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成年发展性阅读障碍者的认知特征:理论启示

Cognitive profiles of adult developmental dyslexics: theoretical implications.

作者信息

Reid Agnieszka A, Szczerbinski Marcin, Iskierka-Kasperek Ewa, Hansen Peter

出版信息

Dyslexia. 2007 Feb;13(1):1-24. doi: 10.1002/dys.321.

DOI:10.1002/dys.321
PMID:17330733
Abstract

The aim of this study was to establish cognitive profiles of dyslexic adults on tests developed within the three main theories of developmental dyslexia: phonological, visual magnocellular and cerebellar and to investigate which theory can account for these profiles. The sample consisted of 15 Polish university students or alumni with a formal diagnosis of dyslexia, without ADHD and 15 controls matched on education, age, gender, IQ and handedness. The results revealed a striking heterogeneity of profiles. Nine dyslexics exhibited only a phonological deficit; one a phonological and a visual magnocellular deficit; a further three a phonological and a cerebellar deficit; two either a cerebellar or a visual magnocellular deficit. None of the three main theories of dyslexia can account for all the cases studied here. It is suggested that the best account of these data is in terms of different sub-types of dyslexia with different underlying causes, such as phonological, visual magnocellular and cerebellar, or a combination of these. However, an account in terms of Ramus' (Trends, Neurosci. 2004; 27(12): 720-726) model, according to which the phonological deficit is a core deficit in dyslexia and other deficits (magnocellular and cerebellar), are just co-morbid markers without a causal relationship to dyslexics' literacy difficulties, cannot currently be ruled out.

摘要

本研究的目的是在发育性阅读障碍的三种主要理论(语音理论、视觉大细胞理论和小脑理论)所开发的测试中,建立阅读障碍成年人的认知概况,并研究哪种理论能够解释这些概况。样本包括15名被正式诊断为阅读障碍的波兰大学生或校友,他们没有注意缺陷多动障碍(ADHD),以及15名在教育程度、年龄、性别、智商和利手方面相匹配的对照组。结果显示出概况的显著异质性。9名阅读障碍者仅表现出语音缺陷;1名表现出语音和视觉大细胞缺陷;另外3名表现出语音和小脑缺陷;2名表现出小脑或视觉大细胞缺陷。阅读障碍的三种主要理论均无法解释此处研究的所有案例。建议对这些数据的最佳解释是存在不同潜在原因的不同阅读障碍亚型,如语音型、视觉大细胞型和小脑型,或这些类型的组合。然而,根据拉姆斯(Ramus)的模型(《神经科学趋势》,2004年;27(12): 720 - 726),语音缺陷是阅读障碍的核心缺陷,而其他缺陷(大细胞和小脑缺陷)只是共病标志物,与阅读障碍者的读写困难没有因果关系,目前不能排除这种解释。

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