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At least 19 recordsLinked to original sources
PubMed2003

[Developmental dyslexia].

Developmental dyslexia makes up an important proportion of the known learning disorders. Until the late 1970s most research on dyslexia was carried out by educators and educational psychologists, but soon after the publication of some dyslexic cases with focal disorders of neuronal migration to the cerebral cortex, interest in the neurobiological and neurocognitive underpinnings of dyslexia grew, especially in Europe and North America. There are at least two types of developmental dyslexia--phonological and surface. Surface dyslexia refers to a disorder in which the difficulty lies in reading irregular words, whereas phonological dyslexia is characterized by difficulty with pseudowords. Phonological dyslexia is the more common of the two types. Surface dyslexia does not present a major problem in a language such as Spanish, where the number of irregular words is indeed very small. Still, in languages such as English, where irregular words are common, the phonological type of developmental dyslexia is much more common. Phonologic dyslexics have problems with phonological awareness, that is, the conscious knowledge and manipulation of speech sounds, which is the most proximate explanation for their difficulty in reading pseudowords. Many, but not all, phonologic dyslexics also have problems processing rapidly changing sounds, even if not linguistic, and some slow sounds, too. The same group tends to have visual problems, especially involving the so-called magnocellular pathway of the visual system, which, among others, has the role of analyzing movement. Accompanying these perceptual and cognitive deficits, phonologic dyslexics also show abnormal brain activation to phonological tasks, as shown in functional magnetic resonance studies (figure). In addition, dyslexic brains show focal malformations, ectopias and microgyria, of the cerebral cortex, involving mainly the left perisylvian region and the word form area in the temporo-occipital junction. There are also changes in the composition of neurons in the lateral and medial geniculate nuclei of the thalamus. Experimental studies indicate that the thalamic changes are a consequence of the focal malformations, and that they are responsible for the sound processing deficits. None of these discoveries have changed the therapeutic modalities in this condition, but it is hoped that this will be the next area of progress.

Brain↗
PubMed1993

Neurology of developmental dyslexia.

Developmental dyslexia was until recently considered to belong solely in the domain of educational psychology. With the advent of better theories on language and reading, and better methods for assessing the structure and function of living human brains and for determining genetic transmission, dyslexia is now poised to become a focal concern of cognitive neuroscience, neurology, and genetic research. Still unresolved are questions relating to how much a reading disability represents a normal variation or a separate pathological entity, and whether the cognitive disorder is primarily cognitive, or secondary to a disorder in early perception. Recent findings from neuroanatomy, neurophysiology, neuropsychology, and genetics research are reviewed. (This review is an updated version of a review first published in Current Opinion In Neurology and Neurosurgery 1992, 5:71-76.)

Brain↗
PubMed2004

Developmental dyslexia.

Developmental dyslexia, or specific reading disability, is a disorder in which children with normal intelligence and sensory abilities show learning deficits for reading. Substantial evidence has established its biological origin and the preponderance of phonological disorders even though important phenotypic variability and comorbidity have been recorded. Diverse theories have been proposed to account for the cognitive and neurological aspects of dyslexia. Findings of genetic studies show that different loci affect specific reading disability although a direct relation has not been established between symptoms and a given genomic locus. In both children and adults with dyslexia, results of neuroimaging studies suggest defective activity and abnormal connectivity between regions crucial for language functions--eg, the left fusiform gyrus for reading--and changes in brain activity associated with performance improvement after various remedial interventions.

Adult↗
PubMed1992

Neurology of developmental dyslexia.

Developmental dyslexia has until recently been considered to belong solely in the domain of educational psychology. With the advent of better theories on language and reading, and better methods for assessing the structure and function of living human brains and for determining genetic transmission, dyslexia is now poised to become a focal concern of cognitive neuroscience and genetic research. Recent findings from neuroanatomy, neurophysiology, neuropsychology, and genetics research are reviewed.

Brain↗
PubMed2002

Mixed lateralization of phonological assembly in developmental dyslexia.

Developmental phonological dyslexia has been characterized as a deficit in phonological assembly. At a neural level, it is possible that this deficit is represented by weak connectivity between anterior and posterior language systems in the left hemisphere. This study used 3-Tesla functional magnetic resonance imaging to investigate phonological assembly in a developmental phonological dyslexic. The phonological dyslexic showed increased activation in the left hemisphere of the inferior frontal gyrus (BA 44/6) and increased activation in the right hemisphere of the parietal cortex (BA 7), occipital cortex (BA 18), and in the cerebellum, as phonological demands were systematically increased. Converging evidence suggests that the core dysfunction in phonological dyslexia resides in and around the angular gyrus of the left hemisphere. This study supports the compensatory role of posterior regions in the right hemisphere together with the left inferior frontal gyrus.

