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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.

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 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 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.

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.

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.

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 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...

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)

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.

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.

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.

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.

We summarize some of the most important findings from research evaluating the hypothesized causes of specific reading disability ('dyslexia') over the past four decades. After outlining components of reading ability, we discuss manifest causes of reading difficulties, in terms of deficiencies in component reading skills that might lead to such difficulties. The evidence suggests that inadequate facility in word identification due, in most cases, to more basic deficits in alphabetic coding is the basic cause of difficulties in learning to read. We next discuss hypothesized deficiencies in reading-related cognitive abilities as underlying causes of deficiencies in component reading skills. The evidence in these areas suggests that, in most cases, phonological skills deficiencies associated with phonological coding deficits are the probable causes of the disorder rather than visual, semantic, or syntactic deficits, although reading difficulties in some children may be associated with general language deficits. Hypothesized deficits in general learning abilities (e.g., attention, association learning, cross-modal transfer etc.) and low-level sensory deficits have weak validity as causal factors in specific reading disability. These inferences are, by and large, supported by research evaluating the biological foundations of dyslexia. Finally, evidence is presented in support of the idea that many poor readers are impaired because of inadequate instruction or other experiential factors. This does not mean that biological factors are not relevant, because the brain and environment interact to produce the neural networks that support reading acquisition. We conclude with a discussion of the clinical implications of the research findings, focusing on the need for enhanced instruction.

The existing literature on developmental dyslexia (hereafter: dyslexia) often focuses on isolating cognitive skills which differ across dyslexic and control participants. Among potential correlates, previous research has studied group differences between dyslexic and control participants in performance on statistical learning tasks. A statistical learning deficit has been proposed to be a potential cause and/or a marker effect for early detection of dyslexia. It is therefore of practical importance to evaluate the evidence for a group difference. From a theoretical perspective, such a group difference would provide information about the causal chain from statistical learning to reading acquisition. We provide a systematic review of the literature on such a group difference. We conclude that there is insufficient high-quality data to draw conclusions about the presence or absence of an effect.

The problem of causation has proven particularly elusive in the case of developmental dyslexia (DD). The field has been dominated by very general hypotheses, such as the idea that DD is caused by a phonological deficit and/or an impairment of the magnocellular pathway. Results are contrasting and causal unidirectional links have not been persuasively demonstrated.Some studies in the Research Topic (RT) re-examine these general hypotheses from the critical perspective of more selective predictions. Others focus on less general deficit hypotheses and stay closer to reading by investigating specific aspects of the reading process such as orthographic learning ability or the ability to deal with multiple-stimulus displays. Studies benefit from new research paradigms as well as new information from research areas such as neuroimaging or genetics. Below, we sketch the general questions tackled by these studies.

Developmental dyslexia is a reading disorder—but what are the underlying cognitive and neurobiological mechanisms? The variety of different explanations in the literature ranges from phonological abilities via sensory (auditory, visual) processing to attention, learning, and cross-modal integration. Here, we suggest that it is advantageous to accept the variability encountered in dyslexia. Different cognitive profiles, or “fingerprints”, characterise groups of dyslexic individuals. Most importantly, these fingerprints have a repercussion in differential brain activation patterns in dyslexia, supporting the notion of a neurobiological basis. We conclude that considering the neurocognitive fingerprint of a dyslexic reader may be helpful to plan an individually targeted training, which, in turn, may optimise the outcome of remediation.

We used fMRI to explore the extent of the anatomical overlap of three neural systems that the literature on developmental dyslexia associates with reading: the auditory phonological, the visual magnocellular, and the motor/cerebellar systems. Twenty-eight normal subjects performed four tasks during fMRI scans: word and pseudoword reading, auditory rhyming for letter names, visual motion perception, and a motor sequence learning task. We found that the left occipitotemporal cortex (OTC), which previous studies reported to be dysfunctional in dyslexia, can be fractionated into different functional areas: an anterior and lateral area that was activated by both reading and auditory rhyming tasks; a posterior area that was commonly activated by both the reading and the motion perception task and a medial/intermediate area, including the so-called Visual Word Form Area, which was specifically activated by the reading task. These results show that the left OTC is an area of segregated convergence of different functional systems. We compared our results with the hypoactivation pattern reported for reading in a previous cross-cultural PET study on 36 dyslexic subjects from three countries. The region of decreased activation in dyslexia overlapped with regions that are specific for reading and those activated during both the auditory rhyming task and the single word and pseudoword reading task described in the present fMRI study. No overlap was found with the activation patterns for the visual motion perception task or for the motor sequence learning task. These observations challenge current theories of dyslexia.

