Background: Dyslexia is a developmental brain-based type of learning disability that affects a person's ability to read and spell words. Best estimates place 5 percent to 10 percent of the population with the condition, but the incidence of dyslexia is challenging to pinpoint, as the definition of dyslexia varies throughout research. Objective: The purpose of this article is to provide an overview of dyslexia, its characteristics, assessment and identification, and intervention techniques for the condition. Results: Although the disorder varies from person to person, common characteristics among people with dyslexia include difficulty with phonological skills, low accuracy and fluency of reading, poor spelling, and/or rapid visual-verbal responding. Dyslexia is a neurological condition and can be inherited, and recent studies have identified a number of genes that may predispose an individual to developing dyslexia. Identification of dyslexia early requires recognition of characteristics such as difficulty associating sounds with letters, reading dysfluencies, spelling difficulties, challenges with written expression and poor handwriting. Dyslexia assessments can guide professions in ways to best administer treatment, such as via strategies to enhance word training and improve decoding skills. All of these interventions have shown to benefit the reading and writing abilities of persons with dyslexia. Conclusions: The unique nature and presentation of dyslexia varies among individuals. The importance of understanding as much as possible and keeping abreast of the assessment and intervention strategies available is critical to minimizing the long-term effects of dyslexia.
The primary aim of this study was to explore the overlaps between dyslexia and a range of neurodevelopmental disorders and problems (NDPs), specifically symptoms of attention-deficit/hyperactivity disorder, autism spectrum disorder, atypical sensory perception and developmental coordination disorder. Capitalizing on a population-based sample of twins, secondary aims included estimating the heritability of dyslexia and reporting on the measurement characteristics of the scale used to assess dyslexia. A telephone interview regarding symptoms of dyslexia and other NDPs was conducted with parents of 1,688 nine-year-old twins. The prevalence and the heritability of dyslexia were estimated at 8 and 52%, respectively. The boy: girl ratio was 1.5:1. Results revealed that there was more than an eight-fold increase in (diagnostic proxy) NDPs prevalence in the dyslexia group as compared to typical readers. Quantitatively measured symptoms of inattention, oral language problems and atypical sensory perception significantly predicted dyslexia status in a multivariate analysis. By contrast, ASD-related inflexibility was inversely associated with dyslexia in the multivariate model. In sum, dyslexia often overlaps with other NDPs. The current study provides new knowledge supporting the position to move beyond isolated diagnostic categories into behavioural profiles of co-occurring problems when trying to understand the pattern of strengths and needs in individuals with dyslexia.
BACKGROUND: Dyslexia is one of the most common neurodevelopmental disorders. There have been many definitions over the past century, and debate continues as to how dyslexia should be defined. This debate contributes to confusion and misinformation. We move beyond the debate by establishing areas of consensus among a wide range of experts. METHODS: We conducted a Delphi study with a panel of dyslexia experts, including academics, specialist teachers, educational psychologists, and individuals with dyslexia, asking them for their views on a set of key statements about dyslexia. We carried out two survey rounds, in each case accepting statements with greater than 80% consensus and reviewing and revising other statements using feedback from the expert panel. This was followed by discussion with a subset of the panel around a few statements with marginal consensus. RESULTS: Forty-two statements were ultimately accepted. In the current paper we review those statements that pertain to a definition of dyslexia, demonstrate how they align with the research literature, and build on previous definitions of dyslexia. CONCLUSIONS: There was considerable consensus in our expert panel that dyslexia is a difficulty in reading and spelling, associated with multiple factors, and that it frequently co-occurs with other developmental disorders. It was agreed that difficulties in reading fluency and spelling are key markers of dyslexia across different ages and languages. We conclude with a proposed new definition of dyslexia.
BACKGROUND: The present study concerns literacy and its underlying cognitive skills in Dutch children who differ in familial risk (FR) for dyslexia. Previous studies with FR-children were inconclusive regarding the performance of FR-children without dyslexia as compared to the controls. Moreover, van Bergen et al. (2011) recently showed that FR-children with and without dyslexia differed in parental reading skills, suggesting that those who go on to develop dyslexia have a higher liability. The current study concerned 1) the comparison of three groups of children at the end of second grade and 2) the intergenerational transfer of reading and its underlying cognitive skills from parent to child. METHOD: Three groups of children were studied at the end of second grade: FR-dyslexia (n = 42), FR-no-dyslexia (n = 99), and control children (n = 66). Parents and children were measured on naming, phonology, spelling, and word and pseudoword reading. RESULTS: The FR-dyslexia children were severely impaired across all tasks. The FR-no-dyslexia children performed better than the FR-dyslexia children, but still below the level of the controls on all tasks; the only exception was rapid naming (RAN), on which they were as fast as the controls. Focusing on the FR subsample, parental reading and RAN were related to their offspring's reading status. CONCLUSIONS: We replicated and extended van Bergen et al.'s study in showing that the FR-children who develop dyslexia are likely to have a higher liability. Both the group comparisons and the parent-child relations highlight the importance of good RAN skills for reading acquisition.