Adult↗
PubMed1986

Interhemispheric coordination is compromised in subjects with developmental dyslexia.

Developmental dyslexics (DDs) and good readers (GRs) were tested on measures of interhemispheric coordination. All subjects (ages 16 to 47) demonstrated normal oculomotor control and visual acuity, prior to testing. Subjects were instructed to track three different point-light source patterns (single stimulus in one hemifield, dual stimuli in one hemifield and a pair of simultaneous, symmetric, bihemifield stimuli [SSBS]), presented in random sequence and arrayed horizontally at +/- 5, +/- 10, and +/- 15 degrees of eccentricity. Tested with unihemifield stimuli, all subjects showed normal saccadic latencies and trajectories. In response to SSBS, all GRs had pronounced directional preference, choosing largely to track one side over the other. In contrast, DDs showed reduced laterality bias (p less than .025). DDs exhibited also significantly longer response latencies to SSBS than to unihemifield stimulation (p less than .01) and differed significantly from GRs (p less than .05).

Adolescent↗
PubMed2003

Why theories about developmental dyslexia require developmental designs.

This article examines the importance of developmental designs in dyslexia research using a neuroconstructivist framework. According to neuroconstructivism, the lowest level of impairment should be identified as early as possible, and developmental effects on higher-level cognition examined longitudinally. A number of recent studies proposing candidate low-level impairments have not used such developmental designs. The role of normal variation in postulated causal factors on development is ignored, inadequate control groups are used, and the nature and timing of environmental inputs are not measured, even though reading is taught systematically and both reading acquisition and dyslexia vary with orthography. It is suggested here that only a phonological deficit arising from low-level auditory processing problems meets the criteria for a neuroconstructivist approach.

Journal Article↗
PubMedDate not supplied

Clock drawing in developmental dyslexia.

Although developmental dyslexia is often defined as a language-based reading impairment not attributable to low intelligence or educational or socioeconomic limitations, the behavioral manifestations of dyslexia are not restricted to the realm of language. Functional brain imaging studies have shed light on physiological differences associated with poor reading both inside and outside the classical language areas of the brain. Concurrently, clinically useful tests that elicit these nonlinguistic deficits are few. Specifically, the integrity of the dorsal visual pathway, which predominantly projects to the parietal cortex, remains underinvestigated, lacking easily administered tests. Here we present the Clock Drawing Test (CDT), used to test the visuoconstructive ability of children with and without dyslexia and garden-variety poor readers. Compared to typically reading children, many children with dyslexia and some garden-variety poor readers showed significant left neglect, as measured by the distribution of figures drawn on the left clock face. In the poor readers with dyslexia, we observed spatial construction deficits like those of patients with acquired right-hemisphere lesions. The results suggest that in some children with dyslexia, right-hemisphere dysfunction may compound the phonological processing deficits attributed to the left hemisphere. The CDT provides an easy opportunity to assess skills known to be associated with right-hemisphere parietal function. This test can be easily administered to children for both clinical and research purposes.

Child↗
PubMed1999

A functional lesion in developmental dyslexia: left angular gyral blood flow predicts severity.

Functional imaging studies have shown reduced regional cerebral blood flow (rCBF) in temporal and inferior parietal regions in dyslexia. To relate such abnormalities to the severity of dyslexia, correlations between reading skill and rCBF during a series of reading tasks and visual fixation were mapped for 17 right-handed dyslexic men, ages 18-40, and 14 matched controls. These correlations uniquely identified the left angular gyrus as the most probable site of a functional lesion in dyslexia: Here, higher rCBF was associated with better reading skill in controls (p <.01), but with worse reading skill in dyslexia (p <.01). This suggests that greater reliance on this region normally facilitates reading, but impairs reading in dyslexia. Thus, developmental dyslexia may share a common localization with alexia.

Adolescent↗
PubMedDate not supplied

The use of orthographic and phonological strategies for the decoding of words in children with developmental dyslexia and average readers.

