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Naming speed in children with dyslexia.

A series of tests of naming speed in discrete reaction time format were undertaken by seven groups of children: three groups with dyslexia with mean ages 8, 13, and 17 years; three groups of normally achieving children matched for age and IQ with the dyslexic groups; and a group of 10-year-old children with mild learning difficulties (slow learners) matched for reading age with the youngest dyslexic group. The children with dyslexia were significantly slower than even their chronological age-matched controls, and equivalent to their reading age-matched controls, on naming colors, digits, and letters, and significantly slower than even their reading age-matched controls on naming pictures of common objects. Overall, performance of the 17-year-old children with dyslexia was closest to that of the 8-year-old controls. Performance of the slow learners was equivalent to that of the youngest children with dyslexia. The results show that children with dyslexia have persistent-and unexpectedly severe-problems in naming speed for all stimuli, regardless of whether or not the stimulus requires grapheme-phoneme decoding.

Adolescent↗

Dyslexia: a validation of the concept at two age levels.

The 144 participants were administered tasks with a demonstrated relationship to reading. Both older students (8 to 10 years old) and younger students (6 to 7 years old) included three groups of poor readers (matched on word reading but differing in the discrepancy from expected reading level) and age-matched average readers. Older poor readers also had a control group of reading-matched younger subjects. The study provided no support for the concept of dyslexia at age 6 to 7 years. Among older participants there was support for the concept of dyslexia as a phonological deficit and of nondiscrepant garden-variety poor reading as a developmental lag. More discrepant participants with dyslexia exhibited orthographic and serial naming-speed deficits, as well as phonological deficits, and were a distinctive dyslexic group. Less discrepant participants with dyslexia were more similar to garden-variety poor readers than to the more discrepant participants with dyslexia.

Age Factors↗

Automatization aspects of dyslexia: speed limitations in word identification, sensitivity to increasing task demands, and orthographic compensation.

A study is presented in which three characteristics of dyslexia were examined: (a) speed limitations in word identification, (b) sensitivity to increasing task demands, and (c) orthographic compensation. Ten students with dyslexia (10 years old) were compared to 10 chronological-age controls and 20 reading-age controls on their performance in reading. Response latencies of the students with dyslexia were slower when familiar words, letter clusters, and nonwords had to be named. A larger word-frequency effect and a larger word-length effect in the these students indicates that they have difficulty with increasing task demands. In addition, a subword-frequency effect was found to be larger in the students with dyslexia. These differences among the three groups of students are interpreted in terms of automatization. Furthermore, it is suggested that students with dyslexia may have a preference for large orthographic units, which is used as a compensatory tool in reading.

Automatism↗

Reading and dual-task balancing: evidence against the automatization deficit explanation of developmental dyslexia.

Nicolson and Fawcett (1990) demonstrated specifically impaired balancing performance of children with dyslexia when balancing had to be done simultaneously with a secondary task. This finding was taken as evidence for a general automatization deficit of children with dyslexia. We attempted to replicate this finding with German children with dyslexia, whose characteristic reading difficulty is a fluency problem quite in correspondence with the automatization deficit explanation. Because we were concerned about a potential confound between dyslexia and attention-deficit/hyperactivity disorder (ADHD), we also collected teacher ratings on ADHD symptoms. We found that poor dual-task balancing was limited to children with higher ADHD ratings and that children with dyslexia without higher ADHD ratings performed as well on dual-task balancing as age-matched control children. This finding supports the aforementioned confound. Together with other findings from our research group, it supports the position that, even in consistent orthographies, difficulties in learning to read are caused by a specific phonological deficit.

Attention Deficit Disorder with Hyperactivity↗

Developmental pathways of children with and without familial risk for dyslexia during the first years of life.

Comparisons of the developmental pathways of the first 5 years of life for children with (N = 107) and without (N = 93) familial risk for dyslexia observed in the Jyväskylä Longitudinal study of Dyslexia are reviewed. The earliest differences between groups were found at the ages of a few days and at 6 months in brain event-related potential responses to speech sounds and in head-turn responses (at 6 months), conditioned to reflect categorical perception of speech stimuli. The development of vocalization and motor behavior, based on parental report of the time of reaching significant milestones, or the growth of vocabulary (using the MacArthur Communicative Development Inventories) failed to reveal differences before age 2. Similarly, no group differences were found in cognitive and language development assessed by the Bayley Scales of Infant Development and the Reynell Developmental Language Scales before age 2.5. The earliest language measure that showed lower scores among the at-risk group was maximum sentence length at age 2. Early gross motor development had higher correlation to later language skills among the at-risk group rather than the control children. The most consistent predictor of differential development between groups was the onset of talking. Children who were identified as late talkers at age 2 were still delayed at the age 3.5 in most features of language-related skills-but only if they belonged to the group at familial risk for dyslexia. Several phonological and naming measures known to correlate with reading from preschool age differentiated the groups consistently from age 3.5. Our findings imply that a marked proportion of children at familial risk for dyslexia follow atypical neurodevelopmental paths. The signs listed previously comprise a pool of candidates for early predictors and precursors of dyslexia, which await validation.

