发展性阅读障碍的噪音抑制缺陷

发展性阅读障碍的缺陷本质一直是研究者们关注和争论的焦点。近些年, 有研究者提出了一种新的理论假设——噪音抑制缺陷假设, 并得到了许多研究证据的支持。这种缺陷在视觉和听觉通道中均存在, 说明阅读障碍具有多感觉/一般性噪音抑制缺陷。但也有研究者指出知觉噪音抑制本质上反映了注意的功能, 因而这种缺陷可能是由注意缺陷导致的。目前还缺乏直接证据支持汉语阅读障碍存在噪音抑制缺陷。最后本文对该领域未来的发展方向做出展望。     

发展性阅读障碍的ERP研究

发展性阅读障碍,ERP,语音缺陷假说,Oddball范式。行为实验已经发现,语音能力的缺损是拼音文字发展性阅读障碍的核心。然而近年来行为研究和神经生理学的研究也发现,发展性阅读障碍与基本知觉障碍有关。事件相关电位（event-related potentials ,简称ERP）作为一种独特的电生理学研究手段,从一个更为直观的角度验证了行为实验的结果,推动了发展性阅读障碍的进展。语言认知水平ERP研究表明,发展性阅读障碍者在存在语音加工和信息整合的缺陷。感知觉加工层次的ERP研究结果则不尽一致,有的研究发现,阅读障碍存在着基本的听觉加工缺陷;有的研究则发现发展性阅读障碍存在言语声音加工的缺陷,而对非言语声音的加工与正常读者没有显著差别;有的研究支持大细胞通路受损假说,发现阅读障碍在低对比度和低空间频率上存在视觉加工的缺陷,有的研究结果则没有发现发展性阅读障碍者与正常读者在不同对比度和空间频率上的差异。     

汉语发展性阅读障碍儿童的视觉大细胞-背侧通路功能

发展性阅读障碍是一种在获得阅读技能方面的特殊困难,其致病原因一直是该领域的核心问题。越来越多的研究表明视觉大细胞-背侧通路功能与阅读技能之间存在紧密联系。视觉大细胞-背侧通路缺陷可能是导致阅读障碍的主要原因之一。一些研究发现汉语阅读障碍儿童同样存在视觉大细胞-背侧通路缺陷。本文将回顾近些年汉语发展性阅读障碍儿童视觉大细胞-背侧通路功能的相关研究成果,并对该领域未来的发展方向做出展望。     

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。     

不同阅读水平儿童中央执行系统比较研究

本研究通过两部分实验探讨汉语发展性阅读障碍儿童与正常儿童中央执行系统的容量差异和这种差异的性质。通过比较匹配生理年龄的不同阅读水平儿童在自定步速和固定步速的复杂阅读广度测验中的成绩,发现发展性阅读障碍儿童在两种阅读广度测验中都表现出中央执行系统容量的缺陷,这种缺陷既不能用加工效率理论,也不能用资源分配理论来解释,而符合一般容量假设。因此,本研究支持发展性阅读障碍儿童存在实时加工和存储信息的一般容量缺陷。     

获得性阅读障碍的“主要系统”假说

认知神经心理学为阅读机制的探讨提供了大量的证据,认为不同阅读障碍是不同加工通道选择性受损的结果。近年来,基于联结主义的三角模型理论,研究者提出了主要系统假说（primary system hypothesis）,认为阅读障碍是主要的认知系统（如视觉、语义和语音系统）受损导致的：表层障碍是因为语义系统受损导致的阅读困难,语音和深层障碍是语音和语义系统同时受损时综合症状的连续体。该理论认为各主要系统可能同时是多个认知活动的加工成分,一个系统的受损会影响所有与之相关的认知过程,从而把阅读障碍与其它认知功能障碍联系起来。统一的主要系统受损下对各种获得性阅读障碍形成机制在文中得到详细的解释     

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。     

发展性阅读障碍的视听时间敏感性缺陷及其脑神经机制

阅读是一个视听加工过程,阅读障碍的产生可能是过程中视听时间敏感性缺陷的结果。视听时间敏感性指个体对视觉和听觉刺激出现时间的感知能力,可通过同时性判断、时间顺序判断和视听整合考察。研究发现,阅读障碍者在这一能力上表现出行为和脑层面异常。而这些研究多是拼音文字背景,汉语文字下该领域研究相当少。未来需要丰富实验设计,扩大对汉语背景下视听时间敏感性研究,并以此开发干预手段,为阅读障碍的机制和治疗提供借鉴。     