Children with developmental dyslexia are known to have problems with phonological awareness and, in particular, with phonological decoding. This study was aimed at determining the relationship between orthographic and phonological decoding strategies used by a group of children with developmental dyslexia and two groups of children who were average readers (matched on reading age and chronological age, respectively). The three groups of children, 12 in each, were presented with single words, either visually or orally. The children were asked to pronounce these words using either an orthographic (spelling) strategy following mental deletion of one letter, or a phonological (sounding) strategy following mental deletion of one sound. Analysis of variance (ANOVA) revealed that the reading age control group were more accurate when using phonological strategies than when using orthographic strategies, whereas the chronological age control group generally showed superior orthographic and phonological processing abilities compared with both the developmental dyslexia and reading age control groups. Compared with both chronological and reading age control groups, children in the developmental dyslexia group had more difficulty when using a phonological strategy, particularly when words were presented auditorily. However, compared with their performance on phonological tasks, the developmental dyslexia group performed at a level commensurate with their age when carrying out the orthographic tasks.

Child↗
PubMed2005

Strong evidence that KIAA0319 on chromosome 6p is a susceptibility gene for developmental dyslexia.

Linkage between developmental dyslexia (DD) and chromosome 6p has been replicated in a number of independent samples. Recent attempts to identify the gene responsible for the linkage have produced inconsistent evidence for association of DD with a number of genes in a 575-kb region of chromosome 6p22.2, including VMP, DCDC2, KIAA0319, TTRAP, and THEM2. We aimed to identify the specific gene or genes involved by performing a systematic, high-density (approximately 2-3-kb intervals) linkage disequilibrium screen of these genes in an independent sample, incorporating family-based and case-control designs in which dyslexia was defined as an extreme representation of reading disability. Using DNA pooling, we first observed evidence for association with 17 single-nucleotide polymorphisms (SNPs), 13 of which were located in the KIAA0319 gene (P<.01-.003). After redundant SNPs were excluded, 10 SNPs were individually genotyped in 223 subjects with DD and 273 controls. Those SNPs that were significant at P</=.05 were next genotyped in a semi-independent sample of 143 trios of probands with DD and their parents, to control for possible population stratification. Six SNPs showed significant evidence of association in both samples (P</=.04-.002), including a SNP (rs4504469) in exon 4 of the KIAA0319 gene that changes an amino acid (P=.002; odds ratio 1.5). Logistic regression analysis showed that two SNPs (rs4504469 and rs6935076) in the KIAA0319 gene best explained DD status. The haplotype composed of these two markers was significantly associated with DD (global P=.00001 in the case-control sample; P=.02 in trios). This finding was largely driven by underrepresentation of the most common haplotype in cases (P=.00003 in the case-control sample; P=.006 in trios; 1-degree-of-freedom tests). Our data strongly implicate KIAA0319 as a susceptibility gene for dyslexia. The gene product is expressed in brain, but its specific function is currently unknown.

Adolescent↗
PubMed2004

Two visual motion processing deficits in developmental dyslexia associated with different reading skills deficits.

Developmental dyslexia is associated with deficits in the processing of visual motion stimuli, and some evidence suggests that these motion processing deficits are related to various reading subskills deficits. However, little is known about the mechanisms underlying such associations. This study lays a richer groundwork for exploration of such mechanisms by more comprehensively and rigorously characterizing the relationship between motion processing deficits and reading subskills deficits. Thirty-six adult participants, 19 of whom had a history of developmental dyslexia, completed a battery of visual, cognitive, and reading tests. This battery combined motion processing and reading subskills measures used across previous studies and added carefully matched visual processing control tasks. Results suggest that there are in fact two distinct motion processing deficits in developmental dyslexia, rather than one as assumed by previous research, and that each of these deficits is associated with a different type of reading subskills deficit. A deficit in detecting coherent motion is selectively associated with low accuracy on reading subskills tests, and a deficit in discriminating velocities is selectively associated with slow performance on these same tests. In addition, evidence from visual processing control tasks as well as self-reports of ADHD symptoms suggests that these motion processing deficits are specific to the domain of visual motion, and result neither from a broader visual deficit, nor from the sort of generalized attention deficit commonly comorbid with developmental dyslexia. Finally, dissociation between these two motion processing deficits suggests that they may have distinct neural and functional underpinnings. The two distinct patterns of motion processing and reading deficits demonstrated by this study may reflect separable underlying neurocognitive mechanisms of developmental dyslexia.

Adult↗
PubMed2003

Contrast sensitivity in subgroups of developmental dyslexia.

