JARA-BRAIN, Jülich and Aachen, Germany.
Dyslexia. 2010 Aug;16(3):258-82. doi: 10.1002/dys.409.
We investigated whether phonological deficits are a consequence of magnocellular processing deficits in dyslexic and control children. In Experiment 1, children were tested for reading ability, phonological awareness, visuo-magnocellular motion perception, and attention shifting (sometimes considered as magnocellular function). A two-step cluster analysis of the behavioural scores revealed four clusters of children. Phonological awareness was correlated with attention (cluster musical sharp1) or motion detection (cluster musical sharp2), whereas attention and motion detection were correlated in cluster musical sharp3. In cluster musical sharp4, all variables were uncorrelated. In Experiment 2, the same variables plus auditory discrimination were tested with fMRI in a sub-sample of Experiment 1. Although dyslexics had reduced activation in visual or auditory cortex during motion detection or auditory discrimination, respectively, they had increased right frontal activation in areas 44 and 45 in all 'magnocellular' (including auditory) tasks. In contrasts, during phonological decisions, there was higher activation for good readers than dyslexics in left areas 44 and 45. Together, the two experiments give insight into the interplay of phonological and magnocellular processing during reading. Distinct left versus right frontal effects reveal partly different underlying neural mechanisms. These data contradict the view that phonological processing deficits in dyslexia necessarily result from impaired magnocellular functioning.
我们研究了语音缺陷是否是阅读障碍儿童和对照组儿童的巨细胞处理缺陷的结果。在实验 1 中,对儿童的阅读能力、语音意识、视-巨细胞运动知觉和注意力转移(有时被认为是巨细胞功能)进行了测试。对行为得分的两步聚类分析显示,儿童分为四个聚类。语音意识与注意力(集群音乐 sharp1)或运动检测(集群音乐 sharp2)相关,而注意力和运动检测在集群音乐 sharp3 中相关。在集群音乐 sharp4 中,所有变量均不相关。在实验 2 中,使用 fMRI 对实验 1 的子样本测试了相同的变量加上听觉辨别力。尽管阅读障碍者在运动检测或听觉辨别力方面的视觉或听觉皮层激活减少,但在所有“巨细胞”(包括听觉)任务中,右额区 44 和 45 区域的激活增加。相比之下,在语音决策过程中,与阅读障碍者相比,优秀读者的左 44 和 45 区域的激活更高。这两个实验共同深入了解阅读过程中语音和巨细胞处理的相互作用。左半球和右半球的明显差异揭示了部分不同的潜在神经机制。这些数据反驳了阅读障碍中语音处理缺陷必然源于巨细胞功能受损的观点。