Krause Margaret B
University of South Florida, 4202 E Fowler Ave, Tampa, FL, 33620, USA.
Dyslexia. 2015 Nov;21(4):285-303. doi: 10.1002/dys.1505. Epub 2015 Sep 3.
The aim of this review is to provide a background on the neurocognitive aspects of the reading process and review neuroscientific studies of individuals with developmental dyslexia, which provide evidence for amodal processing deficits. Hari, Renvall, and Tanskanen (2001) propose amodal sluggish attentional shifting (SAS) as a causal factor for temporal processing deficits in dyslexia. Undergirding this theory is the notion that when dyslexics are faced with rapid sequences of stimuli, their automatic attentional systems fail to disengage efficiently, which leads to difficulty when moving from one item to the next (Lallier et al., ). This results in atypical perception of rapid stimulus sequences. Until recently, the SAS theory, particularly the examination of amodal attentional deficits, was studied solely through the use of behavioural measures (Facoetti et al., ; Facoetti, Lorusso, Cattaneo, Galli, & Molteni, ). This paper examines evidence within the literature that provides a basis for further exploration of amodal SAS as an underlying deficit in developmental dyslexia.
本综述的目的是提供阅读过程的神经认知方面的背景知识,并回顾对发育性阅读障碍个体的神经科学研究,这些研究为非模态加工缺陷提供了证据。哈里、伦瓦尔和坦斯卡宁(2001年)提出非模态注意力转移迟缓(SAS)是阅读障碍中时间加工缺陷的一个因果因素。该理论的基础是,当阅读障碍者面对快速的刺激序列时,他们的自动注意力系统无法有效地脱离,这导致从一个项目转移到下一个项目时出现困难(拉利耶等人)。这导致对快速刺激序列的非典型感知。直到最近,SAS理论,特别是对非模态注意力缺陷的研究,仅通过行为测量来进行(法科埃蒂等人;法科埃蒂、洛鲁索、卡塔内奥、加利和莫尔泰尼)。本文考察了文献中的证据,这些证据为进一步探索非模态SAS作为发育性阅读障碍的潜在缺陷提供了基础。