Acquired dyslexia syndromes

Question 1

who studied mr C

Answer 1

French neurologist Joseph-Jules Déjerine and Monsieur C. (1892

Question 2

who was mr C

Answer 2

Mr C. is a 68 year-old intelligent, cultured, wealthy retired Parisian textile merchant, whom following a stroke wakes up one day of 1887 with the inability to read. He is unable to recognize words or letters, however:

Oral language AND spelling are intact.

Object, face, drawing and even number recognition largely preserved.

Pure verbal blindness

Question 3

where did Mr C’s pure verbal blindness stem from

Answer 3

After postmortem, Déjerine concludes that Mr C.’s ‘pure verbal blindness’ results from a disconnection between primary visual areas and an other occipital area dealing specifically with letters and words.

Question 4

there is a linear relationship between…

Answer 4

the linear relationship between word length (in number of letters) and reading time in ms for alexia patient Mr C

Question 5

what are they Two types of acquired reading disorder?

Answer 5

the peripheral dyslexias and the central dyslexias.

Question 6

what is peripheral dyslexia

Answer 6

Peripheral dyslexias refers to any reading disorder in which visual word form fails to be achieved

Question 7

what is central dyslexia

Answer 7

Central dyslexias refers to any reading disorder in which impairment occurs after the stage of visual word form.

Question 8

what does central dyslexia concern

Answer 8

In that sense, central dyslexias concern the reading system per se. psycho/neurolinguistic in nature

Question 9

what does peripheral dyslexia concernq

Answer 9

In contrast, peripheral dyslexias are due to a failure at an earlier stage (i.e., before recognizing the linguistic relevance of the stimulus).

Question 10

examples of peripheral dyslexia

Answer 10

Pure alexia/alexia without agraphia/letter-by-letter reading (Déjerine, 1892)
 	 Attentional dyslexia (Shallice & Warrington, 1977)
 	 Neglect dyslexia (Ellis, Flude & Young, 1987)

Question 11

examples of central dyslexia

Answer 11

Phonological dyslexia (Beauvois & Derouesné, 1979)
 	 Deep dyslexia (Marshall & Newcombe, 1973)
 	 Semantic dyslexia (Schwartz, Marin & Saffran, 1980) 
 	 Surface dyslexia (Marshall & Newcombe, 1973)

Question 12

what is pure alexia

Answer 12

Other names: ‘alexia without agraphia’ (i.e. no concurrent spelling impairment), ‘letter-by-letter reading’
Many cases described, and Mr C. was the first!
Main symptom: Word identification impossible, except via explicit sequential identification of individual letters (slow and painful).
Hence, substantial length effect and almost a linear relation between length in letters and reading time.

Question 13

what is the saffran effect

Answer 13

The ‘Saffran effect’ (Saffran & Coslett, 1998):
Pure alexics are well above chance in categorizing the meaning of a word (is it an animal?) or lexical status of a letter string (is it a real word?), despite their inability to “consciously” identify the word.
Cerebral area involved: visual word form area (VWFA; ventral occipito-temporal region) damaged or disconnected.

-The Saffran effect demonstrates that some parallel processing of the string is taking place, even though the patient is unable to read the word.

Question 14

what is hemi-alexia

Answer 14

As you know, information from the left visual hemi-field, initially processed in the right hemisphere, needs to cross to the left hemisphere to be combined with the right hemi-field information in the visual word-form area. But if the corpus callosum, which allows communication between the hemispheres, is damaged, then this transfer may no longer be possible. As a result, the patient has difficulty reading only words that are presented in the left visual field. This condition has been termed ‘hemi-alexia’

Question 15

who was patient AC

Answer 15

In patient AC the visual word-form area (i.e., left hemisphere) is NOT activated by strings presented in the left visual field, unlike controls. By comparison, for strings presented in the right visual field, AC lights up his/her visual word form area normally.

Question 16

what is attentional dyslexia (Shallice adn Warrignton)

Answer 16

Very rare!
Associated with left parietal lesion.
Difficulty in identifying letters or words when flanked by other items of the same category
However, naming of a letter or a word in isolation preserved.
‘o’ on its own is fine, but error prone in ‘word’;
‘word’ on its own is fine, but error prone in ‘when the word is in a sentence’.
- Basically, attentional dyslexics are highly sensitive to crowding from same-level items (e.g., words from words, letters from letters, numbers from numbers, etc.)

Also, migration of letters to analogous position in other words, i.e. left hemisphere >

‘

heft hemisphere

’

.
Disorder of the

‘

attentional filter

’

: the window of attention is larger than the target part of the visual field, and this lets other information in.
It is specific to reading, as it does not hold for pictures (Warrington, 1993).
The nature of the flankers modulates the manifestation of the disorder: less interference with different-category than with same-category distractors!

