Successful behavioral genetic studies require precise definition of a homogenous phenotype. This study searched for anatomical markers that might restrict variability in the reading disability phenotype. The subjects were 15 college students (8 male/7 female) diagnosed with a reading disability (RD) and 15 controls (8 males/7 females). All subjects completed a cognitive and reading battery. Only 11 of the RD subjects had a phonological deficit [phonological dyslexia (PD): pseudo word decoding scores < 90 (27th percentile)]. Thirteen RD (9 PD) and 15 controls received a volumetric MRI scan. Four anatomical measures differentiated the PD group from the remainder of the subjects: (i) marked rightward cerebral asymmetry, (ii) marked leftward asymmetry of the anterior lobe of the cerebellum, (ii) combined leftward asymmetry of the planum and posterior ascending ramus of the sylvian fissure, and (iv) a large duplication of Heschl's gyrus on the left. When these four measures were normalized and summed, the resulting variable predicted short- and long-term phonological memory. By contrast, oral and written comprehension skills were predicted by a different anatomical variable: low cerebral volume. These findings provide neurobiological support for an RD phenotype characterized by phonological deficits in the presence of normal or superior comprehension. The study of individual variation in cortical structure may provide a useful link between genotype and behavior.
In this chapter we have considered ways in which the cerebellum may contribute to language, and in particular, reading and dyslexia. First we reviewed the evidence for the cerebellum as a specialized structure for temporal processing in movement and perception, relating this to speech production and perception. We then reviewed some of the evidence for cerebellar involvement in two linguistic processes: lexical retrieval and verbal rehearsal. We focused on the latter process as providing a possible functional link between the cerebellum and developmental dyslexia.
The fMRI pictures showed clearly that a different part of the brain, the left middle front gyrus, is activated among Chinese people with dyslexia rather than the left temporoparietal region. The researchers... believe that this region is implicated because reading Chinese is a different mental task compared with reading an alphabetic language. With an alphabetic language, reading is done sequentially -- the letters are recognised, broken up into phonemes which are then matched to a known meaning. But with Chinese, the reading is more like parallel processing, in which the brain has to seize the meaning of the pictogram almost as simultaneously as it figures out its sound. "Rather than having a universal origin, the biological abnormality of impaired reading is dependent on culture," the authors claim.
Dyslexia research now faces an intriguing paradox. It is becoming increasingly clear that a significant proportion of dyslexics present sensory and/or motor deficits; however, as this 'sensorimotor syndrome' is studied in greater detail, it is also becoming increasingly clear that sensory and motor deficits will ultimately play only a limited role in a causal explanation of specific reading disability.
Studies show a biological basis for this disability that affects millions of American children and adults. One line of research indicates that dyslexics use the brain regions that process written language differently than those without the disorder.
All four genes thus far linked to developmental dyslexia participate in brain development, and abnormalities in brain development are increasingly reported in dyslexia. Comparable abnormalities induced in young rodent brains cause auditory and cognitive deficits, underscoring the potential relevance of these brain changes to dyslexia. Our perspective on dyslexia is that some of the brain changes cause phonological processing abnormalities as well as auditory processing abnormalities; the latter, we speculate, resolve in a proportion of individuals during development, but contribute early on to the phonological disorder in dyslexia. Thus, we propose a tentative pathway between a genetic effect, developmental brain changes, and perceptual and cognitive deficits associated with dyslexia.
Research studies suggest that the left hemisphere is involved in the pathophysiology of dyslexia. Thus far, the exact location and nature of the purported lesion(s) remain a matter of contention. The present study describes the distribution of structural abnormalities as related to brain symmetry in the brains of dyslexic individuals. High-resolution three-dimensional magnetic resonance images (MRIs) were analyzed in 16 dyslexic men and 14 controls matched for sex, age, educational level, and handedness. A computerized image analysis system was used to assess the volumetric deformations required to match each brain with its left-right mirror image. The results showed significant abnormalities in five left hemisphere structures involving the extrapyramidal and limbic systems: amygdala, hippocampus proper, parahippocampal gyrus, putamen, and globus pallidus. The left hemisphere is thought to play a major role in the temporal analysis of information. This stream of temporal analysis is of importance in motor movements. Reading might have evolved as an exaptation to motor movements requiring the sequential analysis of information.
