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100 years of research on specific reading and spelling disorder - what is our knowledge today?
... During the last decade, research on developmental dyslexia has accumulated, and yet the theories about mechanisms underlying this deficit are still controversial (Ramus et al., 2003;Witruk, Friederici, & Lachmann, 2002;Habib, 2000;von Suchodoletz, 1999). We will start by briefly reviewing two of the most prominent theories in current research on developmental dyslexia, the phonological deficit hypothesis and the auditory deficit hypothesis. ...
... During the last decade, research on developmental dyslexia has accumulated, and yet the theories about mechanisms underlying this deficit are still controversial (Ramus et al., 2003;Witruk, Friederici, & Lachmann, 2002;Habib, 2000;von Suchodoletz, 1999). We will start by briefly reviewing two of the most prominent theories in current research on developmental dyslexia, the phonological deficit hypothesis and the auditory deficit hypothesis. ...
In the present study, event-related brain potentials (ERPs) were used to compare auditory sentence comprehension in 16 children with developmental dyslexia (age 9–12 years) and unimpaired controls matched on age, sex, and nonverbal intelligence. Passive sentences were presented, which were either correct or contained a syntactic violation (phrase structure) or a semantic violation (selectional restriction). In an overall sentence correctness judgment task, both control and dyslexic children performed well. In the ERPs, control children and dyslexic children demonstrated a similar N400 component for the semantic violation. For the syntactic violation, control children demonstrated a combined pattern, consisting of an early starting bilaterally distributed anterior negativity and a late centro-parietal positivity (P600). Dyslexic children showed a different pattern that is characterized by a delayed left lateralized anterior negativity, followed by a P600. These data indicate that dyslexic children do not differ from unimpaired controls with respect to semantic integration processes (N400) or controlled processes of syntactic reanalyses (P600) during auditory sentence comprehension. However, early and presumably highly automatic processes of phrase structure building reflected in the anterior negativity are delayed in dyslexic children. Moreover, the differences in hemispheric distribution of the syntactic negativity indicate different underlying processes in dyslexic children and controls. The bilateral distribution in controls suggests an involvement of right hemispherically established prosodic processes in addition to the left hemispherically localized syntactic processes, supporting the view that prosodic information may be used to facilitate syntactic processing during normal comprehension. The left hemispheric distribution observed for dyslexic children, in contrast, suggests that these children do not rely on information about the prosodic contour during auditory sentence comprehension as much as controls do. This finding points toward a phonological impairment in dyslexic children that might hamper the development of syntactic processes.
The phonemic discrimination of subjects with developmental dyslexia was investigated in the present study. Two adult developmental phonological dyslexics are first reported. Both were good at reading real words but had difficulty reading and spelling novel stimuli. Further testing revealed a perceptual discrimination problem that was restricted to a narrow range of phonemes in both subjects. In order to test the generality of this finding, 20 further developmental dyslexics were tested on their nonword reading skill and phonemic discrimination ability. There was a significant association between the two variables…subjects poor at phonemic discrimination were also very likely to be poor at nonword reading. It is suggested that phonemic discrimination problems at an early age may disrupt the normal acquisition of alphabetic processing skills for reading and spelling. Remedial implications of the findings are discussed.
Eight measures of cognitive and language functions in 232 children were subjected to multiple methods of cluster analysis in an effort to identify subtypes of reading disability. Clustering yielded 9 reliable subtypes representing 90% of the sample, including 2 nondisabled subtypes, and 7 reading-disabled subtypes. Of the reading-disabled subtypes, 2 were globally deficient in language skills, whereas 4 of the 5 specific reading-disabled subtypes displayed a relative weakness in phonological awareness and variations in rapid serial naming and verbal short-term memory. The remaining disabled subtype was impaired on verbal and nonverbal measures associated with rate of processing, including rate and accuracy of oral reading. Studies showed evidence for discriminative validity among the 7 reading-disabled subtypes. Results support the view that children with reading disability usually display impairments on phonological awareness measures, with discriminative variability on other measures involving phonological processing, language, and cognitive skills. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The present study assessed reading difficulties and cognitive impairments of German-speaking dyslexic children at grade levels 2, 3, and 4. It was found that German dyslexic children suffered from a pervasive speed deficit for all types of reading tasks, including text, high frequency words, and pseudowords, but at the same time showed generally rather high reading accuracy. For pseudowords, reading refusals or word responses were absent, and the majority of errors was close to the target pronunciation. Reading speed seemed to be most impaired for pseudowords and function words that did not allow the children to take a short-cut from phonemically mediated word processing. The discussion offers a developmental framework for the interpretation of these reading difficulties. For the cognitive tasks, dyslexic children did not differ from age-matched control children on the pseudoword repetition task or the digit span task, indicating that auditory perception and memory were not impaired. On phonological awareness tasks (rhyme oddity detection, vowel substitution, and pseudoword spelling), dyslexic children scored lower than age-matched control children, but not lower than younger reading-level control children. The performance of the dyslexic children on the phonemic segmentation tasks (pseudoword spelling and vowel substitution) was high in absolute terms. In contrast, marked differences between dyslexic and age-matched controls were found on rapid naming tasks: dyslexic grade 4 children showed lower numeral-naming speed than reading-level grade 2 children. Numeral-naming speed turned out to be the most important predictor of reading speed differences. These findings are discussed in relation to the phonological impairment explanation of dyslexia and to recent alternative explanations that posit an underlying impairment in automatizing skills which demand the fast execution of low-level cognitive processes.