Child↗

No evidence for association between dyslexia and DYX1C1 functional variants in a group of children and adolescents from Southern Italy.

Recently, DYX1C1, a candidate gene for developmental dyslexia, encoding a nuclear tetratricopeptide repeat domain protein dynamically regulated in brain, has been characterized through a translocation breakpoint in a Finnish family. Two putatively functional variants, -3G/A and 1249G/T, have been reported to be significantly associated with dyslexia in this population. Further studies, conducted on different ethnic groups (English and Canadian), have not confirmed a role for DYX1C1 variants in increasing the risk for dyslexia. We investigated the role of these variants in dyslexic children and adolescents from Southern Italy. No significant evidence for association between dyslexia and these DYX1C1 putative functional variants has been shown. We argue that the different DYX1C1 allele frequencies shown among Italian and Finnish subjects with dyslexia could be attributable to the different linkage disequilibrium structure of these populations.

Adolescent↗

Dyslexia and classic pathognomic signs.

The classic pathognomic signs of dyslexia, such as reversals and rotations, appear to be associated with poor reading, not diagnosed developmental dyslexia. 26 8th and 9th grade dyslexia with poor perceptual/attentional ability were matched with 19 reading-retarded subjects with age-equivalent perceptual/attentional test scores for age, IQ, and degree of reading retardation and compared both with each other and with 96 adequate readers for reversals, rotations, insertions, substitutions, omissions, poor handwriting and visual ability on the Gray test, the WRAT Spelling Test, a writing task, and the star-tracing mirror test. On 46 of 49 variables, the dyslexia and retarded readers performed comparably. Together they made more classic errors and had lower achievement scores than the adequate readers on 44 of 49 variables. Classic errors clustered with poor reading but not diagnosed dyslexia. The hypothesis that reading acquisition trains perceptual test-taking ability is advanced.

Adolescent↗

The effects of dyslexia on the work of nurses and healthcare assistants.

AIM: To explore the effects of being dyslexic on the working lives of nurses and healthcare assistants (HCAs), and to identify what might be done to improve their working lives. METHOD: A qualitative approach was taken comprising semi-structured interviews and interpretative data analysis. Seven nurses and HCAs took part in the study. FINDINGS: Dyslexia affects each individual differently and may affect career choice and career progression. Appropriate support from colleagues and employers is important. The participants identified dyslexia-friendly practices and made suggestions for improvements. CONCLUSION: Nurses and HCAs with dyslexia can make a major contribution to patient care, although dyslexia can affect their work in many different ways. Establishing a dyslexia-friendly workplace would help them to achieve their maximum potential.

Adaptation, Psychological↗

[Neuroanatomical, neuroradiological and functional magnetic resonance imaging correlates of developmental dyslexia].

Neuropathological data in dyslexia has demonstrated alterations in the symmetry normally present in the planum temporale, as well as microdysgenesis in superficial cortical layers and disruption of the cytoarchitecture in subcortical structures. Neuroradiological and functional neuroimaging studies in dyslexia are consistent with localization of dysfunction to the temporoparietal junction. Present neuropathological and neuroimaging data support the concept that the fundamental problem in developmental dyslexia is a phonologic deficit. Present neuroimaging technology has increased our understanding of the pathophysiology of dyslexia. Functional neuroimaging may allow for the investigation of the effects that treatment of dyslexia has on brain plasticity.

Child↗

Neurophysiological studies in dyslexia.

Using sophisticated computer graphics technologies and sensitive methods, our original dyslexia study of dyslexic boys delineated specific areas of the brain which in combination could constitute a "physiological signature" of dyslexia. In addition to identifying aberrant brain function in the traditional language-associated left posterior region, we also observed medial frontal lobe differences from normals, a finding confirmed by others in recent research. Our subsequent study sought to refine further current definitional subgroupings within the broad entity known as dyslexia-pure. Indeed language-based subgroups appear to have identifiable and differing topographic signatures. Furthermore, based on correlations between neuropsychological test scores and neurophysiological measurements, we suggest that subgroup electrophysiological differences may reflect compensatory as well as pathological brain activity. We believe that the currently expanding understanding of the neurophysiology of dyslexia will lead eventually to improved diagnosis and remediation of this learning disability. The detailed mapping of brain electrical activity shows promise of providing the neuropsychologist and learning disability specialist with another "perspective" on reading disability. This technique may prove valuable in the diagnosis of dyslexia at an early age and in the tailoring of the learning experience to a child's specific deficits and capabilities.

