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PubMedDate not supplied

Outstanding questions about phonological processing in dyslexia.

It is widely accepted that developmental dyslexia results from some sort of phonological deficit. Yet, it can be argued that phonological representations and their processing have been insufficiently tested in dyslexia research. Firstly, claims about how tasks tap into certain kinds of representations or processes are best appreciated in the light of an explicit information-processing model. Here, a cognitive model of lexical access is described, incorporating speech perception, reading and object recognition. The model emphasizes that phonological forms of lexical items are distinct from non-lexical phonological representations. Secondly, phonology, as a linguistic discipline, teaches us that there is much more to it than phonemic categorization and awareness. The phonological level of representation also embodies phonotactic regularities, patterns of phoneme assimilation and alternation, as well as supra-segmental knowledge pertaining to syllable structure, stress, intonation and rhythm. All these aspects are in part language-dependent, and therefore must be learnt by children in order to become proficient native speakers and listeners. If phonological representations were affected in dyslexia, dyslexic children would presumably have difficulties acquiring these aspects of their language. This prediction is as yet untested. A possible research agenda is outlined, aiming to provide a more comprehensive assessment of the phonological theory of dyslexia.

Child↗
PubMedDate not supplied

Comments on 'The dyslexia ecosystem': a reply to Nicolson.

The central issue facing the dyslexia community, and the underlying theme of Nicolson's 'The Dyslexia Ecosystem' (Nicolson, 2002, Dyslexia, 8, 55-66), is how we can best translate what we know about this particular developmental disorder into practice to give each child the greatest opportunity of acquiring the enabling skill of literacy. To achieve this, and notwithstanding Nicolson's caveat on this point, we have to consider how we can best move from our sphere of expertise to a greater sphere of influence, both as individuals and as a community of research practitioners. In our response, we first consider aspects of Nicolson's general analysis of 'The Dyslexia Ecosystem' and then examine some of the specific objectives that have been proposed.

Dyslexia↗
PubMed2004

Early language development in children with a genetic risk of dyslexia.

We report on a prospective longitudinal research programme exploring the connection between language acquisition deficits and dyslexia. The language development profile of children at-risk for dyslexia is compared to that of age-matched controls as well as of children who have been diagnosed with specific language impairment (SLI). The experiments described concern the perception and production of grammatical morphology, categorical perception of speech sounds, phonological processing (non-word repetition), mispronunciation detection, and rhyme detection. The results of each of these indicate that the at-risk children as a group underperform in comparison to the controls, and that, in most cases, they approach the SLI group. It can be concluded that dyslexia most likely has precursors in language development, also in domains other than those traditionally considered conditional for the acquisition of literacy skills. The dyslexia-SLI connection awaits further, particularly qualitative, analyses.

Child, Preschool↗
PubMed2004

Early development of children at familial risk for dyslexia--follow-up from birth to school age.

We review the main findings of the Jyväskylä Longitudinal study of Dyslexia (JLD) which follows the development of children at familial risk for dyslexia (N = 107) and their controls (N = 93). We will illustrate the development of these two groups of children at ages from birth to school entry in the skill domains that have been connected to reading and reading disability in the prior literature. At school entry, the highest score on the decoding task among the poorer half (median) of the at risk children--i.e. of those presumably being most likely genetically affected--is 1 SD below the mean of the control group. Thus, the familial risk for dyslexia shows expected consequences. Among the earliest measures in which group differences as well as significant predictive associations with the first steps in reading have emerged, are indices of speech processing in infancy. Likewise, various measures of early language including pronunciation accuracy, phonological, and morphological skills (but not performance IQ) show both group differences and predictive correlations, the majority of which become stronger as the reliability of the measures increases by age. Predictive relationships tend to be strong in general but higher in the at risk group because of its larger variance in both the predictor variables and in the dependent measures, such as early acquisition of reading. The results are thus promising in increasing our understanding needed for early identification and prevention of dyslexia.

