Monaghan Padraic, Shillcock Richard
Department of Psychology, University of York, York YO105DD, UK.
Brain Lang. 2008 Dec;107(3):185-93. doi: 10.1016/j.bandl.2007.12.005. Epub 2008 Jan 22.
There are several causal explanations for dyslexia, drawing on distinctions between dyslexics and control groups at genetic, biological, or cognitive levels of description. However, few theories explicitly bridge these different levels of description. In this paper, we review a long-standing theory that some dyslexics' reading impairments are due to impairments in hemispheric transfer. We test this theory in a computational model of reading, implementing anatomical features of the visual system. We demonstrate that, when callosal transfer is impaired, the model reads nonwords as well as an unimpaired model, but reads exception words poorly: a pattern of behaviour similar to surface dyslexia. This computational modelling provides a causal link between brain-based theories of dyslexia to cognitive-level theories that refer specifically to phonological impairments within the reading system.
关于阅读障碍有多种因果解释,这些解释基于阅读障碍者与对照组在基因、生物学或认知描述层面的差异。然而,很少有理论能明确地将这些不同的描述层面联系起来。在本文中,我们回顾了一个长期存在的理论,即一些阅读障碍者的阅读障碍是由于半球间传递受损所致。我们在一个阅读计算模型中对这一理论进行了测试,该模型实现了视觉系统的解剖学特征。我们证明,当胼胝体传递受损时,该模型对非单词的阅读能力与未受损模型相当,但对例外词的阅读能力较差:这种行为模式类似于表层阅读障碍。这种计算建模在基于大脑的阅读障碍理论与具体涉及阅读系统中语音障碍的认知层面理论之间建立了因果联系。