Biologising the problems of reading has a long tradition. However, modern and non-invasive techniques, like functional magnetic resonance imaging (fMRI), that allow the mapping of changes in brain hemodynamic that corresponds to mental operations, boosted a wave of new research on the subject. This paper traces the history of treating a problem in teaching/learning as a disease-like condition. It also examines the beliefs of professionals in relation to dyslexia, and how they are biased by published research and the imbalance between biological and educational perspectives in published research. Overall, the educational perspective is underrepresented in published research about dyslexia, while the biological perspective is overrepresented. This is puzzling since to date biological perspectives have not produced any effective interventions for dyslexia, and almost all major claims for the biological view remain unproven. Nevertheless, biological models have a great influence on the beliefs of practitioner...

Long-standing issues with the conceptualization, identification and subtyping of developmental dyslexia persist. This study takes an alternative approach to examine the heterogeneity of developmental dyslexia using taxometric classification techniques. These methods were used with a large sample of 671 children ages 6-8 who were diagnosed with severe reading disorders. Latent characteristics of the sample are assessed in regard to posited subtypes with phonological deficits and naming speed deficits, thus extending prior work by addressing whether these deficits embody separate classes of individuals. Findings support separate taxa of dyslexia with and without phonological deficits. Different latent structure for naming speed deficits was found depending on the definitional criterion used to define dyslexia. Non-phonologically based forms of dyslexia showed particular difficulty with naming speed and reading fluency.

Previous research into the cognitive processes involved in reading Chinese and developmental dyslexia in Chinese, revealed that the single most important factor appears to be orthographic processing skills rather than phonological skills. Also some studies have indicated that even in alphabetic languages some dyslexic individuals reveal deficits in orthographic processing skills, which are linked to a deficit in the visual magnocellular pathway. The current study therefore employed a visual psychophysical experiment together with visual and auditory event-related potential (ERP) experiments eliciting mismatch negativity (MMN) to investigate the link between visual magnocellular functional abnormalities and developmental dyslexia in Chinese. The performance levels of Chinese children with developmental dyslexia (DD) from the behavioural and electrophysiological experiments were compared to those of the chronological age-matched (CA) children and those of the reading level matched (RL) younger children. Both the behavioural and electrophysiological results suggest that the orthographic processing skills were compromised in the Chinese developmental dyslexics, which in turn is linked to a deficit in the visual magnocellular system.

SummaryFirst described over 100 years ago, developmental dyslexia (reading disability) has been a controversial subject. There has been much confusion regarding the definition, the psychological basis, the conceptualisation and even the name. Recent research has helped us to understand the main underlying cognitive deficits that lead to poor reading. Brain imaging studies conducted during the performance of reading tasks have shed light on its biological basis and genetic studies have identified a number of genes that are associated with reading difficulties. Together, these studies have led to a redefinition and new understanding of developmental dyslexia. This article examines these recent findings. A second article to appear in Advances will focus on clinical aspects of the disorder.

Contains fulltext : 90398.pdf (Publisher’s version ) (Open Access) Phonological theories of dyslexia assume a specific deficit in representation, storage and recall of phonemes. Various brain imaging techniques, including qEEG, point to the importance of a range of areas, predominantly the left hemispheric temporal areas. This study attempted to reduce reading and spelling deficits in children who are dyslexic by means of neurofeedback training based on neurophysiological differences between the participants and gender and age matched controls. Nineteen children were randomized into an experimental group receiving qEEG based neurofeedback (n = 10) and a control group (n = 9). Both groups also received remedial teaching. The experimental group improved considerably in spelling (Cohen’s d = 3). No improvement was found in reading. An indepth study of the changes in the qEEG power and coherence protocols evidenced no fronto-central changes, which is in line with the absence of reading improvements. A significant increase of alpha coherence was found, which may be an indication that attentional processes account for the improvement in spelling. Consideration of subtypes of dyslexia may refine the results of future studies. 7 p.

