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PubMed2005

Developmental dyslexia in a regular orthography: a single case study.

This study of an adult case examined in detail with eye movement measures the reading speed problem which is characteristic for developmental dyslexia in regular orthographies. A dramatic length effect was found for low frequency words and for pseudowords, but not for high frequency words. However, even for high frequency words it was found that reading times were substantially prolonged although number of fixations did not differ. A neurocognitive assessment revealed no visual deficits (parallel processing, precedence detection, coherent motion detection) but speed impairments for certain verbal and phonological processes. We propose that the reading difficulties are phonological in nature, but these difficulties become manifest as inefficiency and not as inability.

Adult↗

PubMed1988

Developmental dyslexia and word retrieval deficits.

Developmental dyslexics, selected on the basis of very slow naming rates on the Rapid Automatic Naming Tasks (RAN), were compared to normal readers on oral language, picture categorization, and reading tasks. Findings indicated that the dyslexics' word retrieval deficits were one symptom of a more generalized, however subtle, oral language deficit which involved both receptive and expressive oral language functioning. The dyslexics' word retrieval problem also seemed chiefly related to language processing and not to deficits in semantic memory as there were no significant differences between dyslexics and controls on a nonverbal semantic memory task (picture categorization). In naming and identifying printed words, the dyslexics appeared to rely considerably upon the "indirect" or "assembly-of-phonology" route; they were slower in naming irregularly spelled words compared to regularly spelled words and on a lexical decision task, the dyslexics were slower in making negative decisions for "pseudohomophones" (e.g., "braik") than for other matched nonwords. Results are discussed in terms of the logogen model with some consideration of a developmental model as well.

Anomia↗

PubMed2000

The neurological basis of developmental dyslexia: an overview and working hypothesis.

Five to ten per cent of school-age children fail to learn to read in spite of normal intelligence, adequate environment and educational opportunities. Thus defined, developmental dyslexia (hereafter referred to as dyslexia) is usually considered of constitutional origin, but its actual mechanisms are still mysterious and currently remain the subject of intense research endeavour in various neuroscientific areas and along several theoretical frameworks. This article reviews evidence accumulated to date that favours a dysfunction of neural systems known to participate in the normal acquisition and achievement of reading and other related cognitive functions. Historically, the first arguments for a neurological basis of dyslexia came from neuropathological studies of brains from dyslexic individuals. These early studies, although open to criticism, for the first time drew attention towards a possible abnormality in specific stages of prenatal maturation of the cerebral cortex and suggested a role of atypical development of brain asymmetries. This has prompted a large amount of subsequent work using in vivo imaging methods in the same vein. These latter studies, however, have yielded less clear-cut results than expected, but have globally confirmed some subtle differences in brain anatomy whose exact significance is still under investigation. Neuropsychological studies have provided considerable evidence that the main mechanism leading to these children's learning difficulties is phonological in nature, namely a basic defect in segmenting and manipulating the phoneme constituents of speech. A case has also been made for impairment in brain visual mechanisms of reading as a possible contributing factor. This approach has led to an important conceptual advance with the suggestion of a specific involvement of one subsystem of vision pathways (the so-called magnosystem hypothesis). Both phonological and visual hypotheses have received valuable contribution from modern functional imaging techniques. Results of recent PET and functional MRI studies are reported here in some detail. Finally, one attractive interpretation of available evidence points to dyslexia as a multi-system deficit possibly based on a fundamental incapacity of the brain in performing tasks requiring processing of brief stimuli in rapid temporal succession. It is proposed that this so-called 'temporal processing impairment' theory of dyslexia could also account for at least some of the perceptual, motor and cognitive symptoms very often associated with the learning disorder, a coincidence that has remained unexplained so far.

Articulation Disorders↗

PubMed2005

Do children with developmental dyslexia have an implicit learning deficit?

