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We provide a meta-analytic review of all group-comparison studies that used reading-level match design, were conducted in highly consistent European orthographies, included children with dyslexia younger than 13 years of age as participants, and included measures of one or more of the potential causes of dyslexia. We identified 21 studies meeting these criteria that examined one or more of phonological awareness, rapid naming, verbal short-term memory, or auditory temporal processing. A random effects model analysis showed first that the groups were matched imperfectly and they differed significantly in word reading measures not used for matching. Second, there were no significant differences between the individuals with dyslexia and their reading-level-matched controls in rapid naming, phonological memory, and auditory temporal processing. Finally, the analyses for phonological awareness showed a significant effect for comparisons that involved manipulating phonemes but not for tasks that involved manipulating syllables. The results are compatible with phonological deficit theories of dyslexia, but this conclusion is qualified by observed differences in reading skills and sample selection concerns.

Competing theories of dyslexia posit that reading difficulties arise from impaired visual, auditory, phonological, or statistical learning mechanisms. Importantly, many theories posit that dyslexia reflects a cascade of impairments emanating from a single “core deficit”. Here we report two studies evaluating core deficit and multifactorial models. In Study 1, we use publicly available data from the Healthy Brain Network to test the accuracy of phonological processing measures for predicting dyslexia diagnosis and find that over 30% of cases are misclassified (sensitivity = 66.7%; specificity = 68.2%). In Study 2, we collect a battery of psychophysical measures of visual motion processing and standardized measures of phonological processing in 106 school‐aged children to investigate whether dyslexia is best conceptualized under a core‐deficit model, or as a disorder with heterogenous origins. Specifically, by capitalizing on the drift diffusion model to analyze performance on a visual motion discrimination experiment, we show that deficits in visual motion processing, perceptual decision‐making, and phonological processing manifest largely independently. Based on statistical models of how variance in reading skill is parceled across measures of visual processing, phonological processing, and decision‐making, our results challenge the notion that a unifying deficit characterizes dyslexia. Instead, these findings indicate a model where reading skill is explained by several distinct, additive predictors, or risk factors, of reading (dis)ability., Using predictors from a visual motion processing experiment and linguistic measures, we show that a single‐mechanism model of reading disability cannot account for the range of linguistic and sensory processing outcomes observed in children. We propose an additive risk factor model where different aspects of sensory, cognitive and language function each contribute independently to reading development.

Two themes have puzzled the research on developmental and learning disorders for decades. First, some of the risk and protective factors behind developmental challenges are suggested to be shared and some are suggested to be specific for a given condition. Second, language-based learning difficulties like dyslexia are suggested to result from or correlate with non-linguistic aspects of information processing as well. In the current study, we investigated how adults with developmental dyslexia or ADHD as well as healthy controls cluster across various dimensions designed to tap the prominent non-linguistic theories of dyslexia. Participants were 18–55-year-old adults with dyslexia (n = 36), ADHD (n = 22), and controls (n = 35). Non-linguistic theories investigated with experimental designs included temporal processing impairment, abnormal cerebellar functioning, procedural learning difficulties, as well as visual processing and attention deficits. Latent profile analysis (LPA) was used to investigate the emerging groups and patterns of results across these experimental designs. LPA suggested three groups: (1) a large group with average performance in the experimental designs, (2) participants predominantly from the clinical groups but with enhanced conditioning learning, and (3) participants predominantly from the dyslexia group with temporal processing as well as visual processing and attention deficits. Despite the presence of these distinct patterns, participants did not cluster very well based on their original status, nor did the LPA groups differ in their dyslexia or ADHD-related neuropsychological profiles. Remarkably, the LPA groups did differ in their intelligence. These results highlight the continuous and overlapping nature of the observed difficulties and support the multiple deficit model of developmental disorders, which suggests shared risk factors for developmental challenges. It also appears that some of the risk factors suggested by the prominent non-linguistic theories of dyslexia relate to the general level of functioning in tests of intelligence., SCOPUS: ar.j, info:eu-repo/semantics/published

Although schizophrenia and developmental dyslexia are considered distinct disorders in terms of clinical presentation and functional outcome, they both involve disruption in the processes that support skilled reading, including language, auditory perception, visual perception, oculomotor control, and executive function. Further, recent work has proposed a common neurodevelopmental basis for the two disorders, as suggested by genetic and pathophysiological overlap. Thus, these lines of research suggest that reading may be similarly impacted in schizophrenia and dyslexia. In this review, we survey research on reading abilities in individuals with schizophrenia, and review the potential mechanisms underlying reading deficits in schizophrenia that may be shared with those implicated in dyslexia. Elucidating the relationship between reading impairment in schizophrenia and dyslexia could allow for a better understanding of the pathophysiological underpinnings of schizophrenia, and could facilitate remediation of cognitive deficits that impact day-to-day functioning.

