24/7 writing help on your phone
Any discussion of the causes of dyslexia must, as we shall see, be a complex and controversial undertaking; even the title may raise controversy: what is ‘dyslexia’? Is it the same as ‘specific learning difficulties’? Can it be defined as a single problem? Is there a continuum of dyslexic-type difficulties? Should we be using a label at all? The questions are many, and with very few satisfactory answers. For this reason, it is necessary to begin with a working definition of dyslexia, before discussing what may cause it.
Once this has been established, it will be seen that the cited causes may be usefully grouped into several categories (genetic, perceptual, neurological and linguistic). Each of these areas will be examined in some depth, and the evidence evaluated. It will be found that, as yet, no single cause can be definitively established, but that studies into information and language processing in the brain seem to offer the most promising possibilities for the future.
Due to the complex nature of the problem, and the many different ways in which it manifests itself, it is impossible to find a definition upon which everyone may agree. Nevertheless, several definitions exist which may serve as a starting point. An early definition by Critchley is that dyslexia is “a disorder of children who, despite conventional classroom experience, fail to attain the language skills of reading, writing and spelling commensurate with their intellectual abilities.” This raises two main points: what is conventional classroom experience’, and how can we prove which level of language skills is ‘commensurate with intellectual ability’? This definition was improved upon in 1978 by Critchley and Critchley: “children with specific learning difficulties are those who in the absence of sensory defect or overt organic damage, have an intractable learning problem in one or more of reading, spelling or maths, and who do not respond to normal teaching,” (see also, Critchley and Critchley in Augur, 1981).
Several issues are raised here – the label ‘specific learning difficulties’ is introduced, ‘sensory defects’ and ‘organic damage’ are mentioned, and dismissed, and so is ‘normal teaching’. It is hoped that the issues of sensory defect and organic damage will be dealt with later, so that it shall be possible to consider whether this definition is accurate. The use of the term ‘specific learning difficulties’ (SpLD) is outside the scope of this essay, and so the more widely known ‘dyslexia’ will be used for convenience, even though its use is still controversial (Stanovich, 1994). Dyslexia covers a group of symptoms, any or all of which may be seen in one individual, and which can be briefly summarised as: visual perceptual difficulties, directional confusion, sequencing problems, short term and long term memory problems, difficulties in naming, organisational problems, and general literacy skills (Robertson, 1994).
The question of whether dyslexia is genetically determined has a long history, going back to 1900 when Hinshelwood, Morgan and Kerr noted that with two boys they saw who were intelligent but could not read, there were several cases in each family, which lead him to suggest the term ‘congenital word blindness’, (see Huston, 1987). More recent research has supported the view that dyslexia runs in families, and is therefore at least partly genetically determined, for example, Dr Beve Hornsby reported that 88% of children seen by her had a family history of dyslexia (Osmond, 1993 and Hornsby, 1992). However, these conclusions were based on observation rather than scientific method. Jorm (1983) quotes a study by Finucci et al (1976), who conducted a more stringent test and found that in 45% of cases, immediate family members of the dyslexic person were also retarded readers, confirming the strong tendency for dyslexia to run in families. However, it is important to consider whether one explanation for this apparent ‘genetic’ cause may be that those in families share the same environment i.e. if one or both parents don’t read very well, then it is not unexpected that their children have difficulties. To try and clear up this confusion, we turn to twin studies, of which many have been conducted. Twin studies are important because they allow
comparison between monozygotic twins (who share 100% genes) and dizygotic twins (who share 50%), but where both have been brought up in the same environment, so that any difference between dizygotic twins may conclude to be based on genes rather than environment. Using this method, Herman (1959) found a 100% concordance for monozygotic twins, and 33% for dizygotic twins: this is a summary of three studies undertaken in Scandinavia in the 1950s. Jorm (1983) states that all twin studies show greater similarity between MZ than DZ twins, suggesting a role for genetic factors. However, as Young and Tyre (1983) point out, this is not absolutely conclusive, unless we can be sure that these MZ twins have not been subject to perinatal disturbances, which are more likely than in single births. A related question is why more boys are affected than girls (the ratio is 3:1) – some researchers have suggested that dyslexia may be sex-linked genetically (for example on the X chromosome), although there appears to be little medical or scientific evidence for this as yet. A recent article in The Daily Telegraph (January 5th, 1996) quoted a study from 1994 in which an American team linked dyslexia to chromosome 6, suggesting a biological basis; future research should provide more information. The only reliable conclusion which can be drawn, is that genetics do appear to play a part in the causation of dyslexia, but they do not fully explain it: a combination of factors need to operate together for dyslexia to manifest itself. In addition, genetics offer no explanation for cases in which there is no family history of dyslexia.
