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PubMed1999

A candidate phenotype for familial dyslexia.

The probative analysis of genotype-phenotype relations in familial dyslexia requires operationally defined psychobiological outcome variables that are not confounded by cultural differences of orthography or other factors that may influence the clinical ascertainment and diagnosis of dyslexia. Timing precision, as expressed in coordinated motor action, was used as an objective behavioral measure that can be mapped on current knowledge of central nervous system functions as well as on the most salient non-reading deficits in developmental dyslexia. Dyslexia families with four distinct pedigrees and a normally reading reference group were the study subjects. The results indicated that impaired timing precision in bimanual coordination and in motor speech were transmitted vertically in affected members of about half of dyslexia families. Motor coordination deficits were associated with a disposition to make dysphonemic spelling errors. It is proposed that impaired timing precision identifies a behavioral phenotype in some familial dyslexia subtypes. The detailed analysis of coarticulation in speech production may be one pathway by which impaired timing precision in motor action impinges on reading and writing deficits in developmental dyslexia.

Adolescent↗
PubMed2005

Clinicians and dyslexia--a computer-based assessment of one of the key cognitive skills involved in drug administration.

AIMS: This research investigates the relationship between dyslexia traits and nurse performance on a laboratory task designed to assess one of the key cognitive skills involved in drug administration. The potential moderating role of perceived performance control was also assessed, based on previous work demonstrating the importance of self-belief as a facilitator of vocational success. BACKGROUND: Dyslexia within the health care professions has been the subject of wide and emotionally charged debate but has not yet been scientifically examined. Those who fear clinicians with dyslexia do so because of a presumed or potential risk to patient health and safety posed by dyslexia-induced performance error (e.g. problems with drug administration). DESIGN, SAMPLE AND METHODS: 46 nurses (40 student nurses and 6 qualified nurses) volunteered to complete a battery of computerised tasks assessing for dyslexia traits (using four accuracy tasks measuring different types of literacy skill), a paired association task designed to measure one of the key cognitive skills involved in drug administration) and a self-report questionnaire (Learning Styles Questionnaire, self-reported reading difficulty and a history of educational support, perceived control over performance). The performance criterion measure was constructed after detailed job analysis (involving analysis of official documentation, in-depth interviews and field observation across a variety of clinical settings) and involved matching drug names to patient names and vice versa. RESULTS: The results showed that the dyslexia indicators (objective and self-report) were significantly correlated with performance on the paired association task. Contrary to expectation however, the perceived control variable was not associated with performance. CONCLUSION: The findings provide tentative support for the idea that some tasks might be problematic for the clinician with dyslexia. Taken in isolation however, it would be inappropriate to conclude that this will necessarily translate into true performance errors without taking into consideration the entire performance context. Suggestions are made for replicating and extending the study to provide a more solid and constructive basis for intervention (e.g. support measures, a built-in checking process).

Adaptation, Psychological↗
PubMed2003

Dyslexia linked to talent: global visual-spatial ability.

Dyslexia has long been defined by deficit. Nevertheless, the view that visual-spatial talents accompany dyslexia has grown, due to reports of individuals with dyslexia who possess visual-spatial strengths, findings of elevated incidence of dyslexia in certain visual-spatial professions, and the hypothesis that left-hemisphere deficits accompany right-hemisphere strengths. Studies have reported superior, inferior, and average levels of visual-spatial abilities associated with dyslexia. In two investigations, we found an association between dyslexia and speed of recognition of impossible figures, a global visual-spatial task. This finding suggests that dyslexia is associated with a particular type of visual-spatial talent-enhanced ability to process visual-spatial information globally (holistically) rather than locally (part by part).

Aptitude↗
PubMed2004

Familial cancer and developmental dyslexia: an observational pilot study.

The aim of the study was to test the hypothesis that raised platelet-activating factor (PAF) may contribute to the aetiology of developmental dyslexia. PAF is a potent proinflammatory mediator which signals cell damage and facilitates natural killer cell activity. Raised PAF may help protect against tumourigenesis. As dyslexia has a partial genetic basis, the PAF hypothesis predicts that dyslexia may be negatively associated with a family history of cancer. To test this prediction, children with dyslexia (n=163) and children without dyslexia (n=154), with (n=152) and without (n=165) a family history of cancer (total n=317; mean age 11 years 5 months, SD 2 years 11 months), were compared on standard psychometrics (British Ability Scales subtests). Results showed that proportionately fewer children with dyslexia (38%) than controls (58.4%) had a family history of cancer, and there was some evidence of a 'dose' effect: children who had more relatives with cancer showed better reading and spelling. It was concluded that children at genetic risk of dyslexia who have a family history of cancer have better reading and spelling than those without a family history of cancer, confirming the prediction of the PAF hypothesis.