Repeated reading of meaningful text has been shown to produce improvements in reading rate, fluency, and comprehension in readers of varying ability. The assisted repeated reading (ARR) method, which provides a fluent and expressive (i.e., prosodic) model, has been proposed as being particularly helpful in this regard. However, it is unclear which component of the ARR method (prosodic modeling or reading practice with intact text) is the most influential factor. The present study examined the effects of text practice and prosodic modeling on the reading rate, accuracy, expressiveness, and comprehension of 40 grade 5 disabled readers. Text practice and prosodic modeling were systematically varied to create four training conditions. Each subject read the first half of a set of stories three times under one of the four experimental conditions. Pretest and posttest measures of the dependent variables were analyzed for both the training passages and the second half of each story, on which no training occurred (transfer passages). While reading performance improved across all conditions, substantial additional gains were produced by the conditions that included the practice of intact text. Modeling of prosody did not produce significant additional gains. Transfer effects were limited, with only the ARR condition producing improved accuracy on the second half of the stories.
To address the question of a possible magnocellular visual deficit in children with reading problems (dyslexia), we examined
pattern ERG and VEP responses to stimulation with checks of 24′, 49′ and 180′ in size and of 5%, 42% and 100% contrast level.
Neurophysiological difference between children with reading problems and those without them was found confined to VEP which
showed a significant prolongation of P100 wave in dyslexic children at highest contrast (100%) and smallest checks (24′).
Pattern ERG was normal. These results support the assumption of a visual deficit in dyslexic children. However, they are not
consistent with an isolated deficit of the magnocellular function, which, theoretically, would cause VEP changes to lower
contrast and largest check stimuli.
Studies have shown the existence of minor developmental cortical malformations, including microgyria, in the brains of dyslexics. Concomitant studies have shown that language-impaired individuals exhibit severe deficits in the discrimination of rapidly presented auditory stimuli, including phonological and nonverbal stimuli (i.e., sequential tones). In an effort to relate these results, male rats with neonatally induced microgyria were tested in an operant paradigm for auditory discrimination of stimuli consisting of two sequential tones. Subjects were shaped to perform a go/no-go target identification, using water reinforcement. Stimuli were reduced in duration from 540 to 249 msec across 24 d of testing. Results showed that all subjects were able to discriminate at longer stimulus durations. However, bilaterally lesioned subjects showed specific impairment at stimulus durations of 332 msec or less, and were significantly depressed in comparison to shams. Right- and left-lesioned subjects were significantly depressed in comparison to shams at the shortest duration (249 msec). These results suggest a possible link between the neuropathologic anomalies and the auditory temporal processing deficits reported for language-impaired individuals.
Several behavioral studies have shown that developmental dyslexics do poorly in tests requiring rapid visual processing. In primates fast, low-contrast visual information is carried by the magnocellular subdivision of the visual pathway, and slow, high-contrast information is carried by the parvocellular division. In this study, we found that dyslexic subjects showed diminished visually evoked potentials to rapid, low-contrast stimuli but normal responses to slow or high-contrast stimuli. The abnormalities in the dyslexic subjects' evoked potentials were consistent with a defect in the magnocellular pathway at the level of visual area 1 or earlier. We then compared the lateral geniculate nuclei from five dyslexic brains to five control brains and found abnormalities in the magnocellular, but not the parvocellular, layers. Studies using auditory and somatosensory tests have shown that dyslexics do poorly in these modalities only when the tests require rapid discriminations. We therefore hypothesize that many cortical systems are similarly divided into a fast and a slow subdivision and that dyslexia specifically affects the fast subdivisions.
