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Neuropsychological assessment and treatment of movement and language disorders > Written Language Disorders > Flashcards

Written Language Disorders Flashcards

1
Q

Language disorders are primarily based on a theoretical framework of language processing routes.
There is much debate about which model is most fitting.
Which model does this chapter use?

A

Three-route model: Holds that reading incorporates 3 computational routes: two lexical routes and a non-lexical route when processing written language.

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2
Q

What does the nonlexical route compute?

A

Computes pronunciation of a word on the basis of sub-lexical grapheme-phoneme correspondences (letter-sound association).

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3
Q

What does the lexical-semantic route entail?

A

The route between visual analysis and semantic memory of words. Through this path we access a word’s meaning.

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4
Q

What is the purpose of the direct-lexical route?

A

This route is a direct connection between the visual analysis elements and the corresponding representation in a phonological lexicon. (Reading aloud).

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5
Q

What is Pure Alexia? (Alexia without Agraphia)

A

Complete inability to read despite maintained auditory language comprehension, language production and intact visual modality.

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6
Q

What are the anatomical issues of Pure Alexia?

A

Debate over which lesions can cause these symptoms.
Dejerine(1892) argues that a left hemisphere lesion produces a right-sided hemianopia, which means visual information cannot be processed.
Geschwind argues that lesions in corpus callosum prevents visual information the left visual field from crossing to the right hemisphere.
It is argued that there is a rudimentary reading system in the right hemisphere.

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7
Q

What are the hopes of remediation for patients suffering from pure alexia?

A

Unfortunately there is not much hope for betterment in these cases. In some cases it was possible to teach patients letter naming to such a degree that they could do letter-by-letter reading. (Letter-naming tasks)

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8
Q

How can pure alexia be assessed?

A

Specific tests in Psycholinguistic Assessment of Language Processing in Aphasia. nr. 22/29

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9
Q

Letter-by-letter reading is characterized by?

A

Reading each individual letter in order to read a word.

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10
Q

Is speed of reading words related to word length?

A

Yes. The longer the word is the slower recognition is. Can only recognise words by naming each of its component letters.

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11
Q

What is argued to be the core impairment in LBL-readers?

A

Processing letters in parallel to each other.
There can also additionally be deficits in word level processing.
Much debated issue.

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12
Q

Which regions are implicated in LBL-reading deficits?

A

Lesions to posterior parts of the left hemisphere frequently associated with LBL-reading
Damage to left occipito-temporal junction probable cause of word recognition deficits.
Lesions affecting left V1 or its geniculostraite afferents can cause similar but treatable impairments. (Hemianopic Alexia)
It is debated whether deficits reflect damage to a left system leads to right side inhibition, or if deficits reflects damage to a single shared system.

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13
Q

What are the options of remediation for LBL-reading?

A

´Following treatments yielded significant increased
Multiple Oral re-reading (MOR) read same passages several time
Cross-case matching decisions about pairs of letters in different sized fonts.
Identify letters at the end of a word before reading them loud.

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14
Q

How is it assessed?

A

Measure of reading speed on a word list which manipulates letter length (PALPA #29)

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15
Q

What is Neglect dyslexia?

A

Reminiscent of visual neglect except only when reading words. Neglect in side contra-lateral to lesion. Usually associated with other features of neglect, but patients without other features have been observed.

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16
Q

Which type of reading does it affect?

A

Both word reading and sentence reading.

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17
Q

What is the theory behind neglect dyslexia?

A

Damage to any three distinct levels of representation, Retina-centered, Stimulus-centered, word-centered, might be affected in neglect dyslexia.

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18
Q

Lesions to which areas can cause neglect dyslexia?

A

Left or right Occipito-parietal lesions.

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19
Q

Which kind of words are effective when assessing neglect dyslexia?

A

Words that becomes different words when starting or ending letter is omitted. (cage, lever, peach, etc.)

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20
Q

What is deep dyslexia?

A

Almost complete inability to read nonwords and novel words aloud.

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21
Q

Which words are deep dyslexics most likely to read aloud?

A

Words with a high concreteness/imageability rating.

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22
Q

What are the three different theoretical accounts of the imageability effect in deep dyslexia?

