Atypical Balance between Occipital and Fronto-Parietal Activation for Visual Shape Extraction in Dyslexia

Reading requires the extraction of letter shapes from a complex background of text, and an impairment in visual shape extraction would cause difficulty in reading. To investigate the neural mechanisms of visual shape extraction in dyslexia, we used functional magnetic resonance imaging (fMRI) to examine brain activation while adults with or without dyslexia responded to the change of an arrow’s direction in a complex, relative to a simple, visual background. In comparison to adults with typical reading ability, adults with dyslexia exhibited opposite patterns of atypical activation: decreased activation in occipital visual areas associated with visual perception, and increased activation in frontal and parietal regions associated with visual attention. These findings indicate that dyslexia involves atypical brain organization for fundamental processes of visual shape extraction even when reading is not involved. Overengagement in higher-order association cortices, required to compensate for underengagment in lower-order visual cortices, may result in competition for top-down attentional resources helpful for fluent reading.     

发展性阅读障碍的脑机制——来自脑成像研究的证据

发展性阅读障碍是一种特殊的学习障碍,发展性阅读障碍的脑机制一直是研究者们关心的一个重要问题．随着脑成像技术的应用,人们在发展性阅读障碍的脑机制研究方面取得了重大进展．脑结构研究发现,发展性阅读障碍者在颞-顶叶、颞-枕叶、额下回、小脑等区域都存在一定的脑结构异常,这些脑结构异常要么表现在某个脑区的结构上,要么表现某个脑区结构的左右不对称性上．脑功能研究发现,发展性阅读障碍者出现脑结构异常的区域也大多表现出脑功能的异常．脑功能连接的研究发现,发展性阅读障碍者脑功能连接的异常不仅涉及到同侧脑区前后部分的连接,还涉及双侧脑区相应部分的连接．另外,中文发展性阅读障碍的研究发现了与拼音文字发展性阅读障碍不同的脑机制．这些研究成果为进一步揭示发展性阅读障碍的脑机制以及拓展中文发展性阅读障碍的研究提供了借鉴．     

A Common Left Occipito-Temporal Dysfunction in Developmental Dyslexia and Acquired Letter-By-Letter Reading?

Background

We used fMRI to examine functional brain abnormalities of German-speaking dyslexics who suffer from slow effortful reading but not from a reading accuracy problem. Similar to acquired cases of letter-by-letter reading, the developmental cases exhibited an abnormal strong effect of length (i.e., number of letters) on response time for words and pseudowords.

Results

Corresponding to lesions of left occipito-temporal (OT) regions in acquired cases, we found a dysfunction of this region in our developmental cases who failed to exhibit responsiveness of left OT regions to the length of words and pseudowords. This abnormality in the left OT cortex was accompanied by absent responsiveness to increased sublexical reading demands in phonological inferior frontal gyrus (IFG) regions. Interestingly, there was no abnormality in the left superior temporal cortex which—corresponding to the onological deficit explanation—is considered to be the prime locus of the reading difficulties of developmental dyslexia cases.

Conclusions

The present functional imaging results suggest that developmental dyslexia similar to acquired letter-by-letter reading is due to a primary dysfunction of left OT regions.     

The neural basis of hyperlexic reading: an FMRI case study

Children with autism spectrum disorders in very rare cases display surprisingly advanced "hyperlexic" reading skills. Using functional magnetic resonance imaging (fMRI), we studied the neural basis of this precocious reading ability in a 9-year-old hyperlexic boy who reads 6 years in advance of his age. During covert reading, he demonstrated greater activity in the left inferior frontal and superior temporal cortices than both chronological age- and reading age-matched controls. Activity in the right inferior temporal sulcus was greater when compared to reading age-matched controls. These findings suggest that precocious reading is brought about by simultaneously drawing on both left hemisphere phonological and right hemisphere visual systems, reconciling the two prevailing, but seemingly contradictory, single hemisphere theories of hyperlexia. Hyperlexic reading is therefore associated with hyperactivation of the left superior temporal cortex, much in the same way as developmental dyslexia is associated with hypoactivation of this area.     