OBJECTIVE: The purpose of this study was to investigate the effects of specific types of tasks on the efficiency of implicit procedural learning in the presence of developmental dyslexia (DD). METHODS: Sixteen children with DD (mean (SD) age 11.6 (1.4) years) and 16 matched normal reader controls (mean age 11.4 (1.9) years) were administered two tests (the Serial Reaction Time test and the Mirror Drawing test) in which implicit knowledge was gradually acquired across multiple trials. Although both tests analyse implicit learning abilities, they tap different competencies. The Serial Reaction Time test requires the development of sequential learning and little (if any) procedural learning, whereas the Mirror Drawing test involves fast and repetitive processing of visuospatial stimuli but no acquisition of sequences. RESULTS: The children with DD were impaired on both implicit learning tasks, suggesting that the learning deficit observed in dyslexia does not depend on the material to be learned (with or without motor sequence of response action) but on the implicit nature of the learning that characterises the tasks. CONCLUSION: Individuals with DD have impaired implicit procedural learning.

Child↗

PubMedDate not supplied

[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↗

PubMed2006

Impaired duration mismatch negativity in developmental dyslexia.

A mismatch negativity event-related potential protocol was administered to dyslexic children and their respective controls to test whether a specific auditory deficit concerning phonetic processing or a lower level auditory processing deficit was present in developmental dyslexia. Three different contrast conditions were explored, including nonphonological sounds, contrasted in pitch and duration, and phonemes. Mismatch negativity amplitudes differed significantly between groups in the duration condition, whereas no differences were found in the frequency and phoneme conditions. Moreover, the dyslexic children had delayed mismatch negativity latencies in the three contrast conditions. Our results suggest a deficit in low-level auditory discrimination in dyslexic children, in particular when detecting stimulus duration, and support the rapid auditory processing theory of dyslexia.

Acoustic Stimulation↗

PubMed2006

Supporting dyslexic adults--a need for clarity (and more research): a critical review of the Rice report 'Developmental Dyslexia in Adults: A Research Review'.

Evidence based teaching methods are desirable not only for economic efficiency but also important for ensuring the learner is engaged in meaningful activity. Therefore, a review of the research that could inform both teaching practice and future research is to be welcomed. However, the NRDC review 'Developmental Dyslexia in Adults: A Research Review' contains so many methodological flaws, including the highly selective way in which the research has been used, that the overall value of the report is questionable. In this paper the authors have attempted to highlight the main issues of why this report appears to fall short of being a full 'Research Review'.

Achievement↗

PubMed2000

Functional neuroimaging studies of reading and reading disability (developmental dyslexia).

Converging evidence from a number of neuroimaging studies, including our own, suggest that fluent word identification in reading is related to the functional integrity of two consolidated left hemisphere (LH) posterior systems: a dorsal (temporo-parietal) circuit and a ventral (occipito-temporal) circuit. This posterior system is functionally disrupted in developmental dyslexia. Reading disabled readers, relative to nonimpaired readers, demonstrate heightened reliance on both inferior frontal and right hemisphere posterior regions, presumably in compensation for the LH posterior difficulties. We propose a neurobiological account suggesting that for normally developing readers the dorsal circuit predominates at first, and is associated with analytic processing necessary for learning to integrate orthographic features with phonological and lexical-semantic features of printed words. The ventral circuit constitutes a fast, late-developing, word identification system which underlies fluent word recognition in skilled readers.

Cerebral Cortex↗

PubMed2002

Planum temporale asymmetry and ear advantage in dichotic listening in Developmental Dyslexia and Attention-Deficit/Hyperactivity Disorder (ADHD).

The planum temporale is clearly involved in language processing, for it serves as the auditory association cortex. Research has consistently demonstrated that 60 to 70% of the population has leftward asymmetry of the planum temporale. Research has also suggested that dyslexic individuals tend to have either rightward asymmetry or symmetrical plana. Moreover, many studies have found a relationship between the presence of dyslexia and/or language impairment and deficits in the normal right ear advantage found in dichotic listening paradigms. In this context, this study examined the relationship between planum temporale asymmetry and ear preference in dichotic listening performance in children with Developmental Dyslexia and Attention-Deficit/Hyperactivity Disorder (ADHD). Subjects included 19 children with dyslexia (10 of whom had a comorbid diagnosis of ADHD), 23 children with ADHD, and 12 diagnosed normal control children. Dichotic listening data were not collected for 8 of the 12 normal control children and for 3 of the 23 ADHD children. Results revealed no significant difference between ADHD and dyslexic subjects in regard to ear advantage on the free recall dichotic listening task. In addition, although the directed dichotic listening tasks were not related to degree of planum asymmetry, as predicted, results indicated that subjects who consistently displayed an atypical left ear advantage tended to have larger right bank lengths than those who consistently displayed a typical right ear advantage. These findings support the notion that some individuals with dyslexia or language deficits tend to have a larger right planum temporale and that performance on dichotic listening tasks may reflect this relatively unusual pattern.