Adolescent↗
PubMedDate not supplied

Visual half-field contrast sensitivity in children with dyslexia.

We address the question whether left-hemispheric and/or right-hemispheric contrast thresholds differ between children with dyslexia and controls, and whether there are interhemispheric differences. In order to answer these questions we examined [1] thresholds for the detection of Contrast-Defined (CD) forms to left and right half-field stimulation, and [2] half-field pattern onset Evoked Potentials (EPs) as a function of stimulus contrast in 21 children with dyslexia of 8-15 years of age and in 17 age-matched healthy controls. It was found that (A) children with dyslexia were less sensitive to CD forms than controls irrespective of half field of stimulation. In children with dyslexia as well as controls the forms were more easily detected in the right visual half-field than in the left one: (B) Peak latencies of the pattern onset EPs to contrast levels above 20% were up to 10 ms longer in children with dyslexia than in controls irrespective of half field of stimulation, and (C) children with dyslexia had smaller mean amplitudes for all contrast levels used. (D) Neither children with dyslexia nor controls showed hemispheric differences in the pattern onset EPs.

Adolescent↗
PubMed2004

In search of the auditory, phonetic, and/or phonological problems in dyslexia: context effects in speech perception.

There is a growing consensus that developmental dyslexia is associated with a phonological-core deficit. One symptom of this phonological deficit is a subtle speech-perception deficit. The auditory basis of this deficit is still hotly debated. If people with dyslexia, however, do not have an auditory deficit and perceive the underlying acoustic dimensions of speech as well as people who read normally, then why do they exhibit a categorical-perception deficit? A potential answer to this conundrum lies in the possibility that people with dyslexia do not adequately handle the context-dependent variation that speech signals typically contain. A mathematical model simulating such a sensitivity deficit mimics the speech-perception deficits attributed to dyslexia. To assess the nature of the dyslexic problem, the authors examined whether children with dyslexia handle context dependencies in speech differently than do normal-reading individuals. Contrary to the initial hypothesis, children with dyslexia did not show less context sensitivity in speech perception than did normal-reading individuals at auditory, phonetic, and phonological levels of processing, nor did they reveal any categorization deficit. Instead, intrinsic properties of online phonological processes, not phonological representations per se, may be impaired in dyslexia.

Acoustic Stimulation↗
PubMed2004

Genomewide scan identifies susceptibility locus for dyslexia on Xq27 in an extended Dutch family.

CONTEXT: Dyslexia is a common disorder with a strong genetic component, but despite significant research effort, the aetiology is still largely unknown. OBJECTIVE: To identify loci contributing to dyslexia risk. METHODS: This was a genomewide linkage analysis in a single large family. Dutch families with at least two first degree relatives suffering from dyslexia participated in the study. Participants were recruited through an advertisement campaign in papers and magazines. The main outcome measure was linkage between genetic markers and dyslexia phenotype. RESULTS: Using parametric linkage analysis, we found strong evidence for a locus influencing dyslexia on Xq27.3 (multipoint lod = 3.68). Recombinations in two family members flanked an 8 cM region, comprising 11 currently confirmed genes. All four males carrying the risk haplotype had very low scores on the reading tests. The presentation in females was more variable, but 8/9 females carrying the risk haplotype were diagnosed dyslexic by our composite score, so we considered the putative risk allele to be dominant with reduced penetrance. Linkage was not found in an additional collection of affected sibling pairs. CONCLUSIONS: A locus influencing dyslexia risk is probably located between markers DXS1227 and DXS8091 on the X chromosome, closely situated to a locus indicated by a published genome scan of English sibling pairs. Although the locus may not be a common cause for dyslexia, the relatively small and gene poor region offers hope to identify the responsible gene.

Adolescent↗
PubMedDate not supplied

Visual-spatial strength in dyslexia: rapid discrimination of impossible figures.

It has often been conjectured that visual-spatial talents accompany dyslexia. But do individuals with dyslexia have unusual visual-spatial talents? Individuals with dyslexia were compared to controls on two computer-based visual-spatial tasks in two studies. In accordance with a diverging ability hypothesis, it was predicted that the dyslexia group would perform better on a global task, identifying impossible figures, and worse on a feature-oriented task, matching figures. These hypotheses were partially supported. On the global task, the dyslexia group was faster but no more accurate than the control group at identifying impossible objects. On the feature-oriented task, the control group outperformed the dyslexia group. The results indicate that the diverging ability hypothesis of dyslexia merits further investigation.