发展性阅读障碍的视觉空间注意加工能力

鉴于阅读起始于基础视觉加工阶段, 越来越多的研究者开始关注阅读障碍者的视觉空间注意加工能力。视觉空间注意是指个体对视觉刺激的空间位置的注意, 可通过线索提示、视觉搜索和视觉注意广度等视觉任务来考察。大量国内外研究发现, 发展性阅读障碍者在视觉空间注意任务下表现出行为和神经活动方面的异常。其中的神经机制问题不仅反映在与视觉空间注意有关的顶叶区域激活异常, 还存在于脑区间功能连接异常(如顶叶区域与字形加工区的功能连接)。未来研究还需利用横断和追踪研究探讨阅读障碍与视觉空间注意能力发展关系的内在机制, 以及探究语言特性对阅读障碍者视觉空间注意缺陷的可能调节作用。     

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。     

On the prevalence of magnocellular deficits in the visual system of non-dyslexic individuals

Numerous studies have found visual deficits associated with dyslexia. This has made it important to understand how these deficits may be related to reading difficulties. A widely held theory is that dyslexia is the result of a deficit in the magnocellular part of the visual system (earlier called the transient system). In support for this theory, the prevalence of magnocellular deficits has been reported to be high among dyslexic readers and very low among non-dyslexic ones. This creates the impression that in the population as a whole dyslexic individuals have magnocellular deficits and non-dyslexic individuals do not. However, we show that because the prevalence of dyslexia itself is low this need not be the case. On the basis of previously published data we have estimated the number of non-dyslexic and dyslexic individuals with magnocellular deficits. Our estimates indicate that there should be a large number of non-dyslexic individuals with magnocellular deficits. Paradoxically more individuals without dyslexia have magnocellular deficits than individuals with dyslexia. This poses a challenge to the view that dyslexia is the result of a magnocellular deficit.     

On using Vernier acuity to assess magnocellular sensitivity

A recent study [Keri, S., & Benedek, G. (2009). Visual pathway deficit in female fragile × premutation carriers: A potential endophenotype. Brain and Cognition, 69, 291–295] has found Vernier acuity deficiencies together with contrast sensitivity defects consistent with a magnocellular deficit in female fragile × premutation carriers. This may appear to support the notion that Vernier acuity may serve as a test of magnocellular sensitivity. However, Vernier acuity deficiencies have been reported in other conditions (e.g., schizophrenia, amblyopia and cortical visual impairment) where there is little evidence for magnocellular deficits. The observation that Vernier acuity deficiencies can occur without magnocellular deficits indicates that Vernier acuity is not a reliable test of magnocellular sensitivity.     

Visual pathway deficit in female fragile X premutation carriers: a potential endophenotype

Previous studies indicated impaired magnocellular (M) and relatively spared parvocellular (P) visual pathway functioning in patients with fragile X syndrome. In this study, we assessed M and P pathways in 22 female fragile X premutation carriers with normal intelligence and in 20 healthy non-carrier controls. Testing procedure included visual contrast sensitivity and vernier threshold measurements. Results revealed that carriers were selectively impaired on tests of M pathways (low spatial/high temporal frequency contrast sensitivity and frequency-doubling vernier), whereas they showed intact performance on P pathway tests. These results suggest that the deficit of the M pathway is an endophenotype of fragile X syndrome.     

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.     

The time course of attentional focusing in dyslexic and normally reading children

A cue size procedure was used to evaluate the time course of visuo-spatial attention in dyslexic and normally reading children. When a stimulus target is presented inside a large cue vs a small cue the identification time is slower. In the present study two cue-target delays (100 and 500 ms) were used. Results showed a slower time course of attentional focusing in dyslexics vs normal readers. Indeed, dyslexics exhibited no cue size effect at a shorter cue-target delay (100 ms), while it was present at a longer cue-target delay (500 ms). In contrast, a cue size effect was found at both cue-target delays in normally reading children. These results further support the hypothesis of sluggish automatic focusing of visual attention in dyslexics. This impairment could be a consequence of a general magnocellular deficit demonstrated previously in dyslexics.     

