Acquired Dyslexia And Agraphia Research Paper

Marshall and Newcombe (1973) described three forms of acquired dyslexia; at least three other forms have subsequently been identified, and all six will be described here.

1.1 Phonological Dyslexia

Beauvois and Derouesne (1979) were the first to report that in cases of acquired dyslexia the ability to read nonwords aloud could be selectively impaired relative to the ability to read words aloud. They reported six cases of previously literate readers of French for whom this was the case, and numerous other cases have been reported since then; see Coltheart (1996) for a recent comprehensive review. The most extreme of these cases was WB (Funnell 1983) who scored 0 20 correct on reading aloud very simple nonwords such as nust or cobe, while achieving scores of 85–90 percent correct in reading aloud long low-frequency morphemically complex abstract words such as satirical or preliminary.

When the ability to read aloud pseudohomophones ( printed nonwords whose pronunciations are real words, such as FAKT) is compared to the ability to read aloud nonpseudohomophonic nonwords such as FANT, some phonological dyslexics show a clear advantage for the pseudohomophonic items while others clearly show no difference here (see e.g., Berndt et al. 1996). These results are not only obviously relevant for any attempts to offer a theoretical interpretation of phonological dyslexia; they also show that this condition is not a homogeneous one. Selective difficulty in reading nonwords aloud must occur for different reasons in different patients, if some patients’ nonword reading shows an advantage for pseudohomophones while other patients’ nonword reading does not.

1.2 Surface Dyslexia

If, after brain damage, word reading can be spared while nonword reading is selectively impaired (that is, if phonological dyslexia can occur), it is natural to wonder whether the reverse pattern might also arise: worse reading of words than nonwords. Here it is important to distinguish between regular and irregular words. Regular words are those that respect the standard relationships between letters or letter groups and their corresponding pronunciations; irregular words are those whose spelling–sound relationships violate at least one such correspondence. Thus the word steak is irregular because of the way the letter group ea is pronounced in that word; in almost all words containing this spelling, the ea is pronounced as in steam or freak, both of which are regular words. On all extant models of the reading system, the procedure people use to read nonwords also allows perfectly accurate reading of regular words: so all theories predict that one would never find a person with acquired dyslexia who could read nonwords but was impaired at reading of regular words.

Irregular words could be a different matter, however. According to at least some models of reading, irregular words cannot be read correctly by the procedure that is used to read nonwords—the application of knowledge about typical relationships between segments of spelling and their most common pronunciations would produce correct reading of nonwords but incorrect reading of irregular words. So one might expect to come across patients with acquired dyslexia who are good at reading nonwords but bad at reading irregular words—and such patients have indeed been described.

This form of acquired dyslexia is known as surface dyslexia, first described by Marshall and Newcombe (1973) and reviewed by Patterson et al. (1985). The most extreme cases so far reported are MP (Bub et al. 1985) and KT (McCarthy and Warrington 1986), both of whom were normal in speed and accuracy of reading regular words and nonwords while severely impaired in reading exception words.

If patients with surface dyslexia are erring with exception words because they are reading these words via the application of knowledge about typical relationships between segments of spelling and their most common pronunciations, then one would expect their reading errors to demonstrate this. Precisely this type of error is indeed very frequent in surface dyslexia, and it is known as the ‘regularization error’—for example, reading broad to rhyme with ‘code,’ or steak to rhyme with ‘meek.’ Some patients with surface dyslexia are not perfect at reading regular words: at least some of these patients produce what might be called ‘irregularization errors’ with regular words, such as reading hoot as if it rhymed with ‘foot’ or heat as if it rhymed with ‘threat’ (Patterson et al. 1996).

The deficit in irregular-word reading by surface dyslexics is frequency-sensitive, with performance much worse for low-frequency irregular words than for high-frequency irregular words.

As with phonological dyslexia, there is more than one form of surface dyslexia. Reading errors such as gauge → ‘That is something about a railway…that’s as much as I’ve got, train,/g d /’ (Kay and Patterson 1985; patient EST) clearly show that the problem here is not in visual word recognition (since the printed word has been comprehended correctly, it must first have been recognized correctly) but instead is a failure in retrieval of stored information about the correct pronunciation of that particular word. Since the patient is being asked to read aloud— i.e., to produce a spoken response—he can only fall back on the procedure used for reading nonwords aloud, which of course will yield a regularization error with this irregular word. This is ‘output surface dyslexia.’

A different form, ‘input surface dyslexia,’ is demonstrated when patients asked to define printed exception words produce such responses as bear ‘a drink, beer’ (Coltheart et al. 1985; patient CD). Here the patient has not recognized the word as an orthographic whole (which is necessary for normal reading comprehension) so has had to attempt the reading comprehension task by first translating the word from orthography to phonology via the application of knowledge about typical relationships between segments of spelling and their most common pronunciations. Since bear is an irregular word, a regularization error (translating bear into the pronunciation of ‘beer’) will occur here. The use of this regularized phonological form to access semantics is responsible for the specific comprehension error made here.