Adolescent↗
PubMed1995

Hemisphere-specific treatment of dyslexia subtypes: better reading with anxiety-laden words?

Twenty children (12 boys, 8 girls; mean age = 10.4 years) with P-type dyslexia (accurate but slow and fragmented reading) and 20 children (12 boys, 8 girls; mean age = 10.3 years) with L-type dyslexia (hurried, inaccurate reading) were treated with visual hemisphere-specific stimulation employing the HEMSTIM computer program. Stimulation was produced by presenting words to the left (L-dyslexia) or to the right (P-dyslexia) visual field. Children in the control condition received treatment with neutral words, whereas children in the experimental condition received treatment with anxiety-laden words. After treatment, the children with L-dyslexia in the experimental group made fewer substantive errors and more fragmentations on a text-reading task than did the children with L-dyslexia in the control group. The results are explained as being the consequence of additional activation of the right hemisphere caused by the anxiety-laden words. It is concluded that children with L-dyslexia can benefit from the use of such words in the HEMSTIM program.

Anxiety↗
PubMed2004

Psychophysical indexes of temporal processing abnormalities in children with developmental dyslexia.

Children with dyslexia and children progressing normally in reading performed several perceptual tasks to determine (a) the psychophysical measures that best differentiate children with dyslexia from children with average reading abilities; (b) the extent of temporal processing deficits in a single, well-defined group of children with dyslexia; and (c) the co-occurrence of visual and auditory temporal processing deficits in children with dyslexia. 4 of our 12 psychophysical tasks indicated differences in temporal processing ability between children with dyslexia and children with good reading skills. These included 2 auditory tasks (dichotic pitch perception and FM tone discrimination) and 2 visual tasks (global motion perception and contrast sensitivity). The battery of 12 tasks successfully classified 80% of the children into their respective reading-level groups. Within the group of children with dyslexia who had temporal processing deficits, most were affected in either audition or vision; few children were affected in both modalities. The observed deficits suggest that impaired temporal processing in dyslexia is most evident on tasks that require the ability to synthesize local, temporally modulated inputs into a global percept and the ability to extract the resultant global percept from a noisy environment.

Adolescent↗
PubMed2003

Instructional treatment associated with changes in brain activation in children with dyslexia.

OBJECTIVE: To assess the effects of reading instruction on fMRI brain activation in children with dyslexia. BACKGROUND: fMRI differences between dyslexic and control subjects have most often involved phonologic processing tasks. However, a growing body of research documents the role of morphologic awareness in reading and reading disability. METHODS: The authors developed tasks to probe brain activation during phoneme mapping (assigning sounds to letters) and morpheme mapping (understanding the relationship of suffixed words to their roots). Ten children with dyslexia and 11 normal readers performed these tasks during fMRI scanning. Children with dyslexia then completed 28 hours of comprehensive reading instruction. Scans were repeated on both dyslexic and control subjects using the same tasks. RESULTS: Before treatment, children with dyslexia showed less activation than controls in left middle and inferior frontal gyri, right superior frontal gyrus, left middle and inferior temporal gyri, and bilateral superior parietal regions for phoneme mapping. Activation was significantly reduced for children with dyslexia on the initial morpheme mapping scan in left middle frontal gyrus, right superior parietal, and fusiform/occipital region. Treatment was associated with improved reading scores and increased brain activation during both tasks, such that quantity and pattern of activation for children with dyslexia after treatment closely resembled that of controls. The elimination of group differences at follow-up was due to both increased activation for the children with dyslexia and decreased activation for controls, presumably reflecting practice effects. CONCLUSION: These results suggest that behavioral gains from comprehensive reading instruction are associated with changes in brain function during performance of language tasks. Furthermore, these brain changes are specific to different language processes and closely resemble patterns of neural processing characteristic of normal readers.

Adolescent↗
PubMed1999

A new gene (DYX3) for dyslexia is located on chromosome 2.

Developmental dyslexia is a specific reading disability affecting children and adults who otherwise possess normal intelligence, cognitive skills, and adequate schooling. Difficulties in spelling and reading may persist through adult life. Possible localisations of genes for dyslexia have been reported on chromosomes 15 (DYX1), 6p21.3-23 (DYX2), and 1p over the last 15 years. Only the localisation to 6p21.3-23 has been clearly confirmed and a genome search has not previously been carried out. We have investigated a large Norwegian family in which dyslexia is inherited as an autosomal dominant trait. A genome wide search for linkage with an average 20 cM marker density was initiated in 36 of the 80 family members. The linkage analysis was performed under three different diagnostic models. Linkage analysis in the family identified a region in 2p15-p16 which cosegregated with dyslexia. Maximum lod scores of 3.54, 2.92, and 4.32 for the three different diagnostic models were obtained. These results were confirmed by a non-parametric multipoint GENEHUNTER analysis in which the most likely placement of the gene was in a 4 cM interval between markers D2S2352 and D2S1337. Localisation of a gene for dyslexia to 2p15-16, together with the confirmed linkage to 6p21.3-23, constitute strong evidence for genetic heterogeneity in dyslexia. Since no gene for dyslexia has been isolated, little is known about the molecular processes involved. The isolation and molecular characterisation of this newly reported gene on chromosome 2 (DYX3) and DYX1 will thus provide new and exciting insights into the processes involved in reading and spelling.

