Acquired Dyslexia Essay, Research Paper Acquired Dyslexia Presenters: Kerri Whalen, Angela Munroe, Jeff Collins http://acsweb.ucis.dal.ca/psych3130/Lecture_notes/feb_19.html1. Kerri Whalen
Acquired Dyslexia Essay, Research Paper
Presenters: Kerri Whalen, Angela Munroe, Jeff Collins
http://acsweb.ucis.dal.ca/psych3130/Lecture_notes/feb_19.html1. Kerri Whalen
Acquired Dyslexia: Surface Dyslexia (grapheme-phoneme)
Two +problems+ associated with surface dyslexia:
1. (Luria, 1947) Difficulty in remembering the phonemes represented by different letters: much; monk
2. Difficulty in reading groups of letters forming sequential patterns, for he has lost the schemata whereby letters appearing in
sequences unite to form syllables: congratulations (shons) and congratulations (eye-oh-nn-ss)
-This disorder may also influence writing skills: Man who was fluent in Russian, but French was his first language-lost his French
spelling skills after accident.
-The structural organization of language skills in the brain is sufficiently +tight+ to place restrictions upon types of possible
problems. The analysis centres around…A Functional Analysis
How does each type fit into this model?
-Visual Dyslexia- Patient makes frequent visually based errors in word recognition despite being able to name component
letters: Probably functional relationship +ab+; (stimuli word-stimulus entry).
-Deep Dyslexia- Semantic errors in single-word reading. Inability to read non-words: Several components of the reading
-Surface Dyslexia- Patient attempts pronunciation with +phonic+ errors. Deficits appear to be visual/ semantic together:
Probably +bd+ (stimulus entry-semantic meanings) and +cd+ (phonics-semantic meaning).
-Deep Dyslexics are more likely than surface dyslexics to say +don+t know+ or refuse to give a response; greater visual
disability? or greater tendency to give up?
-Case Studies: +JC+ and +ST+
1. Ambiguous consonants
2. Unvoiced Consonants
3. Phonetic value to silent graphemic consonants
4. The so-called +rule of e+ rarely applied
5. Vowel digraphs; two graphemes represent one sound which is not of either in isolation
6. Consonant clusters; read: consonant-vowel-consonant
7. Shift stress of word
8. Neologisms (new word)
9. Sequences of responses including both words and neologisms to single stimulus; trial and error
10. Loss of whole syllable
11. Consonants misplaced in the vowel sequence
12. Nominalize verbs
13. Spontaneously spell out words: +spelling reading+ -punish and punch (Holmes, 1971)
Question on Aquired Surface Dyslexia
What are the two main problems associated with Aquired Surface Dyslexics?
In the first type, the subject’s difficulty arises from impairment of the ability to remember the phonemes represented by different
letters: ie., m o nk and m u ch. In the second type, the patient+s difficulty arises when he is required to read grups of letters
forming sequential patterns, for he has lost the the schemata whereby letters appearing in sequences unite to form syllables. He
is unable to look ahead and by noting the context of a given letter, pronounce it correctly:ie., starvation (shon) and starvation
(tee-eye-oh-nn). (Luria 1947).
2. Angela Munroe
Deep Dyslexia is one of the many types of Acquired Dyslexias. In most cases of deep dyslexia the patient has damage
occurring in the left temporal-parietal region of the brain which may interfere with the function of Wernicke’s area for
comprehension and production of speech. Evidence for deep dyslexia comes from case studies of individuals with brain injuries.
Deep Dyslexia is a complex reading disorder, in which the prominent symptom is the occurrence of semantic errors in single
word reading. There are five types of deep dyslexic reading errors; semantic (ape as “monkey”), visual (soul as “soup”),
derivational (lovely as “loving”), visual- then- semantic (symphony as “orchestra”), and finally function word substitution errors
(the as “is”). The degree of deep dyslexic impairments differ substantially from individual to individual.