Dyslexia can have different manifestations: this has motivated different theories on its nature, on its underlying brain bases and enduring controversies on how to best treat it. The relative weight of the different manifestations has never been evaluated using both behavioural and fMRI measures, a challenge taken here to assess the major systems called into play in dyslexia by different theories. We found that adult well-compensated dyslexics were systematically impaired only in reading and in visuo-phonological tasks, while deficits for other systems (e.g., motor/cerebellar, visual magnocellular/motion perception) were only very occasional. In line with these findings, fMRI showed a reliable hypoactivation only for the task of reading, in the left occipito-temporal cortex (l-OTC). The l-OTC, normally a crossroad between the reading system and other systems, did not show the same level of intersection in dyslexics; yet, it was not totally silent because it responded, in segregated parts, during auditory phonological and visual motion perception tasks. This minimal behavioural and functional anatomical comorbidity demonstrates that a specific deficit of reading is the best description for developmental dyslexia, at least for adult well-compensated cases, with clear implications for rehabilitation strategies. The reduced intersection of multiple systems in the l-OTC suggests that dyslexics suffer from a coarser connectivity, leading to disconnection between the multiple domains that normally interact during reading.

Dyslexia also known as specific reading disorder is a complex heritable disorder with unexpected difficulty in learning to read and spell despite adequate intelligence, education, environment, and normal senses. Over past decades, researchers have attempted to characterize dyslexia neurobiological and genetic levels and unfold its pathophysiology. The genetic research on dyslexia has received attention in Asia from the last decade. Though limited by different constraints the studies from Asia have been able to gather significant evidence in this field. We present a review of studies of genetics in Asian population and suggest future directions.

Dyslexia is a developmental disorder characterized by reading and phonological difficulties, yet important questions remain regarding its underlying neural correlates. In this study, we used partial least squares (PLS), a multivariate analytic technique, to investigate the neural networks used by dyslexics while performing a word-rhyming task. Although the overall reading network was largely similar in dyslexics and typical readers, it did not correlate with behavior in the same way in the two groups. In particular, there was a positive association between reading performance and both right superior temporal gyrus and bilateral insula activation in dyslexic readers but a negative correlation in typical readers. Together with differences in lateralization unique to dyslexics, this suggests that the combination of poor reading performance with high insula activity and atypical laterality is a consistent marker of dyslexia. These findings emphasize the importance of understanding right-hemisphere activation in dyslexia and provide promising directions for the remediation of reading disorders.

It is generally agreed that there are individual differences in the severity of the reading deficit in dyslexia. The purpose of this review is to discuss whether recent research strengthens claims that there are also qualitative differences in the type of reading impairment that individual dyslexic children experience. Recent research suggests that surface dyslexia exists in larger numbers than has previously been assumed and that different subtypes of surface dyslexia exist in English as well as in Hebrew. Bilinguals with surface dyslexia in English also show the hallmarks of surface dyslexia when reading a more transparent orthography. The developmental reading impairments that have been observed in children with phonological dyslexia and in children with letter position dyslexia can also be found in several different orthographies and are quite distinct from those seen in surface dyslexia. Surface dyslexia, phonological dyslexia, and letter position dyslexia represent qualitatively different types of developmental reading impairments and can all be seen in both opaque and more transparent alphabetic orthographies.

The aim of this study was to investigate the prosody abilities on top of phonological and visual abilities in children with dyslexia in Spanish that can be considered a syllable-timed language. The...

Contains fulltext : 178945.pdf (Publisher’s version ) (Open Access) The present study aimed to explore the nature of developmental dyslexia in a language considered to have a transparent orthography, namely, Dutch. We assessed the accuracy and efficiency of decoding words and pseudowords with four lengths as well as three types of phonological ability in 2,760 typical children and 397 peers with dyslexia across Grades 3-6. For typical readers, decoding levels across the grades were found to be largely a matter of increasing speed. For the readers with dyslexia, difficulties manifested themselves for both accuracy and efficiency of decoding but more for pseudowords than for words. The readers with dyslexia were also more sensitive to word-length effects on decoding. The phonological abilities of the children with dyslexia lagged behind as well. It is concluded that in Dutch, children with dyslexia show a phonological deficit and persistent problems with assembling phonology during the phonological recoding of orthographic representations. 17 p.

The phonological theory of dyslexia makes it difficult to distinguish developmental dyslexia from social causes of reading failure, because, whatever their cause, all poor readers seem to have similar phonological problems. In order to understand why children with dyslexia fail, we need to understand the physiological mechanisms that underlie their failure to acquire phonological skills. An important cause is probably impaired development of the brain’s rapid temporal processing systems; these are required for sequencing accurately the order of the sounds and letters in a word. Such temporal, “transient”, processing is probably carried out in all parts of the brain primarily by a distinct set of “magnocellular” neurones, and the development of these has been found to be impaired in many people with dyslexia. Therefore measuring poor readers’ auditory and temporal processing skills should enable dyslexia to be reliably distinguished from other causes of phonological deficits.