It has been proposed that developmental dyslexia is associated with a deficit in the magnocellular pathway of the visual system. Other research focuses upon the heterogeneous nature of developmental dyslexia, and evidence that subgroups of dyslexia may be identified based on selective deficits in specific component reading skills. This study tested the hypothesis that visual processing deficits may be present in different subgroups of developmental dyslexia by comparing the visual contrast sensitivity of three subgroups of dyslexic children (phonological, surface and mixed) and controls. The stimulus designed to measure magnocellular visual function was a low spatial frequency Gaussian blob, flickered sinusoidally at a temporal frequency of 8.33 Hz. The control stimulus, designed to measure parvocellular visual function, was a relatively high spatial frequency Gaussian windowed grating (8 c/deg) slowly ramped on and off. There were no significant differences between the groups of dyslexic and control children in contrast sensitivity to either stimulus. The findings do not support the existence of a magnocellular system deficit in dyslexia.

Child↗
PubMedDate not supplied

The magnocellular theory of developmental dyslexia.

Low literacy is termed 'developmental dyslexia' when reading is significantly behind that expected from the intelligence quotient (IQ) in the presence of other symptoms--incoordination, left-right confusions, poor sequencing--that characterize it as a neurological syndrome. 5-10% of children, particularly boys, are found to be dyslexic. Reading requires the acquisition of good orthographic skills for recognising the visual form of words which allows one to access their meaning directly. It also requires the development of good phonological skills for sounding out unfamiliar words using knowledge of letter sound conversion rules. In the dyslexic brain, temporoparietal language areas on the two sides are symmetrical without the normal left-sided advantage. Also brain 'warts' (ectopias) are found, particularly clustered round the left temporoparietal language areas. The visual magnocellular system is responsible for timing visual events when reading. It therefore signals any visual motion that occurs if unintended movements lead to images moving off the fovea ('retinal slip'). These signals are then used to bring the eyes back on target. Thus, sensitivity to visual motion seems to help determine how well orthographic skill can develop in both good and bad readers. In dyslexics, the development of the visual magnocellular system is impaired: development of the magnocellular layers of the dyslexic lateral geniculate nucleus (LGN) is abnormal; their motion sensitivity is reduced; many dyslexics show unsteady binocular fixation; hence poor visual localization, particularly on the left side (left neglect). Dyslexics' binocular instability and visual perceptual instability, therefore, can cause the letters they are trying to read to appear to move around and cross over each other. Hence, blanking one eye (monocular occlusion) can improve reading. Thus, good magnocellular function is essential for high motion sensitivity and stable binocular fixation, hence proper development of orthographic skills. Many dyslexics also have auditory/phonological problems. Distinguishing letter sounds depends on picking up the changes in sound frequency and amplitude that characterize them. Thus, high frequency (FM) and amplitude modulation (AM) sensitivity helps the development of good phonological skill, and low sensitivity impedes the acquisition of these skills. Thus dyslexics' sensitivity to FM and AM is significantly lower than that of good readers and this explains their problems with phonology. The cerebellum is the head ganglion of magnocellular systems; it contributes to binocular fixation and to inner speech for sounding out words, and it is clearly defective in dyslexics. Thus, there is evidence that most reading problems have a fundamental sensorimotor cause. But why do magnocellular systems fail to develop properly? There is a clear genetic basis for impaired development of magnocells throughout the brain. The best understood linkage is to the region of the Major Histocompatibility Complex (MHC) Class 1 on the short arm of chromosome 6 which helps to control the production of antibodies. The development of magnocells may be impaired by autoantibodies affecting the developing brain. Magnocells also need high amounts of polyunsaturated fatty acids to preserve the membrane flexibility that permits the rapid conformational changes of channel proteins which underlie their transient sensitivity. But the genes that underlie magnocellular weakness would not be so common unless there were compensating advantages to dyslexia. In developmental dyslexics there may be heightened development of parvocellular systems that underlie their holistic, artistic, 'seeing the whole picture' and entrepreneurial talents.

Brain↗
PubMed2006

[Role of the organ of vision in the course of developmental dyslexia].

PURPOSE: To present and describe the role of the organ of vision in the course of developmental dyslexia. MATERIAL AND METHODS: A comprehensive review of contemporary literature about the etiopathogenesis and the clinical symptoms of dyslexia was conducted. RESULTS: Developmental dyslexia in other words is the specific difficulty of a person with reading and writing caused by a deficit in the development of perceptive and motoric functions as well as the coordination of these functions. The etiopathogenesis of dyslexia is not definitely determined. Currently developmental dyslexia is thought to be determined by environmental and genetic factors. In accessible literature it is noted that a total of 5-17.5% of all people is effected by dyslexia. It is widely regarded that 63% of all sufferers of dyslexia develop the auditory type of dyslexia with an additional 9% having the visual type of dyslexia, while the rest develop a mixed type. The basis of visual dyslexia lies in the disorder of visual perception linked to the disorders of visual and motoric coordination as well as visual and spatial integration. People with developmental dyslexia tend to evolve numerous changes in the magnocellular pathway, eyeball movements, accommodation as well as binocular vision.

