Recent research and development in dyslexia in · Web viewIn educational terms, this means that children with dyslexia need longer to read a word that is familiar to them (van der

Dyslexia:at school: a review of research for the DfES

Recent research and development1 in dyslexia in relation to children of school age: a quarterly review for the Department for Education and Skills, the British Dyslexia Association and the Dyslexia Institute. Review 1, September 2001

Angela Fawcett, Department of Psychology, University of Sheffield

Disclaimer: The material presented here reflects the views of the reviewer, not necessarily those of the University of Sheffield, the DfES, the BDA and the DI. In this first review of the series, I will concentrate on recent developments in the theoretical basis of dyslexia. My brief is to concentrate on school aged children. • explain the theories clearly in language appropriate to a lay audience, • explain the links between theories• outline their implications for policy and practice• consider areas for further research.

Recent research and research currently in progressI shall introduce these theories in the order in which they have emerged. I shall present the background, followed by examples of interesting recent research within each framework. There have been striking developments in dyslexia in the last ten years, with each theory filling in part of the jigsaw for the complex problem of dyslexia, which can extend far beyond literacy skills and impact on an individual throughout their life. The UK is at the forefront in this theoretical research. In my view there is a synergy between these theoretical developments leading to a more satisfactory explanation of the symptoms of dyslexia than the individual theories on their own. I shall return to the theories in the section dealing with links and emerging themes, where I suggest that the most productive way forward is to work together to design studies where each research group tests out all the theories within the population of children they work with, and within school-based samples.

i) Background - Phonological deficit. This is the most well developed and supported of the theories of dyslexia. It has been widely researched, both in the UK (York group) and in the US. The US researchers have united in adopting the phonological deficit hypothesis since the early 1980’s, and this united front has led to the investment of more than $15 million annually by the US government, via the National Institute for Child Health and Human Development (NICHD).

There is unanimous agreement that problems with phonology are associated with dyslexia, however, it is becoming clear that phonology is not the only problem. Phonology is a skill underlying the analysis of both spoken and written language; breaking down words into their parts, or segmenting them, so first knowing that ‘cat’ is made up of the onset and rime c-at, and then recognising the individual sounds (phonemes) are c-a-t. Phonological awareness is also used in hearing a sound (a phoneme) and translating it into a letter which represents it (a grapheme). These skills need to develop around the age of 5, if young children are to learn to read successfully. Otherwise, they are limited to reading words they recognise as a whole

1 Note that by definition research in progress and material under review, although promising, may not yet have satisfied the peer review procedure.

1


(orthography) and are limited in their ability to learn new words. There is solid evidence dating from the work of Bradley and Bryant, 1983, that rhyming is impaired in children with dyslexia. In a research programme spanning many years, Snowling and colleagues have investigated phonological deficits over the life span, in particular the ability to read nonsense words, which depend on both the ability to segment and grapheme/phoneme translation.

There is a clear brain basis for phonological difficulties, based on a difference in areas involved in language (the sylvian fissure and the planum temporale). This is found in both the anatomical structure (Galaburda) and the function (work by Chris Frith and colleagues at UCL). Training helps in improving phonological skills, but even high achieving dyslexic adults still show deficits. Despite all the evidence, Frith concludes (1997, p11) “the precise nature of the phonological deficit remains tantalizingly elusive.”

Recent and ongoing research - PhonologyIn my view, some of the most interesting studies from the York group fall into 2 groups: • Predicting which children from an ‘at risk’ population are likely to develop dyslexia (a)• Longitudinal data on outcomes of childhood disorders (b). These studies provide evidence that phonology is crucial but not necessarily the whole story, and identify other important predictors of progress.a) Examining pre-school children with a family history of dyslexia for early indications of dyslexia (Gallagher et al, 2001). There is strong genetic evidence that children with dyslexia in the family have a 50% chance of having difficulties themselves (see Fisher et al, 2001), so this is an important group to target in order to find out more about pre-school development. Letter recognition at 45 months proved the best predictor of literacy at 6 years.b) A longitudinal study of children identified with language deficits pre-school in terms of their literacy outcomes as teenagers (Snowling et al, 2001). This shows the overlap between Specific Language Impairment (SLI) and Dyslexia, but suggests that around 35% of children with phonological problems develop literacy skills in the normal range, although the gap for less successful children widens. Interestingly, strengths in non-verbal intelligence proved the most protective factor here against continuing difficulties, which may suggest that processing speed is an important factor. The York group are currently establishing comparative data for phonological and sensory deficits, and naming speed and phonology.

(ii) Sensory Deficit.

This theory is broader than the phonological deficit, because it can potentially account for both visual and auditory deficits in dyslexia. The auditory ‘rapid processing deficit’ was introduced by Tallal in the US, whereas the visual magnocellular deficit comes from Stein and his group in Oxford.