Dyslexia affects 5-10% of school-aged children and is therefore one of the most common learning disorders. Research on auditory event related potentials (AERP), particularly the mismatch negativity (MMN) component, has revealed anomalies in individuals with dyslexia to speech stimuli. Furthermore, candidate genes for this disorder were found through molecular genetic studies. A current challenge for dyslexia research is to understand the interaction between molecular genetics and brain function, and to promote the identification of relevant endophenotypes for dyslexia. The present study examines MMN, a neurophysiological correlate of speech perception, and its potential as an endophenotype for dyslexia in three groups of children. The first group of children was clinically diagnosed with dyslexia, whereas the second group of children was comprised of their siblings who had average reading and spelling skills and were therefore "unaffected" despite having a genetic risk for dyslexia. The third group consisted of control children who were not related to the other groups and were also unaffected. In total, 225 children were included in the study. All children showed clear MMN activity to/da/-/ba/contrasts that could be separated into three distinct MMN components. Whilst the first two MMN components did not differentiate the groups, the late MMN component (300-700 ms) revealed significant group differences. The mean area of the late MMN was attenuated in both the dyslexic children and their unaffected siblings in comparison to the control children. This finding is indicative of analogous alterations of neurophysiological processes in children with dyslexia and those with a genetic risk for dyslexia, without a manifestation of the disorder. The present results therefore further suggest that the late MMN might be a potential endophenotype for dyslexia.
For languages other than English there is a lack of empirical evidence about the cognitive profile of students entering higher education with a diagnosis of dyslexia. To obtain such evidence, we compared a group of 100 Dutch-speaking students diagnosed with dyslexia with a control group of 100 students without learning disabilities. Our study showed selective deficits in reading and writing (effect sizes for accuracy between d = 1 and d = 2), arithmetic (d≈1), and phonological processing (d>0.7). Except for spelling, these deficits were larger for speed related measures than for accuracy related measures. Students with dyslexia also performed slightly inferior on the KAIT tests of crystallized intelligence, due to the retrieval of verbal information from long-term memory. No significant differences were observed in the KAIT tests of fluid intelligence. The profile we obtained agrees with a recent meta-analysis of English findings suggesting that it generalizes to all alphabetic languages. Implications for special arrangements for students with dyslexia in higher education are outlined.
BACKGROUND: Developmental dyslexia is a specific cognitive disorder in reading acquisition that has genetic and neurological origins. Despite histological evidence for brain differences in dyslexia, we recently demonstrated that in large cohort of subjects, no differences between control and dyslexic readers can be found at the macroscopic level (MRI voxel), because of large variances in brain local volumes. In the present study, we aimed at finding brain areas that most discriminate dyslexic from control normal readers despite the large variance across subjects. After segmenting brain grey matter, normalizing brain size and shape and modulating the voxels' content, normal readers' brains were used to build a 'typical' brain via bootstrapped confidence intervals. Each dyslexic reader's brain was then classified independently at each voxel as being within or outside the normal range. We used this simple strategy to build a brain map showing regional percentages of differences between groups. The significance of this map was then assessed using a randomization technique. RESULTS: The right cerebellar declive and the right lentiform nucleus were the two areas that significantly differed the most between groups with 100% of the dyslexic subjects (N = 38) falling outside of the control group (N = 39) 95% confidence interval boundaries. The clinical relevance of this result was assessed by inquiring cognitive brain-based differences among dyslexic brain subgroups in comparison to normal readers' performances. The strongest difference between dyslexic subgroups was observed between subjects with lower cerebellar declive (LCD) grey matter volumes than controls and subjects with higher cerebellar declive (HCD) grey matter volumes than controls. Dyslexic subjects with LCD volumes performed worse than subjects with HCD volumes in phonologically and lexicon related tasks. Furthermore, cerebellar and lentiform grey matter volumes interacted in dyslexic subjects, so that lower and higher lentiform grey matter volumes compared to controls differently modulated the phonological and lexical performances. Best performances (observed in controls) corresponded to an optimal value of grey matter and they dropped for higher or lower volumes. CONCLUSION: These results provide evidence for the existence of various subtypes of dyslexia characterized by different brain phenotypes. In addition, behavioural analyses suggest that these brain phenotypes relate to different deficits of automatization of language-based processes such as grapheme/phoneme correspondence and/or rapid access to lexicon entries.