Before one can read, it is necessary to hear the spoken word (audition), and see the written word (vision): these abilities may be grouped under the term ‘perception’. Galaburda (1993) has described perception as “the gateway to cognition” i.e. we cannot think about something until we have perceived it. Faulty perception was one of the first areas of research about the causation of dyslexia: Hinshelwood used the term ‘word blindness’ (Bryant and Bradley, 1985), and Samuel Orton coined the term ‘strephosymbolia’ (Bryant and Bradley, 1985). He Has observed the directional confusion which is common in dyslexia (for example, b/d confusion, word reversals such as saw/was etc.), and suggested that dyslexics sometimes perceived written symbols in a twisted way (Snowling, 1987). Orton explained this by using the mirror-image arrangement of the brain’s hemispheres: the child is presented with the image and the mirror image, and the dyslexic child’s difficulty is in perceiving which image is correct. However, as Bryant and Bradley (1985) point out, this does not explain dyslexia, because directional confusions account for less than 15% of dyslexic reading errors, and in fact, dyslexic children are no more prone to making this kind of error than are normal readers. Perception as a possible cause can not be dismissed, because much of the recent work is more convincing. This can be divided into two main strands- visuo-perceptual processing, and audio-perceptual processing, with some necessary overlap.
It may be that dyslexics have general difficulties with distinguishing and discriminating between visual patterns (Bryant and Bradley, 1985), or that they have problems in storing visual information in memory. However, Bryant and Bradley (1985) are emphatic in stating that backward readers do not suffer an overall visual deficit, and suggest that the evidence which does point to it is flawed, because it uses a mental-age match on subjects, rather than a reading-age match: this means that any apparent problems may be a result rather than a cause of reading difficulties. Vellutino (1979) also attacks the visual deficit notion, showing, for example, that backward readers copy unfamiliar Hebrew letters as well as normal readers, i.e. when the information is solely visual, there is not a problem. An alternative suggestion made by Ellis (1981) is that dyslexics have problems when visual stimuli have to be named: an experiment was conducted in which dyslexics made physical visual matches as quickly as controls, but took significantly longer when letters matched only in their names (see
Snowling, 1987 for a full description). These results also rule out the possibility of a basic visual perceptual problem, and suggest that the problem emerges when name-coding is required. Hornsby (1992) mentions two further possibilities involving visual perception. One is that some backward readers do not have a fixed reference eye (30%), and so have problems with convergence, i.e. the images of the two eyes do not match on the retina, so making accurate perception very difficult, although the Dunlop test, used to establish eye dominance, has received some criticism because subjects respond verbally to a visual test. Secondly, Hornsby quotes Pavlidis (1979), who noted that dyslexics’ make larger, jerkier eye movements when reading than do normal readers, which may partly account for reversals. Very recent research is supporting the view of a visual problem being at least partially responsible for dyslexia (Lovegrove et al, 1986 and Eden et al, 1995). These point, together with the existence of ‘scotopic sensitivity syndrome’ (Irlen syndrome), where backward readers’ reading can be improved by placing a coloured acetate overlay on the page, suggest that visual perceptual difficulties may be one of the causes of dyslexia.