It is now clear that a number of children with dyslexia have problems in processing information coming in via the senses (sensory information). This includes information from both the eyes (visual) and the ears (auditory). This was first identified by Lovegrove, 1993, who found that if you showed a flickering pattern to dyslexic children (think of the lines on a television screen), they needed a more defined flicker before they were aware of it. In more recent work Talcott et al. (1998) showed that dyslexic children needed more information to detect a pattern of stimuli

2


moving together like clouds against a randomly moving background (known as coherent motion sensitivity). Tallal and her colleagues (1993) have claimed that, like language disordered children, children with dyslexia take longer to process sounds which change rapidly. This is tested with high and low tones, or the sounds ba and da, which are only different in the first few milliseconds. Children with dyslexia (and SLI) can’t tell the difference between the sounds if they are presented close together, and this means that they are likely to have problems with phonological awareness.

This type of processing is controlled by the large cells in the magnocellular pathways, which go to a part of the brain known as the thalamus. There are differences in the dyslexic brain anatomy in both visual and auditory magnocellular pathways (Galaburda, Menard and Rosen, 1994; Livingstone, Rosen, Drislane and Galaburda, 1991).

Differences in the visual magnocellular pathway, Stein (e.g., Stein and Walsh, 1997) may cause what is known as ‘visual persistence’ during eye movements. The effect in reading would be that letters in a word drift and blur, because when you try to look at the next letter there is an after image from the previous letter. This explanation seemed to give a good account of the symptoms of blurred vision and letters that move around, which some dyslexic children report. However, it has now become clear that the magnocellular system is not to blame for visual persistence (Stein, 2000). A magnocellular deficit would affect most types of rapid processing, which can be difficult for dyslexic children because it is more demanding for anyone to process material quickly. This is not the easiest theory to get to grips with, because magnocellular deficits cause different problems for vision and audition. In vision, deficits are found for low contrast and/or slowly moving stimuli (Eden et al., 1996; Stein and Walsh, 1997), in audition for rapidly changing stimuli (Tallal, Merzenich, Miller and Jenkins, 1998).

Recent and ongoing research - sensoryTallal, Merzenich and colleagues (2001) in the US and the Oxford group are producing some of the best work in the area• Comparing phonological deficits with magnocellular deficits (i)• Analysing both vision and audition in the same children (ii).• Sensory development in Infancy (iii). i) In two recent fMRI studies, Tallal examines the brain basis of rapid auditory processing and links it to phonology, identifying deficits in orthographic (visual pattern matching skills) in dyslexia, in addition to phonological deficits. ii) Work by Talcott and colleagues (2000, 2001 in preparation) links sensory processing skills to subtypes of reading disability in 350 normal 7-12 year olds. Phonology was tested by reading nonsense words (like ‘torlep’), and orthography by reading irregular words (like yatch). 3.7% of the sample had orthographic problems only (they could read nonsense) and showed delay. 7.4 % of the sample had phonological difficulties only (they could read irregular words) and showed poorer sensitivity to sound frequency; those with difficulties in both tasks (8.9% of the poor readers) showed reduced sensitivity to visual motion. This approach will shortly be applied to children with dyslexia.

iii) Sensory processing in infancy. The Finnish and Dutch infancy studies are examining learning in infancy in terms of both language and sensory development. The work is reviewed in

3


Van der Leij, Lyytinen and Zwarts (2001). In brief the Finnish study looked at the development of 100 children with a family history of dyslexia in comparison with controls in an intensive study from birth. Interesting findings by age 3.5 include the persistence of language deficits and significant associations between motor and language skill development in the familial group. These studies try not only to identify pre-cursors of dyslexia, but also any environmental protective factors which can ‘innoculate’ children against failure. In the US, Molfese (2000) found that infants who were shown to be dyslexic at age 8 could be identified at birth by differences in their brain waves in response to speech and non-speech sounds (see the section on evoked potentials below).

(iii) Speed of processing

Wolf and Bowers (1999) have brought together the phonological and speed problems in the double-deficit hypothesis, which suggests that there are two separate sources of difficulty in dyslexia, phonology and processing speed. Children with both speed and phonology problems have the most severe problems. This is one of the more recently developed theories (for a review see Wolf, 2001).

There is evidence of speed problems for dyslexic children in almost all areas, including those where rapid sensory processing is not needed. This has been known since the 70’s based on ‘Rapid Automatized Naming’ tests (RAN - Denckla and Rudel, 1976), in which dyslexic children show speed deficits in simply saying the names on a page full of simple pictures (or colours). Problems are found even when language is not involved, so children with dyslexia are slower to simply press a button when choosing between a high and a low tone (Nicolson and Fawcett, 1994). In a study which measures the speed of brain waves to see whether the problem lay in registering the tone (sensory) or categorising it as high/low, (using EEG evoked potentials Fawcett et al., 1993) slowed central auditory information processing was found (see recent cerebellar research below). In educational terms, this means that children with dyslexia need longer to read a word that is familiar to them (van der Leij and van Daal,1999) and this may lead to a strategy of trying to process large chunks of letters in reading, rather than breaking the word down phonologically in order to read unfamiliar words. This approach makes heavy demands on working memory, and limits the new words which can be tackled.