This observational, cross-sectional study investigates cortical signatures of developmental dyslexia, particularly from the perspective of behavioral remediation. We employed resting-state fMRI, and compared intrinsic functional connectivity (iFC) patterns of known reading regions (seeds) among three dyslexia groups characterized by (a) no remediation (current reading and spelling deficits), (b) partial remediation (only reading deficit remediated), and (c) full remediation (both reading and spelling deficits remediated), and a group of age- and IQ-matched typically developing children (TDC) (total N = 44, age range = 7-15 years). We observed significant group differences in iFC of two seeds located in the left posterior reading network - left intraparietal sulcus (L.IPS) and left fusiform gyrus (L.FFG). Specifically, iFC between L.IPS and left middle frontal gyrus was significantly weaker in all dyslexia groups, irrespective of remediation status/literacy competence, suggesting that persistent dysfunction in the fronto-parietal attention network characterizes dyslexia. Additionally, relative to both TDC and the no remediation group, the remediation groups exhibited stronger iFC between L.FFG and right middle occipital gyrus (R.MOG). The full remediation group also exhibited stronger negative iFC between the same L.FFG seed and right medial prefrontal cortex (R.MPFC), a core region of the default network These results suggest that behavioral remediation may be associated with compensatory changes anchored in L.FFG, which reflect atypically stronger coupling between posterior visual regions (L.FFG-R.MOG) and greater functional segregation between task-positive and task-negative regions (L.FFG-R.MPFC). These findings were bolstered by significant relationships between the strength of the identified functional connections and literacy scores. We conclude that examining iFC can reveal cortical signatures of dyslexia with particular promise for monitoring neural changes associated with behavioral remediation.
Numerous arguments in the recent neuroscientific literature support the use of musical training as a therapeutic tool among the arsenal already available to therapists and educators for treating children with dyslexia. In the present study, we tested the efficacy of a specially-designed Cognitivo-Musical Training (CMT) method based upon three principles: (1) music-language analogies: training dyslexics with music could contribute to improve brain circuits which are common to music and language processes; (2) the temporal and rhythmic features of music, which could exert a positive effect on the multiple dimensions of the "temporal deficit" characteristic of some types of dyslexia; and (3) cross-modal integration, based on converging evidence of impaired connectivity between brain regions in dyslexia and related disorders. Accordingly, we developed a series of musical exercises involving jointly and simultaneously sensory (visual, auditory, somatosensory) and motor systems, with special emphasis on rhythmic perception and production in addition to intensive training of various features of the musical auditory signal. Two separate studies were carried out, one in which dyslexic children received intensive musical exercises concentrated over 18 h during 3 consecutive days, and the other in which the 18 h of musical training were spread over 6 weeks. Both studies showed significant improvements in some untrained, linguistic and non-linguistic variables. The first one yielded significant improvement in categorical perception and auditory perception of temporal components of speech. The second study revealed additional improvements in auditory attention, phonological awareness (syllable fusion), reading abilities, and repetition of pseudo-words. Importantly, most improvements persisted after an untrained period of 6 weeks. These results provide new additional arguments for using music as part of systematic therapeutic and instructional practice for dyslexic children.
We report on a prospective longitudinal research programme exploring the connection between language acquisition deficits and dyslexia. The language development profile of children at-risk for dyslexia is compared to that of age-matched controls as well as of children who have been diagnosed with specific language impairment (SLI). The experiments described concern the perception and production of grammatical morphology, categorical perception of speech sounds, phonological processing (non-word repetition), mispronunciation detection, and rhyme detection. The results of each of these indicate that the at-risk children as a group underperform in comparison to the controls, and that, in most cases, they approach the SLI group. It can be concluded that dyslexia most likely has precursors in language development, also in domains other than those traditionally considered conditional for the acquisition of literacy skills. The dyslexia-SLI connection awaits further, particularly qualitative, analyses.