Auditory perceptual difficulties may also be a cause: dyslexics tend to confuse the order of syllables and numbers which they hear spoken aloud, due to the way the brain interprets nerve impulses sent by the ears. If there is a problem in the hearing process, then speech perception may become confused (Hornsby, 1992). The siting of the language areas in the dyslexic’s brain (as will be explained later) plays an important role in their ability to decipher spoken words. In normal readers, the right ear is usually better at interpreting speech sounds because it connects to the left hemisphere (specialising in language), but many dyslexics show no dominance, thereby creating confusion in interpretation. Galaburda (1995) suggests that there may be anomalies in the early development of the auditory system for the fast processing of information, which may account for auditory perception difficulties. Thomson and Watkins (1991) state that there is much evidence for difficulties in serial and sequencing skills, particularly where sound encoding is involved. As with visual perception, there appears to be reason to believe that auditory perception may be one factor in causing dyslexia.
Probably the most widely researched area in dyslexia in recent years has been cognitive and neuropsychology, as there appear to be differences between the brains of dyslexic and normal readers. It seems that the way in which the brain is organised is relevant to this field; the human brain is divided into two cerebral hemispheres, each of which has its own highly specialised functions to perform, and which are connected by a bundle of fibres called the corpus callosum. Broadly speaking, the right hemisphere is specialised for non-verbal reasoning, practical skills, music, intuition etc., while the left hemisphere, which is usually larger in size, is specialised for language. Within the left hemisphere, there is yet greater specialisation, for example, Broca’s area (expressive language), Wernicke’s area (receptive language) and the angular gyrus (which associates a written symbol with a sound), (see Hornsby, 1992). There is also a very inefficient language area in the right hemisphere. Whilst this accounts for the majority of the population, a small minority show the reversed pattern, with language being based in the right hemisphere (Jorm, 1983) – this is more often the case with people who are left handed. Zangwill (1967) found that 98% of right handers experienced severe speech difficulties after damage to the left hemisphere, but speech was affected in less than 2% of those whose right hemisphere was damaged There are two possible descriptions of the brains of dyslexics: either they do not have a dominant hemisphere for language, or the language centre in the left hemisphere is smaller. Miles (1974) conducted an experiment whose results suggested that in dyslexic brains, language is shared more equally between the two hemispheres, and that this means that more messages
have to be passed from one hemisphere to the other, resulting in a confusing ‘traffic jam’ of nerve signals in the corpus callosum connecting the two language areas. To support this, Galaburda and Kemper (1981) examined the brain of a young dyslexic man who had been killed, and found unusual arrangements of cells that suggested that the language areas were distributed more evenly. Recent research supports the idea that initial reading is right hemisphere based and transfers to the left hemisphere when graphemic-phonemic relationships become automatic; it is even suggested that there are two subtypes of dyslexia –
linguistic’ (who rely on the left hemisphere) and perceptual’ (who rely on the right hemisphere), (Licht et al, 1988, Bakker et al, 1990, and Strien et al, 1995). The second explanation focuses on the fact that the brain of ‘normal’adults is asymmetrical, with the left hemisphere being larger at the back. Both Sherman (1993) and Hier et al (1978) have found a reversed pattern of asymmetry, or no asymmetry at all, in the brains of dyslexic patients, meaning that their language areas are smaller. The research has shown that these differences happen early on in the pre-natal developing foetus. Jorm (1983) also cites research using computerised tomography and evoked potentials which indicates that retarded reading can be associated with the deficient functioning if the left hemisphere.
