics refers to the meaning or the interpretation of a word, sentence, or other language form, it is the language lexicon.

32
Q

What is syntax?

A

Syntax is the system of rules, grammar, implicit in a language, viewed as a mechanism for generating all sentences possible in that language.

33
Q

What is prosody?

A

Prosody refers to tone, inflection, volume of words and sentences that add meaning to language. For example you might say John went to the movies (with differing inflections) to convey different meaning.

34
Q

This slide attempts to provide you with some understanding of how semantics and syntax mold a language.

The upper set of symbols have neither semantic nor syntactic rules; they are a group of unrelated symbols. The lower set of symbols, although not interpretable by you, have rules governing semantics and syntax. If you examine these symbols you’ll note a pattern of recurrence of several symbols. Given sufficient time, a good code breaker could translate these symbols into the phrase appearing below the symbols.

A
35
Q

This slide presents two important figures in the discovery of language dysfunction in neurologic disease.

On the left is a photo of the French neurologist, Paul Broca who is credited with discovering the frontal language area responsible for motor language.

On the right is the German neurologist, Karl Wernicke, who at the age of 26 published a book in which he accurately described sensory language dysfunction residing in the temporal-parietal lobe. He is also credited with recognizing the dominance of the left hemisphere in language function.

A
36
Q

What connects Wernicke’s and Broca’s areas?

A

the arcuate fasciculus and other peri–Sylvian fibers

It does not show the connections between the main language areas (Broca and Wernicke) and the other association areas of the frontal, temporal, and parietal lobes. It also does not demonstrate connections to the non-dominant hemisphere that provide emotional color to language. Lesions of these connecting fibers will cause aphasia with unique characteristics that will be defined on later slides.

37
Q

What is Broca aphasia?

A

expressive or motor aphasia marked by nonfluent speech, difficulty with syntax, grammar, and production of individual words

Comprehension is intact

38
Q

What is Wernicke aphasia?

A

receptive or sensory aphasia marked by fluent speech, syntax, and grammer, and intact word structure but with difficulty with comprehension of speech so that the result is the production of nonsensical words and phrases

39
Q

What is Conductive aphasia?

A

difficulty repeating words- both comprehension and rpoduction of language are intact

40
Q

Lateralization of language

A

Greater than 95% of right-handed persons are left hemisphere dominant. About 65% of left-handed persons are also left hemisphere dominant, 15 to 20% are right hemisphere dominant and the remainder have mixed dominance.

41
Q

This slide depicts a young man who has been treated for intractable seizures by sectioning the corpus callosum thus creating a so-called ‘split brain’ subject.

These rare subjects provide the cognitive neuroscientist with the opportunity to test the function of each hemisphere independently.

A

Thus when this right-handed split brain subject is asked to name small geometric objects without seeing them he provides the correct answer when he handles the object with his right hand (the sensory information having been registered in the left hemisphere which then connects with the language area). However, when he handles the objects with his left hand (sensory information to the right hemisphere which is disconnected from the language areas in the left hemisphere) he is unable to name the objects. By the way, the cut corpus callosum prevents a seizure originating in one hemisphere from generalizing to the other side, and while unilateral focal seizures still occur, they are no longer complicated by a generalized convulsion which is much more disabling.

42
Q

This slide presents another method for testing split brain subjects using visual input that is restricted to either the left or right calcarine or visual cortex. The same results are obtained as described on the previous slide, that is information transmitted to the right visual cortex cannot reach the language areas in the left hemisphere. Although the subject can see the objects he cannot name them.

What effect on reading, writing and speaking would you expect if a stroke caused damage of the left visual cortex and the splenium of the corpus callosum?

A

Note that the patient would be able to speak normally since the language areas and their connections to motor centers controlling voice are intact.

The patient would also write normally since the left sided language centers and their connections to the left hand motor area remain unaffected. However, the left occipital cortex no longer receives visual information from the right visual field. The right visual cortex is still functioning and receives information from the left visual field but there is no way to transfer this information to the language center because its usual path through the splenium has been destroyed. Thus the patient speaks and writes normally but cannot read what he has just written. This is called alexia without agraphia.

43
Q

What was previously known about language areas was derived from post mortem studies of patients with aphasic disorders.

Now it is possible to investigate activation of brain images via SPECT scanning and so-called functional MRI during various language related tasks.

