Theories Of Dyslexia Research Articles

The perceptual span in dyslexic reading and visual search.

Many studies have attempted to identify the root cause of dyslexia. Different theories of dyslexia have proposed either a phonological, attentional, or visual deficit. While research has used eye-tracking to study dyslexia, only two previous studies have used the moving-window paradigm to explore the perceptual span in dyslexic reading, and none have done so in visual search. The present study analysed the perceptual span using both reading and visual search tasks to identify language-independent attentional impairments in dyslexics. We found equivocal evidence that the perceptual span was impaired in dyslexic reading and no evidence of impairment in visual search. However, dyslexic participants did show deficits in the visual search task, with lower search accuracy and shorter saccades compared with controls. These results lend support for a visual, rather than attentional or phonological, account of dyslexia.

Development of Dyslexia: The Delayed Neural Commitment Framework.

It is now evident that explanations of many developmental disorders need to include a network perspective. In earlier work, we proposed that developmental dyslexia (DD) is well-characterized in terms of impaired procedural learning within the language networks, with the cerebellum being the key structure involved. Here, we deepen the analysis to include the child’s developmental process of constructing these networks. The “Delayed Neural Commitment (DNC)” framework proposes that, in addition to slower skill acquisition, dyslexic children take longer to build (and to rebuild) the neural networks that underpin the acquisition of reading. The framework provides an important link backwards in time to the development of executive function networks and the earlier development of networks for language and speech. It is consistent with many theories of dyslexia while providing fruitful suggestions for further research at the genetic, brain, cognitive and behavioral levels of explanation. It also has significant implications for assessment and teaching.

Impaired Driving Performance as Evidence of a Magnocellular Deficit in Dyslexia and Visual Stress.

High comorbidity and an overlap in symptomology have been demonstrated between dyslexia and visual stress. Several researchers have hypothesized an underlying or causal influence that may account for this relationship. The magnocellular theory of dyslexia proposes that a deficit in visuo-temporal processing can explain symptomology for both disorders. If the magnocellular theory holds true, individuals who experience symptomology for these disorders should show impairment on a visuo-temporal task, such as driving. Eighteen male participants formed the sample for this study. Self-report measures assessed dyslexia and visual stress symptomology as well as participant IQ. Participants completed a drive simulation in which errors in response to road signs were measured. Bivariate correlations revealed significant associations between scores on measures of dyslexia and visual stress. Results also demonstrated that self-reported symptomology predicts magnocellular impairment as measured by performance on a driving task. Results from this study suggest that a magnocellular deficit offers a likely explanation for individuals who report high symptomology across both conditions. While conclusions about the impact of these disorders on driving performance should not be derived from this research alone, this study provides a platform for the development of future research, utilizing a clinical population and on-road driving assessment techniques.

A Mini-Review: Toward a Comprehensive Theory of Dyslexia

Current research suggests that the neurobiological substrate of dyslexia involves the dysfunctional orchestration of a multi-dimensional and hierarchical circuitry of at least three neuronal networks. This circuitry principally involves the posterior corpus callosum, left arcuate fasciculous, and the right frontostriatal attentional control network. The key to understanding the disability and in forging a comprehensive theory of dyslexia may be found in investigations aimed at interactions among all three networking territories.