Recent and ongoing research – double deficitThe double deficit has become a major focus for research, with the majority of papers presented at the 2001 conference including naming speed. This is largely because it has been clear to practitioners for some time that accuracy is not enough to make a child a good reader, and that they clearly need to develop fluency as well. However, it is not surprising that dyslexic children are slower to name letters and numbers, because they find it more difficult to acquire these in the first place. Some of the most interesting research looks at picture naming, which less predictably is also slowed in dyslexia. The most diagnostic test is the RAN, because it tests the following areas; speed of access to the name of the picture, articulation, eye movements to the next picture, ability to keep your place, and maintain concentration for the whole set of stimuli. However, there are differences in the way some tests are administered which makes them not directly comparable. A standardised methodology is needed to allow comparison in further research.

4


(iv) Cerebellar Deficit

In the early 1990s, the Sheffield group found that dyslexic children in their panel had severe problems with a wide range of skills, including balance (Fawcett and Nicolson, 1992; Nicolson and Fawcett, 1990); motor skill (Fawcett and Nicolson, 1995b); phonological skill (Fawcett and Nicolson, 1995a) and rapid processing (Fawcett and Nicolson, 1994,b). Many of these skills were not language based, suggesting that the phonological deficit could not explain all the problems in dyslexia. Looking at all the data together (Nicolson and Fawcett, 1995a; Nicolson and Fawcett, 1995b), it was clear that most of the children showed problems ‘across the board’, rather than with different profiles suggesting sub-types. This pattern of difficulties was in line with the dyslexic automatisation deficit hypothesis (Nicolson and Fawcett, 1990), that dyslexic children have problems in fluency for any skill that should become automatic with extensive practice. This hypothesis could explain dyslexic symptoms in phonological skills, in reading, and in other skills, but did not attempt to specify which brain structure was involved.

Problems in motor skill and automatisation point to the cerebellum, an area at the base of the brain known to be associated with motor skill, but largely dismissed in dyslexia because until recently there were no known links between the cerebellum and language. There is now clear evidence that the cerebellum is involved in both language and cognitive skill, including specific involvement in reading (Fulbright et al., 1999). The human cerebellum has evolved enormously, becoming linked not only with the motor areas at the front of the brain, but also some areas further forward in the frontal cortex, including Broca’s language area.

It seemed to the Sheffield group that cerebellar deficit could possibly explain the range of problems suffered by children with dyslexia, and so this idea was tested out, looking first at behaviour and then at the brain. First, it was shown (Nicolson, Fawcett and Dean, 1995) that dyslexic children showed a pattern of poor performance on time estimation and normal performance on loudness estimation that Ivry and Keele (1989) found only in cerebellar patients. This time estimation task did not involve rapid processing; the children simply had to listen to 2 tones with a second between them, with the first tone also lasting a second, and the second tone either longer or shorter. The control task was very similar, but with the tones either louder or softer. Secondly, it was found that children with dyslexia showed a range of classic cerebellar signs (Fawcett and Nicolson, 1999; Fawcett, Nicolson and Dean, 1996) with problems in muscle tone and balance in 80-90% of the children tested. Direct evidence of cerebellar deficit came from a PET scan study which found that dyslexic adults did not show the normal pattern of activation when performing a motor sequence learning task, with only 10-20% the expected level of activation compared with controls.

Recent research – CerebellarThis falls into 2 groups:• Learning (i and ii)• Anatomy (iii)i) An analysis of how dyslexic children learn (Nicolson and Fawcett, 2001) when asked to blend two simple button pressing tasks, suggests performance can become automatic, but strikingly, a ‘square root rule’, suggests that this takes longer in proportion to the square root of the time normally taken to acquire a skill – see (ii) and Areas for further research below.

5


ii) A recent study on learning suggests that there may also be abnormalities in fundamental learning processes such as classical conditioning, habituation, response ‘tuning’ and error elimination in an eye blink conditioning study (Nicolson et al, 2001, under review).iii) Using the brain bank that Galaburda used to check out the phonological and sensory deficits, evidence has been found for differences in the anatomy of the dyslexic cerebellum (Finch et al, 2001, under review).For a recent review and peer commentary on the cerebellar deficit see Nicolson, Fawcett and Dean (2001).

SummaryAll the theories account for at least some of the symptoms of dyslexia, the deficits they predict have been found in varying percentages of dyslexic children and these deficits are observable in brain scans. These are all real deficits. All the major research groups involved adopt a rigorous approach and produce robust findings.•The phonological deficit explains many of the difficulties which children show linking sounds with symbols in reading and spelling. •The speed or double deficit suggested that there is a speed problem in addition to the phonological deficit, with problems most severe for those with both deficits. •The sensory deficits suggest that these problems are visual as well as auditory, at a basic perceptual level, leading to cerebellar impairment. •The cerebellar deficit suggests that there is a problem in central processing linked to learning and automaticity, which may occur with or without sensory impairment.