Reading text increases binocular disparity in dyslexic children

Children with developmental dyslexia show reading impairment compared to their peers, despite being matched on IQ, socio-economic background, and educational opportunities. The neurological and cognitive basis of dyslexia remains a highly debated topic. Proponents of the magnocellular theory, which postulates abnormalities in the M-stream of the visual pathway cause developmental dyslexia, claim that children with dyslexia have deficient binocular coordination, and this is the underlying cause of developmental dyslexia. We measured binocular coordination during reading and a non-linguistic scanning task in three participant groups: adults, typically developing children, and children with dyslexia. A significant increase in fixation disparity was observed for dyslexic children solely when reading. Our study casts serious doubts on the claims of the magnocellular theory. The exclusivity of increased fixation disparity in dyslexics during reading might be a result of the allocation of inadequate attentional and/or cognitive resources to the reading process, or suboptimal linguistic processing per se.     

Cortical Signatures of Dyslexia and Remediation: An Intrinsic Functional Connectivity Approach

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.     

Reading Performance Is Enhanced by Visual Texture Discrimination Training in Chinese-Speaking Children with Developmental Dyslexia

Background

High order cognitive processing and learning, such as reading, interact with lower-level sensory processing and learning. Previous studies have reported that visual perceptual training enlarges visual span and, consequently, improves reading speed in young and old people with amblyopia. Recently, a visual perceptual training study in Chinese-speaking children with dyslexia found that the visual texture discrimination thresholds of these children in visual perceptual training significantly correlated with their performance in Chinese character recognition, suggesting that deficits in visual perceptual processing/learning might partly underpin the difficulty in reading Chinese.

Methodology/Principal Findings

To further clarify whether visual perceptual training improves the measures of reading performance, eighteen children with dyslexia and eighteen typically developed readers that were age- and IQ-matched completed a series of reading measures before and after visual texture discrimination task (TDT) training. Prior to the TDT training, each group of children was split into two equivalent training and non-training groups in terms of all reading measures, IQ, and TDT. The results revealed that the discrimination threshold SOAs of TDT were significantly higher for the children with dyslexia than for the control children before training. Interestingly, training significantly decreased the discrimination threshold SOAs of TDT for both the typically developed readers and the children with dyslexia. More importantly, the training group with dyslexia exhibited significant enhancement in reading fluency, while the non-training group with dyslexia did not show this improvement. Additional follow-up tests showed that the improvement in reading fluency is a long-lasting effect and could be maintained for up to two months in the training group with dyslexia.

Conclusion/Significance

These results suggest that basic visual perceptual processing/learning and reading ability in Chinese might at least partially rely on overlapping mechanisms.     

Connectionist neuropsychology: uncovering ultimate causes of acquired dyslexia

Acquired dyslexia offers a unique window on to the nature of the cognitive and neural architecture supporting skilled reading. This paper provides an integrative overview of recent empirical and computational work on acquired dyslexia within the context of the primary systems framework as implemented in connectionist neuropsychological models. This view proposes that damage to general visual, phonological or semantic processing abilities are the root causes of different forms of acquired dyslexia. Recent case-series behavioural evidence concerning pure alexia, phonological dyslexia and surface dyslexia that supports this perspective is presented. Lesion simulations of these findings within connectionist models of reading demonstrate the viability of this approach. The commitment of such models to learnt representations allows them to capture key aspects of performance in each type of acquired dyslexia, particularly the associated non-reading deficits, the role of relearning and the influence of individual differences in the premorbid state of the reading system. Identification of these factors not only advances our understanding of acquired dyslexia and the mechanisms of normal reading but they are also relevant to the complex interactions underpinning developmental reading disorders.     