Dissecting Dyslexia and Learning Difficulties in learning to read, despite reasonable effort and instruction, form the basis of dyslexia. Gabrieli (p. 280 ; see the cover) now reviews the latest research into the causes of dyslexia. Neuroimaging studies may give early notice of impending dyslexia, and it is hoped that early interventions may lessen the impact of dyslexia. Learning occurs in many settings. Humans uniquely use the formalized settings of schools and curriculum. Infants and children also do plenty of learning outside these settings, often intermingling social interactions. Meltzoff et al. (p. 284 ) survey the variety of learning contexts that people experience and discuss how recent advances in neuroscience and robotics are driving a new synthesis of learning.

There are several group and case studies that investigate developmental dyslexia in children, and acquired and developmental reading disabilities in adults. To date however, there are few detailed investigations on cases of early acquired dyslexia. The purpose of this study was to examine such a case (participant referred to as SP). The goals of this investigation were to compare SP's reading impairments to the major subtypes of dyslexia, establish SP's specific reading deficits, and consider the neuropsychological variables that may impact on SP's reading disability.

The Jyvaskyla Longitudinal Study of Dyslexia project (JLD) has followed the development of 200 children from birth until 10 years of age. Half the children are from families in which at least one of the parents has dyslexia, thus the child has a high risk of becoming dyslexic, and half have no such risk. Here the main findings of four studies in linguistics from the JLD project are reviewed. The speech processing skills were studied in 6, 18, 24 and 30-month-old children. The findings show that early signs of dyslexia can be detected in speech processing both phonologically and morphosyntactically. These precursors can be seen in perception or production of duration, in the prosody and phonotactics of word production attempts and word structures, as well as in the complexity of morphosyntactic features of expressions. This information can be useful in practice to provide early and appropriate assistance for those children who most likely will face difficulties in learning to read and write at school.

Developmental dyslexia is often characterized by a visual deficit, but the nature of this impairment and how it relates to reading ability is disputed (Brain 2003; 126: 841-865). In order to investigate this issue, we compared groups of adults with and without dyslexia on the Ternus, visual-search and symbols tasks. Dyslexic readers yielded more errors on the visual-search and symbols tasks compared with non-dyslexic readers. A positive correlation between visual-search and symbols task performance suggests a common mechanism shared by these tasks. Performance on the visual-search and symbols tasks also correlated with non-word reading and rapid automatized naming measures, and visual search contributed independent variance to non-word reading. The Ternus task did not discriminate reading groups nor contributed significant variance to reading measures. We consider how visual-attention processes might underlie specific component reading measures.

Extraordinary progress in functional brain imaging, primarily advances in functional magnetic resonance imaging, now allows scientists to understand the neural systems serving reading and how these systems differ in dyslexic readers. Scientists now speak of the neural signature of dyslexia, a singular achievement that for the first time has made what was previously a hidden disability, now visible. Paralleling this achievement in understanding the neurobiology of dyslexia, progress in the identification and treatment of dyslexia now offers the hope of identifying children at risk for dyslexia at a very young age and providing evidence-based, effective interventions. Despite these advances, for many dyslexic readers, becoming a skilled, automatic reader remains elusive, in great part because though children with dyslexia can be taught to decode words, teaching children to read fluently and automatically represents the next frontier in research on dyslexia. We suggest that to break through this “fluency” barrier, investigators will need to reexamine the more than 20-year-old central dogma in reading research: the generation of the phonological code from print is modular, that is, automatic and not attention demanding, and not requiring any other cognitive process. Recent findings now present a competing view: other cognitive processes are involved in reading, particularly attentional mechanisms, and that disruption of these attentional mechanisms play a causal role in reading difficulties. Recognition of the role of attentional mechanisms in reading now offer potentially new strategies for interventions in dyslexia. In particular, the use of pharmacotherapeutic agents affecting attentional mechanisms not only may provide a window into the neurochemical mechanisms underlying dyslexia but also may offer a potential adjunct treatment for teaching dyslexic readers to read fluently and automatically. Preliminary studies suggest that agents traditionally used to treat disorders of attention, particularly attention-deficit/hyperactivity disorder, may prove to be an effective adjunct to improving reading in dyslexic students.