Child↗
PubMed2005

Identification, assessment and intervention--Implications of an audit on dyslexia policy and practice in Scotland.

This article reports on research commissioned by the Scottish Executive Education Department (SEED). It aimed to establish the range and extent of policy and provision in the area of specific learning difficulties (SpLD) and dyslexia throughout Scotland. The research was conducted between January and June 2004 by a team from the University of Edinburgh. The information was gathered from a questionnaire sent to all education authorities (100% response rate was achieved). Additional information was also obtained from supplementary interviews and additional materials provided by education authorities. The results indicated that nine education authorities in Scotland (out of 32) have explicit policies on dyslexia and eight authorities have policies on SpLD. It was noted however that most authorities catered for dyslexia and SpLD within a more generic policy framework covering aspects of Special Educational Needs or within documentation on 'effective learning'. In relation to identification thirty-six specific tests, or procedures, were mentioned. Classroom observation, as a procedure was rated high by most authorities. Eleven authorities operated a formal staged process combining identification and intervention. Generally, authorities supported a broader understanding of the role of identification and assessment and the use of standardized tests was only part of a wider assessment process. It was however noted that good practice in identification and intervention was not necessarily dependent on the existence of a dedicated policy on SpLD/dyslexia. Over fifty different intervention strategies/programmes were noted in the responses. Twenty-four authorities indicated that they had developed examples of good practice. The results have implications for teachers and parents as well as those involved in staff development. Pointers are provided for effective practice and the results reflect some of the issues on the current debate on dyslexia particularly relating to early identification.

Aptitude Tests↗
PubMed2005

The subtypes of developmental dyslexia in Chinese: evidence from three cases.

This study investigated subtypes of developmental dyslexia in Chinese by assessing three cases of Chinese dyslexic children. A battery of screening measures, a character naming and meaning task, and metalinguistic awareness tasks were administered to each child. One of the three children demonstrated characteristics of developmental surface dyslexia, and the other two showed characteristics of developmental deep dyslexia. Moreover, the children's reading problems were found to be specifically related to their deficits in metalinguistic awareness. The dissociation between developmental surface and deep dyslexia provides support to Weekes et al.'s (Neurocase 1997; 3: 51-60) model that a semantic and a nonsemantic pathway exist independently in Chinese reading. The results also suggest that deficits in morphological and phonological awareness may cause developmental delays in the semantic and the nonsemantic pathway.

Adolescent↗
PubMed2000

Deep dyslexia is right-hemisphere reading.

Two views exist concerning the proper interpretation of the form of acquired dyslexia known as deep dyslexia: (a) that it represents reading by a multiply damaged left hemisphere reading system; (b) that it represents reading which relies extensively on right-hemisphere orthographic and semantic processing. Price, Howard, Patterson, Warburton, Friston, and Frackowiak (1998) have recently reported a brain-imaging study whose results, they claim, "preclude an explanation of deep dyslexia in terms of purely right-hemisphere word processing." Their claim conflicts with the conclusions of previous published work, which strongly supports the RH hypothesis, work which they do not mention. Furthermore, I argue that their own results also favor the RH hypothesis (even though they claim otherwise); indeed, their results permit the formulation of a much more detailed version of the RH hypothesis than has hitherto been possible. Hence I conclude that the right-hemisphere interpretation of deep dyslexic reading remains the preferred explanation of deep dyslexia.

Brain↗
PubMed2001

The simultaneous activation hypothesis: explaining recovery from deep to phonological dyslexia.