The rate variable in rapid automatized naming (RAN) was investigated in 50 adolescent and 40 adult students with developmental dyslexia, in matched normal controls, and in learning-disabled students without reading difficulties. Visual stimuli depicting familiar colors and common objects were presented in isolation at three film speeds and three exposure times. Film speed and exposure time contributed as independent variables to error rate; and dyslexic subjects of both age groups made significantly more naming errors than controls. Dyslexic subjects also responded with longer naming latencies than controls when the same RAN stimuli were presented in a continuous sequential mode as a matrix of rows and columns. Naming latencies in the sequential presentation were highly correlated with naming errors in the film version. The implications of reduced naming rates for nongraphological stimuli in developmental dyslexia are discussed.
We report the neuroanatomical findings in 4 consecutively studied brains of men with developmental dyslexia. The patients, who ranged in age between 14 and 32 years, were diagnosed as dyslexic during life. Nonrighthandedness and several autoimmune and atopic illnesses were present in the personal and family histories. All brains showed developmental anomalies of the cerebral cortex. These consisted of neuronal ectopias and architectonic dysplasias located mainly in perisylvian regions and affecting predominantly the left hemisphere. Furthermore, all brains showed a deviation from the standard pattern of cerebral asymmetry characterized by symmetry of the planum temporale. The neuroanatomical findings in these 4 patients are discussed with reference to developmental cortical anomalies, cerebral asymmetries, reorganization of the brain after early lesions, and the association between learning disorders, left handedness, and diseases of the immune system.
A rhyming and short-term memory task with visually presented letters were used to study brain activity in five compensated adult developmental dyslexics. Their only cognitive difficulty was in phonological processing, manifest in a wide range of tasks including spoonerisms, phonemic fluency and digit naming speed. PET scans showed that for the dyslexics, a subset only of the brain regions normally involved in phonological processing was activated: Broca's area during the rhyming task, temporo-parietal cortex during the short- term memory task. In contrast to normal controls these areas were not activated in concert. Furthermore the left insula was never activated. We propose that the defective phonological system of these dyslexics is due to weak connectivity between anterior and posterior language areas. This could be due to a dysfunctional left insula which may normally act as an anatomical bridge between Broca's area, superior temporal and inferior parietal cortex. The independent activation of the posterior and anterior speech areas in dyslexics supports the notion that representations of unsegmented and segmented phonology are functionally and anatomically separate.
It is widely accepted that dyslexics have deficits in reading and phonological awareness, but there is increasing evidence that they also exhibit visual processing abnormalities that may be confined to particular portions of the visual system. In primate visual pathways, inputs from parvocellular or magnocellular layers of the lateral geniculate nucleus remain partly segregated in projections to extrastriate cortical areas specialized for processing colour and form versus motion. In studies of dyslexia, psychophysical and anatomical evidence indicate an anomaly in the magnocellular visual subsystem. To investigate the pathophysiology of dyslexia, we used functional magnetic resonance imaging (fMRI) to study visual motion processing in normal and dyslexic men. In all dyslexics, presentation of moving stimuli failed to produce the same task-related functional activation in area V5/MT (part of the magnocellular visual subsystem) observed in controls. In contrast, presentation of stationary patterns resulted in equivalent activations in V1/V2 and extrastriate cortex in both groups. Although previous studies have emphasized language deficits, our data reveal differences in the regional functional organization of the cortical visual system in dyslexia.
Developmental dyslexics often complain that small letters appear to blur and move around when they are trying to read. Anatomical, electrophysiological, psychophysical and brain-imaging studies have all contributed to elucidating the functional organization of these and other visual confusions. They emerge not from damage to a single visual relay but from abnormalities of the magnocellular component of the visual system, which is specialized for processing fast temporal information. The m-stream culminates in the posterior parietal cortex, which plays an important role in guiding visual attention. The evidence is consistent with an increasingly sophisticated account of dyslexia that does not single out either phonological, or visual or motor deficits. Rather, temporal processing in all three systems seems to be impaired. Dyslexics may be unable to process fast incoming sensory information adequately in any domain.
Induction of microgyria by freezing injury to the developing somatosensory cortex of neonatal rats causes a defect in fast auditory processing in males, but not in females. It was speculated that early damage to the cortex has sexually dimorphic cascading effects on other brain regions mediating auditory processing, which can lead to the observed behavioral deficits. In the current series of experiments, bilateral microgyri were induced by placement of a freezing probe on the skulls of newborn male and female rats, and these animals were tested in adulthood for auditory temporal processing. Control animals received sham surgery. The brains from these animals were embedded in celloidin, cut in the coronal plane and the following morphometric measures assessed: microgyric volume, medial geniculate nucleus (MGN) volume, cell number, and cell size, and, as a control, dorsal lateral geniculate nucleus (dLGN) volume, cell number and cell size. There were no sex differences in the cortical pathology of lesioned animals. However, microgyric males had more small and fewer large neurons in the MGN than their sham-operated counterparts, whereas there was no difference between lesioned and sham-operated females. There was no effect on dLGN cell size distribution in either sex. Microgyric males were significantly impaired in fast auditory temporal processing when compared to control males, whereas lesioned females exhibited no behavioral deficits. These results suggest that early injury to the cerebral cortex may have different effects on specific thalamic nuclei in males and females, with corresponding differences in behavioral effects.