1.3 Visual Dyslexia

There has been curiously little research on this form of acquired dyslexia. Its characteristic symptom is the abundance of visual errors in reading aloud— responses which share many letters with the stimulus but are otherwise unrelated to it, such as reading enigma as ‘image’ or garden as ‘anger.’

1.4 Lexical Nonsemantic Reading

Brain damage sometimes affects the semantic system and so impairs the comprehension of written or spoken words. This can happen as a consequence of head injury, but is more commonly due to a progressive brain deterioration such as dementia of the Alzheimer’s type. Schwartz et al. (1980) studied the reading performance of WLP, a patient of this type. At a point in the evolution of her disorder where she could no longer understand written words reliably, she could still read aloud very well—and that included the ability to read aloud exception words such as blood, shoe, and sweat.

According to some models of reading aloud (Hillis and Caramazza 1991), the procedure by which irregular words can be read correctly is via a pathway from orthography to meaning and then a pathway from meaning to pronunciation. If that were so, then a severe semantic impairment would always be accompanied by an impairment in the reading of irregular words. The data from WLP, and from other reports of patients with severe semantic impairment but good irregular-word reading (Cipolotti and Warrington 1995, Coslett 1991, Lambon Ralph et al. 1995), show that this kind of model of reading cannot be correct; and this form of acquired dyslexia has come to be called ‘lexical nonsemantic reading.’

1.5 Pure Alexia (Letter-By-Letter Reading)

In this form of acquired dyslexia (see Coltheart (1998) for a recent comprehensive review), words and nonwords are read aloud slowly and effortfully, usually by naming each letter in left-to-right order. If all the letters are named correctly, the patient will then usually produce the whole word or nonword correctly. Latency to read aloud increases linearly with the length of the word or nonword, with slopes sometimes as shallow as one letter per five or more seconds, so that a six letter word might require 30 seconds or more before a correct reading response is produced. The term ‘letter-by-letter reading’ is used since it describes the characteristic reading behavior of these patients. The term ‘pure alexia’ (or ‘alexia without agraphia’) is used because writing and spelling is often intact in these patients; this is discussed further below.

Some patients with pure alexia exhibit a phenomenon known as ‘covert reading.’ When letter strings are presented at durations too short for the patient to be able to read them aloud—two seconds or so, for example—and the patient asked to judge whether the letter string was a word or not, or in other studies whether it was the name of an animal or not, performance on these classification tasks can be well above chance, and even sometimes perfect, even though the stimuli cannot be read aloud and the patient may even claim not to have seen them at all (see e.g., Saffran and Coslett 1998). It is argued that in pure alexia ‘the right hemisphere supports performance in covert reading tasks, and…letter-by-letter reading is the product of the left hemisphere operating on information transferred from the right’ (Saffran and Coslett 1998, p. 141). Here it is important to appreciate the lesion sites typically associated with pure alexia. These patients generally have damage to two distinct regions of the brain, the left occipital cortex and the splenium of the corpus callosum. The left occipital lesion means that printed words must be visually processed by the right hemisphere’s occipital cortex. That in itself would not cause reading to be abnormal, however, since intact readers have no difficulty in reading words briefly presented in the left visual field (must be visually processed by the right hemisphere’s occipital cortex). Normal readers read promptly under these conditions by transferring information from right occipital cortex to language systems in the left hemisphere. Pure alexics can’t do that, and the reason must be that the splenium of the corpus callosum is the pathway by which such interhemispheric transfer for reading is normally done. In the patients, the splenial lesion means that some other callosal pathways have to be used for this transfer, and the use of these other pathways may impose a slow and serial letter-by-letter transfer process.

1.6 Deep Dyslexia

This acquired dyslexia is reviewed in detail by Coltheart et al. (1980). Its cardinal symptom is the semantic error in reading aloud. When single isolated words are presented for reading aloud with no time pressure, the deep dyslexic will often produce as a response a word that is related in meaning, but in no other way, to the word he or she is looking at: dinner → ‘food,’ uncle → ‘cousin,’ and close → ‘shut’ are examples of the semantic errors made by the deep dyslexic GR (Coltheart et al. 1980). Visual errors such as quarrel → ‘squirrel’ or angle → ‘angel,’ and morphological errors such as running → ‘runner’ or unreal → ‘real,’ are also seen. 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.

As noted above, Marshall and Newcombe (1973) proposed that different forms of acquired dyslexia might be interpretable as consequences of specific different patterns of breakdown within a multicomponent model of the normal skilled reading system. That kind of interpretation has also been offered for deep dyslexia, by Morton and Patterson (1980). However, this way of approaching the explanation of deep dyslexia was rejected by Coltheart (1980) and Saffran et al. (1980), who proposed that deep dyslexic reading was not accomplished by an impaired version of the normal skilled reading system, located in the left hemisphere of the brain, but relied instead on reading mechanisms located in the intact right hemisphere.