The present study aims to find empirical evidence of deficits in linguistic pragmatic skills and theory of mind (ToM) in children with dyslexia with associated language difficulties or nonverbal learning disabilities (NLD), when compared with a group of typically developing (TD) children matched for age and gender. Our results indicate that children with dyslexia perform less well than TD children in most of the tasks measuring pragmatics of language, and in one of the tasks measuring ToM. In contrast, children with NLD generally performed better than the dyslexia group, and performed significantly worse than the TD children only in a metaphors task based on visual stimuli. A discriminant function analysis confirmed the crucial role of the metaphors subtest and the verbal ToM task in distinguishing between the groups. We concluded that, contrary to a generally-held assumption, children with dyslexia and associated language difficulties may be weaker than children with NLD in linguistic pragmatics and ToM, especially when language is crucially involved. The educational and clinical implications of these findings are discussed.

Competing theories of dyslexia posit that reading disability arises from impaired sensory, phonological, or statistical learning mechanisms. Importantly, many theories posit that dyslexia reflects a cascade of impairments emanating from a “core deficit”. Here we collect a battery of psychophysical and language measures in 106 school-aged children to investigate whether dyslexia is best conceptualized under a core-deficit model, or as a disorder with heterogenous origins. Specifically, by capitalizing on the drift diffusion model to separate sensory encoding from task-related influences on performance in a visual motion discrimination experiment, we show that deficits in motion perception, decision making and phonological processing manifest largely independently. Based on statistical models of how variance in reading skill is parceled across measures of sensory encoding, phonological processing and decision-making, our results challenge the notion that a unifying deficit characterizes dyslexia. Instead, these findings indicate a model where reading skill is explained by several distinct, additive predictors, or risk factors, of reading (dis)ability.Research HighlightsOur research provides direct evidence that a single-mechanism, or core-deficit, model of dyslexia cannot account for the range of linguistic and sensory outcomes in children.Individual differences in visual motion processing, perceptual decision making, phonological awareness and rapid naming each account for unique variance in reading skill.Our data support an additive risk-factor model, in which multiple independent dimensions each confer risk for reading difficulties.

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.

Previous results showed a positive influence of music training on linguistic abilities at both attentive and preattentive levels. Here, we investigate whether six months of active music training is more efficient than painting training to improve the preattentive processing of phonological parameters based on durations that are often impaired in children with developmental dyslexia (DD). Results were also compared to a control group of Typically Developing (TD) children matched on reading age. We used a Test&ndash, Training&ndash, Retest procedure and analysed the Mismatch Negativity (MMN) and the N1 and N250 components of the Event-Related Potentials to syllables that differed in Voice Onset Time (VOT), vowel duration, and vowel frequency. Results were clear-cut in showing a normalization of the preattentive processing of VOT in children with DD after music training but not after painting training. They also revealed increased N250 amplitude to duration deviant stimuli in children with DD after music but not painting training, and no training effect on the preattentive processing of frequency. These findings are discussed in view of recent theories of dyslexia pointing to deficits in processing the temporal structure of speech. They clearly encourage the use of active music training for the rehabilitation of children with language impairments.

Several etiological theories, in particular neuronal noise and impaired auditory sampling, predicted neurotransmission deficits in dyslexia. Neurometabolites also affect white matter microstructure, where abnormalities were previously reported in dyslexia. However findings from only few magnetic resonance spectroscopy studies using diverse age groups, different brain regions, data processing and reference scaling are inconsistent. We used MEGA-PRESS single-voxel spectroscopy in two ROIs: left temporo-parietal and occipital cortex in 36 adults and 52 children, where half in each group had dyslexia. Dyslexics, on average, had significantly lower total N-acetylaspartate (tNAA) than controls in the occipital cortex. Adults compared to children were characterized by higher choline and creatine in both areas, higher tNAA in left temporo-parietal and lower glutamate in the visual cortex, reflecting maturational changes in cortical microstructure and metabolism. Although the current findings do not support the proposed etiological theories of dyslexia, they show, for the first time, that tNAA, considered to be a neurochemical correlate of white matter integrity, is deficient in the visual cortex in both children and adults with dyslexia. They also point that several neurotransmitters, including ones previously used as reference, change with age.

Purpose This paper starts by considering what it means if dyslexia has genetic or environmental causes. The author also explains phrases used by genetic researchers and the kind of things they look for in genetic material. The purpose of this paper is to discuss two recent studies on dyslexia that shed light on either genetic or environmental causes. Design/methodology/approach One study was a thorough exploration of possible genetic differences that could be present in children experiencing reading and language difficulties. The other study examined a large sample of the Canadian public to see whether there was a link between dyslexia and having experienced physical abuse as a child or teenager. Findings The study on genetic differences found no evidence for some previously suggested genetic causes of dyslexia. Although previous studies have suggested dyslexia runs in families, the genetic contribution may have been overestimated. The study on the Canadian public found that people who reported experiencing physical abuse in their younger years were six to seven times more likely also to have a diagnosis of dyslexia. Childhood trauma is known to affect brain development. Originality/value Although this paper only discusses two papers in detail, they are two of the most recent explorations of genetic and environmental links to dyslexia. There could be a case for greater attention to possible traumatic experiences in children identified as dyslexic. Physical abuse is one possibility but should never be assumed. Families can be under strain and may need more support. However, dyslexia and the mental health difficulties that can result from childhood trauma can reduce a child’s current and future social inclusion. Early intervention may avert this outcome.