Developmental dyslexia is a language-based learning disability characterized by persistent difficulty in learning to read. While an understanding of genetic contributions is emerging, the ways the environment affects brain functioning in children with developmental dyslexia are poorly understood. A relationship between the home literacy environment (HLE) and neural correlates of reading has been identified in typically developing children, yet it remains unclear whether similar effects are observable in children with a genetic predisposition for dyslexia. Understanding environmental contributions is important given that we do not understand why some genetically at-risk children do not develop dyslexia. Here, we investigate for the first time the relationship between HLE and the neural correlates of phonological processing in beginning readers with (FHD+, n = 29) and without (FHD−, n = 21) a family history of developmental dyslexia. We further controlled for socioeconomic status to isolate the neurobiological mechanism by which HLE affects reading development. Group differences revealed stronger correlation of HLE with brain activation in the left inferior/middle frontal and right fusiform gyri in FHD− compared to FHD+ children, suggesting greater impact of HLE on manipulation of phonological codes and recruitment of orthographic representations in typically developing children. In contrast, activation in the right precentral gyrus showed a significantly stronger correlation with HLE in FHD+ compared to FHD− children, suggesting emerging compensatory networks in genetically at-risk children. Overall, our results suggest that genetic predisposition for dyslexia alters contributions of HLE to early reading skills before formal reading instruction, which has important implications for educational practice and intervention models.

Dyslexia (or specific reading disability) is the most common and extensively studied of the learning disabilities, affecting 80% of all individuals identified as learning disabled. Not only is dyslexia the most thoroughly characterized of all learning disabilities but it is historically the oldest. In fact, the first description of dyslexia in children preceded the first mention of “learning disability” by over 60 years; dyslexia was first described in 1896 while the term “learning disability” was not used until 1962! As discussed throughout this chapter, the demonstration of an unexpected difficulty in reading in relation to intelligence is a key hallmark of dyslexia. Dyslexia is an unexpected difficulty in reading that is best and most reliably and clearly demonstrated by performance on a test of intelligence, on the WISC-V, most often observed using the VCI, though the Full Scale IQ may also be useful.

International audience; The visual attention (VA) span is defined as the amount of distinct visual elements which can be processed in parallel in a multi-element array. Both recent empirical data and theoretical accounts suggest that a VA span deficit might contribute to developmental dyslexia, independently of a phonological disorder. In this study, this hypothesis was assessed in two large samples of French and British dyslexic children whose performance was compared to that of chronological-age matched control children. Results of the French study show that the VA span capacities account for a substantial amount of unique variance in reading, as do phonological skills. The British study replicates this finding and further reveals that the contribution of the VA span to reading performance remains even after controlling IQ, verbal fluency, vocabulary and single letter identification skills, in addition to phoneme awareness. In both studies, most dyslexic children exhibit a selective phonological or VA span disorder. Overall, these findings support a multi-factorial view of developmental dyslexia. In many cases, developmental reading disorders do not seem to be due to phonological disorders. We propose that a VA span deficit is a likely alternative underlying cognitive deficit in dyslexia.

Studies of basic (nonspeech) auditory processing in adults thought to have developmental dyslexia have yielded a variety of data. Yet there has been little consensus regarding the explanatory value of auditory processing in accounting for reading difficulties. Recently, however, a number of studies of basic auditory processing in children with developmental dyslexia have suggested that a reduced ability to discriminate the rate of change in amplitude envelope onsets (rise time) may be linked to phonological processing difficulties and thereby to reading difficulties. Here, we select a range of different rise-time tasks used with children, and give them to adults with developmental dyslexia, along with 2 other auditory tasks (intensity discrimination and temporal order judgment). Deficits in both rise-time perception and temporal order judgment were found to predict literacy attainment in adults with developmental dyslexia, but the data were suggestive of different causal pathways.