If individuals with dyslexia have difficulties with literacy skills, they might also have problems with musical notation, even though they may have a good musical ear and a good sense of melody and harmony.
Five to ten per cent of school-age children fail to learn to read in spite of normal intelligence, adequate environment and educational opportunities. Thus defined, developmental dyslexia (hereafter referred to as dyslexia) is usually considered of constitutional origin, but its actual mechanisms are still mysterious and currently remain the subject of intense research endeavour in various neuroscientific areas and along several theoretical frameworks. This article reviews evidence accumulated to date that favours a dysfunction of neural systems known to participate in the normal acquisition and achievement of reading and other related cognitive functions. Historically, the first arguments for a neurological basis of dyslexia came from neuropathological studies of brains from dyslexic individuals. These early studies, although open to criticism, for the first time drew attention towards a possible abnormality in specific stages of prenatal maturation of the cerebral cortex and suggested a role of atypical development of brain asymmetries. This has prompted a large amount of subsequent work using in vivo imaging methods in the same vein. These latter studies, however, have yielded less clear-cut results than expected, but have globally confirmed some subtle differences in brain anatomy whose exact significance is still under investigation. Neuropsychological studies have provided considerable evidence that the main mechanism leading to these children's learning difficulties is phonological in nature, namely a basic defect in segmenting and manipulating the phoneme constituents of speech. A case has also been made for impairment in brain visual mechanisms of reading as a possible contributing factor. This approach has led to an important conceptual advance with the suggestion of a specific involvement of one subsystem of vision pathways (the so-called magnosystem hypothesis). Both phonological and visual hypotheses have received valuable contribution from modern functional imaging techniques. Results of recent PET and functional MRI studies are reported here in some detail. Finally, one attractive interpretation of available evidence points to dyslexia as a multi-system deficit possibly based on a fundamental incapacity of the brain in performing tasks requiring processing of brief stimuli in rapid temporal succession. It is proposed that this so-called `temporal processing impairment' theory of dyslexia could also account for at least some of the perceptual, motor and cognitive symptoms very often associated with the learning disorder, a coincidence that has remained unexplained so far.
Genetically determined focal cortical anomalies in specific left perisylvian language areas are the underlying cause of the phonological deficit. This phonological deficit is the primary cause of reading impairment.
Dyslexia, a reading disorder, affects up to 17 percent of the population. Yale researchers identified an inherited component to reading disability, and some potentially responsible chromosome regions. The most widely reported region is on chromosome 6, which contains about 19 genes, most of which are expressed in the brain.
A multiple case study was conducted in order to assess three leading theories of developmental dyslexia: (i) the phonological theory, (ii) the magnocellular (auditory and visual) theory and (iii) the cerebellar theory. Sixteen dyslexic and 16 control university students were administered a full battery of psychometric, phonological, auditory, visual and cerebellar tests. Individual data reveal that all 16 dyslexics suffer from a phonological deficit, 10 from an auditory deficit, four from a motor deficit and two from a visual magnocellular deficit. Results suggest that a phonological deficit can appear in the absence of any other sensory or motor disorder, and is sufficient to cause a literacy impairment, as demonstrated by five of the dyslexics. Auditory disorders, when present, aggravate the phonological deficit, hence the literacy impairment. However, auditory deficits cannot be characterized simply as rapid auditory processing problems, as would be predicted by the magnocellular theory. Nor are they restricted to speech. Contrary to the cerebellar theory, we find little support for the notion that motor impairments, when found, have a cerebellar origin or reflect an automaticity deficit. Overall, the present data support the phonological theory of dyslexia, while acknowledging the presence of additional sensory and motor disorders in certain individuals.
Bruce Pennington, Professor of Psychology at University of Denver, discusses dyslexia, ADHD and speech/language disorders.
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