The magnocellular theory of developmental dyslexia.
The magnocellular theory of developmental dyslexia.
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DOI：
10.1002/dys.186
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发表时间：
2001-01-01
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影响因子：
--
通讯作者：
Stein, J
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作者：
Stein, J
当阅读能力明显落后于智商(IQ)的预期水平，并出现其他症状--协调不协调、左右混乱、排序不良--这些症状将其表征为神经综合征时，识字率低被称为发育性阅读障碍。5%-10%的儿童，尤其是男孩，被发现患有阅读障碍。阅读需要获得良好的拼写技能，以便识别单词的视觉形式，使人能够直接获取单词的含义。它还需要发展良好的语音技能，利用字母发音转换规则的知识来辨别不熟悉的单词。在阅读困难的大脑中，两侧的颞顶语言区域是对称的，没有正常的左侧优势。此外，还发现了脑疣(异位)，特别是聚集在左侧顶叶语言区周围。视觉巨细胞系统负责对阅读时的视觉事件进行计时。因此，如果意想不到的移动导致图像移出中心凹(“视网膜滑动”)，它就会发出任何视觉运动的信号。然后，这些信号被用来将眼睛带回目标。因此，对视觉运动的敏感度似乎有助于决定好的和不好的读者的拼写技能发展得有多好。在阅读困难患者中，视觉大细胞系统的发育受到损害：阅读困难的外侧膝状核(LGN)的大细胞层发育异常；其运动敏感度降低；许多阅读困难患者表现出不稳定的双眼注视；因此视觉定位不良，特别是左侧(左忽视)。因此，阅读困难者的双眼不稳定和视觉感知不稳定会导致他们试图阅读的字母看起来像是四处移动和相互交叉。因此，遮住一只眼睛(单眼遮挡)可以提高阅读能力。因此，良好的大细胞功能对于高运动敏感度和稳定的双眼注视，从而正确地发展矫正技能是必不可少的。许多阅读障碍者也有听觉/语音方面的问题。区分字母发音依赖于捕捉到表征它们的声音频率和幅度的变化。因此，高频(FM)和调幅(AM)敏感性有助于发展良好的语音技能，而低敏感性阻碍了这些技能的获得。因此，阅读困难者对调频和调幅的敏感度明显低于好读者，这就解释了他们在音位方面的问题。小脑是大细胞系统的头部神经节；它有助于双眼注视和发音的内部语言，在阅读困难的人中，它显然是有缺陷的。因此，有证据表明，大多数阅读问题都有根本的感觉运动原因。但为什么巨细胞系统不能正常发育呢？整个大脑的巨噬细胞发育受损有明显的遗传基础。最被理解的连锁是与6号染色体短臂上的主要组织相容性复合体(MHC)1类区域，该区域有助于控制抗体的产生。巨噬细胞的发育可能会受到影响发育中大脑的自身抗体的影响。巨噬细胞还需要大量的多不饱和脂肪酸来保持膜的弹性，这种弹性允许通道蛋白的快速构象变化，这是它们瞬时敏感性的基础。但是，除非阅读障碍有补偿优势，否则导致大细胞缺陷的基因不会如此普遍。在发育性阅读障碍患者中，可能有少量细胞系统的高度发展，这些系统奠定了他们的整体、艺术、‘看到全景’和创业天赋的基础。
Low literacy is termed 'developmental dyslexia' when reading is significantly behind that expected from the intelligence quotient (IQ) in the presence of other symptoms--incoordination, left-right confusions, poor sequencing--that characterize it as a neurological syndrome. 5-10% of children, particularly boys, are found to be dyslexic. Reading requires the acquisition of good orthographic skills for recognising the visual form of words which allows one to access their meaning directly. It also requires the development of good phonological skills for sounding out unfamiliar words using knowledge of letter sound conversion rules. In the dyslexic brain, temporoparietal language areas on the two sides are symmetrical without the normal left-sided advantage. Also brain 'warts' (ectopias) are found, particularly clustered round the left temporoparietal language areas. The visual magnocellular system is responsible for timing visual events when reading. It therefore signals any visual motion that occurs if unintended movements lead to images moving off the fovea ('retinal slip'). These signals are then used to bring the eyes back on target. Thus, sensitivity to visual motion seems to help determine how well orthographic skill can develop in both good and bad readers. In dyslexics, the development of the visual magnocellular system is impaired: development of the magnocellular layers of the dyslexic lateral geniculate nucleus (LGN) is abnormal; their motion sensitivity is reduced; many dyslexics show unsteady binocular fixation; hence poor visual localization, particularly on the left side (left neglect). Dyslexics' binocular instability and visual perceptual instability, therefore, can cause the letters they are trying to read to appear to move around and cross over each other. Hence, blanking one eye (monocular occlusion) can improve reading. Thus, good magnocellular function is essential for high motion sensitivity and stable binocular fixation, hence proper development of orthographic skills. Many dyslexics also have auditory/phonological problems. Distinguishing letter sounds depends on picking up the changes in sound frequency and amplitude that characterize them. Thus, high frequency (FM) and amplitude modulation (AM) sensitivity helps the development of good phonological skill, and low sensitivity impedes the acquisition of these skills. Thus dyslexics' sensitivity to FM and AM is significantly lower than that of good readers and this explains their problems with phonology. The cerebellum is the head ganglion of magnocellular systems; it contributes to binocular fixation and to inner speech for sounding out words, and it is clearly defective in dyslexics. Thus, there is evidence that most reading problems have a fundamental sensorimotor cause. But why do magnocellular systems fail to develop properly? There is a clear genetic basis for impaired development of magnocells throughout the brain. The best understood linkage is to the region of the Major Histocompatibility Complex (MHC) Class 1 on the short arm of chromosome 6 which helps to control the production of antibodies. The development of magnocells may be impaired by autoantibodies affecting the developing brain. Magnocells also need high amounts of polyunsaturated fatty acids to preserve the membrane flexibility that permits the rapid conformational changes of channel proteins which underlie their transient sensitivity. But the genes that underlie magnocellular weakness would not be so common unless there were compensating advantages to dyslexia. In developmental dyslexics there may be heightened development of parvocellular systems that underlie their holistic, artistic, 'seeing the whole picture' and entrepreneurial talents.