NEUROLOGICAL FACTORS IN READING DISABILITY.
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An overview is presented of that portion of the literature on reading disability wherein neurological defect is seen as causal or correlative. From the publication of Hinshelwood's "Congenital Word Blindness" (1917) to the present, investigators have considered the possible association of reading difficulty with genetically determined neurological defect, with cerebral damage, with biochemical imbalance inhibiting synaptic transmission, and with some form of maturational lag. (+info)
Is the perception of brightness different in poor readers?
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The transient system deficit hypothesis (TSDH) of specific reading disability [Percept. Psychophys. 40 (1986) 440] remains contentious. As part of a study examining multiple measures of transient and sustained system function, heterochromatic flicker matching (HFM) and brightness matching (HBM) were assessed in 30 poor readers (9.11+/-0.68 years) and 30 age, grade and sex matched controls (9.24+/-0.73 years). HBM and HFM are known to reflect the processing of brightness and luminance information and have been related to the function of magnocellular and parvocellular visual sub-systems. Flicker and brightness matches were determined for blue, green, yellow and red stimuli on Macintosh colour displays using 2AFC and double interleaved random staircases. A ratio of the luminances for brightness and flicker matches represented performance. A significant difference between controls and poor readers in performance for red and blue stimuli was found indicating different visual function in poor readers. While not providing direct support for the transient system deficit hypothesis, this effect implies a mismatch between those achromatic systems that subserve HFM and those more complex mechanisms involved in HBM. The most important aspect of this finding is that poor readers and normal controls could be differentiated on the basis of a paradigm known to be contingent upon magnocellular and parvocellular functioning. (+info)
Pleiotropic effects of a chromosome 3 locus on speech-sound disorder and reading.
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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. (+info)
Predictors of antisocial personality. Continuities from childhood to adult life.
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BACKGROUND: Antisocial behaviour in adult life has its roots in childhood. AIMS: To explore the independent and joint effects of childhood characteristics on the persistence of antisocial behaviour into adult life. METHOD: A clinical sample of twins who were systematically ascertained in childhood was followed up 10-25 years later. A total of 225 twins were interviewed regarding childhood and adult psychiatric disorder, psychosocial functioning, and psychosocial and cognitive risk factors. RESULTS: In univariate analyses, childhood hyperactivity and conduct disorder showed equally strong prediction of antisocial personality disorder (ASPD) and criminality in early and mid-adult life. Lower IQ and reading problems were most prominent in their relationships with childhood and adolescent antisocial behaviour. In multivariate modelling childhood conduct disorder and hyperactivity predicted adult ASPD even when intervening risk factors were accounted for. The number of hyperactive and conduct symptoms also predicted adult outcome. CONCLUSIONS: Childhood disruptive behaviour has powerful long-term effects on adult antisocial outcomes, which continue into middle adulthood. The importance of number of symptoms, the presence of disruptive disorder, and intermediate experiences highlight three areas where interventions might be targeted. (+info)
Sequential spatial frequency discrimination is consistently impaired among adult dyslexics.
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The degree and nature of dyslexics' difficulties in performing basic visual tasks have been debated for more than thirty years. We recently found that dyslexics' difficulties in detecting temporally modulated gratings are specific to conditions that require accurate comparisons between sequentially presented stimuli [Brain 124 (2001) 1381]. We now examine dyslexics' spatial frequency discrimination (rather than detection), under simultaneous (spatial forced choice) and sequential (temporal forced choice) presentations. Sequential presentation (at SOAs of 0.5, 0.75 and 2.25 s) yielded better discrimination thresholds among the majority of controls (around 0.5 c/ degrees reference), but not among dyslexics. Consequently, there was a (large and significant) group effect only for the sequential conditions. Within the same dyslexic group, performance on a sequential auditory task, two-tone frequency discrimination, was impaired in a smaller proportion of the participants. Taken together, our findings indicate that visual paradigms requiring sequential comparisons are difficult for the majority of dyslexic individuals, perhaps because deficits either in visual perception or in visual memory could both lead to difficulties on these paradigms. (+info)
Learning problems, delayed development, and puberty.
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Language-based learning disorders such as dyslexia affect millions of people, but there is little agreement as to their cause. New evidence from behavioral measures of the ability to hear tones in the presence of background noise indicates that the brains of affected individuals develop more slowly than those of their unaffected counterparts. In addition, it seems that brain changes occurring at approximately 10 years of age, presumably associated with puberty, may prematurely halt this slower-than-normal development when improvements would normally continue into adolescence. The combination of these ideas can account for a wide range of previous results, suggesting that delayed brain development, and its interaction with puberty, may be key factors contributing to learning problems. (+info)
Wider recognition in peripheral vision common to different subtypes of dyslexia.
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Italian children (n = 125) were classified into dyslexics, poor readers and ordinary readers. The dyslexics were further classified into the Boder and Bakker subtypes. The children were tested with the form-resolving field (FRF), which measures central and peripheral visual recognition. Dyslexics show higher correct identification of letters in the periphery, supporting the notion of a different distribution of lateral masking. A numerical characterization of individual FRFs--C2R--reliably distinguishes between dyslexics and ordinary readers. The wider distribution of recognition, similar across the various subtypes of dyslexia, suggests a general characteristic of visual perception, and possibly a different visual-attentional mode. (+info)
Abnormal response recovery in the right somatosensory cortex of dyslexic adults.
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Somatosensory evoked fields (SEFs) to repetitive tactile stimuli were recorded from eight dyslexic and eight normal-reading adults. Three successive stimuli, produced by diaphragms driven by compressed air, were delivered to thumb, index finger and thumb in sequence, with stimulus-onset asynchronies (SOAs) of 100 and 200 ms in different runs. Both hands were stimulated alternatingly with an intertrain interval of 1 s, and the responses were recorded with a whole-scalp neuromagnetometer. Whereas the primary somatosensory cortex responses to the first stimuli of the trains did not differ between dyslexics and controls, responses to the second stimuli (and the ratios of second to first responses) were significantly smaller in dyslexic than in control subjects in the right hemisphere (differences 41 and 28% for response amplitudes at the 100 and 200 ms SOAs). The results agree with the proposed pansensory nature of temporal processing deficits in dyslexia, specifically demonstrating abnormal response recovery in the right somatosensory cortex. (+info)