Linkages, emerging themes and points of interestHaving outlined these theories, it is not intuitively easy for the reader to understand how they link together, and how it can be possible for them all to be supported. Let me first fill you in on the background, and areas of potential controversy.

i) Emerging themes and points of interestA striking analogy, which emerged from the BDA 2001 conference, came from Rod Nicolson, the conference chair. Nicolson pointed out that many of the misunderstandings that have arisen in dyslexia research derive from the different perspectives of the people involved. It is not surprising that teachers, researchers, psychologists, the government, parents, and dyslexics themselves all have different priorities. Nicolson dubbed this the ‘dyslexia eco-system’ with a call for everyone in dyslexia research to work harder in understanding and respecting other people’s viewpoints. This became the emerging theme of the conference, identifying linkages not only between the delegates, but also between the underlying theories.

A further important distinction is between the three ‘levels’ of theory: the biological, the cognitive and the behavioural level (Frith, 1997). Recognition that it is quite possible for all the theories to be right, at different levels of explanation, led to an emerging consensus at the conference. The behavioural level examines the symptoms of dyslexia, such as poor reading or rhyming deficits. Theories are explanations at the cognitive level; for example problems in phonological awareness, automatisation, and slow processing speed. Finally, the underlying brain mechanisms lie at the biological level, with differences in language areas, magnocellular pathways, and the cerebellum. It has been recognised that these levels are different, that none is

6


‘better’ than another, and indeed that any complete explanation must include all three, with the cognitive level providing a necessary link between brain and behaviour.

At the roundtable discussion following the conference (led by van der Leij, Fawcett, Stein, Wolf, and Galaburda with around one hundred dyslexia researchers/practitioners), an emerging consensus was found that it was important to consider the biological level in addition to the cognitive/behavioural level. It was agreed that further investigation is needed of all the major hypotheses, from underlying cerebellar deficits and/or magnocellular deficits to the overarching phonological deficit, and the double deficit hypothesis. Systematic high quality research is needed, based on comparative analyses of the incidence and severity of these deficits in different populations. Marker tasks for different theories of dyslexia should be produced, to aid early identification. In order to establish how far the theories interlink, a non-adversarial approach was advocated, based on listening to other theoretical viewpoints and testing them out.

Linkage between the theoriesIt remains to demonstrate how the theories potentially interlink in producing the known deficits in dyslexia. The figure below outlines how a deficit in the cerebellum could explain the range of symptoms found in dyslexia. Note that the writing, reading and spelling difficulties are all accounted for in different ways, and in particular the natural causal explanation of the poor handwriting typically shown in dyslexia. Handwriting, of course, is a motor skill that requires precise timing and co-ordination of different muscle groups. Literacy difficulties arise from several routes, and here the central route is highlighted. If an infant has a cerebellar impairment, this will first show up as a mild motor difficulty – the infant may be slower to sit up and to walk, and may have problems with fine muscle control.

Cerebro- cerebellar

loop

Problems automatising skill and knowledge

Motor skill impairment

Balance impairment

SPELLING

READING

WRITING

'word recognition

module'

Articulatory skill

Phonological awareness

Cerebellar impairment

Interpretations linking the cerebellum, phonology speed and magnocellular hypothesesOur most complex motor skill, demanding the finest control over a sequence of muscles, is articulation. Consequently, the infant might be slower to start babbling, and, later, talking. Even after speech and walking emerge, one might expect that their skills would be less fluent. If

7


articulation is less fluent than normal, it takes more effort, leaving the child with less spare capacity to process the sensory feedback, in particular the structure of the words spoken. There may, therefore, not be a natural sensitivity to onset, rime, and the structure of language – in short, one would expect early deficits in phonological awareness. Cerebellar impairment would therefore be predicted to cause the ‘phonological core deficit’ leading to the standard explanations of reading difficulties in dyslexia. However, cerebellar impairment could also lead to the ‘double deficit’ because the cerebellum controls learning and automatisation, which would lead to impaired fluency and speed of reading. Similarly for spelling, problems arise from over-effortful reading, poor phonological awareness, difficulties in automatising skills and in eliminating errors. This is what the Americans call a ‘double whammy’. The child with dyslexia tries to build on faulty building blocks, using an impaired learning mechanism which results in a range of abnormally fragile skills, which break down further under time pressures.

The double deficit hypothesis (Wolf & Bowers, 1999) is a cognitive level description. The key question here is ‘where does speed come from?’ No-one really knows the answer. As children get older, their speed of processing and speed of reaction increases, but this is unlikely to be due to sensory mechanisms because the sensory pathways get longer as children grow. Cognitive psychologists think that speed increases reflect more efficient central processing mechanisms – noticing something has happened, classifying this information, making decisions, accessing the motor codes, and carrying them out. The cerebellum is naturally centrally involved in this tuning and automatisation of the central processing machinery. The cerebellar deficit suggests that inefficiencies in this central processing loop may produce most of the difficulties for dyslexic children.