A

SPECT scans register the changes in regional cerebral metabolism as measured with positron emitting isotopes, in this case, radioactive deoxyglucose. When the subject is instructed to passively view the word “Table”, the calcarine cortex lights up indicating increased metabolic activity from neuronal activation. When the subjects listens to the word with no visual input, Hershel’s gyrus and Wernicke’s area light up.

44
Q

When the subject speaks the word “Table”, the facial area of the motor strip and Broca’s area light up.

A

When the subject is asked for a more complex language related task, for example to generate a word association for “Table”, the language association areas light up when he says “Chair”.

45
Q

This slide summarizes the left/right hemisphere functions in a left hemispheric dominant individual.

I have placed an orange box around the specific language functions of the two hemispheres.

A

Note that lexical and syntactic language, writing, and spoken word abilities lie in the left hemisphere while some rudimentary spoken language and the emotional coloring of language (prosody) are functions of the right hemisphere.

Some individuals with a massive left hemispheric stroke are mute except for a rare word, typically an expletive that arises from the right emotional hemisphere. Also, some years ago while I was in residency training in New York city, a famous Metropolitan opera star suffered a right hemispheric stroke that produced little left sided weakness so she could get about the stage just fine. However her ability to place inflections in her voice was lost and her career was ended.

46
Q

This and the next slide describe the six components of language that should be tested when you suspect language dysfunction. Expression is normal when?

A

the verbal output ranges from 100 to 150 words per minute. One assesses this during spontaneous conversation.

Comprehension of spoken language is tested by the ability to follow simple and complex spoken commands.

Repetition is tested by asking the subject to repeat single words and phrases.

  • Reading – Ask subject to read aloud and follow a written command
  • Writing – Ask subject to write a simple sentence
  • Naming – Ask subject to identify common objects
47
Q

Language syndromes can be divided into what?

A

These can be divided into those lying near the perisylvian fissure, the perisylvian syndromes and those more remote from this fissure, the extrasylvian syndromes.

This categorization helps in recalling the neuroanatomical structures involved when one encounters a patient with one of these syndromes.

48
Q

The first of the perisylvian syndromes is Broca’s Aphasia, which can also be described as:

A

a non-fluent, motor or expressive aphasia.

49
Q

How does Broca’s aphasia present?

A
  • Typically verbal output is reduced to less than 50 words per minute.
  • The patient uses single words or short phrases, typically less than 5 words in a phrase, and word use is restricted to nouns, verbs and adjectives.
  • There is limited use of syntactical words such as adverbs, prepositions and articles.
  • Comprehension relatively spared but there is some trouble with understanding complex syntactical language.
  • Repetition is poor and paraphasias are common.

The patient typically feels very frustrated, knowing what he wants to say but he just cannot get the words out.

50
Q

Where is the lesion location for Broca’s aphasia?

A

In the inferior frontal gyrus, Brodmann’s areas 44 & 45, also known as Broca’s area. The causes for Broca’s aphasia can be multiple but most often it is due to ischemic stroke as shown in the inset.

51
Q

The next perisylvian syndrome is Wernicke’s Aphasia, also known as:

A

Fluent, Sensory or Receptive Aphasia.

52
Q

Describe Wernick’e aphasia

A

Fluency is normal.

Verbal output is often increased at about 200 words per minute but may be normal. The sentences are typically unintelligible and devoid of meaningful language.

Most noticeable is the absence of nouns that are replaced by pronouns and prepositions.

Comprehension is severely impaired, and the patient lacks insight into his inability to communicate.

Repetition is poor.
Paraphasic errors and neologisms are common.

53
Q

The lesion producing Wernicke’s aphasia occurs where?

A

in Brodmann’s area 22 near the posterior end of the superior temporal gyrus better known as Wernicke’s area. Causes are multiple but the most common is ischemic stroke as shown in the inset.

54
Q

What is global aphasia?

A

Global aphasia presents with severe impairment of both expressive and receptive language function. There is virtually no verbal output except for the some residual paraphasic errors and sporadic monosyllabic expletives. There is no comprehension of language.

55
Q

What causes global aphasia?

A

The lesion involves a large area of the left hemisphere that affects both Broca’s and Wernicke’s areas. The cause is usually due to a massive stroke involving the left middle cerebral artery (MCA) territory, shown as a “hypodensity” on the CT scan.

56
Q

What is conduction aphasia?

A

Conduction Aphasia is characterized by preserved comprehension and normal fluency but repetition is poor.

Paraphasic errors are common.

57
Q

Where does the lesion casin conduction aphasia lie?

A

In the supramarginal gyrus just anterior to the angular gyrus as shown by the red arrow. It involves the arcuate fasciculus that connects Wernicke’s area with Broca’s area.