Individuals with deep dyslexia read semantically related words in place of the word they are trying to read (e.g. merry as
“christmas”). Nouns are the easiest for these individuals to read, followed by adjectives then verbs. Function words present the
greatest challenge (e.g. the & is). Those who suffer from this disorder also find it easier to read concrete words rather than
abstract ones and are completely unable to read nonsense words aloud. Deep dyslexics are also usually impaired in their
short-term verbal memory as well as in their writing. Individuals with deep dyslexia seem to have an instability of their “central”
language component. A model of reading aloud came about as a result of evidence collected from studies on acquired dyslexia.
This model shows evidence for a parallel processing of language. The model is called the Dual Route Parallel Model.
According to this model, two types of processing of the same input occur simultaneously over two different neural pathways.
According to this model, reading is mediated by a Lexical Procedure, which is based on information acquired about the
pronunciation of specific written words and a Non-Lexical Procedure, that is based on the general rules of pronunciation of a
language. Individuals suffering from deep dyslexia have a dysfunction of the non-lexical route whereby the lexical route is still
(1) Define and Exemplify Deep Dyslexia.
(2) What is the Dual Route Parallel Model? How does this model tie into a deep dyslexic’s reading impairment?
(1) Deep Dyslexia is a complex reading disorder caused by brain damage, in which the prominent symptom is the occupance of
semantic errors in single word reading. There are five types of deep dyslexic errors which differ substantially from person to
person. Adjectives and verbs present the greatest difficulty whereas nouns are the easiest to read. In most cases of deep
dyslexia the patient has damage occurring in the left temporal- parietal area which may interfere with Wernick’s Area and in turn
cause the dyslexia.
(2) The Dual Route Parallel Model is one that describes a parallel processing of language. According to this model two types of
processing of the same input occur all at once over two different neural pathways. Reading aloud is intervened by a lexical route
and a non-lexical route. Individuals suffering from deep dyslexia have a dysfunction of the non-lexical route which is defined as
information acquired about the pronunciation of specific written words. The lexical route, is based on general rules of
pronunciation of a language and the deep dyslexic patient still has this route intact.
3. Jeff Collins
Acquired Visual Dyslexia Patterns of Paralexia: A Psycholinguistic Approach John C. Marshall and Freda
Visual Dyslexia is defined as a pathological reading difficulty caused by a visual impairment. Subtypes of Visual Dyslexia
correspond to the specific nature of the impairment or in other words the nature of the impairment will dictate the sorts of errors
Paralexia is a term used to classify the typical mistakes made by persons with visual dyslexia. Examples include the ability to
recognize individual letters but letters with visual similarity are confused (p,q), whole words are confused (apple, able).
Reading consists of eye scans, scanning the world by making series of fixations and are connected by very fast eye movements
called saccades. The visual system integrates images from these fixations to provide a wide-angled, high acuity, visually colored
perception. A problem then with either scanning or within the fixation characteristic will produce deficits in the visual temporal
A patient was shown to produce errors that consistently involved the ends of words and never their beginning (Beware r
Because) . This patient was shown to have a gross derangement of the normal pattern of scanning movements and fixations in
reading. Right hemisphere lesions have also been shown to disrupt performance on spatial tasks, reading in particular. The left
hemisphere is thought to be responsible for the spatial adjustments of the eyes necessary for smooth pursuit and fixations and
paralexic errors result from lesions of the left hemisphere. Visual confusion tends to be the general explanation of the errors
encountered from dyslexic patients. Paralexic errors can be attributed to a dysfunction of the visual analysis system in the dual
route parallel model of reading.
Two explanation have been put forth to attempt and explain paralexic errors of visual dyslexic patients. The first is that they
have a lack of effective inhibition to produce the wrong answer either at the letter level or word level or within the word level
itself. The second is that they tend to accept a less than perfect overlap between the word presented and the response given
termed ‘Approximate visual access’.
* What is visual dyslexia and how does it affect a persons reading ability?