Deep dyslexia evolved into phonological dyslexia in one patient. Semantic errors resolved while phonological and derivational errors persisted in reading. Nonword reading improved but remained inferior to word reading. Despite a residual semantic deficit naming improved. The Simultaneous Activation Hypothesis explains recovery from deep to phonological dyslexia and the continued dissociation between reading and naming errors. Partial recovery to all three reading routes increased constraints for word selection at the phonological output lexicon (POL) improving word reading. With recovery, the POL receives additional supportive information from the partially recovered direct oral reading route and grapheme-to-phoneme conversion (GPC) eliminating semantic errors in oral reading. Nonword reading also improved because of partial recovery to all three routes. Semantic errors in naming persisted because additional constraints were unavailable at the POL to activate a phonological entry. Phonological and derivational errors were more frequent in reading than in naming the result of incomplete GPC recovery. Residual nonword reading deficits resulted from incomplete GPC recovery, indicated by the persistence of neologisms in nonwords. The Simultaneous Activation Hypothesis readily accounts for the evolution from deep to phonological dyslexia.

Adult↗
PubMed1999

Genetic linkage analysis with dyslexia: evidence for linkage of spelling disability to chromosome 15.

Dyslexia (reading and spelling disability) is one of the most frequently diagnosed disorders in childhood. Twin studies of dyslexia have indicated that deficits in spelling are substantially heritable and that the heritability of spelling deficits is higher than the heritability of reading deficits. We conducted a linkage study for spelling disability in seven multiplex families from Germany. Following previously reported linkage findings of components of dyslexia to chromosome 6p21-p22 and 15q21, we genotyped 26 microsatellite markers covering all of chromosome 6, and 13 microsatellite markers covering all of chromosome 15. While the chromosome 6 data were negative, results from chromosome 15 markers supported a locus on 15q21. The highest two-point LOD score was 1.26 with marker D15S143 at theta = 0. A multipoint LOD score of 1.78 (p = 0.0042) was achieved with a maximum at D15S132. Thus, our results provide independent support for a dyslexia gene on the long arm of chromosome 15.

Child↗
PubMed2002

Eyeblink conditioning indicates cerebellar abnormality in dyslexia.

There is increasing evidence that cerebellar deficit may be a causal factor in dyslexia. The cerebellum is considered to be the major structure involved in classical conditioning of the eyeblink response. In a direct test of cerebellar function in learning, 13 dyslexic participants (mean age 19.5 years) and 13 control participants matched for age and IQ undertook an eyeblink conditioning experiment in which for 60 acquisition trials an 800-ms auditory tone (conditioned stimulus, CS) was presented. On 70% of the trials an 80-ms corneal airpuff (unconditioned stimulus, US) was presented 720 ms after the tone onset. The cerebellar deficit hypothesis, uniquely of the causal hypotheses for dyslexia, predicts that the dyslexic participants would show abnormal performance in the incidence and/or timing of the conditioned response (CR) of an eyeblink in response to the tone (and before the US). Three of the dyslexic group showed no conditioning at all. Furthermore, the dyslexic group showed significantly worse "tuning" of the CR timing, together with significantly reduced habituation of the orienting response (OR) to the CS. Individual analyses indicated that 85% of the dyslexic group showed either no conditioning or abnormally poor CR tuning and/or abnormally low OR habituation. It is concluded that the findings provide further converging evidence of cerebellar abnormality in dyslexia and for the first time demonstrate that there are fundamental abnormalities in the way that dyslexic people learn. Equally important, the eye blink conditioning paradigm provides a method of investigating further both homogeneity and heterogeneity in the learning deficits underlying dyslexia and other developmental disorders.

Adolescent↗
PubMed2005

TDT-association analysis of EKN1 and dyslexia in a Colorado twin cohort.

A candidate gene, EKN1, was recently described in a cohort from Finland for the dyslexia locus on chromosome 15q, DYX1. This report described a (2;15) (q11;21) translocation disrupting EKN1 that cosegregated with dyslexia in a two-generation family. It also characterized a sequence polymorphism in the 5' untranslated region and a missense mutation that showed significant association in 109 dyslexics compared to 195 controls (p=0.002 and p=0.006, respectively). To confirm these results we interrogated the same polymorphisms in a cohort of 150 nuclear families with dyslexia ascertained through the Colorado Learning Disabilities Research Center. Using QTDT analysis with nine individual quantitative tasks and two composite measures of reading performance, we could not replicate the reported association. We conclude that the polymorphisms identified in the Finland sample are unlikely to be functional DNA changes contributing to dyslexia, and that if variation in EKN1 is causal such changes are more likely to be in regulatory regions that were not sequenced in this study. Alternatively, the published findings of association with markers in EKN1 may reflect linkage disequilibrium with variation in another gene(s) in the region.

