Deep Dyslexia Semantic Errors In Single Word example essay topic

Acquired Dyslexia Presenters: Kerri Whalen, Angela Munroe, Jeff Collins web 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 (shows) 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 system. -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 graphemics consonant 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. Nominal ize 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 groups 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 (shown) and starvation (tee-eye-oh-nn).

(Luria 1947). 2. Angela Munroe Deep Dyslexia 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 intact.

Study Questions (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 Answers (1) Deep Dyslexia is a complex reading disorder caused by brain damage, in which the prominent symptom is the occupancy 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 Newcombe 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 encountered. 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 processing. 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'. QUESTION #1 What is visual dyslexia and how does it affect a persons reading ability ANSWER #1 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 fovea l 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. QUESTION #2 What is thought to be the general explanations for these errors, and what is one explanation why these errors arise ANSWER #2 - 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'. web max / Acq Dys / DD. html Introduction 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 Shall ice 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 hemi paresis.

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, 1980 a, 1987 a). 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-image able) 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. Nonword 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 neuro psychologists 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 been abolished. 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 and production.

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 (1980 b, 1987 b) 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 literalized 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, Varga-Kha dem and Pol key (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, He naff 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 deep dyslexia. Treatment 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 Part (1986). 32 a.