Attention Deficit Disorder with Hyperactivity↗

PubMedDate not supplied

Coherence of hemispheric function in developmental dyslexia.

Left parieto-occipital EEG leads record a frequency spectrum in dyslexics that is consistently different from the spectrum obtained from normals. It is suggested that these effects represent significant differences in the functional organization of these areas. EEG coherence values indicate that normals have significantly greater sharing between hemispheres at symmetrical locations. Dyslexics demonstrate significantly greater sharing within hemisphere than do normals. The data supports developmental dyslexia being a functional hemispheric disconnection syndrome.

Brain↗

PubMed2006

Developmental dyslexia in Norwegian: evidence from single-case studies.

This study provides detailed descriptions of the reading impairments in four 10-year-old Norwegian children with dyslexia. In all four cases reading comprehension was well in advance of the children's slow and inaccurate word-recognition skills. Phonological decoding (as assessed by pseudohomophone and nonword reading) appeared relatively unimpaired in three of the dyslexic cases, both in terms of speed and accuracy. However, reading errors showed that these children had particular difficulties with both phoneme length and phoneme quality awareness in reading. A 'phonemic identification deficit' account for developmental dyslexia in Norwegian children is suggested.

Awareness↗

PubMed1987

Defective lateralized attention for non-verbal sounds in developmental dyslexia.

The performance of dyslexic and control children--matched for age, sex, handedness and performance IQ--was compared on a dichotic listening task in which the stimuli were environmental sounds. Two findings emerged. First, the dyslexic group showed a normal, left ear perceptual advantage for these non-verbal materials. Second, the dyslexics were incapable of occluding dichotically presented sounds to the left ear when required to deploy attention only to sounds entering the right ear. This failure of unilateral selective attention was not found in the controls, nor in either group under a condition of left ear only attention. The data were interpreted as undermining the bihemispheric non-verbal processing hypothesis of developmental dyslexia. It was argued that the dyslexics' apparent inability to override voluntarily the reflexive lateral orienting mechanism was most consistent with explanatory models emphasizing defective functioning, or even malformation, of the left cerebral hemisphere alone.

Adolescent↗

PubMed1990

MRI evaluation of the size and symmetry of the planum temporale in adolescents with developmental dyslexia.

MRI technique was used to examine the size and symmetry of the plana temporale in 19 dyslexic students in grade 8 and in carefully matched control subjects. The results demonstrated a high frequency of planum symmetry among the dyslexics (70%) whereas symmetry was observed in only 30% of the control subjects. It was not possible to demonstrate any clear association between symmetry/asymmetry of planum temporale and handedness. Word-reading strategies among the dyslexics and control subjects were investigated with computerized tasks where accuracy and naming latency were recorded. All subjects with pure phonological deficits in reading had symmetrical plana temporale indicating a possible neuroanatomical basis for a characteristic symptom of linguistic processing deficiency in developmental dyslexia.

Adolescent↗

PubMed1995

Family patterns of developmental dyslexia, part II: behavioral phenotypes.

The motor control of bimanual coordination and motor speech was compared between first degree relatives from families with at least 2 dyslexic family members, and families where probands were the only affected family members. Half of affected relatives had motor coordination deficits; and they came from families in which probands also showed impaired motor coordination. By contrast, affected relatives without motor deficits came from dyslexia families where probands did not have motor deficits. Motor coordination deficits were more common and more severe among affected offspring in families where both parents were affected than among affected offspring in families where only one parent was affected. However, motor coordination deficits were also more common and more severe in affected parents when both parents were affected than among affected parents in families where only one parent was affected. We conclude that impaired temporal resolution in motor action identifies a behavioral phenotype in some subtypes of developmental dyslexia. The observed pattern of transmission for motor deficits and reading impairment in about half of dyslexia families was most congruent with a genetic model of dyslexia in which 2 codominant major genes cosegregate in dyslexia pedigrees where the proband is also motorically impaired.

Adolescent↗

PubMed1986

Flicker masking and developmental dyslexia.