Base Sequence↗
PubMed2004

Large-scale neural correlates of developmental dyslexia.

Recent work in the field of developmental dyslexia has emphasized the large-scale neural aspects of the disorder as measured by means of contemporary imaging techniques, electrophysiology, and post-mortem analyses. This article presents findings from these research domains and comprehensively reviews their relevance with respect to the behavioral and cognitive profiles of dyslexia. Large-scale alterations were observed in the perisylvian region across paradigms. Convergent evidence has also been reported in terms of hemispheric balance. Specifically, deviances in cerebral asymmetry associated with atypical organization of the left hemisphere were found in both children and adults with dyslexia. Emerging research encompassing high-temporal resolution methods such as magnetoencephalography (MEG) suggests right-hemisphere involvement and points to the complexity of the developmental disorder. A combined approach of structural imaging and MEG, and most importantly theory driven behavioral tasks may shed light on dynamics and trajectories of the neurobiology of dyslexia.

Adult↗
PubMed2006

Developmental dyslexia: an update.

Dyslexia is the most common and carefully studied of the learning disabilities in school-age children. It is characterized by a marked impairment in the development of reading skills, and affects a large number of people (5-10%). Reading difficulties may also arise from poor vision, emotional problems, decreased hearing ability, and behavioral disorders, such as attention-deficit hyperactivity (ADHD). Although many areas of the brain are involved in reading, analysis of postmortem brain specimens by a variety of imaging techniques most consistently suggests that deficiency within a specific component of the language system - the phonologic module - in the temporo-parietal-occipital brain region underlies dyslexia. It is a highly familial and heritable disorder with susceptibility loci on chromosomes 1, 2, 3, 6, 11, 13, 15 and 18. Recently, four candidate genes (KIAA 0319, DYX1C1, DCDC2 and ROBO1) are shown to be associated with dyslexia. Although some of these results are controversial because of the genetic heterogeneity of the disorder, the available evidence suggests that dyslexia could be due to the abnormal migration and maturation of neurons during early development. Interestingly, in spite of genetic heterogeneity, the pathology appears to involve common phonological coding deficits. The condition can be managed by a highly structured educational training exercise.

Child↗
PubMed2004

The development of children at familial risk for dyslexia: birth to early school age.

Children at risk for familial dyslexia (n = 107) and their controls (n = 93) have been followed from birth to school entry in the Jyvaskyla Longitudinal study of Dyslexia (JLD) on developmental factors linked to reading and dyslexia. At the point of school entry, the majority of the at-risk children displayed decoding ability that fell at least 1 SD below the mean of the control group. Measures of speech processing were the earliest indices to show both group differences in infancy and also significant predictive associations with reading acquisition. A number of measures of language, including phonological and morphological skill collected repeatedly from age three, revealed group differences and predictive correlations. Both the group differences and the predictive associations to later language and reading ability strengthened as a function of increasing age. The predictions, however, tend to be stronger and the spectrum of significant correlations wider in the at-risk group. These results are crucial to early identification and intervention of dyslexia in at-risk children.

Case-Control Studies↗
PubMed1994

An investigation of some sensory and refractive visual factors in dyslexia.