Grey Matter Alterations Co-Localize with Functional Abnormalities in Developmental Dyslexia: An ALE Meta-Analysis

The neural correlates of developmental dyslexia have been investigated intensively over the last two decades and reliable evidence for a dysfunction of left-hemispheric reading systems in dyslexic readers has been found in functional neuroimaging studies. In addition, structural imaging studies using voxel-based morphometry (VBM) demonstrated grey matter reductions in dyslexics in several brain regions. To objectively assess the consistency of these findings, we performed activation likelihood estimation (ALE) meta-analysis on nine published VBM studies reporting 62 foci of grey matter reduction in dyslexic readers. We found six significant clusters of convergence in bilateral temporo-parietal and left occipito-temporal cortical regions and in the cerebellum bilaterally. To identify possible overlaps between structural and functional deviations in dyslexic readers, we conducted additional ALE meta-analyses of imaging studies reporting functional underactivations (125 foci from 24 studies) or overactivations (95 foci from 11 studies ) in dyslexics. Subsequent conjunction analyses revealed overlaps between the results of the VBM meta-analysis and the meta-analysis of functional underactivations in the fusiform and supramarginal gyri of the left hemisphere. An overlap between VBM results and the meta-analysis of functional overactivations was found in the left cerebellum. The results of our study provide evidence for consistent grey matter variations bilaterally in the dyslexic brain and substantial overlap of these structural variations with functional abnormalities in left hemispheric regions.     

Gray and White Matter Distribution in Dyslexia: A VBM Study of Superior Temporal Gyrus Asymmetry

In the present study, we investigated brain morphological signatures of dyslexia by using a voxel-based asymmetry analysis. Dyslexia is a developmental disorder that affects the acquisition of reading and spelling abilities and is associated with a phonological deficit. Speech perception disabilities have been associated with this deficit, particularly when listening conditions are challenging, such as in noisy environments. These deficits are associated with known neurophysiological correlates, such as a reduction in the functional activation or a modification of functional asymmetry in the cortical regions involved in speech processing, such as the bilateral superior temporal areas. These functional deficits have been associated with macroscopic morphological abnormalities, which potentially include a reduction in gray and white matter volumes, combined with modifications of the leftward asymmetry along the perisylvian areas. The purpose of this study was to investigate gray/white matter distribution asymmetries in dyslexic adults using automated image processing derived from the voxel-based morphometry technique. Correlations with speech-in-noise perception abilities were also investigated. The results confirmed the presence of gray matter distribution abnormalities in the superior temporal gyrus (STG) and the superior temporal Sulcus (STS) in individuals with dyslexia. Specifically, the gray matter of adults with dyslexia was symmetrically distributed over one particular region of the STS, the temporal voice area, whereas normal readers showed a clear rightward gray matter asymmetry in this area. We also identified a region in the left posterior STG in which the white matter distribution asymmetry was correlated to speech-in-noise comprehension abilities in dyslexic adults. These results provide further information concerning the morphological alterations observed in dyslexia, revealing the presence of both gray and white matter distribution anomalies and the potential involvement of these defects in speech-in-noise deficits.     

A sibling-pair based approach for mapping genetic loci that influence quantitative measures of reading disability

Family and twin studies consistently demonstrate a significant role for genetic factors in the aetiology of the reading disorder dyslexia. However, dyslexia is complex at both the genetic and phenotypic levels, and currently the nature of the core deficit or deficits remains uncertain. Traditional approaches for mapping disease genes, originally developed for single-gene disorders, have limited success when there is not a simple relationship between genotype and phenotype. Recent advances in high-throughput genotyping technology and quantitative statistical methods have made a new approach to identifying genes involved in complex disorders possible. The method involves assessing the genetic similarity of many sibling pairs along the lengths of all their chromosomes and attempting to correlate this similarity with that of their phenotypic scores. We are adopting this approach in an ongoing genome-wide search for genes involved in dyslexia susceptibility, and have already successfully applied the method by replicating results from previous studies suggesting that a quantitative trait locus at 6p21.3 influences reading disability.     