58
Q

When a sentence is heard and processed by Heschel’s gyrus, it is sent where?

A

to the nearby Wernicke’s area where comprehension of its content is made possible. However, in conductive aphasia the command to repeat cannot reach Broca’s area for its expression, and so repetition fails.

Other internal instructions travelling by different pathways to Broca’s area are unaffected so that spontaneous language output is possible.

59
Q

The most common cause of conduction aphasia is:

A

stroke due to occlusion of the angular branch of the left middle cerebral artery. The inset, however, shows an MRI lesion due to multiple sclerosis causing this syndrome.

60
Q

What is transcorticla motor aphasia?

A

extra-sylvian:

•uncommon aphasia similar to Broca’s except that subjects are able to repeat

61
Q

Where does the lesion causing transcortical motor aphasia occur?

A

Left anterior frontal lobe, either superior or inferior to Broca’s area, (lesions of the left basal ganglia may be a rare lesion site)

• causes similar to Broca’s

62
Q

What is transcortical sensory aphasia?

A

•uncommon aphasia similar to Wernicke’s except that subjects are able to repeat

63
Q

Where is the lesion causing transcortical sensory aphasia located?

A

The border zone between the left middle cerebral and posterior cerebral arteries

• causes similar to Wernicke’s but also severe hypotension

64
Q

The Mixed Transcortical Aphasia is similar to Global Aphasia except that:

A

subjects are able to repeat.

65
Q

Mixed transcortical aphasia is sometimes called “isolation aphasia”. Why?

A

because the language centers, Broca’s, Wernicke’s and the connecting arcuate fasciculus, remain intact in the face of destruction surrounding them.

The language center is disconnected or isolated from projection input from other areas of the brain.

66
Q

How does mixed transcortical aphasia present?

A

There is no comprehension or spontaneous output of speech but patients retain the ability to repeat and will do so in a parrot-like manner.

67
Q

What causes mixed transcortical aphasia?

A

Achieving a donut-like injury around the language center is not easy given the typical infarction patterns following occlusion of the cerebral arteries. This can occasionally happen with hypotension that produces uneven drops in blood flow to the hemisphere affecting watershed zones “just so” because the intracranial atheromatous disease happened to be distributed “just so”. This is the rarest of the transcortical aphasias.

68
Q

What are anomica aphasias?

A

Anomic Aphasias (extra-sylvian) are poorly defined since most aphasias have some problems with naming. However there is a very specific syndrome called Gerstman’s syndrome

69
Q

What is Gerstmann Syndrome (of the angular gyrus)?

A

In Gerstman’s syndrome, individuals have difficulty naming objects, difficulty reading and difficulty writing. They have right-left disorientation. They have problems with calculations, and curiously they have great difficulty in identifying their individual fingers.

The lesion is very specifically localized to the left angular gyrus.

70
Q

What is subcortical aphasia?

A

Subjects with lesions of the left basal ganglia of the left thalamus may be associated with variable forms of aphasia

71
Q

What is alexia without agraphia?

A

• inability to read but preserved ability to write

72
Q

Where would a lesion producing alexia without agraphia be located?

A

The left medial occipital and medial temporal lobe involving the splenium of the corpus callosum

73
Q

What causes alexia without agraphia?

A

branch occlusion of the left posterior cerebral artery

74
Q

This slide presents the axial section of a brain from an individual who demonstrated ‘alexia’, that is the inability to read, without ‘agraphia’, that is the inability to write. Reading and writing typically are linked language functions and patients with aphasia who have difficulty reading also have difficulty writing.

In this special case of alexia without agraphia, patients cannot read but they can write.

A

The lesion that produces this syndrome is shown in purple and involves the left visual cortex and splenium of the corpus callosum.

75
Q

The language areas of the left hemisphere are undisturbed in alexia without agraphia, and thus patients are able to speak normally and write normally but why can’t they read?

A

Because of the left occipital lesion, they have a right visual field deficit, that is a right homonymous hemianopia. The only vision getting through is from the left visual field and right occipital cortex. However, there is no way for that visual information to reach the language center on the left since the crossing pathway is blocked by destruction of the splenium of the corpus callosum. Thus, the patient is unable to read and unable to identify objects presented in his visual field.

76
Q

This slide presents a color coded algorithm for identifying the type of aphasia and the lesion location. Testing the patient for fluency, comprehension, and the ability to repeat simple phrases permits the categorization of all aphasic syndromes.

A
77
Q
A