The relationship between brain activity and reading performance was examined to test the hypothesis that dyslexia involves a deficit in a specific visual pathway known as the magnocellular (M) pathway. Functional magnetic resonance imaging was used to measure brain activity in dyslexic and control subjects in conditions designed to preferentially stimulate the M pathway. Dyslexics showed reduced activity compared with controls both in the primary visual cortex and in a secondary cortical visual area (MT+) that is believed to receive a strong M pathway input. Most importantly, significant correlations were found between individual differences in reading rate and brain activity. These results support the hypothesis for an M pathway abnormality in dyslexia and imply a strong relationship between the integrity of the M pathway and reading ability.
The relationship between reading ability and psychophysical performance was examined to test the hypothesis that dyslexia is associated with a deficit in the magnocellular (M) pathway. Speed discrimination thresholds and contrast detection thresholds were measured under conditions (low mean luminance, low spatial frequency, high temporal frequency) for which psychophysical performance presumably depends on M pathway integrity. Dyslexic subjects had higher psychophysical thresholds than controls in both the speed discrimination and contrast detection tasks, but only the differences in speed thresholds were statistically significant. In addition, there was a strong correlation between individual differences in speed thresholds and reading rates. These results support the hypothesis for an M pathway abnormality in dyslexia, and suggest that motion discrimination may be a more sensitive psychophysical predictor of dyslexia than contrast sensitivity.
Learning a specific skill during childhood may partly determine the functional organization of the adult brain. This hypothesis led us to study oral language processing in illiterate subjects who, for social reasons, had never entered school and had no knowledge of reading or writing. In a brain activation study using PET and statistical parametric mapping, we compared word and pseudoword repetition in literate and illiterate subjects. Our study confirms behavioural evidence of different phonological processing in illiterate subjects. During repetition of real words, the two groups performed similarly and activated similar areas of the brain. In contrast, illiterate subjects had more difficulty repeating pseudowords correctly and did not activate the same neural structures as literates. These results are consistent with the hypothesis that learning the written form of language (orthography) interacts with the function of oral language. Our results indicate that learning to read and write during childhood influences the functional organization of the adult human brain.
Im deutschsprachigen Teil der Schweiz haben sich in den letzten Jahren zwei eigenartige Richtungen mit orthoptischer und operativer Behandlung der Legasthenie befaßt. Prof. Otto führte zur Erzielung eines Führungsauges eine Okklusionsbehandlung durch und hat bei 300 so behandelten Kinder 147 wegen einer Exoabweichung operiert. Dr. Pestalozzi führt zur Erreichung eines vollwertigen Binokularsehens mittels Untersuchungen am Poltest eine Prismenkorrektur durch und hat bei 175 so behandelten Kindern 43 wegen einer konvergenten Augenstellung operiert. Die Grundlagen dieser Behandlungsmethoden werden kritisch beleuchtet und abgelehnt.
Summary
In the German speaking part of Switzerland in the last few years there have been two singular trends in orthoptic and surgical treatment of dyslexia. Professor Otto performs occlusion to achieve dominance in one eye. Of 300 cases treated he has operated on 147 for an exodeviation. Dr. Pestalozzi prescribes prismes based on the Polatest to reach perfect binocular vision. In 175 cases he operated on 43 dyslectic children for an esodeviation. Both treatments are critically analysed and refused.
MRI technique was used to examine the size and symmetry of the plana temporale in 19 dyslexic students in grade 8 and in carefully matched control subjects. The results demonstrated a high frequency of planum symmetry among the dyslexics (70%) whereas symmetry was observed in only 30% of the control subjects. It was not possible to demonstrate any clear association between symmetry/asymmetry of planum temporale and handedness. Word-reading strategies among the dyslexics and control subjects were investigated with computerized tasks where accuracy and naming latency were recorded. All subjects with pure phonological deficits in reading had symmetrical plana temporale indicating a possible neuroanatomical basis for a characterstic symptom of linguistic processing deficiency in developmental dyslexia.