A causal link between visual spatial attention and reading acquisition

Reading is a unique, cognitive human skill crucial to life in modern societies, but, for about 10% of the children, learning to read is extremely difficult. They are affected by a neurodevelopmental disorder called dyslexia. Although impaired auditory and speech sound processing is widely assumed to characterize dyslexic individuals, emerging evidence suggests that dyslexia could arise from a more basic cross-modal letter-to-speech sound integration deficit. Letters have to be precisely selected from irrelevant and cluttering letters by rapid orienting of visual attention before the correct letter-to-speech sound integration applies. Here we ask whether prereading visual parietal-attention functioning may explain future reading emergence and development. The present 3 year longitudinal study shows that prereading attentional orienting--assessed by serial search performance and spatial cueing facilitation--captures future reading acquisition skills in grades 1 and 2 after controlling for age, nonverbal IQ, speech-sound processing, and nonalphabetic cross-modal mapping. Our findings provide the first evidence that visual spatial attention in preschoolers specifically predicts future reading acquisition, suggesting new approaches for early identification and efficient prevention of dyslexia.     

Pleiotropic effects of a chromosome 3 locus on speech-sound disorder and reading

Speech-sound disorder (SSD) is a complex behavioral disorder characterized by speech-sound production errors associated with deficits in articulation, phonological processes, and cognitive linguistic processes. SSD is prevalent in childhood and is comorbid with disorders of language, spelling, and reading disability, or dyslexia. Previous research suggests that developmental problems in domains associated with speech and language acquisition place a child at risk for dyslexia. Recent genetic studies have identified several candidate regions for dyslexia, including one on chromosome 3 segregating in a large Finnish pedigree. To explore common genetic influences on SSD and reading, we examined linkage for several quantitative traits to markers in the pericentrometric region of chromosome 3 in 77 families ascertained through a child with SSD. The quantitative scores measured several processes underlying speech-sound production, including phonological memory, phonological representation, articulation, receptive and expressive vocabulary, and reading decoding and comprehension skills. Model-free linkage analysis was followed by identification of sib pairs with linkage and construction of core shared haplotypes. In our multipoint analyses, measures of phonological memory demonstrated the strongest linkage (marker D3S2465, P=5.6 x 10(-5), and marker D3S3716, P=6.8 x 10(-4)). Tests for single-word decoding also demonstrated linkage (real word reading: marker D3S2465, P=.004; nonsense word reading: marker D3S1595, P=.005). The minimum shared haplotype in sib pairs with similar trait values spans 4.9 cM and is bounded by markers D3S3049 and D3S3045. Our results suggest that domains common to SSD and dyslexia are pleiotropically influenced by a putative quantitative trait locus on chromosome 3.     

Brain mechanisms in normal and dyslexic readers

Developmental dyslexics, individuals with an unexplained difficulty reading, have been shown to have deficits in phonological processing -- the awareness of the sound structure of words -- and, in some cases, a more fundamental deficit in rapid auditory processing. In addition, dyslexics show a disruption in white matter connectivity between posterior and frontal regions. These results give continued support for a neurobiological etiology of developmental dyslexia. However, more research will be required to determine the possible causal relationships between these neurobiological disruptions and dyslexia.     

Absence of linkage of phonological coding dyslexia to chromosome 6p23-p21.3 in a large family data set.

Previous studies have suggested that a locus predisposing to specific reading disability (dyslexia) resides on chromosome 6p23-p21.3. We investigated 79 families having at least two siblings affected with phonological coding dyslexia, the most common form of reading disability (617 people genotyped, 294 affected), and we tested for linkage with the genetic markers reported to be linked to dyslexia in those studies. No evidence for linkage was found by LOD score analysis or affected-sib-pair methods. However, using the affected-pedigree-member (APM) method, we detected significant evidence for linkage and/or association with some markers when we used published allele frequencies with weighting of rarer alleles. APM results were not significant when we used marker allele frequencies estimated from parents. Furthermore, results were not significant with the more robust SIMIBD method using either published or parental marker frequencies. Finally, family-based association analysis using the AFBAC program showed no evidence for association with any marker. We conclude that the APM method should be used only with extreme caution, because it appears to have generated false-positive results. In summary, using a large data set with high power to detect linkage, we were unable to find evidence for linkage or association between phonological coding dyslexia and chromosome 6p markers.     