Interpretations in terms of magnocellular deficitIt should be noted, however, that there may be alternative explanations of these findings. Stein (2001) suggests that ‘cerebellar impairment’ might be based on faulty input to the cerebellum from impaired magnocellular pathways, noting that there are magnocells both in the cerebellum and in the motor output systems. It is therefore difficult to distinguish the magnocellular from the cerebellar theory. However, if the task is simple, the cerebellar deficit predicts there need be no problems in speed or accuracy of sensory processing. The obvious point is that dyslexic children are known to have problems in detecting rhymes, which do not involve analysis of rapidly changing waveforms. There is no obvious magnocellular explanation of why dyslexic children react at normal speed when asked to simply press a button in response to a tone, but are slow with the same response when a choice needs to be made (Nicolson & Fawcett, 1994); no explanation of difficulties in time estimation; no explanation of why muscle tone should be lowered; and no explanation of why there should be abnormal cerebellar activation in the motor sequence learning task.

It may be that in due course it will be found that there is a ‘magnocellular’ sub-type (or two), a ‘cerebellar’ sub-type, and various ‘mixed’ sub-types, and that most subtypes show phonological deficits. However, it is not yet clear how many dyslexic children suffer from each deficit. These are topics for further research. In the next section I highlight the general directions that in my view research should take. I am optimistic that we have reached a real turning point in our understanding of the area.

8


Areas for further researchThere are a range of interesting questions which still need to be answered, and which dyslexia researchers are well equipped to address. The areas of research that are proving exciting to me are subtypes, co-morbidity, and pre-school development. The major step in this work is the initial recognition that these issues are important, and that further research is worthy of funding.

This analysis falls into 2 sections: • Approaches for investigating the theories further (i-ii)• Individual topics which warrant further attention.

i) Subtypes. Do some dyslexic children show a cerebellar or magnocellular deficit, and others show only a speed or a phonological deficit, or do most children show a profile with elements of all the deficits, but with some deficits more striking than others? We do not know this. It is important to bear in mind here that there may be differences between the research groups, based on the type of child recruited into the study. For example, if a child has any problems with vision, it is natural that they would be referred to the Oxford group, while children with language difficulties might well be referred to the York group. One might predict therefore, that the proportions of children with different deficits would vary between groups. This may well be the origin of the mixed results in terms of sensory deficits which have been identified in the literature (Skottun, 2000).

There are many examples of good practice in linking theories, but the concept of investigating all four major theories is only just emerging. Two examples of good practice in ongoing research should be mentioned here. a) The Oxford lab is collaborating in running a new Sheffield panel through a series of tests of auditory and visual magnocellular function. The children tested have already undertaken a full series of tests of speed, phonology, and cerebellar function. The incidence of deficits reflecting all four theories will then be established in the Sheffield children. b) A phonological group led by Ramus, Frith and colleagues at UCL, are adopting a similar approach. Ramus accepts that the theories are compatible with each other, but he expects to find evidence of different subtypes. In this study, performance of university students is examined on cerebellar, magnocellular, speed and phonological skills, so the deficits found may be less clear-cut than those in children.

ii) Co-morbidity. There is clear evidence of overlap between different developmental disorders, with large percentages of children (30% or more) showing language impairments, dyspraxia, attention deficit or conduct disorders, in addition to their dyslexia. There is still an exceptional amount of work to do in this area – for example there has been no systematic research on the behavioural effects of cerebellar or sensory impairment in dyspraxia, ADHD or conduct disorders, By contrast, there is a clear profile of phonological deficits in children with mild to moderate learning disabilities, but preliminary evidence suggests no cerebellar deficits in balance or muscle tone for this group (Fawcett et al, 2001).

3 stages of research (controlled studies)• Major research groups pool techniques for cerebellar, magnocellular phonological and speed tasks and apply to panels. Low cost

9


• School studies of poor readers using same techniques (incidence in children not referred- drawn from several schools) Moderate cost• Comparative study using same techniques with groups of dyslexia plus. Higher cost Individual Topics• i) Learning – a targeted topicThis is a surprisingly neglected area, considering that dyslexia was originally known as ‘specific learning disability’, and that this seems to be the crux of the difficulty. Interestingly enough, some children with dyslexia learn to read and develop their phonological skills, areas with which they have the greatest difficulty. However, their skills tend to remain less fluent, more demanding and more error prone, particularly in areas such as spelling. So, a study by Nicolson et al, 2001 shows that a simple skill that normally takes 4 sessions to master, would take a dyslexic child 8 sessions, whereas if it normally took 400 sessions, it would take the dyslexic child 8000 sessions! This suggests that it is important to monitor learning in small, easily assimilated steps for dyslexics, providing theoretical support for existing good practice, and distinguishing dyslexia support from that necessary for other poor readers. Naturally, further research is needed to address these issues, but in my view, learning is the key,.