The visual correlates of dyslexia are the subject of controversy, and much evidence suggests that they may include some aspects of binocular and accommodative function. These factors were investigated in 43 control and 39 dyslexic children, who were matched for age, sex and performance intelligence quotient. The dyslexic group exhibited significantly lower positive and negative vergence reserves, and vergence instability when the eyes were dissociated at near. Their amplitudes of accommodation also were significantly reduced. However, other measures including dissociated and associated heterophoria and accommodative lag and facility were similar in both groups. The stability of motor ocular dominance, as assessed with a modified Dunlop test, was similar in both groups. The results of a simulated reading visual search task suggested that the vergence and accommodative dysfunction were not a major cause of the dyslexia. Further analyses, using reading-age matched groups, suggested that these ocular motor correlates were not attributable to the better reading performance in the control group. The most likely remaining explanation is that they are, in most cases, non-causal correlates of the dyslexia.
Children at risk for reading disability were evaluated as kindergartners and again as first graders to determine (1) intercorrelations among phonological processing tasks and (2) the relationship of such tasks to word identification and word attack. With IQ controlled, there were no intercorrelations among measures of phonological awareness, phonetic recoding in working memory, and phonological recoding in lexical access. Thus, these results failed to substantiate the concept of a general phonological processing ability. Partial correlations controlling for IQ revealed no relationship between reading and phonological awareness or phonetic recoding in working memory. In contrast, lexical access measures were significantly, albeit moderately, correlated with word identification but not word attack. Word attack and word identification were predicted by different combinations of variables. These results suggest that lexical access ability is an important factor in reading acquisition and that different combinations of phonological processes may be related to different aspects of reading.
Placement of a freezing probe on the skull of neonatal rats produces four-layered microgyria, complete with a lamina dissecans and microsulcus. We studied the developmental course of this induced microgyria under light microscopy by examining changes in neurons, glia, and macrophages following a focal freezing insult on the day of birth (postnatal day [P]0). The destruction of neurons and glia induced by the freezing probe extends through the cortical plate and occasionally through the subplate, but the pial membrane appears undamaged and radial glial cells, while damaged, are not eliminated. Reactive astrocytes and macrophages arrive in the damaged area within 24 hours of the injury, and repair of the damaged tissue peaks within the first week. Damaged radial glial fibers regrow, and supragranular neurons migrate through this damaged area, also within the first week. The newly formed supragranular layer overlies the cell-free area. The damaged cortex begins to assume its adult-like microgyric appearance from P5 to P10. On P15 and P32, long glial fibers, resembling radial glia, are present and are immunoreactive for glial fibrillary acidic protein and radial glial fiber antibodies (vimentin and Rat-401). No such fibers appear at this age in the non-microgyric areas or in normal brains. We conclude that microgyria formation may be the consequence of brain repair mechanisms occurring during neuronal migration to the neocortex, and that it appears to preserve primitive features characteristic of the developing cortex.
The present research represents the final 2 years of a 5-year longitudinal investigation of (a) confrontation-based, word-retrieval deficits in dyslexic children; (b) the role of vocabulary development in these deficits; (c) the relationship between confrontation naming performance and three carefully defined aspects of reading performance in the general population and in eight dyslexic case studies; and (d) the possible specificity of word-retrieval deficits in dyslexia. Results indicate enduring problems in word-retrieval processes for dyslexic children across the primary grades and into middle childhood. Second, these deficits cannot be explained by simple vocabulary deficits. Third, these results in conjunction with our earlier data consolidate a pattern of differential relationships between specific reading and confrontation naming skills that are based on development and on the level of processes involved. Trends within case studies suggest the more pronounced the retrieval deficit, the more global the reading impairment. And fourth, there appear to be some specific differences in the basis of word-retrieval problems between dyslexic and garden-variety or lower achieving readers. Results are discussed within a speculative framework that implicates problems in timing as a possible predetermining condition in the dyslexias.
This article presents 4 experiments aimed at defining the primary underlying phonological processing deficit(s) in adult dyslexia. 5 phonological processes, all involving spoken language, were studied: phoneme perception, phoneme awareness, lexical retrieval of phonology, articulatory speed, and phonetic coding in verbal short-term memory. 2 differently ascertained adult dyslexic groups, familial dyslexics (n = 15) and clinic dyslexics (n = 15), were the subjects in each experiment. These dyslexic groups were chosen because deficits that persist until adulthood and that are found in differently ascertained dyslexic groups are more likely to be primary. Each dyslexic group was compared to 2 control groups, chronological age (CA) controls who were similar in age and sex, and younger reading age (RA) controls who were similar in reading age and sex. The main finding was a clear deficit in phoneme awareness in both dyslexic groups, with each dyslexic group performing significantly worse than both CA and RA controls. Moreover, performance on the 2 phoneme awareness tasks together uniquely accounted for substantial variance in nonword reading. The clinic but not the familial dyslexics appeared to have an additional deficit in verbal short-term memory. No clear deficits were found in either dyslexic group in phoneme perception, lexical retrieval, or articulatory speed.
