14Centre référent pour le diagnostic des troubles du langage et des apprentissages, Département de pédiatrie, CHU Nord, Grenoble, France; Background: The relationship between phoneme awareness, rapid automatized naming (RAN), verbal short-term/working memory (ST/WM) and diagnostic category is investigated in control and dyslexic children, and the extent to which this depends on orthographic complexity. Methods: General cognitive, phonological and literacy skills were tested in 1,138 control and 1,114 dyslexic children speaking six different languages spanning a large range of orthographic complexity (Finnish, Hungarian, German, Dutch, French, English). Results: Phoneme deletion and RAN were strong concurrent predictors of developmental dyslexia, while verbal ST/WM and general verbal abilities played a comparatively minor role. In logistic regression models, more participants were classified correctly when orthography was more complex. The impact of phoneme deletion and RAN-digits was stronger in complex than in less complex orthographies. Conclusions: Findings are largely consistent with the literature on predictors of dyslexia and literacy skills, while uniquely demonstrating how orthographic complexity exacerbates some symptoms of dyslexia.
Speech perception deficits in developmental dyslexia were investigated in quiet and various noise conditions. Dyslexics exhibited clear speech perception deficits in noise but not in silence. Place-of-articulation was more affected than voicing or manner-of-articulation. Speech-perception-in-noise deficits persisted when performance of dyslexics was compared to that of much younger children matched on reading age, underscoring the fundamental nature of speech-perception-in-noise deficits. The deficits were not due to poor spectral or temporal resolution because dyslexics exhibited normal 'masking release' effects (i.e. better performance in fluctuating than in stationary noise). Moreover, speech-perception-in-noise predicted significant unique variance in reading even after controlling for low-level auditory, attentional, speech output, short-term memory and phonological awareness processes. Finally, the presence of external noise did not seem to be a necessary condition for speech perception deficits to occur because similar deficits were obtained when speech was degraded by eliminating temporal fine-structure cues without using external noise. In conclusion, the core deficit of dyslexics seems to be a lack of speech robustness in the presence of external or internal noise.
Although the causes of dyslexia are still debated, all researchers agree that the main challenge is to find ways that allow a child with dyslexia to read more words in less time, because reading more is undisputedly the most efficient intervention for dyslexia. Sophisticated training programs exist, but they typically target the component skills of reading, such as phonological awareness. After the component skills have improved, the main challenge remains (that is, reading deficits must be treated by reading more—a vicious circle for a dyslexic child). Here, we show that a simple manipulation of letter spacing substantially improved text reading performance on the fly (without any training) in a large, unselected sample of Italian and French dyslexic children. Extra-large letter spacing helps reading, because dyslexics are abnormally affected by crowding, a perceptual phenomenon with detrimental effects on letter recognition that is modulated by the spacing between letters. Extra-large letter spacing may help to break the vicious circle by rendering the reading material more easily accessible.
Specific language impairment (SLI) is one of the most common childhood disorders, affecting 7% of children. These children experience difficulties in understanding and producing spoken language despite normal intelligence, normal hearing, and normal opportunities to learn language. The causes of SLI are still hotly debated, ranging from nonlinguistic deficits in auditory perception to high-level deficits in grammar. Here, we show that children with SLI have poorer-than-normal consonant identification when measured in ecologically valid conditions of stationary or fluctuating masking noise. The deficits persisted even in comparison with a younger group of normally developing children who were matched for language skills. This finding points to a fundamental deficit. Information transmission of all phonetic features (voicing, place, and manner) was impaired, although the deficits were strongest for voicing (e.g., difference between͞b͞and͞p͞). Children with SLI experienced perfectly normal ''release from masking'' (better identification in fluctuating than in stationary noise), which indicates a central deficit in feature extraction rather than deficits in low-level, temporal, and spectral auditory capacities. We further showed that speech identification in noise predicted language impairment to a great extent within the group of children with SLI and across all participants. Previous research might have underestimated this important link, possibly because speech perception has typically been investigated in optimal listening conditions using non-speech material. The present study suggests that children with SLI learn language deviantly because they inefficiently extract and manipulate speech features, in particular, voicing. This result offers new directions for the fast diagnosis and remediation of SLI.phonetic deficit ͉ auditory deficit ͉ speech intelligibility ͉ masking noise ͉ specific language impairment M any children experience unexpected difficulties in understanding and producing spoken language despite normal intelligence, normal hearing, normal opportunities to learn language, and in the absence of any obvious neurological problems (for review, see ref. 1). This disorder is typically called specific language impairment (SLI). In the past years, research on SLI has experienced a growth of interest partially because it has become clear that more children than initially thought show language learning difficulties. Indeed, recent epidemiological studies estimate the incidence of SLI to be Ϸ7.4% in a population of monolingual English-speaking kindergarten children (2). Children with SLI exhibit deficits in several aspects of language, including phonology, morphology, and syntax (1, 3). One of the hallmarks of SLI is a deficit in the use of function morphemes (e.g., the, a, and is) and other grammatical morphology (e.g., plural -s, past tense -ed). Children with SLI also are at high risk for subsequent literacy problems (4).The causes of SLI are still hotly debated. Current theories of SLI fall into two categ...
In this study, we concurrently investigated 3 possible causes of dyslexia-a phonological deficit, visual stress, and a reduced visual attention span-in a large population of 164 dyslexic and 118 control French children, aged between 8 and 13 years old. We found that most dyslexic children showed a phonological deficit, either in terms of response accuracy (92.1% of the sample), speed (84.8%), or both (79.3%). Deficits in visual attention span, as measured by partial report ability, affected 28.1% of dyslexic participants, all of which also showed a phonological deficit. Visual stress, as measured by subjective reports of visual discomfort, affected 5.5% of dyslexic participants, not more than controls (8.5%). Although phonological variables explained a large amount of variance in literacy skills, visual variables did not explain any additional variance. Finally, children with comorbid phonological and visual deficits did not show more severe reading disability than children with a pure phonological deficit. These results (a) confirm the importance of phonological deficits in dyslexia; (b) suggest that visual attention span may play a role, but a minor one, at least in this population; (c) do not support any involvement of visual stress in dyslexia. Among the factors that may explain some differences with previously published studies, the present sample is characterized by very stringent inclusion criteria, in terms of the severity of reading disability and in terms of exclusion of comorbidities. This may exacerbate the role of phonological deficits to the detriment of other factors playing a role in reading acquisition. (PsycINFO Database Record
Dyslexia is one of the most common childhood disorders with a prevalence of around 5-10% in school-age children. Although an important genetic component is known to have a role in the aetiology of dyslexia, we are far from understanding the molecular mechanisms leading to the disorder. Several candidate genes have been implicated in dyslexia, including DYX1C1, DCDC2, KIAA0319, and the MRPL19/C2ORF3 locus, each with reports of both positive and no replications. We generated a European cross-linguistic sample of school-age children -the NeuroDys cohort -that includes more than 900 individuals with dyslexia, sampled with homogenous inclusion criteria across eight European countries, and a comparable number of controls. Here, we describe association analysis of the dyslexia candidate genes/locus in the NeuroDys cohort. We performed both case-control and quantitative association analyses of single markers and haplotypes previously reported to be dyslexia-associated. Although we observed association signals in samples from single countries, we did not find any marker or haplotype that was significantly associated with either case-control status or quantitative measurements of word-reading or spelling in the meta-analysis of all eight countries combined. Like in other neurocognitive disorders, our findings underline the need for larger sample sizes to validate possibly weak genetic effects.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.