Subsequent research has strongly favored the right-hemisphere interpretation of deep dyslexia. Patterson et al. (1987) report the case of an adolescent girl who developed a left-hemisphere pathology that necessitated removal of her left hemisphere. Before the onset of the brain disorder, she was apparently a normal reader for her age; after the removal of her left hemisphere, she was a deep dyslexic. Michel et al. (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. They studied his ability to read tachistoscopically displayed words presented to the left or right visual hemifields. With right hemifield (left hemisphere) presentation, his reading was normal. With left hemifield (right hemisphere) presentation, his reading showed all the symptoms of deep dyslexia. In a brain imaging study, Weekes et al. (1997) found that brain activation associated with visual word recognition was greater in the right than the left hemisphere for a deep dyslexic, but not for a surface dyslexic, nor for two normal readers.

It seems clear, then, that deep dyslexia is unlike all the other patterns of acquired dyslexia discussed here, in that deep dyslexics do not read via some damaged version of the normal (left-hemisphere) reading system, whereas patients with other forms of acquired dyslexia do.

2. Forms Of Acquired Dysgraphia And Their Relationship To Acquired Dyslexia

Just as damage to the left hemisphere of the brain can sometimes specifically affect reading, so too left-hemisphere damage can sometimes specifically affect spelling and/or writing. Such an impairment of writing or spelling in a previously literate person is referred to as an acquired dysgraphia; and various different forms of patterns of acquired dysgraphia have been reported. There is a selective difficulty in spelling nonwords relative to words, known as ‘phonological agraphia’ or ‘phonological dysgraphia’ (e.g., Shallice 1981). There is a selective difficulty in spelling irregular words relative to regular words and nonwords, known as ‘lexical agraphia’ or ‘surface dysgraphia’ (e.g., Beauvois and Derouesne 1981). There are cases in which semantic errors are made in spelling to dictation, and spelling of nonwords to dictation is impossible, known as ‘deep dysgraphia’ (Bub and Kertesz 1982). There is also ‘lexical nonsemantic spelling’ (Patterson 1986)

Almost all patients with acquired dyslexia also exhibit acquired dysgraphia—the only clear exception here is for pure alexia (letter-by-letter reading), in which writing and spelling are often intact. Patients with acquired dyslexia and acquired dysgraphia offer unique opportunities for learning more about the relationships between the systems intact people use to read and to spell. For example, when one sees a patient who reads yacht as ‘/jætt/’ and spells ‘yacht’ as yot—a patient with surface dyslexia and surface dysgraphia—it is exceedingly tempting to take this as evidence that the body of orthographic knowledge we use to recognize familiar printed words is the same as the body of orthographic knowledge we use when retrieving familiar spellings. If this were so, then loss of the representation of the word yacht from this body of knowledge would force the word to be both read and spelled via the application of knowledge about typical relationships between segments of spelling and their most common pronunciations. This method of reading and of spelling would generate the particular erroneous reading and spelling responses just described. Here one would be arguing against the view that there are distinct bodies of orthographic knowledge for orthographic input (reading) and for orthographic output (spelling and writing) (as proposed by many (e.g., Morton 1980) and for the view that there is just a single body of orthographic knowledge used both for reading and for spelling and writing (as proposed by Allport and Funnell 1981).

But the relationships between the form of acquired dyslexia a person has and the form of acquired dysgraphia accompanying it are unfortunately much more complicated than this. Most people with surface dysgraphia also show surface dyslexia, but not all do: RG (Beauvois and Derouesne 1979) was a surface dysgraphic but a phonological dyslexic. Most people with deep dysgraphia also show deep dyslexia, but not all: MK (Howard and Franklin 1988) was a deep dysgraphic but a surface dyslexic, and JC (Bub and Kertesz 1982) was a deep dysgraphic but essentially normal at reading.

Thus the relationships between acquired dyslexia and acquired dysgraphia are simply not understood at present. But as has been documented above acquired dyslexia itself is rather well understood. Various types of acquired dyslexia have been clearly delineated, as have subvarieties of each type, and we have very clear ideas about how to interpret these patterns of impaired reading in relation to an information-processing theory of the normal reading system.

3. Computational Cognitive Neuropsychology Of Reading

Currently a number of information-processing theories of reading aloud are expressed as computational models—that is, as executable computer programs which turn print into phonology and do so by using the specific information-processing procedures posited by the particular theory. Some of these models are in the connectionist tradition and are built up via connectionist learning algorithms such as backpropagation (Plaut et al. 1996, Zorzi et al. 1998). Others are nonconnectionist, with their architectures specified by the modeler rather than by a learning algorithm (Coltheart et al. 2001). This is an area of much ongoing theoretical development.

One way to test such models is to investigate their ability to simulate different patterns of acquired dyslexia. The way this is done is to try to ‘lesion’ particular components of the program so as to cause the computational model to exhibit the same kinds of errors as do patients with particular forms of acquired dyslexia—to cause the program to make regularization errors with irregular words, especially low-frequency ones, for example, whilst still being good at reading nonwords (thus simulating surface dyslexia) or to cause the program to be poor at reading nonwords while still being able to read words (thus simulating phonological dyslexia). The computational cognitive neuropsychology of reading is currently being pursued both in the connectionist tradition (Plaut 1997) and in the nonconnectionist tradition (Coltheart et al. 2001)

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