The aim of this study was to see whether patterns of neuro-cognitive assets and deficits seen in dyslexia also would lead to different patterns of reading and writing. A group of dyslexic children was subgrouped by language comprehension and mathematics skills in accordance with the definition of the British Dyslexia Association of 1998. This yielded three subgroups that showed three distinct neuro-cognitive profiles depicted within the Multi-Component Model of Working Memory. The participants were tested with single word reading and spelling tasks. The scores varied only to a minor degree between the subgroups. The results were discussed in view of developmental phases into literacy. Only one subgroup could be defined within the orthographic phase, while the other two were within the alphabetic phase. Thus, patterns at the neuro-cognitive level seen in the subgroups were to a limited degree reflected at the behavioural level. The results were also discussed in view of different orthographies. Since using information from phonological testing only, as currently appears to be common practice in many contexts, may result in intervention with little effect for some dyslexics, it was concluded that assessing neuro-cognitive assets and deficits targeting dyslexia is essential to intervention and the understanding of dyslexia. Copyright © 2006 John Wiley & Sons, Ltd.

Developmental dyslexia is commonly thought to arise from specific phonological impairments. However, recent evidence is consistent with the possibility that phonological impairments arise as symptoms of an underlying dysfunction of procedural learning. The nature of the link between impaired procedural learning and phonological dysfunction is unresolved. Motivated by the observation that speech processing involves the acquisition of procedural category knowledge, the present study investigates the possibility that procedural learning impairment may affect phonological processing by interfering with the typical course of phonetic category learning. The present study tests this hypothesis while controlling for linguistic experience and possible speech-specific deficits by comparing auditory category learning across artificial, nonlinguistic sounds among dyslexic adults and matched controls in a specialized first-person shooter videogame that has been shown to engage procedural learning. Nonspeech auditory category learning was assessed online via within-game measures and also with a post-training task involving overt categorization of familiar and novel sound exemplars. Each measure reveals that dyslexic participants do not acquire procedural category knowledge as effectively as age- and cognitive-ability matched controls. This difference cannot be explained by differences in perceptual acuity for the sounds. Moreover, poor nonspeech category learning is associated with slower phonological processing. Whereas phonological processing impairments have been emphasized as the cause of dyslexia, the current results suggest that impaired auditory category learning, general in nature and not specific to speech signals, could contribute to phonological deficits in dyslexia with subsequent negative effects on language acquisition and reading. Implications for the neuro-cognitive mechanisms of developmental dyslexia are discussed.

The hallmark of developmental surface dyslexia in English and French is inaccurate reading of words with atypical spelling-sound correspondences. According to Douklias, Masterson and Hanley (2009), surface dyslexia can also be observed in Greek (a transparent orthography for reading that does not contain words of this kind). Their findings suggested that surface dyslexia in Greek can be characterized by slow reading of familiar words, and by inaccurate spelling of words with atypical sound-spelling correspondences (Greek is less transparent for spelling than for reading). In this study, we report seven adult cases whose slow reading and impaired spelling accuracy satisfied these criteria for Greek surface dyslexia. When asked to read words with atypical grapheme-phoneme correspondences in English (their second language), their accuracy was severely impaired. A co-occurrence was also observed between impaired spelling of words with atypical phoneme-grapheme correspondences in English and Greek. These co-occurrences provide strong evidence that surface dyslexia genuinely exists in Greek and that slow reading of real words in Greek reflects the same underlying impairment as that which produces inaccurate reading of atypical words in English. Two further individuals were observed with impaired reading and spelling of nonwords in both languages, consistent with developmental phonological dyslexia. Neither of the phonological dyslexics read words slowly. In terms of computational models of reading aloud, these findings suggest that slow reading by dyslexics in transparent orthographies is the consequence of a developmental impairment of the lexical (Coltheart, Rastle, Perry, Langdon, & Zeigler, 2001; Perry, Ziegler, & Zorzi, 2010) or semantic reading route (Plaut, McClelland, Seidenberg, & Patterson, 1996). This outcome provides evidence that the neurophysiological substrate(s) that support the lexical/semantic and the phonological pathways that are involved in reading and spelling are the same in both Greek and English.