Modelling relations between sensory processing, speech perception, orthographic and phonological ability, and literacy achievement

The general magnocellular theory postulates that dyslexia is the consequence of a multimodal deficit in the processing of transient and dynamic stimuli. In the auditory modality, this deficit has been hypothesized to interfere with accurate speech perception, and subsequently disrupt the development of phonological and later reading and spelling skills. In the visual modality, an analogous problem might interfere with literacy development by affecting orthographic skills. In this prospective longitudinal study, we tested dynamic auditory and visual processing, speech-in-noise perception, phonological ability and orthographic ability in 62 five-year-old preschool children. Predictive relations towards first grade reading and spelling measures were explored and the validity of the global magnocellular model was evaluated using causal path analysis. In particular, we demonstrated that dynamic auditory processing was related to speech perception, which itself was related to phonological awareness. Similarly, dynamic visual processing was related to orthographic ability. Subsequently, phonological awareness, orthographic ability and verbal short-term memory were unique predictors of reading and spelling development.     

Cortical locus of coherent motion deficits in deaf poor readers

Samar and Parasnis [Samar, V. J., & Parasnis, I. (2005). Dorsal stream deficits suggest hidden dyslexia among deaf poor readers: correlated evidence from reduced perceptual speed and elevated coherent motion detection thresholds. Brain and Cognition, 58, 300-311.] reported that correlated measures of coherent motion detection and perceptual speed predicted reading comprehension in deaf young adults. Because deficits in coherent motion detection have been associated with dyslexia in the hearing population, and because coherent motion detection is strongly dependent on extrastriate cortical area MT, these results are consistent with the claim that hidden dyslexia occurs within the deaf population and is associated with deficits in MT. However, coherent motion detection can also be influenced by subcortical deficits in both magnocellular and parvocellular pathways. To confirm the putative cortical locus of coherent motion perception deficits, we measured contrast thresholds for detecting the direction of movement of drifting sine wave gratings in the same participant group as [Samar, V. J., & Parasnis, I. (2005). Dorsal stream deficits suggest hidden dyslexia among deaf poor readers: correlated evidence from reduced perceptual speed and elevated coherent motion detection thresholds. Brain and Cognition, 58, 300-311.], under stimulus conditions that selectively biased for input from the subcortical magnocellular and parvocellular pathways, respectively. Contrast thresholds were not related to reading comprehension performance under either the magnocellular or parvocellular conditions. Furthermore, the previously reported correlations among reading comprehension, coherent motion thresholds, and perceptual speed remained significant even after contrast thresholds and non-verbal IQ were controlled in partial correlation analyses. In addition, coherent motion detection thresholds were found to correlate specifically with a reading-IQ discrepancy score, one commonly used indicator of dyslexia. These results provide direct psychophysical evidence that the previously reported deficit in coherent motion detection in deaf poor readers does not involve subcortical pathway deficits, but rather is associated with a cortical deficit likely involving area MT. They also strengthen the argument for the existence of hidden dyslexia in the deaf adult population.     

Visual temporal processing in dyslexia and the magnocellular deficit theory: the need for speed?

A controversial question in reading research is whether dyslexia is associated with impairments in the magnocellular system and, if so, how these low-level visual impairments might affect reading acquisition. This study used a novel chromatic flicker perception task to specifically explore temporal aspects of magnocellular functioning in 40 children with dyslexia and 42 age-matched controls (aged 7-11). The relationship between magnocellular temporal resolution and higher-level aspects of visual temporal processing including inspection time, single and dual-target (attentional blink) RSVP performance, go/no-go reaction time, and rapid naming was also assessed. The Dyslexia group exhibited significant deficits in magnocellular temporal resolution compared with controls, but the two groups did not differ in parvocellular temporal resolution. Despite the significant group differences, associations between magnocellular temporal resolution and reading ability were relatively weak, and links between low-level temporal resolution and reading ability did not appear specific to the magnocellular system. Factor analyses revealed that a collective Perceptual Speed factor, involving both low-level and higher-level visual temporal processing measures, accounted for unique variance in reading ability independently of phonological processing, rapid naming, and general ability.