发展性阅读障碍与知觉加工

近年来许多行为实验和神经生理学实验都发现 ,发展性阅读障碍与基本知觉障碍有关。在视觉领域研究者提出了巨细胞障碍假设 ,这种假设认为阅读障碍者视觉神经系统中的巨细胞障碍导致他们对某种类型的视觉刺激加工存在困难 ,进而影响阅读。在听觉领域研究发现阅读障碍者加工快速、系列、短暂呈现的声音刺激存在障碍。研究者认为阅读障碍者加工快速刺激输入障碍反映了普遍的时间知觉障碍。这方面的研究发展非常迅速 ,理论观点非常明确 ,并且直接与内在的神经机制相联系 ,形成了与传统的“语言障碍”理论迥然不同的“知觉障碍”理论。“知觉障碍”理论综合了行为、认知和神经等多个层次的研究 ,反映了神经科学发展所带来的巨大影响和认知加工模块化理论的渐渐衰退。     

动作视频游戏对发展性阅读障碍者阅读技能的影响及其内在机制

发展性阅读障碍是一种在获得阅读技能方面的特殊困难, 这种障碍会严重影响个体的发展, 如何帮助发展性阅读障碍者改善其阅读技能是近年来研究的焦点。传统的干预方法主要针对发展性阅读障碍者的语音缺陷, 这类方法存在一些问题, 如费时费力、给阅读障碍者带来阅读压力等。近年来, 大部分研究表明通过趣味性的动作视频游戏训练可以显著地提高发展性阅读障碍者的阅读技能, 但是其背后的机制尚不明确。基于大细胞通路缺陷理论框架, 从视觉空间注意、注意跨通道转换、视觉运动加工等方面来梳理动作视频游戏与阅读之间的关系, 揭示了动作视频游戏训练对阅读效率影响的可能内在机制。未来的研究可以在大细胞通路缺陷理论的框架下, 深入分析动作视频游戏改善阅读的神经机制, 并尝试开发更适合发展性阅读障碍者的干预程序。     

基于PASS模型的汉语阅读障碍认知加工特点的实验研究

研究以智力的PASS认知模型为基础,考察了3-5年级阅读障碍组和正常对照组的PASS认知加工特点,探究汉语阅读障碍儿童的PASS认知缺陷模式,为后期的干预提供理论上的支持和帮助。结果发现,PASS四个认知加工均存在明显的年级差异,低年级儿童的PASS认知加工能力明显不如中高年级儿童。汉语阅读障碍儿童在DN: CAS 12项分任务上的成绩均低于正常对照组儿童。同时,大多数汉语阅读障碍儿童存在不止一种的PASS认知加工缺陷,即汉语发展性阅读障碍内部是一个异质群体;阅读障碍儿童在继时性加工上存在的问题最为严重,存在缺陷的人数也最多。     

阅读障碍的巨细胞系统缺陷理论之争

近几年诸多研究者认为阅读障碍是由于视觉系统巨细胞功能缺陷引起的。他们从对比度敏感性研究、巨细胞抑制功能研究与视觉运动知觉功能的研究结果中得到了支持证据。就这个问题的研究进行综述,表明不论是巨细胞功能缺陷理论的支持者还是反对者,都从巨细胞的对比度敏感性、视觉运动知觉与巨细胞抑制功能上得到了一些研究结果的支持。巨细胞功能缺陷理论的支持者还从阅读障碍的神经生理学研究和阅读的脑功能研究中得到了一些支持性的证据。新的研究结果揭示了巨细胞系统缺陷理论与阅读之间的关系以及巨细胞系统缺陷理论的应用价值。在巨细胞系统缺陷理论的进一步研究中,还需要统一实验方法与实验标准以获得更多的证据,同时需要有新的方法来有效区分小细胞系统与巨细胞系统     

Dyslexia and dyscalculia: Two learning disorders with different cognitive profiles

This study tests the hypothesis that dyslexia and dyscalculia are associated with two largely independent cognitive deficits, namely a phonological deficit in the case of dyslexia and a deficit in the number module in the case of dyscalculia. In four groups of 8- to 10-year-olds (42 control, 21 dyslexic, 20 dyscalculic, and 26 dyslexic/dyscalculic), phonological awareness, phonological and visual-spatial short-term and working memory, naming speed, and basic number processing skills were assessed. A phonological deficit was found for both dyslexic groups, irrespective of additional arithmetic deficits, but not for the dyscalculia-only group. In contrast, deficits in processing of symbolic and nonsymbolic magnitudes were observed in both groups of dyscalculic children, irrespective of additional reading difficulties, but not in the dyslexia-only group. Cognitive deficits in the comorbid dyslexia/dyscalculia group were additive; that is, they resulted from the combination of two learning disorders. These findings suggest that dyslexia and dyscalculia have separable cognitive profiles, namely a phonological deficit in the case of dyslexia and a deficient number module in the case of dyscalculia.     