A

Plaut & Shallice (1993): Computational model of deep dyslexic. Postulates that abastract words contain fewer semantic features, and are less resistant to semantic feature loss than concrete words.
Newton & Barry (1997): Abstract words tend to be more ambiguous than concrete words. Ambiguity makes lexicalisation more difficult for abstract words.
Crutch & Warrington (2005): Abstract words tend to be represented in semantic memory in terms of their associations with related concepts. Concrete words are represented in tersms of similarity to other members of the same category. Qualitatively different representational systems.

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23
Q

Which errors are common in deep dyslexia patients?

A

Semantic errors: The hallmark; reading uncle -> cousin; hurt -> injure.
Visual errors: Confusing words which share similar letters. Crown -> Crowd
Both of the above: Stream -> train
Derivational errors: Confusing words with similar morphological elements. Heat -> Hot.

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24
Q

What damages are believed to cause deep dyslexia?

A

Anatomically there is evidence that lesions or infarcts to the left fronto-temporo-parietal region cause deficits.
Usually there is severe damage to the nonlexical route and the direct-lexical route that connects words to the phonological lexicon when reading aloud.

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25
Q

It is argued that three types of deep dyslexia exists:

A

Input deep dyslexia: Deficits in access to word representations
Central deep dyslexia: Deficits in the representations themselves
Output deep dyslexia: Problems accessing speech output from semantic representations.

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26
Q

How can possible remediation happen?

A

Teaching phoneme blending

Re-teaching grapheme-phoneme correspondences.

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27
Q

How is deep dyslexia assessed?

A

Investigate reading accuracy on low/high imageability words.

Investigate evidence of semantic errors.

28
Q

What is the defining characteristic of phonological dyslexia

A

The selective impairment of the ability to read nonwords relative to real words.
nonword reading is usually more preserved than in deep dyslexia

29
Q

Which processes do patients experience errors in?

A

Graphemic parsing (how many phonemes does auk contain)
Grapheme-phoneme knowledge.
Blending auditorily presented phonemes.

30
Q

It said that there is a spectrum of severity. Describe this spectrum

A

It is argued that deep dyslexia and phonological dyslexia are a spectrum of severity ranging from relatively severe (deep dyslexia) to relatively mild (Phonological).

31
Q

It is argued that which route is damaged?

A

Nonlexical route

32
Q

What are the anatomical issues of phonological dyslexia?

A

Lesions focused around the the anterior perisylvian areas ranging from left inferior, posteror frontal lobes to extensive damage to fronto-temporo-parietal areas. Usually associated with a form of cerebrofascular accident.

33
Q

Phonological dyslexia is a less severe pathology and thus has a good prognosis. What are the treatment options?

A

Teaching phoneme-grapheme correspondances.

Teaching phonological awareness skills.

34
Q

How is phonological dyslexia assessed?

A

By investigating reading accuracy on nonwords. (PALPA test 36).
Compare reading aloud accuracy on matched words and nonwords

35
Q

What characterises surface dyslexia?

A

In english language or in languages with irregular words patients will regularise the irregular words.

36
Q

Surface dyslexia stems from damage to which route?

A

Lexical route

37
Q

What is interesting about surface dyslexia?

A

Surface dyslexia patients provde evidence consistent with the view that reading systems contains functionally distinct lexical and nonlexical reading routes.

38
Q

Where do the anatomical damages which lead to surface dyslexia arise?

A

Surface dyslexia usually occurs following a tumour, head trauma, and strokes. Damage to left temporal regions frequently including putamen and the insula

39
Q

There are two succesful remediation techniques:

A

Repeatedly presenting words that patients cannot read together with a picture that provides information about the meaning of the word.

Immediately hearing the spoken word after reading it incorrectly.

40
Q

Results from various studies reveal a very strong dissociation between surface dyslexia and semantic dementia.

A

51/51 studies of semantic dementia cases became surface dyslexic as their disease progressed.

41
Q

Which anatomical area is related to semantic representation of irregular words?

A

The left temporal pole provides a gateway to semantic representations

42
Q

There are some dementia patients who do no develop surface dyslexia. How can this be interpreted?