Morphometric magnetic resonance imaging techniques were used to compare the convolutional surface area of the planum temporale, temporal lobe volume and superior surface area, and an estimate of overall brain volume in a homogeneous sample of 17 dyslexic children (7 girls) and 14 nonimpaired children (7 girls). Substantial sex differences were apparent for all measured regions, with all the measurements in boys being significantly larger. Age, even within the narrow range employed here (7.5-9.7 years), was positively correlated with the size of each brain region. While initial analyses suggested smaller left hemisphere structures in dyslexics compared to control subjects, subsequent analyses controlling for age and overall brain size revealed no significant differences between dyslexics and nonimpaired children on a variety of measures, in particular surface area and symmetry of the planum temporale. We suggest that differences in subject characteristics (i.e., sex, age, handedness, and definition of dyslexia) as well as procedural variations in the methods used to acquire images and to define and measure anatomical regions of interest such as the planum temporale all may play an important role in explaining apparent discrepant results in the neuroimaging literature on dyslexia.
To test the hypothesis of anomalous anatomy in posterior brain regions associated with language and reading, the corpus callosum was imaged in the midsagittal plane with magnetic resonance. The areas of the anterior, middle, and posterior segments were measured in 21 dyslexic men (mean age 27 yrs, SD 6) and in 19 matched controls. As predicted, the area of the posterior third of the corpus callosum, roughly equivalent to the isthmus and splenium, was larger in dyslexic men than in controls. No differences were seen in the anterior or middle corpus callosum. The increased area of the posterior corpus callosum may reflect anatomical variation associated with deficient lateralization of function in posterior language regions of the cortex and their right-sided homologues, hypothesized to differ in patients with dyslexia.
This study examined whether dyslexic children learning to read German show the same nonword reading deficit, which is characteristic of dyslexic children learning to read English (Rack, Olson, & Snowling, 1992), a deficit which is taken as evidence for a phonological impairment underlying dyslexia. Because the German writing system, in contrast to English, exhibits comparatively simple and straightforward grapheme-phoneme correspondences, the generality of the nonword reading deficit across different alphabetic systems seemed questionable. Actually, it was found that 10-year-old dyslexic children learning to read German exhibited rather high reading accuracy for nonwords when compared to that typically found among dyslexic children learning to read English. Nevertheless, the children learning German did exhibit a nonword reading deficit. Specifically, their speed for nonwords was impaired in relation to younger control (nondyslexic) children matched on reading speed for frequent words. This nonword reading deficit was observed for nonwords with little similarity to existing German words as well as for nonwords which were analogous to short, frequent content words. It is hypothesized that dyslexic children learning German do not differ from dyslexic children learning English in their underlying phonological impairment, but that they do differ with respect to the expression of this impairment.
The major trends in current research on developmental dyslexia assume that impaired phonological processing is the core deficit in this disorder. Our earlier studies indicated that half of all dyslexic persons have significant deficits of bimanual motor coordination, and that impaired temporal resolution in motor action may identify a vertically transmitted behavioral phenotype in familial dyslexia. This report examines the relationship between spelling errors as a measure of impaired phonological processing and motor coordination deficits in the same dyslexia families. Affected family members with motor coordination deficits made significantly more dysphonetic spelling errors than dyslexic family members without motor deficits, but there was no evidence that dysphonetic spelling is vertically transmitted in dyslexia families. On the other hand, affected offspring of affected parents with motor coordination deficits made relatively more dysphonetic spelling errors than the affected offspring of parents without motor coordination deficits. We suggest that dysphonetic spelling may be one outward expression of a vertically transmitted behavioral phenotype of impaired temporal resolution that is clearly expressed in coordinated motor action.
Livingstone et al. [Livingstone, M. S., Rosen, G. D., Drislane, F. W. and Galaburda, A. M. Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia. Proceedings of the National Academy of Science U.S.A. 88, 7943-7947, 1991] presented evidence for a defect of the magnocellular visual processing stream in developmental dyslexia. We attempted to replicate this effect using transient and steady-state VEPs to checkerboard reversal stimuli in a group of adult developmental dyslexics. Several different reversal rates and contract levels were utilized. No differences were found between the dyslexic and control groups for the low-contrast, rapidly reversing patterns, nor for any combination of stimulus rate or contrast that was tested. Thus, these findings do not support a magnocellular processing deficit in developmental dyslexia.