* Visual dyslexia is a pathological reading difficulty cause by visual impairment. The different motor functions involved in normal
reading such as eye scanning, fixations, and saccades performed to integrate foveal images may be disrupted as a result of an
acquired lesion to the right (spatial) or left hemisphere (spatial adjustments of eyes). Impairments called paralexic errors include,
confusion of letters with similarity, or errors may be whole words.
* What is thought to be the general explanations for these errors, and what is one explanation why these errors arise?
- Simple visual confusions are thought the be the best explanation and may be a result of the patient willing to accept a less than
perfect overlap between the word present and the response given termed ‘approximate visual access’.
The first systematic study of deep dyslexia was by Marshall and Newcombe (1966), although the
condition had been sporadically mentioned in the neuropsychological literature at least since
1931.Marshall and Newcombe (1973) and Shallice and Warrington (1975) also published early systematic
studies. An entire book on deep dyslexia was published in 1980 (Coltheart, Patterson and Marshall,
1980), and much work on deep dyslexia has appeared since then.
The symptoms of deep dyslexia.
All patients so far reported with deep dyslexia have had extensive left-hemisphere damage sufficient to
produce aphasia (normally Broca’s aphasia) and normally also a left hemiparesis. This acquired dyslexia is
identified by the occurrence of semantic errors in reading aloud. Single words are presented, without
context and without time pressure, for reading aloud; even in this simple situation the deep dyslexic will
often produce a reading response that is related in meaning to the stimulus word but may be quite
different from it in spelling and pronunciation, such as reading the word canary as “parrot”. Although the
semantic error in reading aloud is the key symptom of deep dyslexia, many other reading symptoms are
also seen in this form of acquired dyslexia (for review see Coltheart, 1980a, 1987a).Deep dyslexics
generally show all of the following symptoms in reading-aloud tasks:
Semantic errors, such as “tartan” read as “kilt” or”anchor” read as “boat”.
Visual errors: a visual error in reading is when the response shares many letters with the stimulus,
such as quarrel read as “squirrel” or angle read as “angle”.
Morphological errors: a morphological error in reading is when a prefixed or suffixed word is read
with the root of the word correct but the prefix or suffix wrong, such as running read as”runner” or
unreal read as “real”.
Concreteness effect: concrete (highly-imageable) words such as tulip or green are much more
likely to be successfully read than abstract (difficult-to-image) words such as idea or usual.
Function words such as and, the or or are very poorly read.
Nonwords such as vib or ap cannot be read aloud at all.
Spelling/writing may be impossible; if it is at all possible, then it usually shows the spelling
equivalent of the above 6 symptoms.
Deep dyslexia as left-hemisphere reading.
Cognitive neuropsychologists seek to understand cases of acquired dyslexia by investigating how one
could selectively damage a component or some components of a model of reading so that the model
would exhibit the same symptoms as the patient.
For deep dyslexia,this was attempted by Morton and Patterson (1980, 1987) as follows: First, since
nonword reading is completely abolished in deep dyslexia, the letter-to-sound rules system must have
Second, since word reading is much less than 100% accurate, the direct connection from the Orthographic
Input Lexicon to the Phonological Output Lexicon must be impaired. Take function words, for example.
The deep dyslexic can recognize these as words (since visual lexical decision performance with such
words can be very good) and can produce them (since the usual error response to a function word is
another function word). Hence the problem in reading them must be a disconnection between recognition
Third, since reading is worse for abstract words than for concrete words, there must also be an
impairment of the Semantic System that is worse for abstract than for concrete words.
Fourth, the Semantic System must be impaired in such a way that semantic errors occur e.g. that “parrot”
and “canary” are not successfully distinguished in the semantic system.
Fifth, since sometimes the deep dyslexic will correctly understand a printed word but make a semantic
error in reading it aloud, the connection between the Semantic System and the Phonological Output
Lexicon must be damaged in such a way that a correct semantic representation yields an incorrect
(semantically related) reading response.
Sixthly, there must be damage to whatever the syntactic system is that is used for processing prefixes and
suffixes, to account for morphological errors in reading affixed words.