A

Evidence that the reading system contains a direct-lexical reading route that does not require access to a word’s meaning.
This however debatable.

43
Q

There is shown to be word length effects in the reading speed of semantic dementia patients. Which other dyslexic condition is heavily affected by word length?

A

Letter-By-Letter dyslexia.

44
Q

How is developing surface dyslexia in dementia patients assessed?

A

The National Adult Reading Test was designed to provide a measure of pre-morbid IQ based on the assumption that irregular word reading is relatively immune to the effects of dementia.

45
Q

What is the goal of the assessment of writing?

A

To examine the status of the components necessary to support written communication.

46
Q

There are two categories of processes related to writing disorders what are they?

A

Central processes and peripheral processes

47
Q

What are the central processes engaged during written language production?

A 
Semantic system: word meaning
Orthographic lexicon: spelling
Phonological lexicon: word sounds
Graphemes: Letters that represent a single sound
Phonemes: Smallest meaningful sounds
48
Q

What are the peripheral processes engaged during written language production?

A

Allographic conversion: Converting representations into letters
Graphic motor programs: Motor programmes required to write.
Graphic innervatory patterns: Motor commands to specific muscles.

49
Q

The dual-route model which is very helpful for understanding can be found on what page?

A

p. 324

50
Q

Input from the phonological lexicon is referred to as what route?

A

Lexical-semantic spelling route.

51
Q

What is the graphemic buffer?

A

Working memory system which stores information by lexical-semantic and sublexical routes while converting it into handwriting.

52
Q

What is the initial goal of assessment?

A

To determine whether an individual can meet their daily needs for written language production.

53
Q

Writing abilities are considered relative to what?

A

Relative to premorbid language skills.

54
Q

How can it be assessed?

A

A variety of tasks to sample writing performance and comparative performance across tasks to isolate damaged components.
Batteries such as Western Aphasia Battery, Boston Diagnostic Aphasia Examination, Psycholinguistic Assessment of Language Processing in Aphasia.

55
Q

What does single word dictation allow?

A

Examination of various linguistic variables known to affect spelling performance.
Tests like PALPA contain a standardized word list which controls for various variables.

56
Q

How is semantic processing assessed?

A

When words are spelled to dictation. Also narrative and naming tasks.

57
Q

Orthographic representations is assessed how?

A

Its activation regardless of output modality is required to support spelling.

58
Q

Seblexical spelling procedures rely on what?

A

Knowledge of phoneme-grapheme correspondence rules. Tested directly withspelling of pronouncable nonwords.

59
Q

The graphenuc buffer holds orthographic information in short term memory. How is it examined?

A

Spelling words of increasing length

60
Q

Allographic conversion refers to the ability to assign each grapheme to letter shape. How is it assessed?

A

ASking patients to trasnscribe letters from upper to lower case and vice versa. Copying words in different case or style.

61
Q

How is sensorimotor control assessed?

A

Can be done through the simple act of observing a patients proces of handwriting. Deficits may be very apparent. Asking patient to copy words or letters may work. If they write in more of a drawing manner than in a writing manner.

62
Q

How is language skills compared with motor skills during assessment?

A

Examining single-word comprehension auditory and reading,
Examining reading aloud capabilities.
Examining spoken picture naming vs written naming.
General examination of limb praxis.

63
Q

There are two categories of agraphia:

A

Central Agraphia Syndromes: Reflect damage to lexical-semantic, sublexical spelling routes, and/or graphemic buffer. Impairments across modalities.

Peripheral Agraphia Syndromes: Reflect damage to writing processes distal to the graphemic buffer.

64
Q

There are three peripheral agraphia syndromes:

A

Apraxic agraphia, allographic disorders, and non-apraxic disorders of neuromuscular execution

65
Q

What are the four central agraphia syndromes?

A

Lexical/surface agraphia, phonological agraphia, deep agraphia, and graphemic buffer agraphia.

66
Q

What are the treatment principles of agraphia?

A

In general treatment are designed to strengthen damaged processing components and take advantage of residual abilities

Neuropsychological assessment and treatment of movement and language disorders (2 decks)

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