Related to research into hemispheric dominance, is research which suggests specific functional abnormalities i.e. differences not i the way in which he brain is structured, but in how the different parts of it operate. Here we find considerable overlap with cognitive neuropsychology, for example, research into memory has shown good evidence for a weakness in dyslexics, particularly in relation to short-term strategies (Thomson, 1990). Dyslexics have difficulties in remembering letter strings and sound-symbol correspondences, and in particular, series and sequences of stimuli. Galaburda (1995) has suggested that the mechanisms involved in processing information in parallel and in series in the brain are altered in dyslexic brains; he has found ectopias (clusters of cells out of place in the cortex of the brain, where cognitive activity is controlled, and suggests that this is caused by vascular disturbance early on in development. Watson and Willows (1995) suggest the main differences are in short term auditory/working memory, decoding and encoding, phonological coding and visual sequential memory, and Grogan (1995) also shows that cognitive defects, for example, grapho-phoneme conversion, predate reading problems. This is a very active area of research and as tech niques become more sophisticated and knowledge greater, cognitive neuropsychology should certainly help to improve understanding of what causes many of the problems associated with dyslexia.
Cognitive neuropsychology is closely linked with research into language processing, which many people believe to be a central factor on dyslexia. Heaton and Winterson (1986) go so far as to state simply that dyslexia is “an impairment of language”, and draw on evidence from Vellutino (1979) and Ellis and Miles (1981). The research has focused on two main areas – verbal memory problems and defective phonological processing. The latter are had generated the most work, which supports the idea of phonological awareness difficulties as the main cause of dyslexia.
However, there has been much controversy surrounding the idea if dyslexia as a language deficiency, or as Snowling (1987) puts it, a ‘verbal coding deficit’. She points out that almost all studies show dyslexics to have verbal memory difficulties, i.e. memory for words, particularly in the area of retrieval from long term memory (see Bauer and Emhert, 1984). The problems appear to arise in the way in which dyslexics encode words: normal readers use phonological codes, whereas dyslexics use semantic codes, and if verbal material is to be maintained in memory, this is a less efficient process (Byrne and Shea, 1979). The suggestion
that dyslexics do not use phonological codes for memory storage would obviously have implications for reading. But these suggestions have been refuted by Hall et al (1981) and Olson et al (1984), who claim that the experiments above were faulty invalid; instead, the suggestion is that dyslexics merely lag developmentally in the use of phonological codes. Bryant and Bradley (1985) say that poor verbal memory in tests could be as a result of not being able to read, rather than a cause, and support this by the results of a longitudinal study they carried out. Controversy still seems to surround this area.
There is greater agreement in the area of phonological awareness, i.e. the ability to perceive that words are made up of units of sound which can be combined in different ways to produce thousands more words, and later, that these individual sounds or phonemes) are represented by written symbols (or graphemes) in English. McBride-Chang (1995) states three components of PA – verbal short term memory, speech perception and intelligence. The beginning of the awareness is the ability firstly to divide the speech stream into words, and then segment the words into phonemes. Bryant and Bradley (1985) supported this view but Snowling (1987) put forward the idea that this ability was a consequence not a cause of learning to read, and quotes Morais et al (1979), whose testing of Portuguese former illiterates supported this. In response, Bryant and Bradley carried out further experiments into rhyming ability (which involves phoneme segmentation) and showed quite convincingly, by using reading-age matched subjects, that backward readers are “remarkably insensitive” to rhyme, despite their reading ability, which implies that this ability could hardly be the result of the reading problem, but one of the causes. This is also supported by Tangel and Blachman (1995), who showed that instruction in PA improves reading ability, and Snowling (1995).
An idea related to this is that of the ‘internal lexicon’ or dictionary (Vellutino and Scanlon, 1985), which is, in simple terms, a store of words with which we are familiar. Snowling (1987) suggests that a difficulty with phoneme segmentation and synthesis at an early age would slow down the acquisition of new words into this lexicon, which may explain why, in tests, dyslexics have difficulty in repeating low frequency words, as they do not have these words in their lexicon. The result of this lack of vocabulary places a restriction on the codes available for cognitive tasks such as reading, particularly in accessing and activating phonological memory codes, and in retrieval of words. It would seem that the two areas, of verbal memory problems and phonological awareness, may be linked in dyslexia and that one (phoneme segmentation) may lead to the other (Snowling, 1987). This is evidently an area of great interest, and research is ongoing which should be fruitful in the search for the causes of dyslexia.