The argument is that if the model has these 6 kinds of damage its reading will exhibit all the symptoms of
deep dyslexia. A problem with this argument is that if these are really six different ways in which the
reading system can be damaged, then one would expect to see patients with forms of acquired dyslexia
that represent subsets from this set of six forms of damage. For example, there would be no reason why
someone should not just have the first five impairments: that would mean we should see cases of acquired
dyslexia where there are semantic errors but no morphological errors; similarly.when all but the third form
of damage is present, we would see semantic errors but no advantage for concrete words. Patterns like
these have never been observed. For that, and other, reasons an alternative theoretical account of deep
dyslexia was proposed by Coltheart(1980,1987) and Saffran, Bogyo, Schwartz and Marin (1980, 1987).
They proposed that deep dyslexia was unique amongst the acquired dyslexias in that these patients are not
reading with a damaged version of the normal reading system which is in the left hemisphere. Instead,they
cannot use the left hemisphere at all for reading. Their reading is carried out by a separate reading system,
located in the right hemisphere.
Deep dyslexia as right-hemisphere reading.
Coltheart (1980b, 1987b) and Saffran, Bogyo, Schwartz and Marin(1980, 1987) supported their
arguments that reading in deep dyslexia was carried out by a right-hemisphere reading system by pointing
out a number of resemblances between deep dyslexic reading and what was then known about language in
the right hemisphere: there was evidence, from split-brain patients, of poor syntax in the right hemisphere
(which would impair processing of function words and affixes), and there was evidence from experiments
with lateralized presentation of words to intact subjects of a concrete word superiority with
right-hemisphere (left visual field)presentation. There was also Gott’s report of a young girl who had
learned to read but then had a left-hemispherectomy, after which semantic errors appeared in her reading
aloud of single words.
However, there was much that was inadequate about this evidence.For example, the well-studied
split-brain patients all had bilateral brain damage from birth, so one cannot safely generalize from their
hemispheres to the hemispheres of people who had intact brains in adulthood prior to the damage that
caused deep dyslexia. Similarly,Gott’s patient exhibited an encephalopathy at an age earlier than that at
which language lateralization would have been complete, so she too is not a completely satisfactory source
of evidence. More recently, however, two much more satisfactory pieces of evidence have emerged.
Patterson, Vargha-Khadem and Polkey (1987) report a study of a person who first exhibited signs of a
left-hemisphere abnormality at 13 and had a left hemispherectomy at age 15. Given her age, it is likely
that language development in the two hemispheres would have reached maturity. Prior to the onset of her
left-hemisphere symptoms she was a normal reader for her age. After her hemispherectomy she displayed
all the major symptoms of deep dyslexia:
Semantic errors (arm -> “finger”, pigeon -> “cockatoo”)
Visual errors (bush -> “brush”, frost -> “forest”)
Morphological errors (duck -> ducks”, smoke -> “smoking”)
Very poor reading of function words
Nonword reading impossible.
Michel, Henaff and Intrilligator (1996) report the case of a 23-year-old man who as a result of
neurosurgery was left with a lesion of the posterior half of the corpus callosum. He was able to resume his
college studies in accountancy after recovering from surgery. Michel et al studied his reading by briefly
presenting words to the left hemisphere (i.e. in the right visual hemifield) or the right hemisphere (left
visual hemifield), with these results:
Right visual hemifield: Words were read rapidly, and with 100% accuracy. Judgement of whether
two words rhymed or not was 94% accurate.
Left visual hemifield:
Numerous semantic errors such as bijou -> “perle”, poulet -> “garlic”.
Concrete words read better than abstract words.
Function words poorly read.
Nonword reading virtually impossible.
At chance on judging whether two words rhymed.
These two studies would seem to provide conclusive evidence for the right-hemisphere interpretation of
In deep dyslexia, the brain damage is extensive, the reading impairment is severe, and the patient is
aphasic as well as dyslexic. Nevertheless, the condition responds to appropriate and intensive treatment;
this has been demonstrated by de Partz (1986).
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