Neural changes following remediation in adult developmental dyslexia

Brain imaging studies have explored the neural mechanisms of recovery in adults following acquired disorders and, more recently, childhood developmental disorders. However, the neural systems underlying adult rehabilitation of neurobiologically based learning disabilities remain unexplored, despite their high incidence. Here we characterize the differences in brain activity during a phonological manipulation task before and after a behavioral intervention in adults with developmental dyslexia. Phonologically targeted training resulted in performance improvements in tutored compared to nontutored dyslexics, and these gains were associated with signal increases in bilateral parietal and right perisylvian cortices. Our findings demonstrate that behavioral changes in tutored dyslexic adults are associated with (1) increased activity in those left-hemisphere regions engaged by normal readers and (2) compensatory activity in the right perisylvian cortex. Hence, behavioral plasticity in adult developmental dyslexia involves two distinct neural mechanisms, each of which has previously been observed either for remediation of developmental or acquired reading disorders.     

The interface between genetics and psychology: lessons from developmental dyslexia

Developmental dyslexia runs in families, and twin studies have confirmed that there is a substantial genetic contribution to poor reading. The way in which discoveries in molecular genetics are reported can be misleading, encouraging us to think that there are specific genes that might be used to screen for disorder. However, dyslexia is not a classic Mendelian disorder that is caused by a mutation in a single gene. Rather, like many other common disorders, it appears to involve combined effects of many genes and environmental factors, each of which has a small influence, possibly supplemented by rare variants that have larger effects but apply to only a minority of cases. Furthermore, to see clearer relationships between genotype and phenotype, we may need to move beyond the clinical category of dyslexia to look at underlying cognitive deficits that may be implicated in other neurodevelopmental disorders.     

Spatial and temporal measurements of eye movement in children with dyslexia

This paper presents the first reading data in Croatian collected with an eye-tracking device. The eye-tracking method allows for research into two crucial levels underlying reading: the visual and the cognitive. The aim of this paper is to show the differences in eye movements in children with dyslexia using the principles of cognitive-control view. Despite the well-known definitions and vast literature on dyslexia, the neural basis of dyslexia varies greatly on the individual level. The three children studied in this paper were tested behaviorally using set of language tests for language behavior assessment on all language levels: phonology, morphology, syntax, lexicon and pragmatics. Two children had low scores on most language tests, and all three children had poor reading and writing level. Each of the children had to read two texts silently while their eye movements were recorded by means of an infrared eye-tracking system. We analyzed the number, position, and duration of fixations and the number and position of regressive (or back) saccades. Our results show intergroup differences (between a typically developing child and the three children with dyslexia), and intragroup differences (among all three children with dyslexia). The great number of fixations, longer duration of fixations, and great number of regression saccades are the main features that differentiate the children with dyslexia form the typically developing child. The only difference found between language and visual subtypes of dyslexia was a shorter duration of fixations for the child with a visual processing disorder.     

The psycholinguistic analysis of acquired dyslexias: some illustrations

Three approaches to the neuropsychology of cognitive function are distinguished: the neuroanatomical (where the primary concern is to correlate particular disorders of cognitive function with particular lesion sites), the 'general-cognitive' (in which associations are sought between impairments of performance on specific cognitive tasks and general disorders of broadly defined cognitive processes) and the model-building (in which one attempts to interpret the pattern of impairments and preservations of some cognitive function produced by brain damage in terms of an explicit model of the normal operation of this function). I claim that the model-building approach to the neuropsychology of cognitive function must take precedence over the other two. One reason for this is that any disorder of cognitive function can only be defined with reference to some model of that function. I illustrate this claim with reference to acquired disorders of reading, describing current work of a psycholinguistic nature dealing with two acquired disorders of reading: phonological dyslexia and surface dyslexia. A psycholinguistic account of normal reading is used as a theoretical framework to define and to explain the patterns of deficit and preservation observed in these two dyslexias. The detailed account of surface dyslexia in English provided by this framework is then used to make predictions about the nature of surface dyslexia in other languages: alphabetically written languages where all words are regularly spelled, or where homophones cannot occur, as well as ideographically and syllabically written languages. A case of surface dyslexia in an English-Spanish bilingual, in which such predictions were confirmed, is described.     

Improvements in Spelling after QEEG-based Neurofeedback in Dyslexia: A Randomized Controlled Treatment Study

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.