Auditory Perception↗
PubMed2006

Directional motion contrast sensitivity in developmental dyslexia.

The present study compared the perception of visual motion in two dyslexia classification schemes; the [Boder, E. (1973). Developmental dyslexia: a diagnostic approach based on three atypical reading-spelling patterns. Developmental Medicine and Child Neurology, 15, 663-687.] dyseidetic, dysphonetic and mixed subgroups and [Williams, M. J., Stuart, G. W., Castles, A., & McAnally, K. I. (2003). Contrast sensitivity in subgroups of developmental dyslexia. Vision Research, 43, 467-477.] surface, phonological and mixed subgroups by measuring the contrast sensitivity for drifting gratings at three spatial frequencies (1.0, 4.0, and 8.0 c/deg) and five drift velocities (0.75, 3.0, 6.0, 12.0, and 18.0 cyc/s) in a sample of 32 children with dyslexia and 32 matched normal readers. The findings show that there were no differences in motion direction perception between normal readers and the group with dyslexia when dyslexia was taken as a homogeneous group. Motion direction perception was found to be intact in the dyseidetic and surface dyslexia subgroups and significantly lowered in both mixed dyslexia subgroups. The one inconsistency in the findings was that motion direction perception was significantly lowered in the [Boder, E. (1973). Developmental dyslexia: a diagnostic approach based on three atypical reading-spelling patterns. Developmental Medicine and Child Neurology, 15, 663-687.] dysphonetic subgroup and intact in the [Williams, M. J., Stuart, G. W., Castles, A., & McAnally, K. I. (2003). Contrast sensitivity in subgroups of developmental dyslexia. Vision Research, 43, 467-477.] phonological subgroup. The findings also provide evidence for the presence of a disorder in sequential and temporal order processing that appears to reflect a difficulty in retaining sequences of non-meaningful auditory and visual stimuli in short-term working memory in children with dyslexia.

Adolescent↗
PubMed2004

Cognitive profiling and preliminary subtyping in Chinese developmental dyslexia.

The present study examined the cognitive profile and subtypes of developmental dyslexia in a nonalphabetic script, Chinese. One hundred and forty-seven Chinese primary school children with developmental dyslexia were tested on a number of literacy and cognitive tasks. The results showed that rapid naming deficit and orthographic deficit were the two most dominant types of cognitive deficits in Chinese developmental dyslexia, and that rapid naming and orthographic processing had significant unique contributions to literacy performance. Seven subtypes of dyslexia--global deficit, orthographic deficit, phonological memory deficit, mild difficulty, and three other subtypes with rapid-naming-related deficits--were identified using scores of the cognitive tasks as classification measures in cluster analyses. These subtypes were validated with a behaviour checklist and three literacy measures. The authors suggested that orthographic and rapid naming deficits in Chinese dyslexic children might pose an interrelated problem in developing orthographic knowledge and representation. Therefore, orthographic-related difficulties may be the crux of the problem in Chinese developmental dyslexia.

Child↗
PubMed2005

Measurement error: Implications for diagnosis and discrepancy models of developmental dyslexia.

The diagnosis of developmental dyslexia (DD) is reliant on a discrepancy between intellectual functioning and reading achievement. Discrepancy-based formulae have frequently been employed to establish the significance of the difference between 'intelligence' and 'actual' reading achievement. These formulae, however, often fail to take into consideration test reliability and the error associated with a single test score. This paper provides an illustration of the potential effects that test reliability and measurement error can have on the diagnosis of dyslexia, with particular reference to discrepancy models. The roles of reliability and standard error of measurement (SEM) in classic test theory are also briefly reviewed. This is followed by illustrations of how SEM and test reliability can aid with the interpretation of a simple discrepancy-based formula of DD. It is proposed that a lack of consideration of test theory in the use of discrepancy-based models of DD can lead to misdiagnosis (both false positives and false negatives). Further, misdiagnosis in research samples affects reproducibility and generalizability of findings. This in turn, may explain current inconsistencies in research on the perceptual, sensory, and motor correlates of dyslexia.

Child↗