Brain↗

[Clinical diagnosis of dyslexia].

In 5 years of experience at the Instituto Nacional de la Comunicacion Humana, 302 clinical histories showed the diagnosis of dyslexia. The following parameters were studied: age, sex, heredofamilial history, gestation, psychomotor development, clinical picture, examination of the language (type, reading, spontaneous writing, dictation, mathematic concepts), laterality, scholarship, scholar failures, psychological study. The following results were obtained: Dyslexia was more important or frequent between 5 to 8.9 years of age. Males predominated 3:1. The heredofamilial history was important. Dyslexia prevailed in products of the first gestations. A high disturbance was found in the psychomotor development of a large percent of dyslexic patients. Examination of language was also important. Dyslexia was more frequent in right-handed patients. Scholar failures in one or more instances were found. The psychological study must be done. If dyslexia is diagnosed on time, it may be prevented and all unwanted sequelae may be avoided.

Dyslexia↗

Dyslexia: a neuroscientific puzzle.

The initial assumptions as to the existence of neurodevelopmental disorders have been confirmed by almost a century of studies focused on the nature and causes of reading disability. Dyslexia is an umbrella term for the various manifestations of reading disabilities, each of which is related to its own complex of neuropsychological dysfunctions, sometimes accompanied by neurological symptoms that can be indicative of the specific location involved. Electro-physiology and neuro-imaging in relation to metabolic activity have also confirmed that, to some extent, there is dysfunction in various cerebral areas, more frequently in the left than in the right hemisphere, less often between the hemispheres (corpus callosum) and outside the classical language areas. The rather rare subtype referred to as visual dyslexia and the inter-modal disconnection type resembling alexia are eclipsed by dyslexias related to spoken language: the dysphonemic (auditory-phonological) subtype and the subtypes that are concerned with the production of speech (fluency, word-finding, syntax, sequences), semantics (language comprehension) and linguistic memory. Although it is considered that there are basic brain dysfunctions in dyslexics such as deficits in sequential information processing, there is no "grand unified theory" of dyslexia. There are some new insights as regards the aetiology. In addition to indications of such possible causes as perinatal brain damage, genetic or chromosomal anomalies that manifest themselves in the substrate in an unclear manner, there is also the possibility that the cortical language areas can be disturbed in their development (migration disorders and abnormal asymmetry) due to genetic or epigenetic hormonal and/or immunological factors, so that the normal left hemispheric dominance does not develop. The diagnosis and treatment of dyslexia should begin at an early age and should be acknowledged as being of great social importance.

Brain↗

Standard EEG and dyslexia in children--new evidence for specific correlates?

Contrary to the current assumption that there are no specific correlates of dyslexia in the standard clinical EEG, we have often noted a spontaneous "intermittent left parietal alpha desynchronization" (ILPAD) when visually evaluating the standard EEGs of children with delayed speech and language development and/or dyslexia. Visual evaluations of EEGs, as well as computer-assisted frequency analysis of three pairs of matched groups (healthy and hyperkinetic children with vs. without relatively "low levels" of verbal performance, as well as children with other child psychiatric disorders with vs. without dyslexia), revealed that healthy children did not display the ILPAD phenomenon. It was seen neither in healthy children with a homogeneous performance profile ("high level" of verbal performance) nor in those with a relatively "low level" of verbal performance. However, the ILPAD phenomenon was evident mainly in children with psychiatric disorders who suffered from dyslexia. Its intermittent occurrence prevented its detection by means of the usual computer-supported analyses of EEG power spectra. Nevertheless, auditory cognitive loading was accompanied by a decrease in alpha power in both healthy and hyperkinetic children with "high" or "low" levels of verbal performance. In a further group of 8-year-old children with dyslexia, but otherwise healthy, the ILPAD phenomenon was also observed if their CNS maturation as reflected in the EEG was normal for their age. These results seemed to indicate at least a deficit-specificity of the ILPAD phenomenon, which is interpreted as an electrophysiological correlate of a "brain-electrical developmental deviation" with regard to the "functions of communication": speech, language, reading and spelling.

Alpha Rhythm↗

Acquired and developmental spelling dyslexia.

Two cases of acquired spelling dyslexia and one case of developmental spelling dyslexia are described along with accounts of their performance on various psycholinguistic tasks. It is argued that there is some evidence that spelling dyslexia may exist in developmental form but that parallels are difficult to draw because of the very different histories of child and adult cases. It is also suggested that features of surface dyslexia exist in at least a proportion of spelling dyslexic cases and that this may be influenced by level of premorbid reading skill.

Aged↗

A magnetic resonance imaging study of planum temporale asymmetry in men with developmental dyslexia.