The cognitive profile and multiple-deficit hypothesis in Chinese developmental dyslexia

The present study was conducted to examine the cognitive profile and multiple-deficit hypothesis in Chinese developmental dyslexia. Thirty Chinese dyslexic children in Hong Kong were compared with 30 average readers of the same chronological age (CA controls) and 30 average readers of the same reading level (RL controls) in a number of rapid naming, visual, phonological, and orthographic tasks. Chinese dyslexic children performed significantly worse than the CA controls but similarly to the RL controls on most of the cognitive tasks. The rapid naming deficit was found to be the most dominant type of cognitive deficit in Chinese dyslexic children. Over half of the dyslexic children exhibited deficits in 3 or more cognitive areas, and there was a significant association between the number of cognitive deficits and the degree of reading and spelling impairment. The present findings support the multiple-deficit hypothesis in Chinese developmental dyslexia.     

发展性阅读障碍亚类型研究进展

发展性阅读障碍是一种特殊的学习障碍,伴有多种认知缺陷并且存在不同的亚类型。依据相关的阅读模型理论,阅读障碍可划分为语音型和表层型。从认知缺陷角度出发,语音加工缺陷是主要的缺陷表现,以此为特征形成一种主要的阅读障碍的亚类型,同时还有以正字法加工缺陷和快速命名缺陷为主的其他亚类型。而以基本感知觉缺陷为标准,主要有以视觉加工缺陷和以听觉加工缺陷为主的两种亚类型。在汉语条件下,依据同样的阅读模型理论,语音型阅读障碍亚类型比例明显低于拼音文字条件下的。汉语阅读障碍也具有分别以语音加工缺陷、快速命名缺陷和正字法加工缺陷为主要认知缺陷的亚类型。未来有必要从神经机制角度进一步明确不同亚类型的神经基础。     

The Effect of Parents’ Literacy Skills and Children’s Preliteracy Skills on the Risk of Dyslexia

The combination of investigating child and family characteristics sheds light on the constellation of risk factors that can ultimately lead to dyslexia. This family-risk study examines plausible preschool risk factors and their specificity. Participants (N?=?196, 42 % girls) included familial risk (FR) children with and without dyslexia in Grade 3 and controls. First, we found impairments in phonological awareness, rapid naming, and letter knowledge in FR kindergartners with later dyslexia, and mild phonological-awareness deficits in FR kindergartners without subsequent dyslexia. These skills were better predictors of reading than arithmetic, except for rapid naming. Second, the literacy environment at home was comparable among groups. Third, having a dyslexic parent and literacy abilities of the non-dyslexic parent related to offspring risk of dyslexia. Parental literacy abilities might be viewed as indicators of offspring’s liability for literacy difficulties, since parents provide offspring with genetic and environmental endowment. We propose an intergenerational multiple deficit model in which both parents confer cognitive risks.     

Can a temporal processing deficit account for dyslexia?

In this comment, we argue that although Farmer and Klein (1995) have provided a valuable review relating deficits in nonreading tasks and dyslexia, their basic claim that a “temporal processing deficit” is one possible cause of dyslexia is somewhat vague. We argue that “temporal processing deficit” is never clearly defined. Furthermore, we question some of their assumptions concerning an auditory temporal processing deficit related to dyslexia, and we present arguments and data that seem inconsistent with their claims regarding how a visual temporal processing deficit would manifest itself in dyslexic readers. While we agree that some dyslexics have visual problems, we conclude that problems with reading caused by the visual mechanisms that Farmer and Klein postulate are quite rare.     

On the use of metacontrast to assess magnocellular function in dyslexic readers

It has been proposed that dyslexia is the result of a deficit in the magnocellular system. Reduced metacontrast masking in dyslexic readers has been taken as support for this view. In metacontrast, a masking stimulus reduces the visibility of a spatially adjacent target stimulus when the target stimulus precedes the masking stimulus by about 30–100 msec. Recent evidence indicates that the latency difference between the magnocellular and parvocellular subcortical pathways is at most 20 msec and may be as small as only 5 msec, or even less. This makes it difficult to attribute the latency in metacontrast to the latency differences between the magnocellular and parvocellular systems. It is therefore problematic to attribute reduced metacontrast masking to a deficit in the magnocellular system.     

On the use of metacontrast to assess magnocellular function in dyslexic readers.