There is a growing consensus that developmental dyslexia is associated with a phonological-core deficit. One symptom of this phonological deficit is a subtle speech-perception deficit. The auditory basis of this deficit is still hotly debated. If people with dyslexia, however, do not have an auditory deficit and perceive the underlying acoustic dimensions of speech as well as people who read normally, then why do they exhibit a categorical-perception deficit? A potential answer to this conundrum lies in the possibility that people with dyslexia do not adequately handle the context-dependent variation that speech signals typically contain. A mathematical model simulating such a sensitivity deficit mimics the speech-perception deficits attributed to dyslexia. To assess the nature of the dyslexic problem, the authors examined whether children with dyslexia handle context dependencies in speech differently than do normal-reading individuals. Contrary to the initial hypothesis, children with dyslexia did not show less context sensitivity in speech perception than did normal-reading individuals at auditory, phonetic, and phonological levels of processing, nor did they reveal any categorization deficit. Instead, intrinsic properties of online phonological processes, not phonological representations per se, may be impaired in dyslexia.
Dyslexia is a highly heritable learning disorder with a complex underlying genetic architecture. Over the past decade, researchers have pinpointed a number of candidate genes that may contribute to dyslexia susceptibility. Here, we provide an overview of the state of the art, describing how studies have moved from mapping potential risk loci, through identification of associated gene variants, to characterization of gene function in cellular and animal model systems. Work thus far has highlighted some intriguing mechanistic pathways, such as neuronal migration, axon guidance, and ciliary biology, but it is clear that we still have much to learn about the molecular networks that are involved. We end the review by highlighting the past, present, and future contributions of the Dutch Dyslexia Programme to studies of genetic factors. In particular, we emphasize the importance of relating genetic information to intermediate neurobiological measures, as well as the value of incorporating longitudinal and developmental data into molecular designs.
Studies have converged in their findings of relatively less gray matter volume (GMV) in developmental dyslexia in bilateral temporoparietal and left occipitotemporal cortical regions. However, the interpretation of these results has been difficult. The reported neuroanatomical differences in dyslexia may be causal to the reading problems, following from, for example, neural migration errors that occurred during early human development and before learning to read. Alternatively, less GMV may represent the consequence of an impoverished reading experience, akin to the experience-dependent GMV differences attributed to illiterate compared with literate adults. Most likely, a combination of these factors is driving these observations. Here we attempt to disambiguate these influences by using a reading level-matched design, where dyslexic children were contrasted not only with age-matched controls, but also with younger controls who read at the same level as the dyslexics. Consistent with previous reports, dyslexics showed less GMV in multiple left and right hemisphere regions, including left superior temporal sulcus when compared with age-matched controls. However, not all of these differences emerged when dyslexics were compared with controls matched on reading abilities, with only right precentral gyrus GMV surviving this second analysis. When similar analyses were performed for white matter volume, no regions emerged from both comparisons. These results indicate that the GMV differences in dyslexia reported here and in prior studies are in large part the outcome of experience (e.g., disordered reading experience) compared with controls, with only a fraction of the differences being driven by dyslexia per se.
PURPOSE: This study investigated whether adults with dyslexia show evidence of a consistent speech perception deficit by testing phoneme categorization and word perception in noise. METHOD: Seventeen adults with dyslexia and 20 average readers underwent a test battery including standardized reading, language and phonological awareness tests, and tests of speech perception. Categorization of a pea/bee voicing contrast was evaluated using adaptive identification and discrimination tasks, presented in quiet and in noise, and a fixed-step discrimination task. Two further tests of word perception in noise were presented. RESULTS: There were no significant group differences for categorization in quiet or noise, across- and within-category discrimination as measured adaptively, or word perception, but average readers showed better across- and within-category discrimination in the fixed-step discrimination task. Individuals did not show consistent poor performance across related tasks. CONCLUSIONS: The small number of group differences, and lack of consistent poor individual performance, suggests weak support for a speech perception deficit in dyslexia. It seems likely that at least some poor performances are attributable to nonsensory factors like attention. It may also be that some individuals with dyslexia have speech perceptual acuity that is at the lower end of the normal range and exacerbated by nonsensory factors.