A recent functional magnetic resonance imaging (fMRI) study concluded that the motion-specific visual area V5 is not activated in dyslexic subjects. We report here opposing evidence based on whole-scalp neuromagnetic recordings. Apparent-motion stimuli elicited similar activation of V5 in both dyslexic and control subjects, with a trend for longer latencies in dyslexics. Both high- and low-contrast stimuli activated the V5 region in dyslexics. The lack of significant blood flow changes despite modified neuronal synchrony would explain the absence of fMRI signals and the presence of neuromagnetic signals in dyslexic subjects.
The claim that the well-documented difficulties shown by dyslexic children in phonological awareness tasks may arise from deficits in the accuracy and the segmental organization of the phonological representations of words in their mental lexicons is receiving increasing interest from researchers. In this experiment, two versions of the phonological representations hypothesis were investigated by using a picture naming task and a battery of phonological measures at three linguistic levels (syllable, onset-rime, phoneme). The picture naming task was used to identify words for which dyslexic and control children had accurate vs inaccurate phonological representations, and performance in the phonological awareness tasks was then compared for the words which had precise vs imprecise representations. Findings indicated that frequency effects in the phonological awareness tasks at all levels disappeared for dyslexic and control children once representational quality was taken into account, and that the availability of sublexical units for analysis appeared to differ according to (1) the accuracy and retrieval of the phonological representation and (2) the linguistic level tapped by the phonological awareness task.
Abnormal functioning of the transient visual pathway (the M-pathway) has been implicated in specific reading disability (SRD). The aim of this study is to examine the contrast thresholds for flicker-defined form discrimination in primary school children, and to compare its development with reading and mentation development as a means of identifying children at risk of SRD.
One hundred eighty-seven children (aged 4 to 13 years) and 22 adults (aged 18 to 45 years) were assessed for contrast sensitivity to an illusory, flicker contrast-defined form (the letter 'E')--a task which was designed to rely to a large extent on magnocellular pathway function. Reading age (Neale Analysis of Reading) and mental age (Raven's Coloured Progressive Matrices) were assessed in the children, who had been previously screened for clinically normal binocular vision and refractive anomalies.
The ability of primary school-age children to discriminate the orientation of the low contrast flickered letters (from a choice of 4) showed a significant improvement from kindergarten (ages 4 to 6 years) to grade 3 (ages 8 to 10 years) and older age groups. No significant difference was found between good and disabled readers (at least 1-year lag in reading readiness for the kindergarten group and 2-year lag in reading performance for 8 to 10 and 10 to 12-year-olds).
It appears that there is a developmental improvement in perceptual capacity for tasks attributed to magnocellular function, which plateaus at the age of about 8 to 10 years. However, despite the reported reduction of magnocellular function in specific reading disabled children, no significant difference in contrast threshold for flicker-defined letter discrimination was found between good and poor readers.
Learning to read requires an awareness that spoken words can be decomposed into the phonologic constituents that the alphabetic characters represent. Such phonologic awareness is characteristically lacking in dyslexic readers who, therefore, have difficulty mapping the alphabetic characters onto the spoken word. To find the location and extent of the functional disruption in neural systems that underlies this impairment, we used functional magnetic resonance imaging to compare brain activation patterns in dyslexic and nonimpaired subjects as they performed tasks that made progressively greater demands on phonologic analysis. Brain activation patterns differed significantly between the groups with dyslexic readers showing relative underactivation in posterior regions (Wernicke's area, the angular gyrus, and striate cortex) and relative overactivation in an anterior region (inferior frontal gyrus). These results support a conclusion that the impairment in dyslexia is phonologic in nature and that these brain activation patterns may provide a neural signature for this impairment.
The classical notion that developmental dyslexia may somehow relate to impaired communication between hemispheres has not yet received convincing support. Sixteen dyslexic adults and 12 controls received a high resolution brain MRI scan for morphometric study of the corpus callosum. Automatized measurements of callosal area and calculation of indices defining the general morphology of the callosal mid-surface were performed. Each participant received global intelligence and reading achievement evaluation; dyslexics were further proposed specific neuropsychological tests specially designed to explore the mechanisms of reading impairment. It just appears from the group comparisons (1) that the dyslexics' corpus callosum displays a more circular and evenly thicker general shape, and (2) that the midsagittal surface is on the average larger than in controls, in particular in the isthmus. Moreover, the different morphometric characteristics of the dyslexic brain correlated with the degree of impairment on various tests exploring phonological abilities. In vivo morphometry of the corpus callosum may provide valuable hints for understanding developmental learning disorders and their consequences in adults.