It has been proposed that dyslexia is the result of a deficit in the magnocellular system. Reduced metacontrast masking in dyslexic readers has been taken as support for this view. In metacontrast, a masking stimulus reduces the visibility of a spatially adjacent target stimulus when the target stimulus precedes the masking stimulus by about 30-100 msec. Recent evidence indicates that the latency difference between the magnocellular and parvocellular subcortical pathways is at most 20 msec and may be as small as only 5 msec, or even less. This makes it difficult to attribute the latency in metacontrast to the latency differences between the magnocellular and parvocellular systems. It is therefore problematic to attribute reduced metacontrast masking to a deficit in the magnocellular system.     

Deaf poor readers' pattern reversal visual evoked potentials suggest magnocellular system deficits: implications for diagnostic neuroimaging of dyslexia in deaf individuals

Deafness and developmental dyslexia in the same individual may jointly limit the acquisition of reading skills for different underlying reasons. A diagnostic marker for dyslexia in deaf individuals must therefore detect the presence of a neurobiologically based dyslexia but be insensitive to the ordinary developmental influences of deafness on reading skill development. We propose that the functional status of the magnocellular visual system in deaf individuals is potentially such a marker. We present visual evoked potential (VEP) evidence that adult deaf poor readers as a group display magnocellular system deficits not observed in deaf good readers. We recorded pattern-reversal VEPs to high- and low-contrast checkerboard stimuli, which primarily activate the parvocellular and magnocellular pathways, respectively. Principal components analysis of these VEPs produced a time-ordered sequence of three early components that displayed interactions between reading skill and stimulus contrast across multiple scalp recording sites. Deaf poor readers displayed an abnormal absence of contrast-sensitive VEP responses at occipital sites during early visual processing (75 ms poststimulus), whereas deaf good readers showed the expected early contrast-sensitive occipital VEP responses. Over the subsequent 225 ms, the occipital VEP behavior of deaf poor readers closely approximated that of deaf good readers. The VEPs of deaf poor readers were apparently characterized by delayed responses to low-contrast stimuli compared with deaf good readers. Our results provide the first neurobiological evidence that developmental dyslexia exists within the deaf population and is associated with the same underlying magnocellular system deficit that has been observed in hearing dyslexics. Direct neural imaging of the status of the magnocellular visual system in deaf individuals may eventually provide differential diagnosis of developmental dyslexia in the deaf population.     

阅读障碍儿童的技能自动化能力

以自动化缺陷假说为理论背景,采用系列反应时学习任务,探讨了41名五、六年级的汉语发展性阅读障碍儿童和41名正常儿童的技能自动化能力,通过比较对系列刺激和随机刺激的反应时差异,发现障碍组儿童的反应时虽然普遍长于正常组,但两组儿童都表现出了相同模式的系列学习效应,不支持发展性阅读障碍的技能自动化缺陷假说.     

发展性阅读障碍书写加工缺陷及其神经机制

发展性阅读障碍是学习障碍的主要类型之一, 严重影响个体认知、情感与社会适应性的发展。书写与阅读关系密切, 阅读障碍者常常表现出书写加工缺陷。在行为层面, 阅读障碍者书写缺陷表现在书写质量差、速度慢和停顿多等多个方面。在脑机制层面, 脑成像研究发现, 阅读障碍者书写加工缺陷与字形加工脑区活动, 以及字形与运动区脑功能与结构连接异常有关。总体而言, 阅读障碍者书写过程中的字形通达缺陷的证据比较充分, 但字形与运动编码的衔接以及运动执行是否存在困难, 尚缺乏研究证据。相对于字母语言, 书写与阅读的关系在汉语中更为紧密, 汉语阅读障碍的书写研究将为开发汉语特色的诊治方案提供重要指导。     

汉语发展性阅读障碍儿童的视知觉学习*

研究采用知觉学习经典范式中的视觉搜索任务探讨汉语发展性阅读障碍儿童的知觉学习过程。研究考察了阅读障碍儿童与正常儿童在简单搜索任务、复杂搜索任务和限制时间的复杂搜索任务上的知觉学习特点。结果发现,阅读障碍儿童在复杂搜索任务中初始搜索时间显著长于正常控制组;在限制时间的复杂搜索任务中更进一步发现阅读障碍儿童的反应正确率显著低于正常控制组儿童;而且两组儿童视觉搜索任务的正确率与汉语阅读的识字量成绩存在显著相关。上述结果表明,汉语发展性阅读障碍儿童存在复杂搜索的知觉学习缺陷,这种缺陷可能在某种程度上与儿童的阅读技能发展有关。     

Rapid processing of letters,digits and symbols: what purely visual‐attentional deficit in developmental dyslexia?