Clearly, the value of any theory—dyslexia or otherwise—depends entirely on its encompassing and explanatory powers as well as its ability to lead to new insights and discoveries.

Objective Individuals with dyslexia experience reading difficulties, whereas their other cognitive abilities seem normal. The purpose of this study was to investigate the event-related potential (ERP) patterns of children with dyslexia during a target-detection task. Methods Seventeen children with dyslexia and 18 children without this disorder participated in this study. We evaluated their writing and reading ability, symptoms of attention-deficit/hyperactivity disorder, and intelligence quotient. ERPs were recorded while participants performed a target-detection task, and the peak amplitude and latency of P100 and P300 were analyzed. The lateral asymmetry index (LAI) was calculated for each ERP component. Results The dyslexic group exhibited longer reaction times and larger P100 amplitudes than the non-dyslexic group in the right hemisphere. The P100 latency was also significantly delayed in the right hemisphere of those in the dyslexic group compared with those in the non-dyslexic group. The P300 amplitude was larger in the right hemisphere compared with left hemisphere in the dyslexic group, whereas no interhemispheric differences were observed with respect to the P300 latency. The LAI for P100 showed a significant right hemispheric dominance, whereas the LAI for P100 was significantly correlated with the accuracy of target detection in children with dyslexia. Conclusion Our results suggest that right hemispheric dominance acts as an ancillary system that compensates for poor reading in children with dyslexia.

Developmental dyslexia is an unexplained inability to acquire accurate or fluent reading that affects approximately 5-17% of children. Dyslexia is associated with structural and functional alterations in various brain regions that support reading. Neuroimaging studies in infants and pre-reading children suggest that these alterations predate reading instruction and reading failure, supporting the hypothesis that variant function in dyslexia susceptibility genes lead to atypical neural migration and/or axonal growth during early, most likely in utero, brain development. Yet, dyslexia is typically not diagnosed until a child has failed to learn to read as expected (usually in second grade or later). There is emerging evidence that neuroimaging measures, when combined with key behavioral measures, can enhance the accuracy of identification of dyslexia risk in pre-reading children but its sensitivity, specificity, and cost-efficiency is still unclear. Early identification of dyslexia risk carries important implications for dyslexia remediation and the amelioration of the psychosocial consequences commonly associated with reading failure.

The purpose of this theoretical analysis and synthesis is to indicate how left-eye sighting dominance may lead to reading failure through dysfunctional right hemisphere letter encoding. Differing compensatory strategies are postulated to lead to outcomes that include the development of the phonologically impaired and phonologically proficient subtypes of dyslexia as well as specific spelling disability. Evidence is presented indicating that these disorders might be prevented by delaying the introduction of letter writing until the age of 8 years. Early childhood speech categorization in children genetically at-risk of developing dyslexia is also considered from this perspective. Convergent support for this premature writing hypothesis is provided by a comparison with the development of the left-hand inverted writing posture.

The aim of this review is to provide a background on the neurocognitive aspects of the reading process and review neuroscientific studies of individuals with developmental dyslexia, which provide evidence for amodal processing deficits. Hari, Renvall, and Tanskanen (2001) propose amodal sluggish attentional shifting (SAS) as a causal factor for temporal processing deficits in dyslexia. Undergirding this theory is the notion that when dyslexics are faced with rapid sequences of stimuli, their automatic attentional systems fail to disengage efficiently, which leads to difficulty when moving from one item to the next (Lallier et al., ). This results in atypical perception of rapid stimulus sequences. Until recently, the SAS theory, particularly the examination of amodal attentional deficits, was studied solely through the use of behavioural measures (Facoetti et al., ; Facoetti, Lorusso, Cattaneo, Galli, & Molteni, ). This paper examines evidence within the literature that provides a basis for further exploration of amodal SAS as an underlying deficit in developmental dyslexia.

Developmental dyslexia (DD) or reading disability is characterized by unexpected problems in reading acquisition, despite average intelligence. It is considered the most common neurodevelopmental disorder, and many researchers aimed to identify the cognitive, neurobiological and genetic etiology of DD. At the cognitive level, the hypothesis of auditory temporal processing deficit has been widely investigated. The aim of this review is to present some of the most exciting researches on DD in the domains of this theory that will help future studies to follow.

Background: The Japanese writing system has two distinctive orthographies: morphographic Kanji and syllabographic Kana. The difference between Kanji and Kana in terms of both character–sound correspondences (i.e., pronunciation predictability) and the character–meaning relationship is quite striking. Research on acquired dyslexia in Japanese means studying “monolingual-bi-scriptal readers” with brain damage, giving us a rare chance to examine whether the identical brain damage has similar or discrepant effects on the processes of reading aloud in different orthographies.Aims: This article mainly reviews cognitive neuropsychological research on Japanese acquired dyslexia and proposed reading models for Japanese, then asks how well existing reading models can explain patterns of impaired oral reading in Japanese.Main Contribution: This review attempts to provide a comprehensive picture of research on Japanese acquired dyslexia, which is still not especially well-known in the English literature and has not e...