Considerable evidence exists that some reading-disabled children have disordered visual processing, specifically in the fast processing magnocellular (M) pathway.
The extent that varying luminance and temporal frequency affect amplitude and latency of visual evoked potentials (VEPs) in normally achieving and reading-disabled children grades 4 to 6 was measured. Each group consisted of approximately 30 subjects. Monocular and binocular single channel VEPs were recorded using a sinusoidal checkerboard pattern of spatial frequency 14 min arc at 3 different temporal frequencies (1, 4, and 8 Hz), and an 8 Hz flicker fusion stimulus. Stimuli were presented under high and low luminance conditions. The peak of the major positive wave component (P100) of each waveform and the trough of the previous major negative wave component were identified, and the peak to trough amplitude was measured.
Statistical analysis of the VEP amplitudes and latencies in response to different experimental conditions was performed using a repeated measure analysis of variance (MANOVA). VEP amplitudes were significantly higher for normal readers across all conditions. Within all subjects, significant effects were found for monocular vs. binocular viewing, temporal frequencies, and high vs. low luminance. Similar analysis of latencies revealed no significant differences.
The presence of a weaker VEP response in reading-disabled children suggests a deficit early in visual processing. The significant difference in VEP amplitudes between the two reading groups provides an objective measure of a deficit in the M pathway that has been implicated in this condition. Whether serial VEP recordings might help to assess the effects of optometric therapy by providing an independent index of therapeutic efficiency is of special interest.
Neurological and physiological deficits have been reported in the brain in developmental dyslexia. The temporoparietal cortex has been directly implicated in dyslexic dysfunction, and substantial indirect evidence suggests that the cerebellum is also implicated. We wanted to find out whether the neurological and physiological deficits manifested as biochemical changes in the brain.
We obtained localised proton magnetic resonance spectra bilaterally from the temporo-parietal cortex and cerebellum of 14 well-defined dyslexic men and 15 control men of similar age.
We found biochemical differences between dyslexic men and controls in the left temporo-parietal lobe (ratio of choline-containing compounds [Cho] to N-acetylaspartate [NA] p< or =0.01) and right cerebellum (Cho/NA, p< or = 0.01; creatine [Cre] to NA p< or =0.05; (not significant). We found lateral biochemical differences in dyslexic men in both these brain regions (Cho/NA in temporo-parietal lobe, left vs right, p< or =0.01; Cre/NA in cerebellum, left vs right, p< or =0.001). We found no such lateral differences in controls. There was no significant relation between the degree of contralateral chemical difference and handedness in dyslexic or control men.
We suggest that the observed differences reflect changes in cell density in the temporo-parietal lobe in developmental dyslexia and that the altered cerebral structural symmetry in dyslexia is associated with abnormal development of cells or intracellular connections or both. The cerebellum is biochemically asymmetric in dyslexic men, indicating altered development of this organ. These differences provide direct evidence of the involvement of the cerebellum in dyslexic dysfunction.
The classic neurologic model for reading, based on studies of patients with acquired alexia, hypothesizes functional linkages between the angular gyrus in the left hemisphere and visual association areas in the occipital and temporal lobes. The angular gyrus also is thought to have functional links with posterior language areas (e.g., Wernicke's area), because it is presumed to be involved in mapping visually presented inputs onto linguistic representations. Using positron emission tomography , we demonstrate in normal men that regional cerebral blood flow in the left angular gyrus shows strong within-task, across-subjects correlations (i.e., functional connectivity) with regional cerebral blood flow in extrastriate occipital and temporal lobe regions during single word reading. In contrast, the left angular gyrus is functionally disconnected from these regions in men with persistent developmental dyslexia, suggesting that the anatomical disconnection of the left angular gyrus from other brain regions that are part of the "normal" brain reading network in many cases of acquired alexia is mirrored by its functional disconnection in developmental dyslexia.
Visual factors in specific learning difficulties (SpLD) are reviewed. People with SpLD fail to achieve at a level that is commensurate with their intelligence. The commonest SpLD is dyslexia, which usually results from phonological processing/decoding deficits. Additionally, there are several optometric correlates of SpLD which may, in some cases, contribute to the learning difficulty. These correlates include binocular instability and a low amplitude of accommodation. Some people with reading difficulties and perceptual distortions/eyestrain can be helped by individually prescribed coloured filters. A visual processing anomaly is also often present in the form of a deficit of the transient visual system. The role of the optometrist is discussed.