The magnocellular theory of dyslexia

The magnocellular theory of dyslexia

DYSLEXIA RESEARCH AT THE TURN OF THE 21ST CENTURY: BEHAVIOURAL, NEUROIMAGING AND GENETIC FINDINGS

Behavioural studies have shown that dyslexics are a heterogeneous population and between-group comparisons are thus inadequate. Some subjects do not develop dyslexia despite having a deficit implicated in this disorder, which points to protective factors. Dyslexia co-occurs with ADHD, DCD, SLI, and SSD, so that future behavioural studies will need to screen and/or statistically control for other disorders. Studies of multiple cases of DPs with other developmental disorders are necessary. Neuroimaging findings show structural and/or functional brain abnormalities in language areas, V5/MT and the cerebellum. Future neuroimaging studies need to investigate the whole reading network and multiple cases. Six dyslexia risk genes have been found, mostly involved in neural migration, which may suggest dyslexia is a deficit of neuronal migration. However, it is not clear how these genes can restrict migration to specific brain areas. As a complex and heterogeneous disorder, dyslexia is likely to be associated with several mutated genes. ADHD and SSD are characterised by genetic risk factors which are partially shared with dyslexia, resulting in comorbidity. Future genetic studies need to focus on identifying other risk genes and pleiotropic genes involved in comorbidities, and linking genotypes implicated in dyslexia with brain structure. Any theory of dyslexia needs to take into account a multitude of risk and protective factors across behavioural, neural and genetic domains.

The Orientation Theory of dyslexia: uniting current schisms through an ecological perspective

In earlier work the concept of Orientation (O) was proposed as the key factor in successful literacy acquisition. This article develops that idea further to discuss the potential of Orientation Theory (OT) to unite current conflicts between apparently opposing theories of dyslexia. After briefly outlining these theoretical differences it is proposed that by adopting an ecological paradigm, in place of a “within child” model, the three major theories of dyslexia can be seen to offer valid but partial explanations within the wider concept of orientation. Orientation (O) and Genetic Identity (GI) generated as the two essential factors of OT are described in relation to these three theories. The application of OT in both UK educational policy and early years development are outlined. Finally, some answers to Nicolson's six questions for dyslexia are provided.

Surface and phonological developmental dyslexia in Greek

The present study examined whether equivalents of surface and phonological subtypes of developmental dyslexia could be found among a sample of 84 poor readers aged 9–12 years in Greece. Word reading latency was used as a measure of lexical skill, and nonword reading accuracy was used as a measure of nonlexical skill. A simple regression of word reading latencies on nonword reading accuracy scores was performed for 42 developing readers. A total of 2 poor readers with accurate nonword reading plus slow word reading relative to controls (equivalents of surface dyslexia) and 2 poor readers with inaccurate nonword reading plus fast accurate word reading relative to controls (equivalents of phonological dyslexia) were identified from amongst the sample of poor readers. Further testing of these 4 cases on measures of irregular-word and nonword spelling revealed additional evidence of a dissociation between lexical and nonlexical impairments. These results support the notion that dual-route models can be used to explore individual differences among dyslexic readers in transparent orthographic systems such as Greek. An attempt is also made to interpret the results in terms of a double deficit theory of dyslexia (Wimmer, Mayringer, & Landerl, 2000; Wolf & Bowers, 1999).

Auditory and visual stream segregation in children and adults: An assessment of the amodality assumption of the ‘sluggish attentional shifting’ theory of dyslexia

Among the hypotheses relating dyslexia to a temporal processing disorder, Hari and Renvall (Hari, R., Renvall, H., 2001. Impaired processing of rapid stimulus sequences in dyslexia. Trends. Cognit. Sci. 5, 525–532.) argued that dyslexic individuals would show difficulties at an attentional level, through sluggish attentional shifting (SAS) in all sensory modalities. However, the amodality assumption of the SAS theory was never straightforwardly assessed in the same group of dyslexic participants using similar paradigms in both the visual and auditory modalities. Here, the attentional sequential performance of control and dyslexic participants was evaluated using rapid serial presentation paradigms measuring individual stream segregation thresholds in the two modalities. The first experiment conducted on French dyslexic children with a phonological disorder revealed an SAS only in the auditory modality only which was strongly related to reading performance. The second experiment carried out on British dyslexic young adults with a phonological disorder using the same auditory segregation task but a different visual paradigm revealed an SAS in both the visual and the auditory modalities. In addition, a relationship was found in this group between SAS, poor reading and poor phonological skills. Two further control experiments showed that differences in task design or participants' language between Experiments 1 and 2 could not account for the differences in terms of visual segregation patterns. Overall, our results support the view that the auditory SAS plays a role in developmental dyslexia via its impact on phonological abilities. In addition, a visual temporal disorder in dyslexia might emerge at a later developmental stage, when the visual system normally becomes more expert at rapid temporal processing.