Background Causal theories of dyslexia suggest that it is a heritable disorder, which is the outcome of multiple risk factors. However, whether early screening for dyslexia is viable is not yet known. Methods The study followed children at high risk of dyslexia from preschool through the early primary years assessing them from age 3 years and 6 months (T1) at approximately annual intervals on tasks tapping cognitive, language, and executive-motor skills. The children were recruited to three groups: children at family risk of dyslexia, children with concerns regarding speech, and language development at 3;06 years and controls considered to be typically developing. At 8 years, children were classified as ‘dyslexic’ or not. Logistic regression models were used to predict the individual risk of dyslexia and to investigate how risk factors accumulate to predict poor literacy outcomes. Results Family-risk status was a stronger predictor of dyslexia at 8 years than low language in preschool. Additional predictors in the preschool years include letter knowledge, phonological awareness, rapid automatized naming, and executive skills. At the time of school entry, language skills become significant predictors, and motor skills add a small but significant increase to the prediction probability. We present classification accuracy using different probability cutoffs for logistic regression models and ROC curves to highlight the accumulation of risk factors at the individual level. Conclusions Dyslexia is the outcome of multiple risk factors and children with language difficulties at school entry are at high risk. Family history of dyslexia is a predictor of literacy outcome from the preschool years. However, screening does not reach an acceptable clinical level until close to school entry when letter knowledge, phonological awareness, and RAN, rather than family risk, together provide good sensitivity and specificity as a screening battery.

In voxel-based morphometry studies of dyslexia, the relation between causal theories of dyslexia and gray matter (GM) and white matter (WM) volume alterations is still under debate. Some alterations are consistently reported, but others failed to reach significance. We investigated GM alterations in a large sample of Dutch students (37 dyslexics and 57 non-dyslexics) with two analyses: group differences in local GM and total GM and WM volume and correlations between GM and WM volumes and five behavioural measures. We found no significant group differences after corrections for multiple comparisons although total WM volume was lower in the group of dyslexics when age was partialled out. We presented an overview of uncorrected clusters of voxels (p 200) with reduced or increased GM volume. We found four significant correlations between factors of dyslexia representing various behavioural measures and the clusters found in the first analysis. In the whole sample, a factor related to performances in spelling correlated negatively with GM volume in the left posterior cerebellum. Within the group of dyslexics, a factor related to performances in Dutch-English rhyme words correlated positively with GM volume in the left and right caudate nucleus and negatively with increased total WM volume. Most of our findings were in accordance with previous reports. A relatively new finding was the involvement of the caudate nucleus. We confirmed the multiple cognitive nature of dyslexia and suggested that experience greatly influences anatomical alterations depending on various subtypes of dyslexia, especially in a student sample.

In this chapter we address the underlying causes of dyslexia, the developmental learning disability, rather than reading disability. In our breakthrough research over 25 years ago we demonstrated that the process of skill automatization of skill was a problem for dyslexic children not only in reading-related skills but also in a range of other skills not obviously linked to reading. In this chapter we report the subsequent development of this framework, first with identification of the cerebellum as a key structure in the automatization deficits, then a “neural circuit” analysis suggesting that many developmental disorders are related to proceduralization problems, with dyslexia associated with specific difficulties in the language/cerebellar procedural circuits. Here we bring this research to the present day, extending the analysis to consider how networks are grown from birth onwards, and introduce the concept of Delayed Neural Commitment (DNC) as a powerful explanatory developmental framework, proposing that dyslexic children are slower to build the connectivity networks on which reading acquisition and fluency depend. This analysis links back to the development of executive function and language networks, and is consistent with all the major theories of dyslexia. We hope that DNC will provide a fruitful and integrative framework for further theoretical and applied research.

The cause of developmental dyslexia is still unknown despite decades of intense research. Many causal explanations have been proposed, based on the range of impairments displayed by affected individuals. Here we draw attention to the fact that many of these impairments are also shown by illiterate individuals who have not received any or very little reading instruction. We suggest that this fact may not be coincidental and that the performance differences of both illiterates and individuals with dyslexia compared to literate controls are, to a substantial extent, secondary consequences of either reduced or suboptimal reading experience or a combination of both. The search for the primary causes of reading impairments will make progress if the consequences of quantitative and qualitative differences in reading experience are better taken into account and not mistaken for the causes of reading disorders. We close by providing four recommendations for future research.