Visual‐attentional theories of dyslexia predict deficits for dyslexic children not only for the perception of letter strings but also for non‐alphanumeric symbol strings. This prediction was tested in a two‐alternative forced‐choice paradigm with letters, digits, and symbols. Children with dyslexia showed significant deficits for letter and digit strings but not for symbol strings. This finding is difficult to explain for visual‐attentional theories of dyslexia which postulate identical deficits for letters, digits and symbols. Moreover, dyslexics showed normal W‐shaped serial position functions for letter and digit strings, which suggests that their deficit is not due to an abnormally small attentional window. Finally, the size of the deficit was identical for letters and digits, which suggests that poor letter perception is not just a consequence of the lack of reading. Together then, our results show that symbols that map onto phonological codes are impaired (i.e. letters and digits), whereas symbols that do not map onto phonological codes are not impaired. This dissociation suggests that impaired symbol‐sound mapping rather than impaired visual‐attentional processing is the key to understanding dyslexia.     

Picture naming deficits in developmental dyslexia in German

Recent research with English developmental dyslexics comparing the picture naming performance of these children to the picture naming performance of non-dyslexic (‘garden variety’) poor readers, reading age matched controls and chronological age matched controls has suggested that a selective difficulty in retrieving the phonological codes of known names on demand underlies the picture naming deficit found in developmental dyslexia (Swan & Goswami, Picture naming deficits in developmental dyslexia: the phonological representations hypothesis, Brain and Language, 56 (1997), 334–353). If the underlying causal factors in dyslexia are independent of the orthography that the child is learning to read, then a difficulty in retrieving the phonological codes of known names on demand should also be found in developmental dyslexics who are learning to read other languages. We therefore set out to replicate Swan and Goswami’s study with a group of German developmental dyslexics. We were interested to see whether a phonological deficit is characteristic of dyslexia in all orthographies, even those, such as German, in which high orthographic transparency means that dyslexic children read with considerable accuracy.     

Attentional modulation of visual processing in adult dyslexia: a spatial-cuing deficit

Anumber of researchers have suggested that deficient visual attention may play a causal role in dyslexia. However, traditional methods for investigating this assertion have been limited by the conflation of sensory and attentional factors and the inability to isolate large attentional effects. In this study, we sought to overcome these problems by combining spatial cuing with a visual search task measuring psychophysical thresholds. In normal readers, uncued search performance was characterized by a strong dependence on the number of elements in the stimulus array. Cuing the location of the target removed much of this effect, suggesting attentional facilitation of performance. Although dyslexic participants' performance in uncued search was nearly identical to that of normal readers, all dyslexic participants failed to gain the same effect of cuing that normal readers did. However, dyslexic participants did not differ from normal readers on tests of magnocellular function, suggesting that this spatial-cuing deficit is not merely a secondary consequence of magnocellular dysfunction.     

The Nature of the Automatization Deficit in Chinese Children with Dyslexia

Clarifying whether automatization deficits constitute the primary causes or symptoms of developmental dyslexia, we focused on three critical issues of the dyslexic automatization deficit, namely universality, domain specificity, and severity. Thirty Chinese dyslexic children (mean age 10 years and 5 months), 30 chronological-age-, and 30 reading-level-matched children were tested in 4 areas of automaticity: motor, visual search, Stroop facilitation effects, and automatic word recognition. The results showed that the dyslexic children performed significantly worse than the CA-controls but not the RL-controls in all the tasks except for Stroop congruent-color words, on which they performed worse than children in both control groups. The deficits reflect a lag in reading experiences rather than a persistent cognitive deficit.     

Unilateral implicit motor learning deficit in developmental dyslexia

It has been suggested that developmental dyslexia involves various literacy, sensory, motor skill, and processing speed deficits. Some recent studies have shown that individuals with developmental dyslexia exhibit implicit motor learning deficits, which may be related to cerebellar functioning. However, previous studies on implicit motor learning in developmental dyslexics have produced conflicting results. Findings from cerebellar lesion patients have shown that patients' implicit motor learning performance varied when different hands were used to complete tasks. This suggests that dyslexia may have different effects on implicit motor learning between the two hands if cerebellar dysfunction is involved. To specify this question, we used a one-handed version of a serial reaction time task to compare the performance of 27 Chinese children with developmental dyslexics with another 27 age-matched children without reading difficulties. All the subjects were students from two primary schools, Grades 4 to 6. The results showed that children with developmental dyslexic responded more slowly than nondyslexic children, and exhibited no implicit motor learning in the condition of left-hand response. In contrast, there was no significant difference in reaction time between two groups of children when they used the right hand to respond. This finding indicates that children with developmental dyslexia exhibited normal motor skill and implicit motor learning ability provided the right hand was used. Taken together, these results suggested that Chinese children with developmental dyslexia exhibit unilateral deficits in motor skill and implicit motor learning in the left hand. Our findings lend partial support to the cerebellar deficit theory of developmental dyslexia.