• Migration to an analogous position in another word indicates that knowledge of within-word letter position is preserved, despite the attentional deficit.

Question 17

what is neglect dyslexia (Kinsbourne & Warrington, 1962)

Answer 17

Main symptom: failure to identify the initial or final letter(s) of a word or group of words, resulting in omissions, substitutions or additions.
Often but not necessarily associated with spatial neglect.
Typically, contralateral parietal lesion.
In the most common form, the initial portion of the word is problematic (i.e. right lesion).
e.g. lend > ‘end’, wine > ‘mine’, oat > ‘boat’

Question 18

what are the central dyslexia

Answer 18

• Phonological dyslexia (Beauvois & Derouesné, 1979)

- Deep dyslexia (Marshall & Newcombe, 1973)

Question 19

what is Phonological dyslexia (Beauvois & Derouesné, 1979)

Answer 19

Main symptoms: Impaired ability to read new or made up word (or nonwords), and to sound out individual graphemes.

- The two symptoms point to a damage of print-to-sound correspondences (i.e., the nonlexical route in the DRC model): knowledge of the rules and application of the rules is faulty.
- The fact that in non-imageable words may also be affected demonstrates that the meaning of words take an active part in supporting reading. For those words that do not have a well defined meaning (e.g., abstract words, function words), an intact non-lexical route is crucial. When the latter breaks down, these words are the first in line to suffer. And of course the least frequent is such a word, the more like it will be misread, or not read at all.

Question 20

what is deep dyslexia

Answer 20

Associated with extensive damage to the dominant (L) hemisphere, and consists of:
Impaired ability to read nonwords.
Suggests knwoledge of sound of letters and unable to guess
Semantic errors: ill > ‘sick’, bush > ‘tree’, bad > ‘liar’
Correct but say the wrong output
Visual errors: life >’wife’, sword >’words’
Derivational errors: card > ‘cards’, fleeing > ‘flee’, entertain > ‘entertainment’, beg > ‘beggar’
Effect of syntactical class:
nouns > adjectives > verbs > functors
Effect of imageability: concrete > abstract words

Question 21

why sematnic errors in deep dyslexia

Answer 21

The semantic route is by default inaccurate when it comes to selecting word for speech production.
The patient has no information about the target word other than its meaning.
This would explain imageability effect, and low performance on functors.

Question 22

what is semantic dyslexia

Answer 22

Disorder associated with neurological disease (e.g. Alzheimer, semantic dementia).
Main symptom: ability of patients to read fast and fluently (even irregular words in some patients), but inability to comprehend what they are reading.
‘I don’t know the word, I can only read’ (from McCarthy & Warrington, 1982).
Most patients evolve towards surface dyslexia, which itself is associated with semantic disorders.

Question 23

what is the case of WLP

Answer 23

Patient with semantic dementia.
WLP can read pseudowords (made-up words), match a spoken word (‘brain’) with a written pseudohomophone (brane), and read aloud irregular words (pint), which by contrast she can not define or match with a picture.
BUT she fails in an object naming task (1/70), although she can mimic the use of certain objects (thus poor conceptual knowledge)
-In sum, this is DRC without a semantic system!
-WLP led to a drastic revision of the dual-route theory, which needed to include a direct (nonsemantic) lexical route, to explain the good performance on irregular words in the absence of semantic access.

Before the discovery of this syndrome, reading was thought to involve only a semantic route and a grapho-phonological route.

Question 24

difference between semantic dyslexia and deep dyslexia

Answer 24

deep has semantic route intac

Question 25

what is surface dyslexia

Answer 25

Main symptoms:
Regularisations (typical pronunciation chosen), especially for low frequency irregular words, e.g., ‘pint’ rhyming with ‘mint’
Stress shift, e.g. guiTAR > ‘GUItar’
Comprehension based on pronunciation, e.g., bear as ‘alcoholic beverage’ (beer).
Failures to apply contextual rules, e.g. insect > ‘insist’, guest > ‘just’
Incomplete decoding of digram vowels, e.g. niece > ‘nice’

However, reading of regular words and nonwords spared!
Traditional interpretation: Inability to read via the lexical route; reading reflects the exclusive reliance on the nonlexical route and thus on GPCs.
Indeed, strong sensitivity to regularity as a

‘

critical variable

’

(cf. next Table).

Question 26

Surface dyslexia is one argument for the existence of the ________route

Answer 26

Surface dyslexia is one argument for the existence of the nonlexical route

Question 27

what did cohen 2003 do

Answer 27

tested 5 patients, 3 had pure verbal blindness.

found that ventral occipital-temporal region causes pure verbal blindness