Dyslexia is one of the most common learning disabilities, yet its brain basis and core causes are not yet fully understood. Neuroimaging methods, including structural and functional magnetic resonance imaging, diffusion tensor imaging, and electrophysiology, have significantly contributed to knowledge about the neurobiology of dyslexia. Recent studies have discovered brain differences before formal instruction that likely encourage or discourage learning to read effectively, distinguished between brain differences that likely reflect the etiology of dyslexia versus brain differences that are the consequences of variation in reading experience, and identified distinct neural networks associated with specific psychological factors that are associated with dyslexia., Eunice Kennedy Shriver National Institute of Child Health and Human Development (U.S.) (Grant R01 HD067312)

International audience; This study investigated how deficits in orthographic processing affect movement production during word writing. Children with dyslexia and dysgraphia wrote words and pseudo-words on a digitizer. The words were orthographically regular and irregular of varying frequency. The group analysis revealed that writing irregular words and pseudo-words increased movement duration and dysfluency. This indicates that the spelling processes were active while the children were writing the words. The impact of these spelling processes was stronger for the children with dyslexia and dysgraphia. The analysis of individual performance revealed that most dyslexic/dysgraphic children presented similar writing patterns. However, selective lexical processing deficits affected irregular word writing but not pseudo-word writing. Selective poor sublexical processing affected pseudo-word writing more than irregular word writing. This study suggests that the interaction between orthographic and motor processing constitutes an important cognitive load that may disrupt the graphic outcome of the children with dyslexia/dysgraphia.

A key problem in the field of search interfaces is dyslexic users interaction with the UI. Dyslexia is a widespread specific learning difficult (SpLD) (10% of any population is estimated to have this cognitive disability) which is under researched in the field of information retrieval. The focus here is an analysis of the User Interface (UI) for search, using visual analytical methods on eye tracking data to examine the difference between control and dyslexic searchers. We use a number of visual analytic methods including path similarity analysis (PSA) and clustering of time intervals to demonstrate both similarities and differences between the user groups. Observations of videos are used to augment the visualizations. Results demonstrate a clear difference between the user groups, and a clear memory effect on the user of search interfaces is shown -- this is a key contribution of this paper. We examine the results using of theories of dyslexia, contributing also to the field of dyslexia and search.

Specific reading disability, dyslexia, is a prevalent and heritable disorder impairing reading acquisition characterized by a phonological deficit. However, the underlying mechanism of how the impaired phonological processing mediates resulting dyslexia or reading disabilities remains still unclear. Using ERPs we studied speech sound processing of 30 dyslexic children with familial risk for dyslexia, 51 typically reading children with familial risk for dyslexia, and 58 typically reading control children. We found enhanced brain responses to shortening of a phonemic length in pseudo-words (/at:a/ vs. /ata/) in dyslexic children with familial risk as compared to other groups. The enhanced brain responses were associated with better performance in behavioral phonemic length discrimination task, as well as with better reading and writing accuracy. Source analyses revealed that the brain responses of sub-group of dyslexic children with largest responses originated from a more posterior area of the right temporal cortex as compared to the responses of the other participants. This is the first electrophysiological evidence for a possible compensatory speech perception mechanism in dyslexia. The best readers within the dyslexic group have probably developed alternative strategies which employ compensatory mechanisms substituting their possible earlier deficit in phonological processing and might therefore be able to perform better in phonemic length discrimination and reading and writing accuracy tasks. However, we speculate that for reading fluency compensatory mechanisms are not that easily built and dyslexic children remain slow readers during their adult life. peerReviewed

Recent years have seen the publication of a range of new theories suggesting that the basis of dyslexia might be sensory dysfunction. In this Opinion article, the evidence for and against several prominent sensory theories of dyslexia is closely scrutinized. Contrary to the causal claims being made, my analysis suggests that many proposed sensory deficits might result from the effects of reduced reading experience on the dyslexic brain. I therefore suggest that longitudinal studies of sensory processing, beginning in infancy, are required to successfully identify the neural basis of developmental dyslexia. Such studies could have a powerful impact on remediation.

The developmental dyslexia studies in alphabetic languages usually from the perspectives of cognition, neurobiology and genetics. Since the Chinese language is characterized as a logographic writing system with deep orthography, which is different from alphabetic languages, whether the findings in alphabetic languages are coincident in Chinese remains a question. By comparing theories in the causes of developmental dyslexia in alphabetic language with that in Chinese language, the paper reviews the studies on development dyslexia in L1 Chinese learners and finally reach the conclusion that although developmental dyslexia in Chinese language have been studied from cognition, neurobiology and genetics, which is coincident with those of alphabetic languages, there exits some differences in minor parts of the theories.

Dehaene (in Reading in the Brain) reviews and finds support for the phonological deficit hypothesis of developmental dyslexia, which proposes that dyslexics have a basic deficit in processing the constituents of spoken words. This hypothesis can be seen as reflecting three associated claims: a) there is only one basic kind of dyslexia; b) all (or most) dyslexic children have phonological impairments, and c) these phonological impairments cause their dyslexia. We consider each of these claims, and the evidence presented by Dehaene, and conclude that questions remain about all three. Phonological deficits alone seem unlikely to be able to account for the complexity and heterogeneity of developmental dyslexia.