Recent studies have provided evidence that dyslexic children tend to show longer visual persistence than control children when presented with low-spatial-frequency grating stimuli. The possibility that this phenomenon might reflect an impairment of inhibitory Y-cell activity in the visual system of dyslexics has been investigated. A flicker masking technique was used to mask Y-cell activity selectively in a group of dyslexic boys and a group of age-matched controls. There were no overall differences in reaction times to the offsets of grating patterns of various spatial frequencies between the groups, and no differences between subgroups defined by age, degree of reading impairment, or any other criterion. The results show no evidence of abnormal Y-cell function in developmental dyslexia.

Afterimage↗

PubMed2003

A candidate gene for developmental dyslexia encodes a nuclear tetratricopeptide repeat domain protein dynamically regulated in brain.

Approximately 3-10% of people have specific difficulties in reading, despite adequate intelligence, education, and social environment. We report here the characterization of a gene, DYX1C1 near the DYX1 locus in chromosome 15q21, that is disrupted by a translocation t(2;15)(q11;q21) segregating coincidentally with dyslexia. Two sequence changes in DYX1C1, one involving the translation initiation sequence and an Elk-1 transcription factor binding site (-3G --> A) and a codon (1249G --> T), introducing a premature stop codon and truncating the predicted protein by 4 aa, associate alone and in combination with dyslexia. DYX1C1 encodes a 420-aa protein with three tetratricopeptide repeat (TPR) domains, thought to be protein interaction modules, but otherwise with no homology to known proteins. The mouse Dyx1c1 protein is 78% identical to the human protein, and the nonhuman primates differ at 0.5-1.4% of residues. DYX1C1 is expressed in several tissues, including the brain, and the protein resides in the nucleus. In human brain, DYX1C1 protein localizes to a fraction of cortical neurons and white matter glial cells. We conclude that DYX1C1 should be regarded as a candidate gene for developmental dyslexia. Detailed study of its function may open a path to understanding a complex process of development and maturation of the human brain.

Base Sequence↗

PubMed1992

Language abilities, reading acquisition, and developmental dyslexia: a discussion of hypothetical and observed relationships.

Tests of a model of the expected relationships between language abilities and reading achievement measures from the beginning of kindergarten through third grade are discussed. At kindergarten, more global language abilities influenced early, wholistic measures of reading achievement, including letter and number naming. At Grade 1, these earlier accomplishments had a direct effect on word recognition, but a second direct effect was also apparent for word and pheneme segmentation measured in kindergarten. Comprehension at Grade 1 was influenced primarily by word recognition abilities at the same time. At Grade 2, comprehension influenced word recognition; at Grade 3, word recognition and comprehension were essentially independent. These findings are considered in the context of Frith's three-phase hypothesis of reading acquisition. A rationale for testing the potential of training in auditory segmentation to modulate the effects of developmental dyslexia is presented.

Aptitude↗

PubMed1999

A quantitative-trait locus on chromosome 6p influences different aspects of developmental dyslexia.

Recent application of nonparametric-linkage analysis to reading disability has implicated a putative quantitative-trait locus (QTL) on the short arm of chromosome 6. In the present study, we use QTL methods to evaluate linkage to the 6p25-21.3 region in a sample of 181 sib pairs from 82 nuclear families that were selected on the basis of a dyslexic proband. We have assessed linkage directly for several quantitative measures that should correlate with different components of the phenotype, rather than using a single composite measure or employing categorical definitions of subtypes. Our measures include the traditional IQ/reading discrepancy score, as well as tests of word recognition, irregular-word reading, and nonword reading. Pointwise analysis by means of sib-pair trait differences suggests the presence, in 6p21.3, of a QTL influencing multiple components of dyslexia, in particular the reading of irregular words (P=.0016) and nonwords (P=.0024). A complementary statistical approach involving estimation of variance components supports these findings (irregular words, P=.007; nonwords, P=.0004). Multipoint analyses place the QTL within the D6S422-D6S291 interval, with a peak around markers D6S276 and D6S105 consistently identified by approaches based on trait differences (irregular words, P=.00035; nonwords, P=.0035) and variance components (irregular words, P=.007; nonwords, P=.0038). Our findings indicate that the QTL affects both phonological and orthographic skills and is not specific to phoneme awareness, as has been previously suggested. Further studies will be necessary to obtain a more precise localization of this QTL, which may lead to the isolation of one of the genes involved in developmental dyslexia.

Adolescent↗