COHERENT MOTION, MAGNOCELLULAR SENSITIVITY AND THE CAUSATION OF DYSLEXIA

The central tenet of the magnocellular deficit theory of dyslexia is that dyslexia is caused by a magnocellular deficit. A number of investigators have found deficiencies in visual coherent motion perception among dyslexic readers. These deficiencies have been attributed to magnocellular deficits, which means that they directly reflect the cause of dyslexia. However, similar perceptual deficiencies have been found in association with autism, Williams's syndrome, hemiplegia, and schizophrenia. These findings appear to undermine at least one of the following claims: (1) that a magnocellular deficit is the cause of dyslexia, and (2) that coherent motion is a reliable test of magnocellular sensitivity.

A test of the magnocellular deficit theory of dyslexia in an adult sample

An influential theory of dyslexia is based on the premise that individuals with the disorder have impaired sensitivity to rapidly changing stimuli in the visual and auditory modalities, due to a dysfunction in the magnocellular channel of the visual system and its analogue in the auditory pathway. The deficit in the auditory system is thought to cause difficulties in the segmentation of speech and the formation of accurate phonological representations, leading to problems in making the grapheme–phoneme correspondences necessary for reading. In a sample of 13 adults with a history of severe reading difficulty and 18 controls, visual contrast thresholds were measured in response to an 8-Hz flickering Gaussian blob as well as a slowly modulated 8 cycles/deg Gaussian windowed grating. Auditory thresholds were measured in response to a 4-s burst of white noise, the 2nd or 3rd second of which was amplitude modulated at 100 Hz or 1 Hz. The adult reading difficulty group exhibited normal thresholds to rapidly changing stimuli in both modalities and to the slowly modulated visual stimulus, but some showed reduced sensitivity to the 1-Hz amplitude-modulated auditory stimulus. Sensitivity to amplitude modulation at slower rates has been shown to be important for segmentation of the speech stream and so may be implicated in the reading difficulty of the affected individuals. A magnocellular deficit cannot explain this impaired sensitivity, which may be the result of a reduced echoic memory span.

Longitudinal case-studies of developmental dyslexia in Norwegian

This study examined retrospectively the preschool cognitive and linguistic profiles and emergent literacy skills in four Norwegian dyslexic children. The aim was to identify prognostic indicators that were associated with the reading impairments observed in an earlier study of these children. In comparison to a control group of at-risk children who were normal readers at age 10, three of the four dyslexic children exhibited either stagnation or a decline in speech accuracy in the presence of a vocabulary growth spurt at age 2-3 years. Skills in phonological awareness seemed to vary inconsistently with both early speech development and emergent literacy across the four cases. Delayed development in emergent literacy turned out to be the most potent prognostic indicator of later reading disorders. The study was guided by lexical restructuring theories of dyslexia.

Balancing and pointing tasks in dyslexic and control adults

Developmental dyslexia may affect as much as 15% of the population, but the aetiology of the disorder is still being debated. The cerebellar theory of dyslexia proposes that cerebellar dysfunction could lead to the myriad of symptoms seen in dyslexic individuals, both in literacy and non-literacy domains. The cerebellum is crucial to the fluent performance of motor skills. Previous studies have found that dyslexic children are worse than control children on certain motor and balancing tasks. Here the performance of 28 dyslexic compared to 26 control adults on rapid pointing and balancing measures, tasks which are thought to reflect cerebellar function, was investigated. There were no significant differences between the dyslexic and control participants on the balancing tasks or when the speed and accuracy of pointing were analysed separately. However, when the speed and accuracy of pointing were combined, the dyslexic participants showed poorer performance than the controls (p = 0.045). Furthermore, there were significant relationships between performance on the pointing task and literacy skills, and regression analysis showed that the error and speed of pointing contributed significantly to the variance in literacy skill. The implications for the role of the cerebellum and processing speed in dyslexia are discussed.