Whilst the main factors in the causation of dyslexia have been discussed above, it is necessary to mention some additional possibilities, even if this is merely to exclude them. Social background is one such consideration, and there are two opposing points of view. Some people still view dyslexia as a ‘middle class’ problem, caused by ‘over-anxious’ parents who are concerned that their child is not as brilliant as they expect. I hope that this discussion has at least ruled out this fallacy. Alternatively, it is accepted that in areas of social disadvantage, incidents of learning difficulties form a higher percentage that in more ‘welloff’ areas, a number of factors are involved here, including housing, diet, pollution, poor health etc., but it cannot be said that these actually cause dyslexia – there must be some kind of predisposition’ present aswell. Pennington (1995) carried out a study which, among other things, concluded that there may be a causal relationship between psycho-social correlates and dyslexia, but that these alone were not sufficient to cause dyslexia. Hornsby (1992)
suggests some factors which, similarly, may aggravate dyslexia. One is poor schooling, particularly where this involves changes in teaching methods, which may retard the child’s ability to acquire basic skills. She also controversially suggests that ‘open plan’ education does not suit a child with dyslexia, as he needs a more structured system of education; however, I would argue that a dyslexic child is more likely to receive an individual education programme in an open plan classroom than in one where the children sit in rows and are taught as a class, as long as the IEP has a strong phonic basis. The second and final factor which Hornsby mentions is poor health, as this may mean time missed from school and inability to concentrate; this may particularly be important if it involves some kind of hearing loss such as ‘glue ear’. The factors mentioned here may be said to be aggravating to a child with dyslexia, but they cannot be said to cause it.
The research discussed above has practical implications for teaching. The possibility of a genetic link means that teachers should be particularly aware of any older siblings or parents having reading problems, so that they can pick up on the early signs of a child in their class. The possibility of perceptual problems should be borne in mind, for example, thinking of using coloured paper where possible instead of white, so as to reduce glare. The research into hemispheric differences suggests it is useful to employ different teaching methods for different subtypes of difficulties, for example, visual presentation for ‘linguistic’ dyslexics and tactual for ‘perceptual’ dyslexics (Strien et al, 1995). Grogan (1995) recommends games to train verbal STM skills, such as those already used by the British Dyslexia Institute are worthwhile, as deficiencies in this area are related to reading problems. Perhaps the most frequently stressed factor for teaching is phonic training – Snowling (1995) says that if a child does not have phonemic awareness at entry to school, then they are not ready to benefit from reading instruction, i.e. teachers should ensure that their pupils have a good level of PA before trying to teach reading, and if they do not, then they should try and train this area. All of the suggestions are saying the same thing: Teaching for children with dyslexia should be multisensory, i.e. all the senses should be stimulated and trained in order to give the child the maximum opportunity to improve in reading ability.
It seems apparent from the above discussion that the answer to the cause of dyslexia is still unresolved, although with modern techniques and knowledge, progress is being made all the time. I believe it is limiting to think in terms of a single cause, just as there are many variations of dyslexia, so the causes must be varied. This point is supported by Miles (1970), who suggests a combination of adverse factors, and Thomson and Watkins (1991), who state that there is a point where perception, coding and memory overlap with each other. It mat be that there are different causes for different subtypes (for example, visual, auditory and sequencing; see Watson and Willows, 1995), and that a weakness in one area can adversely affect related areas. Finally, I would like to suggest a model which begins with genetic factors, which affect brain development, which affects perception, which in turn affects language, and thereby, reading and writing. Obviously, this is a simplified pathway and the reality is far more complex, and I will be very interested to see whether future research supports this view.
👋 Hi! I’m your smart assistant Amy!
Don’t know where to start? Type your requirements and I’ll connect you to an academic expert within 3 minutes.get help with your assignment