A recent voice recognition experiment conducted by Perrachione, Del Tufo, and Gabrieli (2011) revealed that, in normal adult readers, the accuracy at identifying human voices was better in the participants’ mother tongue than in an unfamiliar language, while this difference was absent in a group of adults with dyslexia. This pattern favored a view of dyslexia as due to “fundamentally impoverished native-language phonological representations.” To further examine this issue, we conducted two voice recognition experiments, one with children with/without dyslexia, and the other with adults with/without dyslexia. Results revealed that children/adults with dyslexia were less accurate at identifying voices than normal readers and, importantly, this effect was independent of language. These data are more consistent with the assumption of dyslexia as due to a deficit in multisensory integration rather than a deficit based on impoverished native-language phonologically based representations.

Historically, dyslexia research has focused on the literacy aspects of dyslexia on children, and more recent definitions of dyslexia have included the cognitive processing aspects of verbal language, memory and organisation. However, these neuro-cognitive accounts largely conceptualise dyslexia as a neurological dysfunction, with only a small body of work using phenomenology and social disability theory to focus on the individual perceptions of dyslexic learners. This article explores the experiences of adult dyslexic actors through the lens of Mearleu-Ponty's phenomenology of embodiment, discussing their lived experience of both verbal and written language, and the impact of dyslexia on their identity and creative process. Drawing on these experiences and also on neuro-cognitive accounts of dyslexic strengths, the article suggests that dyslexic learners have a different intentional relationship to verbal language which is created as a result of a dynamic brain–body–world interaction. It firstly outlines ...

BackgroundIn this paper we showed predictive relationships between central auditory processes, phonological abilities, and reading abilities in children diagnosed with developmental dyslexia (DD). Both empirical data and theoretical approaches indicate that central auditory processing deficits may contribute to developmental dyslexia; however, associations between reading and phonological skills and central auditory processes remain unclear.Material and MethodsExactly 57 children with dyslexia and 40 age- and gender-matched normal reading children performed reading, phonological, and auditory information processing tests, i.e. the Frequency Pattern Test (FPT), Dichotic Digit Test (DDT), and Gap Detection Test (GDT).ResultsDyslexic children showed parallel reading, phonological, and auditory information processing deficits. Principal component analysis, performed in dyslexic and normal reading children to reduce the data set before exploring the predictors of language skills, revealed three factors: 1) ‘Auditory processing’, which received high loadings from phonological, FPT, and DDT for the right ear; 2) ‘Age and Cognition’, including chronological age as well as measures of fluid intelligence and auditory working memory span; and 3) ‘Dichotic listening’ for the left ear. All three factors together best predicted reading regular words in children diagnosed with DD, while ‘Auditory processing’ and ‘Age and cognition’ together explained most of the variance while predicting pseudo-word reading.ConclusionsThe present study indicates that frequency pattern recognition, dichotic listening for the right year, and phonological awareness are strongly interrelated and constitute the most significant predictor of reading abilities in children diagnosed with dyslexia. The results may have important implications for diagnosis and therapy of language disorders.

Developmental dyslexia is a heterogeneous condition entailing problems with reading and spelling. Several genes have been linked or associated to the disease, many of which contribute to the development and function of brain areas that are important for auditory and phonological processing. Nonetheless, a clear link between genes, the brain, and the symptoms of dyslexia is still pending. The goal of this paper is contributing to bridge this gap. With this aim, we have focused on how the dyslexic brain fails to process speech sounds and reading cues. We have adopted an oscillatory perspective, according to which dyslexia results from a deficient integration of different brain rhythms during reading/spellings tasks. Moreover, we show that some candidates for this condition are related to brain rhythms. This approach should help gain a better understanding of the aetiology and the clinical presentation of developmental dyslexia, but also achieve an earlier and more accurate diagnosis of the disease.

Purpose The specificity of visual channel impairment in dyslexia has been the subject of much controversy. The purpose of this study was to determine if a differential pattern of impairment can be verified between visual channels in children with developmental dyslexia, and in particular, if the pattern of deficits is more conspicuous in tasks where the magnocellular-dorsal system recruitment prevails. Additionally, we also aimed at investigating the association between visual perception thresholds and reading. Methods In the present case-control study, we compared perception thresholds of 33 children diagnosed with developmental dyslexia and 34 controls in a speed discrimination task, an achromatic contrast sensitivity task, and a chromatic contrast sensitivity task. Moreover, we addressed the correlation between the different perception thresholds and reading performance, as assessed by means of a standardized reading test (accuracy and fluency). Group comparisons were performed by the Mann-Whitney U test, and Spearman's rho was used as a measure of correlation. Results Results showed that, when compared to controls, children with dyslexia were more impaired in the speed discrimination task, followed by the achromatic contrast sensitivity task, with no impairment in the chromatic contrast sensitivity task. These results are also consistent with the magnocellular theory since the impairment profile of children with dyslexia in the visual threshold tasks reflected the amount of magnocellular-dorsal stream involvement. Moreover, both speed and achromatic thresholds were significantly correlated with reading performance, in terms of accuracy and fluency. Notably, chromatic contrast sensitivity thresholds did not correlate with any of the reading measures. Conclusions Our evidence stands in favor of a differential visual channel deficit in children with developmental dyslexia and contributes to the debate on the pathophysiology of reading impairments.