• ii) Early development – further research neededInfancy studies involve expensive and complex longitudinal studies, but they are particularly important, because they have the potential to identify marker tasks for subtypes of dyslexia in the youngest groups of all. It may not be necessary for the UK to undertake their own study of infant development, but it is important to take on board the knowledge these studies are producing, and to continue research towards early identification of problems.

• iii) The brain and evoked potentials – an area to watch. There is considerable mileage in looking at the working of different areas of the brain when performing a range of tasks. However, in my view, it is less useful to look at the pattern of activation during reading, because it is well known that dyslexics have difficulty with this task and may be doing it differently. It is more interesting to try to unpick the various components of skills in which dyslexics may achieve a similar level of performance, but use an atypical approach. The study of brain waves using a network of electrodes is a non-invasive procedure which can be used with children of all ages, including infants. A series of studies of very simple auditory or visual stimuli (a tone and a cross) are in progress (Shankerdass, 2001), where the task is to respond to the frequent stimulus and ignore the infrequent. Early perception (magnocellular) and later processing (cerebellar) before deciding not to respond can be seen in the brain waves and will explain the relative contribution of these two deficits.

Possible impact of research outcomes to current and future policiesFor the first time in the UK, research in dyslexia has moved from an adversarial approach to recognition that dyslexia researchers are all working in the same direction, for the good of children with dyslexia. Rather than trying to establish which one theory is right, there is a growing recognition that all the theories are correct at least in part. If a consensus can be reached on the need to investigate major causal theories more systematically, there may be a real opportunity to influence policy and practice. Potential benefits might include:

10


a) Studies of the incidence of visual, phonological, speed and cerebellar deficits in poor readers and controls in the school population would indicate how many children show these problems with and without reading deficits, and the effect on standards generally.b) Protective factors, such as early letter knowledge and speed of processing, are beginning to be identified in children showing phonological or visual deficits who learn to read without undue difficulty. With greater knowledge these factors could be built into the school environment to help other less successful children.c) Identifying the causes of dyslexia can improve both the timing and the tuning of any intervention that might need to be delivered.

I shall return to these theories in December when presenting the 2nd review, on approaches to intervention.

Angela Fawcett, September 2001

11


Appendix 1

Research highlighted (published)

Gallagher, A., Frith, U., Snowling, M. J. (2000). Precursors of literacy delay among children at genetic risk of dyslexia. Journal of Child Psychology and Psychiatry and Allied Disciplines, 41, 2, 203-213.This paper reports the literacy skills of 63 children selected as bring at genetic risk of dyslexia compared with 34 children from families reporting no history of reading impairment. Fifty-seven per cent of the at-risk group were delayed in literacy development at 6 years compared with only 12 % of controls. The " unimpaired " at-risk group were not statistically different from controls on most cognitive and language measures at 45 months, whereas the literacy-delayed group showed significantly slower speech and language development, although they did not differ from controls in nonverbal ability. Letter knowledge at 45 months was the strongest predictor of literacy level at 6 years. In addition, early speech and language skills predicted individual differences in literacy outcome and genetic risk accounted for unique variance over and above these other factors. The results are discussed in terms of an interactive developmental model in which semantic and phonological skills support early reading acquisition.

Molfese, D. L. (2000). Predicting dyslexia at 8 years of age using neonatal brain responses. Brain and Language, 72,3 348-345.Auditory event-related potentials recorded at birth to speech and nonspeech syllables from six scalp electrodes discriminated between newborn infants who 8 years later would be characterized as dyslexic, poor, or normal readers. These findings indicate that reading problems can be identified and possible interventions undertaken up to 9 years earlier than is currently possible.

Snowling, M., Bishop, D. V. M., Stothard, S. E. (2000). Is preschool language impairment a risk factor for dyslexia in adolescence? Journal of Child Psychology and Psychiatry and Allied Disciplines, 41, 5, 587-600.The literacy skills of 56 school leavers from the Bishop and Edmundson (1987) cohort of preschoolers with specific language impairment (SLI) were assessed at 15 years. The SLI group performed worse on tests of reading, spelling, and reading comprehension than age-matched controls and the literacy outcomes were particularly poor for those with Performance IQ less than 100. The rate of specific reading retardation in the SLI group had increased between the ages of 8 1/2 and 15 years and there had been a substantial drop in reading accuracy, relative to age. However, over 35 % had reading skills within the normal range and those who had had isolated impairments of expressive phonology had a particularly good outcome, Our findings highlight the limitations of discrepancy definitions of dyslexia that do not take account of the changing demands of reading over time. We argue that children's phonological difficulties place them at risk of literacy failure at the outset of reading and that later, impairments of other language skills compromise development to adult levels of fluency.