BACKGROUND: Imaging studies have suggested anomalous anatomical asymmetries in language-related regions of the temporal and parietal lobes in individuals with developmental dyslexia. Autopsy studies have reported unusual symmetry of the planum temporale (PT) in patients with dyslexia. Methodological limitations characterize much of this literature, however. OBJECTIVE: To examine the size and asymmetry of the PT and its extension into the parietal lobe (planum parietale [PP]) in men with well-characterized, persistent dyslexia by using magnetic resonance imaging and 3-dimensional surface rendering techniques. METHODS: The brains of 16 right-handed dyslexic men aged 18 to 40 years and 14 matched control subjects were studied with magnetic resonance imaging. Most of these subjects were previously studied with positron emission tomography, which demonstrated functional abnormalities in temporal and parietal brain regions in the dyslexic group. The area of the PT was determined with the aid of 3-dimensional surface-rendering techniques. The size of the PP was estimated by measuring the length of the posterior ascending ramus on 3 parasagittal slices. RESULTS: Approximately 70% to 80% of both groups showed equivalent leftward (left > right) asymmetries of the PT; approximately 50% to 60% showed equivalent rightward (right > left) asymmetries of the PP. These asymmetries showed equivalent moderate inverse correlations with each other in both groups. CONCLUSIONS: These results challenge the notion that anomalous asymmetry of the PT is strongly associated with developmental dyslexia. Given the heterogeneity of the dyslexic population, some subgroup of dyslexic individuals (i.e., those with developmental language disorders) may show unusual symmetry or reversed asymmetry in this region. However, anomalous asymmetry of the planum did not contribute to functional abnormalities demonstrated in these patients by positron emission tomography.

Adolescent↗

Family patterns of developmental dyslexia. Part III: Spelling errors as behavioral phenotype.

The major trends in current research on developmental dyslexia assume that impaired phonological processing is the core deficit in this disorder. Our earlier studies indicated that half of all dyslexic persons have significant deficits of bimanual motor coordination, and that impaired temporal resolution in motor action may identify a vertically transmitted behavioral phenotype in familial dyslexia. This report examines the relationship between spelling errors as a measure of impaired phonological processing and motor coordination deficits in the same dyslexia families. Affected family members with motor coordination deficits made significantly more dysphonetic spelling errors than dyslexic family members without motor deficits, but there was no evidence that dysphonetic spelling is vertically transmitted in dyslexia families. On the other hand, affected offspring of affected parents with motor coordination deficits made relatively more dysphonetic spelling errors than the affected offspring of parents without motor coordination deficits. We suggest that dysphonetic spelling may be one outward expression of a vertically transmitted behavioral phenotype of impaired temporal resolution that is clearly expressed in coordinated motor action.

Child↗

Multilingualism and dyslexia: challenges for research and practice.

Over the last two decades there has been an expansion of activity and substantial progress in research on dyslexia and research on bilingualism and multilingualism. But the study of dyslexia has generally focused on monolingual learners and the study of bilingualism has tended to focus on speakers who do not have special educational needs. This paper will review the strands of research to date that have a bearing on multilingualism and dyslexia and attempt to identify the major challenges that face researchers and teachers. A satisfactory response cannot be developed without a full understanding of the impact that dyslexia has on language learning and the impact that multilingualism has on literacy learning.

Adolescent↗

Linkage analyses of four regions previously implicated in dyslexia: confirmation of a locus on chromosome 15q.

Dyslexia is a common, complex disorder, which is thought to have a genetic component. There have been numerous reports of linkage to several regions of the genome for dyslexia and continuous dyslexia-related phenotypes. We attempted to confirm linkage of continuous measures of (1) accuracy and efficiency of phonological decoding; and (2) accuracy of single word reading (WID) to regions on chromosomes 2p, 6p, 15q, and 18p, using 111 families with a total of 898 members. We used both single-marker and multipoint variance components linkage analysis and Markov Chain Monte Carlo (MCMC) joint segregation and linkage analysis for initial inspection of these regions. Positive results were followed with traditional parametric lod score analysis using a model estimated by MCMC segregation analysis. No positive linkage signals were found on chromosomes 2p, 6p, or 18p. Evidence of linkage of WID to chromosome 15q was found with both methods of analysis. The maximum single-marker parametric lod score of 2.34 was obtained at a distance of 3 cM from D15S143. Multipoint analyses localized the putative susceptibility gene to the interval between markers GATA50C03 and D15S143, which falls between a region implicated in a recent genome screen for attention-deficit/hyperactivity disorder, and DYX1C1, a candidate gene for dyslexia. This apparent multiplicity of linkage signals in the region for developmental disorders may be the result of errors in map and/or model specification obscuring the pleiotropic effect of a single gene on different phenotypes, or it may reflect the presence of multiple genes.

Chromosomes, Human, Pair 15↗