First Published December 21, 2016 It has been proposed that atypical neural oscillations in both the auditory and the visual modalities could explain why some individuals fail to learn to read and suffer from developmental dyslexia. However, the role of specific oscillatory mechanisms in reading acquisition is still under debate. In this article, we take a cross-linguistic approach and argue that both the phonological and orthographic specifics of a language (e.g., linguistic rhythm, orthographic depth) shape the oscillatory activity thought to contribute to reading development. The proposed theoretical framework should allow future research to test cross-linguistic hypotheses that will shed light on the heterogeneity of auditory and visual disorders and their underlying brain dysfunction(s) in developmental dyslexia, and inform clinical practice by helping us to diagnose dyslexia across languages. This research was funded by the European Research Council (ERC Advanced Grant, BILITERACY Project, to M.C.), and the Spanish government (Plan Nacional-PSI2012-32128 and PSI2015-65338-P to M.L., Plan Nacional-PSI2012-32350 and PSI2015-65694-P to N.M., and Plan Nacional-PSI2015-67353-R to M.C.). The Basque Center on Brain Cognition and Language acknowledges funding from Ayuda Centro de Excelencia Severo Ochoa SEV-2015-0490.

Personal narratives derived from insider accounts of schooling can illuminate our understanding of how individuals negotiate their learning; and how teachers and schools might empower or marginalise students on the basis of a specific learning disability. This chapter retrospectively examines the lived experience of one of the authors, Alanna, as a student diagnosed with dyslexia.

An on-going debate surrounds the relationship between specific language impairment and developmental dyslexia, in particular with respect to their phonological abilities. Are these distinct disorders? To what extent do they overlap? Which cognitive and linguistic profiles correspond to specific language impairment, dyslexia and comorbid cases? At least three different models have been proposed: the severity model, the additional deficit model and the component model. We address this issue by comparing children with specific language impairment only, those with dyslexia-only, those with specific language impairment and dyslexia and those with no impairment, using a broad test battery of language skills. We find that specific language impairment and dyslexia do not always co-occur, and that some children with specific language impairment do not have a phonological deficit. Using factor analysis, we find that language abilities across the four groups of children have at least three independent sources of variance: one for non-phonological language skills and two for distinct sets of phonological abilities (which we term phonological skills versus phonological representations). Furthermore, children with specific language impairment and dyslexia show partly distinct profiles of phonological deficit along these two dimensions. We conclude that a multiple-component model of language abilities best explains the relationship between specific language impairment and dyslexia and the different profiles of impairment that are observed.

We investigated the phonological and surface subtypes of developmental dyslexia in light of competing predictions made by two computational models of single word reading, the dual-route cascaded model (DRC; Coltheart, Rastle, Perry, Langdon, & Ziegler, 2001) and Harm and Seidenberg’s connectionist model (HS model; Harm & Seidenberg, 1999). The regression-outlier procedure was applied to a large sample to identify children with disproportionately poor phonological coding skills (phonological dyslexia) or disproportionately poor orthographic coding skills (surface dyslexia). Consistent with the predictions of the HS model, children with “pure” phonological dyslexia, who did not have orthographic deficits, had milder phonological impairments than children with “relative” phonological dyslexia, who did have secondary orthographic deficits. In addition, pure cases of dyslexia were more common among older children. Consistent with the predictions of the DRC model, surface dyslexia was not well conceptualized as a reading delay; both phonological and surface dyslexia were associated with patterns of developmental deviance. In addition, some results were problematic for both models. We identified a small number of individuals with severe phonological dyslexia, relatively intact orthographic coding skills, and very poor real word reading. Further, a subset of controls could read normally despite impaired orthographic coding. The findings are discussed in terms of improvements to both models that might help better account for all cases of developmental dyslexia.

Identification of specific neurophysiological dysfunctions resulting in selective reading difficulty (dyslexia) has remained elusive. In addition to impaired reading development, individuals with dyslexia frequently exhibit behavioral deficits in perceptual adaptation. Here, we assessed neurophysiological adaptation to stimulus repetition in adults and children with dyslexia for a wide variety of stimuli, spoken words, written words, visual objects, and faces. For every stimulus type, individuals with dyslexia exhibited significantly diminished neural adaptation compared to controls in stimulus-specific cortical areas. Better reading skills in adults and children with dyslexia were associated with greater repetition-induced neural adaptation. These results highlight a dysfunction of rapid neural adaptation as a core neurophysiological difference in dyslexia that may underlie impaired reading development. Reduced neurophysiological adaptation may relate to prior reports of reduced behavioral adaptation in dyslexia and may reveal a difference in brain functions that ultimately results in a specific reading impairment., NIH (Grant UL1RR025758)