Temple E, Poldrack RA, Salidis J, Deutsch GK, Tallal P, Merzenich MM, Gabrieli JDE (2001). Disrupted neural responses to phonological and orthographic processing in dyslexic children: an fMRI study, Neuroreport 12, 2, 299-307 Developmental dyslexia, characterized by difficulty in reading, has been associated with phonological and orthographic processing deficits. fMRI was performed on dyslexic and normal-reading children (8-12 years old) during phonological and orthographic taslts of rhyming and matching visually presented letter pairs. During letter rhyming, both normal and dyslexic reading children had activity in left frontal brain regions, whereas only normal-reading children had activity in left temporo-parietal cortex. During letter matching, normal reading children showed activity throughout extrastriate cortex, especially in occipito-parietal regions,whereas dyslexic children had little activity in extrastriate cortex during this task. These results indicate dyslexia may be characterized in childhood by disruptions in the neural bases of both phonological and orthographic processes important for reading.

Poldrack R. A, Temple E., Protopapas A., Nagarajan S., Tallal P., Merzenich M., Gabrieli J. D. E., (2001) Relations between the neural bases of dynamic auditory processing and phonological processing: Evidence from fMRI, Journal of Cognitive Neuroscience 13, 5, 687-697.Functional magnetic resonance imaging (fMRI) was used to examine how the brain responds ri, temporal compression of speech and to determine whether the same regions are also involved in phonological processes associated with reading. Recorded speech was temporally compressed to varying degrees anti presented in a

12


sentence verification task. Regions involved in phonological processing were identified in a separate scan using a rhyming judgment task with pseudo-words compared to a lettercase judgment task. The left inferior frontal and left superior temporal regions (Broca's and Wernicke's areas), along with the right inferior frontal cortex. demonstrated a convex response to speech compression; their activity increased as compression increased, but then decreased when speech became incomprehensible. Other regions exhibited linear increases in activity as compression increased, including the middle frontal gyri bilaterally. The auditory cortices exhibited compression-related decreases bilaterally, primarily reflecting a decrease in activity when speech became incomprehensible. Rhyme judgments engaged two left inferior frontal gyrusregions (pars triangularis and pars opercularis), of which only the pars triangularis region exhibited significant compression-related activity. These results directly demonstrate that a subset of the left inferior frontal regions involved in phonological processing is also sensitive to transient acoustic features within the range of comprehensible speech.

Talcott, JB, Witton, C, McLean, MF, Hansen, PC, Rees, A, Green, GGR, Stein, J (2000). Dynamic sensory sensitivity and children's word decoding skills. Proceedings of the National Academy of Sciences of the United States of America, 97, 6, 2952-2957The relationship between sensory sensitivity and reading performance was examined to test the hypothesis that the orthographic and phonological skills engaged in visual word recognition are constrained by the ability to detect dynamic visual and auditory events. A test battery using sensory psychophysics, psychometric tests, and measures of component literacy skills was administered to 32 unselected 10-year-old primary school children. The results suggest that children's sensitivity to both dynamic auditory and visual stimuli are related to their literacy skills. Importantly, after controlling for intelligence and overall reading ability, visual motion sensitivity explained independent variance in orthographic skill but not phonological ability, and auditory FM sensitivity covaried with phonological skill but not orthographic skill. These results support the hypothesis that sensitivity at detecting dynamic stimuli influences normal children's reading skills. Vision and audition separately may affect the ability to extract orthographic and phonological information during reading.

See Fawcett, A.J. (2001). Dyslexia: Theory and good practice. A series of chapters on the theoretical basis of dyslexia; Stein, Talcott and Witton on the magnocellular system, Nicolson and Fawcett on the cerebellum and learning (including evoked potentials); Wolf on speed of processing; van der Leij and Lyytinen on the infant studies, and Fisher et al on the genetics.

13


References

Bradley, L. & Bryant, P.E. (1983). Categorising sounds and learning to read: A causal connection. Nature, 301, 419-421

Denckla, M. B., & Rudel, R. G. (1976a). Rapid 'Automatized' naming (R.A.N.). Dyslexia differentiated from other learning disabilities. Neuropsychologia, 14, 471-479.

Eden, G.F., Vanmeter, J.W., Rumsey, J.M., Maisog, J.M., Woods, R.P. & Zeffiro, T.A. (1996). Abnormal processing of motion in dyslexia revealed by functional brain imaging. Nature, 382, 66-69.

Fawcett, A. J, Nicolson, R. I. & Dean, P. (1996). Impaired performance of children with dyslexia on a range of cerebellar tasks. Annals of Dyslexia , 46, 259-283.

Fawcett, A. J. & Nicolson, R. I. (1999). Performance of dyslexic children on cerebellar and cognitive tests. Journal of Motor Behavior, 31, 68-78.

Fawcett, A.J., Maclagan, F and Nicolson, R. I (2001). Cerebellar tests differentiate between poor readers with and without IQ discrepancy. Journal of Learning Disabilities, 34, 2, 119-135.