Auditory perceptual grouping and attention in dyslexia

Despite dyslexia affecting a large number of people, the mechanisms underlying the disorder remain undetermined. There are numerous theories about the origins of dyslexia. Many of these relate dyslexia to low-level, sensory temporal processing deficits. Another group of theories attributes dyslexia to language-specific impairments. Here, we show that dyslexics perform worse than controls on an auditory perceptual grouping task. The results show differences in performance between the groups that depend on sound frequency and not solely on parameters related to temporal processing. Performance on this task suggests that dyslexics' deficits may result from impaired attentional control mechanisms. Such deficits are neither modality nor language-specific and may help to reconcile differences between theories of dyslexia.

The relationship between motor control and phonology in dyslexic children.

The goal of this study was to investigate the automaticity/cerebellar theory of dyslexia. We tested phonological skills and cerebellar function in a group of dyslexic 8-12-year-old children and their matched controls. Tests administered included the Phonological Assessment Battery, postural stability, bead threading, finger to thumb and time estimation. Dyslexic children were found to be significantly poorer than the controls at all tasks but time estimation. About 77% of dyslexics were more than one standard deviation below controls in phonological ability, and 59% were similarly impaired in motor skills. However, at least part of the discrepancy in motor skills was due to dyslexic individuals who had additional disorders (ADHD and/or DCD). The absence of evidence for a time estimation deficit also casts doubt on the cerebellar origin of the motor deficiency. About half the dyslexic children didn't have any motor problem, and there was no evidence for a causal relationship between motor skills on the one hand and phonological and reading skills on the other. This study provides partial support for the presence of motor problems in dyslexic children, but does not support the hypothesis that a cerebellar dysfunction is the cause of their phonological and reading impairment.

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.

Stavefejlenes udviklingspsykologi—kreativitet og strukturelle hypoteser I børns stavning

Kihl, P. (1993). The developmental psychology of spelling errors—creativity and structural hypotheses in children's spelling. Nordisk Psykologi, 45, 186–202. The paper reviews and describes current Danish and Anglo-American research on children's spelling errors at different developmental stages. The stages are characterized by the most frequent spelling error type occuring at a given time even if there is overlap between error types. Based on these stages, in particular the transitional period before mature spelling, a model of the spelling process with different cognitive levels is presented. It is argued that other studies of normal and dyslectic spelling support this model. Furthermore, this interpretation of normal children's spelling errors in a natural way accounts for two-category theories of dyslexia. Finally the cognitive nature of children's hypercorrections is discussed.

Visual Persistence and Adult Dyslexia

Visual persistence was investigated in adults with and without dyslexia in order to determine whether the adults with dyslexia demonstrate problems similar to those found in childhood dyslexia. Using a temporal separation threshold measure and procedures derived from signal detection theory, sensitivity to sequentially presented form information was determined for the two types of adults. The results showed that the sensitivity of the adults with dyslexia was impaired relative to that of the nondisabled adults when parts of a test stimulus were presented to adjacent retinal areas. This result suggests that, under certain conditions, visual persistence is longer for adults with dyslexia. The results are discussed within the context of a recent theory of dyslexia (Lovegrove, Martin & Slaghuis, 1986) that incorporates the operation of sustained and transient visual mechanisms.

Initial observations on sensory interaction and the theory of dyslexia

Dyslexia is held to be a disorder of intersensory matching and discrimination. Two very different experiments are reported to test this theory, and the results to indeed support it. (a) The immediate visual recall of dyslexic children is significantly hindered by the presentation of distracting auditory noise during the initial exposure of the visual targets. (b) The bimodally evoked audiovisual brain responses in dyslexic children are most generally slightly reduced in amplitude, i.e. from their uninhibited unimodal ones, in contrast to the bimodal enhancement which we have sometimes found in normal readers. While we do not wish to extrapolate beyond these findings, particularly because the brain study with normals is still in progress, they do in general support the theory of the intersensory basis of dyslexia and suggest many directions for further study.