The role of visual factors in dyslexia has been a long-standing source of controversy. Recent research has suggested that there may be a deficit of the transient visual subsystem in dyslexia. The evidence for this hypothesis comes principally from investigations of spatial and temporal contrast sensitivity and visual persistence. This evidence is reviewed and it is noted that previous work has never applied two of these purported "tests of transient function" to the same subject group. The hypothesised transient system deficit in dyslexia was investigated in a study comparing 43 control with 39 dyslexic children who were matched for age, sex, and intelligence. Comprehensive psychometric and optometric data were obtained, including visual acuities and refractive errors. The spatial contrast sensitivity function was determined in such a way as to investigate further the findings of Lovegrove, Martin, Bowling, Blackwood, Badcock and Paxton [(1982) Neuropsychology, 20, 309-315] and Martin and Lovegrove [(1984) Neuropsychologia, 22, 73-77]. It might be expected, from the work of Merigan and Maunsell [(1990) Neuroscience, 5, 347-352], that a better test of magno-cellular function would be to investigate the modulation threshold for a virtually uniform field that was flickering sinusoidally at 10 Hz. This temporal contrast sensitivity was studied in a similar way to Brannan and Williams [(1988) Clinical Vision Sciences, 3, 137-142]. A non-verbal simulated reading visual search task was used to investigate the effect of any visual deficits on a test that was, in its low-level visual requirements, similar to reading. The following factors were found to be significantly associated with dyslexia: reduced visual acuity, impaired flicker detection at 10 Hz, reduced low spatial frequency contrast sensitivity, and slightly slower performance at a simulated reading visual search task. The two alleged "tests of transient function" were only weakly correlated with one another (r = 0.183), suggesting that these variables do not measure the same function. Much of the dyslexic group's slightly slower performance at the simulated reading task could be accounted for by the psychometric variable of visual sequential memory. Like reading, the simulated reading task requires the accurate perception of sequential characters. Hence, it seems unlikely that the low-level visual deficits in the dyslexic group were major causes of their poor reading performance. Alternative explanations for the results are discussed.

Child↗
PubMed1988

Red is read but eye is blue: a case study of developmental dyslexia and follow-up report.

Recently, analogies have been drawn between the developmental and acquired dyslexias, but there has been no unequivocal report of developmental deep dyslexia. The case is reported here of a 9-year-old child whose reading performance resembles deep dyslexia in several ways. The incidence of errors with a semantic component is shown to be significantly above chance. The pattern of errors is discussed in relation to recent data on error patterns in normal beginning readers. Text reading, spelling, naming, and repetition are described. In contrast to previous case reports, follow-up data are presented which chart the qualitative changes in performance over time despite relatively little quantitative change. The child described has several specific handicaps. Developmental deep dyslexia may not be a prevalent subtype because the multiple impairments necessary to produce the disorder seldom co-occur and may tend to preclude reading development altogether.

Child↗
PubMed2005

Detection of sound rise time by adults with dyslexia.

Low sensitivity to amplitude modulated (AM) sounds is reported to be associated with dyslexia. An important aspect of amplitude modulation cycles are the rise and fall times within the sound. In this study, simplified stimuli equivalent to just one cycle were used and sensitivity to varying rise times was explored. Adult participants with dyslexia or compensated dyslexia and a control group performed a detection task with sound pairs of different rise times. Results showed that the participants with dyslexia differed from the control group in rise time detection and a correlation was found between rise time detection and reading and phonological skills. A subgroup of participants with lower sensitivity to rise time detection characterized by low accuracy in syllable-level phonological skills was found within the dyslexic group. Short stimuli containing only one rise time produced associations with phonological skills and reading, even in a language where the perception of rise time contrasts are not crucial for the signaling of phonemic contrast.

Acoustic Stimulation↗
PubMed2005

Do differences in brain activation challenge universal theories of dyslexia?

It has been commonly agreed that developmental dyslexia in different languages has a common biological origin: a dysfunction of left posterior temporal brain regions dealing with phonological processes. Siok, Perfetti, Jin, and Tan (2004, Nature, 431, 71-76) challenge this biological unity theory of dyslexia: Chinese dyslexics show no deficits in posterior temporal brain regions but a functional disruption of the left middle frontal gyrus. Here, I will argue that these data do not challenge universal cognitive theories of dyslexia according to which weaknesses in the ability to process the phonological features of language are at the origin of dyslexia.

Asian People↗