Finch, A.J., Nicolson, R.I., and Fawcett, A.J. (2001). Evidence for an anatomical difference within the cerebella of dyslexic brains. Submitted to Cortex

Frith, U. (1997). Brain, mind and behaviour in dyslexia. In C. Hulme and M. Snowling (Eds.), Dyslexia: Biology, cognition and intervention. Whurr: London.

Fulbright, R. K., Jenner, A. R., Mencl, W. E., Pugh, K. R., Shaywitz, B. A., Shaywitz, S. E., Frost, S. J., Skudlarski, P., Constable, R. T., Lacadie, C. M., Marchione, K. E., & Gore, J. C. (1999). The cerebellum's role in reading: A functional MR imaging study. American Journal of Neuroradiology, 20, 1925-1930.

Galaburda, A.M., Menard, A.M. and Rosen, G.D. (1994). Evidence for aberrant auditory anatomy in developmental dyslexia. Proceedings of the National Academy of Sciences of the USA, 91, 8010-8013.

Ivry, R.B. and Keele, S.W. (1989). Timing functions of the cerebellum. Journal of Cognitive Neuroscience, 1, 136-152.

Livingstone, M.S., Rosen, G.D., Drislane, F.W., & Galaburda, A.M. (1991). Physiological and anatomical evidence for a magnocellular deficit in developmental dyslexia. Proceedings of the National Academy of Sciences of the USA, 88, 7943-7947

Lovegrove, W. J., Garzia, R. P., & Nicholson, S. B. (1990) Experimental evidence of a transient system deficit in specific reading disability. Journal of the American Optometric Association, 61, 137-146.

Nicolson, R.I and Fawcett, A.J. (1990). Automaticity: a new framework for dyslexia research? Cognition, 30, 159-182.

Nicolson, R.I and Fawcett, A.J. (1994a). Reaction Times and Dyslexia. Quarterly Journal of Experimental Psychology: 47A, 29-48.

Nicolson, R.I. and Fawcett, A.J. (1994b). Comparison of deficits in cognitive and motor skills in children with dyslexia. Annals of Dyslexia, 44, 147-164.

Nicolson, R.I., Fawcett, A.J. and Dean, P. (1995). Time estimation deficits in developmental dyslexia: Evidence for cerebellar involvement. Proceedings of the Royal Society: Biological Sciences, 259, 43-47.

Nicolson, R.I., Fawcett, A.J., Berry, E.L., Jenkins, H., Dean, P. and Brooks, D.J. (1999). Association of abnormal cerebellar activation with motor learning difficulties in dyslexic adults.The Lancet, 353, 1162-7.

14


Nicolson, R.I., Fawcett, A.J., & Dean, P. (2001). Developmental dyslexia: The cerebellar deficit hypothesis. Trends in Neurosciences. 24, 506-514.

Nicolson, R. I., Daum, I., Schugens, M. M., Fawcett, A. J., & Schulz, A. (2001). Abnormal eyeblink conditioning for dyslexic children. Experimental Brain Research, submitted

Paulesu, E., Frith, U., Snowling, M., Gallagher, A., Morton, J., Frackowiak, R. S. J., & Frith, C. D. (1996). Is developmental dyslexia a disconnection syndrome? Evidence from PET scanning. Brain, 119, 143-157

Skottun, B. C. The magnocellular deficit theory of dyslexia: the evidence from contrast sensitivity. Vision Research, 40, 111-127.

Snowling, M. (1995). Phonological processing and developmental dyslexia. Journal of Research in Reading, 18, 132-138

Stein, J. and Walsh, V. (1997). To see but not to read: the magnocellular theory of dyslexia. Trends in Neuroscience, 20, 147-152.

Stein, J. (2000). The neurobiology of reading difficulties. Prostaglandins Leukotrienes and Essential Fatty Acids, 63, 109-116.

Talcott, J. B., Hansen, P. C., Willis-Owen, C., McKinnell. I. W., Richardson. A. F., and Stein, J. F. (1998). Visual magnocellular impairment in adult developmental dyslexics. Neuro-opthalmology, 20, 187-201.

Tallal, P., Miller, S. and Fitch, R.H. (1993). Neurological basis of speech: A case of the preeminence of temporal processing. Annals of the New York Academy of Sciences, 682, 27-47.

Tallal, P., Merzenich, M. M., Miller, S., & Jenkins, W. (1998). Language learning impairments: integrating basic science, technology, an d remediation. Experimental Brain Research, 123, 210-219

Wolf, M. and Bowers, P.G. (1999). The double-deficit hypothesis for the developmental dyslexias. Journal of Educational Psychology, 91,415-438.

Index of archived material

Web of science Search Dyslexia DfES, stored as an Endnote resource.

BDA full abstracts. A complete database of abstracts submitted and accepted for the recent BDA International conference in York, April 2001

BDA speaker’s e-mail list. A complete list of speakers from the recent BDA International conference in York, April 2001.

E-mail list of responses from speakers to invitation

15

Documents

Recent research and development in dyslexia in · Web viewIn educational terms, this means that children with dyslexia need longer to read a word that is familiar to them (van der