Although the neural systems supporting single word reading are well studied, there are limited direct comparisons between typical and dyslexic readers of the neural correlates of reading fluency. Reading fluency deficits are a persistent behavioral marker of dyslexia into adulthood. The current study identified the neural correlates of fluent reading in typical and dyslexic adult readers, using sentences presented in a word-by-word format in which single words were presented sequentially at fixed rates. Sentences were presented at slow, medium, and fast rates, and participants were asked to decide whether each sentence did or did not make sense semantically. As presentation rates increased, participants became less accurate and slower at making judgments, with comprehension accuracy decreasing disproportionately for dyslexic readers. In-scanner performance on the sentence task correlated significantly with standardized clinical measures of both reading fluency and phonological awareness. Both typical readers and readers with dyslexia exhibited widespread, bilateral increases in activation that corresponded to increases in presentation rate. Typical readers exhibited significantly larger gains in activation as a function of faster presentation rates than readers with dyslexia in several areas, including left prefrontal and left superior temporal regions associated with semantic retrieval and semantic and phonological representations. Group differences were more extensive when behavioral differences between conditions were equated across groups. These findings suggest a brain basis for impaired reading fluency in dyslexia, specifically a failure of brain regions involved in semantic retrieval and semantic and phonological representations to become fully engaged for comprehension at rapid reading rates.
Purpose: The purpose of this tutorial is to provide an overview of the benefits and challenges associated with the early identification of dyslexia. Method: The literature on the early identification of dyslexia is reviewed. Theoretical arguments and research evidence are summarized. An overview of response to intervention as a method of early identification is provided, and the benefits and challenges associated with it are discussed. Finally, the role of speech-language pathologists in the early identification process is addressed. Conclusions: Early identification of dyslexia is crucial to ensure that children are able to maximize their educational potential, and speech-language pathologists are well placed to play a role in this process. However, early identification alone is not sufficient-difficulties with reading may persist or become apparent later in schooling. Therefore, continuing progress monitoring and access to suitable intervention programs are essential.
In order to understand why some children are vulnerable to difficulties in their language development and their acquisition of reading skill, the Jyväskylä Longitudinal Study of Dyslexia followed 200 Finnish children from birth to school age. Half of these children had a family history of reading problems and were considered at risk for dyslexia; the other half were not at risk. A novel analysis, mixture modeling, revealed four subgroups with differential developmental trajectories to early reading. The subgroups who showed either a “dysfluent trajectory” (n = 12; 11 at risk vs. 1 control) or a “declining trajectory” (n = 35; 24 vs. 11) contained more children with familial risk for dyslexia. The subgroup showing an “unexpected trajectory” contained equal numbers of at-risk and non-risk children (n = 67; 33 vs. 34). The subgroup displaying a “typical trajectory” (n = 85, 38 vs. 47) contained more children born without dyslexia risk. This differential development of skills revealed that there are at least three troubled routes along which a child may ultimately encounter difficulties in reading acquisition. The most explicit routes are characterized by problems in either phonological awareness, naming speed, or letter knowledge—problems that increase in severity with age.
BACKGROUND: It is well established that phonological awareness, print knowledge and rapid naming predict later reading difficulties. However, additional auditory, visual and motor difficulties have also been observed in dyslexic children. It is examined to what extent these difficulties can be used to predict later literacy difficulties. METHOD: An unselected sample of 267 children at school entry completed a wide battery of tasks associated with dyslexia. Their reading was tested 2, 3 and 4 years later and poor readers were identified (n = 42). Logistic regression and multiple case study approaches were used to examine the predictive validity of different tasks. RESULTS: As expected, print knowledge, verbal short-term memory, phonological awareness and rapid naming were good predictors of later poor reading. Deficits in visual search and in auditory processing were also present in a large minority of the poor readers. Almost all poor readers showed deficits in at least one area at school entry, but there was no single deficit that characterised the majority of poor readers. CONCLUSIONS: Results are in line with Pennington's () multiple deficits view of dyslexia. They indicate that the causes of poor reading outcome are multiple, interacting and probabilistic, rather than deterministic.
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.
Functional imaging studies of developmental dyslexia have reported reduced task-related neural activity in the temporal and inferior parietal cortices. To examine the possible contribution of subtle anatomic deviations to these reductions, volumes were measured for the major lobes of the brain, the subcortical nuclei, cerebellum, and lateral ventricles on magnetic resonance imaging (MRI) scans from 16 right-handed dyslexic men, ages 18 to 40, and 14 matched controls, most of whom had previously undergone PET imaging. A specific decrease in tissue volume was localized to the temporal lobes and was particularly prominent on the left (p < .01). An analysis of tissue composition revealed that this reduction was primarily attributable to decreased gray matter within the left temporal lobe (p < .002). Further segmentation of the temporal lobe showed that this reduction was not confined to the superior temporal gyrus, the primary location of primary auditory cortex. Reductions of temporal lobe gray matter may reflect a regional decrease in neuronal number or neuropil, which in turn may result in reading impairment.