Adult↗
PubMed1991

Evidence for major gene transmission of developmental dyslexia.

OBJECTIVE: --There is strong evidence that developmental dyslexia is both familial and heritable, but the mode of genetic transmission has remained unclear. In this article, we examine specific genetic hypotheses about the mode of transmission of developmental dyslexia by performing complex segregation analyses. DESIGN: --A family study method was applied, whereby the relatives of dyslexic probands were examined for dyslexia. The families studied represent four independently ascertained samples. SETTING: --The four samples of families were primarily from rural and suburban communities of Colorado, Washington State, and Iowa. PARTICIPANTS: --A total of 204 families and 1698 individuals in the four samples combined. MAIN OUTCOME MEASURES: --The complex segregation program, POINTER, was used to test competing genetic hypotheses of how a categorical trait (dyslexia) is transmitted in families. RESULTS: --The results were consistent with major locus transmission in three of four samples and with polygenic transmission in the fourth. In these three samples, the estimates of penetrance for the AA, Aa, and aa genotypes (where A is the abnormal allele) were, respectively, 1.000, 1.000, and 0.001 to 0.039 in males, and 0.560 to 1.000, 0.550 to 0.897, and 0.000 in females. The estimated gene frequency of the major locus was between 3% and 5%. CONCLUSIONS: --Sex-influenced, additive, or dominant transmission occurs in a significant proportion of dyslexic families. Other evidence indicates, however, that dyslexia is etiologically heterogeneous and that there is genetic heterogeneity even among families selected for apparent dominant transmission. Thus, while no single major locus may account for all of dyslexia, it is important to pursue potential major loci for dyslexia using linkage techniques.

Adult↗
PubMed1982

The psycholinguistic analysis of acquired dyslexias: some illustrations.

Three approaches to the neuropsychology of cognitive function are distinguished: the neuroanatomical (where the primary concern is to correlate particular disorders of cognitive function with particular lesion sites), the 'general-cognitive' (in which associations are sought between impairments of performance on specific cognitive tasks and general disorders of broadly defined cognitive processes) and the model-building (in which one attempts to interpret the pattern of impairments and preservations of some cognitive function produced by brain damage in terms of an explicit model of the normal operation of this function). I claim that the model-building approach to the neuropsychology of cognitive function must take precedence over the other two. One reason for this is that any disorder of cognitive function can only be defined with reference to some model of that function. I illustrate this claim with reference to acquired disorders of reading, describing current work of a psycholinguistic nature dealing with two acquired disorders of reading: phonological dyslexia and surface dyslexia. A psycholinguistic account of normal reading is used as a theoretical framework to define and to explain the patterns of deficit and preservation observed in these two dyslexias. The detailed account of surface dyslexia in English provided by this framework is then used to make predictions about the nature of surface dyslexia in other languages: alphabetically written languages where all words are regularly spelled, or where homophones cannot occur, as well as ideographically and syllabically written languages. A case of surface dyslexia in an English-Spanish bilingual, in which such predictions were confirmed, is described.

Adult↗
PubMed2001

Evidence for a susceptibility locus on chromosome 6q influencing phonological coding dyslexia.

A linkage study of 96 dyslexia families containing at least two affected siblings (totaling 877 individuals) has found evidence for a dyslexia susceptibility gene on chromosome 6q11.2-q12 (assigned the name DYX4). Using a qualitative phonological coding dyslexia (PCD) phenotype (affected, unaffected, or uncertain diagnoses), two-point parametric analyses found highly suggestive evidence for linkage between PCD and markers D6S254, D6S965, D6S280, and D6S251 (LOD(max) scores = 2.4 to 2.8) across an 11 cM region. Multipoint parametric analysis supported linkage of PCD to this region (peak HLOD = 1.6), as did multipoint nonparametric linkage analysis (P = 0.012). Quantitative trait linkage analyses of four reading measures (phonological awareness, phonological coding, spelling, and rapid automatized naming speed) also provided evidence for a dyslexia susceptibility locus on chromosome 6q. Using a variance-component approach, analysis of phonological coding and spelling measures resulted in peak LOD scores at D6S965 of 2.1 and 3.3, respectively, under 2 degrees of freedom. Furthermore, multipoint nonparametric quantitative trait sibpair analyses suggested linkage between the 6q region and phonological awareness, phonological coding, and spelling (P = 0.018, 0.017, 0.0005, respectively, for unweighted sibpairs < 18 years of age). Although conventional significance thresholds were not reached in the linkage analyses, the chromosome 6q11.2-q12 region clearly warrants investigation in other dyslexia family samples to attempt replication and confirmation of a dyslexia susceptibility gene in this region.

Adolescent↗
PubMed2004

A dyslexia susceptibility locus (DYX7) linked to dopamine D4 receptor (DRD4) region on chromosome 11p15.5.

Dyslexia is a disability in acquiring reading and spelling skills that is independent of general intelligence and educational opportunity, and is highly heritable. It is known that dyslexia often co-occurs with attention deficit hyperactivity disorder (ADHD), and the 7-repeat allele of the 48-bp tandem repeat in exon 3 of the dopamine D4 receptor (DRD4) has been implicated in ADHD. We, therefore, investigated DRD4 as a candidate gene for dyslexia by testing for linkage and association with 14 markers at and around the DRD4 locus on chromosome 11p15.5. Using 100 families having at least two siblings affected with dyslexia, model-free linkage analysis revealed evidence for linkage to the DRD4-exon 3 repeat (two-point MFLOD = 2.27, P = 0.001) and to HRAS located just proximal to DRD4 (two-point MFLOD = 2.68, P = 0.0004). Evidence for linkage was maximal between DRD4 and HRAS (three-point MFLOD = 3.57, P = 0.00005). However, linkage disequilibrium analysis showed no significant evidence for association between dyslexia and DRD4 or HRAS. In particular, dyslexic subjects showed no significant increase of the DRD4 7-repeat allele associated with ADHD. It is possible that other DRD4 variants, not in strong linkage disequilibrium with the exon 3 repeat polymorphism, or alternatively, another gene very closely linked to DRD4, may influence susceptibility to dyslexia.

Alleles↗
PubMed2004

Confirmation of a dyslexia susceptibility locus on chromosome 1p34-p36 in a set of 100 Canadian families.

Dyslexia is a common and genetically complex trait that manifests primarily as a reading disability independent of general intelligence and educational opportunity. Strong evidence for a dyslexia susceptibility locus on chromosome 1p34-p36 (near marker D1S199) was recently reported, and an earlier study found suggestive evidence for linkage to the same region. We tested for the presence of a dyslexia gene in this region in a sample of 100 Canadian families using both qualitative and quantitative definitions of the phenotype. Using a qualitative definition of dyslexia (affected, unaffected, or uncertain), the largest multipoint Genehunter Maximum LOD-Score (MLS) in 100 core nuclear families was 3.65 at D1S507, distal to D1S199. Quantitative trait locus (QTL) linkage analysis was performed for four measures of dyslexia (phonological awareness, phonological coding, spelling, and rapid automatized naming speed) employing the variance components approach implemented in Genehunter. Using a model with QTL additive and dominance variance and polygenic additive variance, the multipoint LOD scores maximized proximal to D1S199 (between D1S552 and D1S1622), with peaks of 4.01 for spelling and 1.65 for phonological coding (corresponding LOD scores under 1 degree of freedom were 3.30 and 1.13, respectively). In conclusion, our study confirms and strengthens recent findings of a dyslexia susceptibility gene on chromosome 1p34-p36 (now designated DYX8).

Canada↗
PubMed2003

Occupation choices of adults with and without symptoms of dyslexia.

People with the learning disability developmental dyslexia characteristically have difficulties in processing written language. There is some evidence that they may also have talents in other areas such as visuospatial processing. This pattern of strengths and weaknesses may predispose people who have dyslexia towards adopting certain occupations and away from others. Although there is literature on career choice in learning disabled adults in general, relatively little work has been done specifically for dyslexia. We therefore compared the occupations of adults with and without symptoms of developmental dyslexia. Results were analysed using non-parametric statistics and are illustrated with a case study. We found significant differences in the distribution of our samples. Adults with symptoms of dyslexia were much less likely than adults not reporting such symptoms to be involved in professions such as science/computing, management and finance. They were more likely to be involved in people-oriented professions such as nursing or sales. While preliminary, these results suggest that people with dyslexia may indeed show significantly different patterns of occupation choice.

Adult↗