Orgogozo J M, Pere J J, Strube E
Sem Hop. 1979;55(31-32):1389-94.
Two cases of alexia without agraphia are reported, with differences in the characters of the alexia and in the accompanying signs. The visual field defect was limited to quadranopia in both cases which was upper quadrantic and mild in one, lower quadrantic and severe in the other. These differences make it unlikely that a similar anatomical location of the lesion and a unique mechanism are responsible of all cases of alexia without agraphia. Persistance of visual inputs in the right visual field is partial in our cases, but alexia without hemianopsia does exist. These facts are against the mechanism of "splenio-cortical" disconnection proposed by Geschwind as the only explanation. A "cortical", or agnosic mechanism has been also claimed, with lesions of the lingual and fusiform gyri on the dominant side, as well as "subangular", mechanism, with intrahemispheric disconnection by a lesion located between the visual associative areas and the angular gyrus: in these last two situations an hemianopsia is not necessarily associated to the alexia without agraphia.
报告了两例失读不伴失写症的病例，失读的特征及伴随症状存在差异。两例患者的视野缺损均局限于象限盲，其中一例为上象限轻度象限盲，另一例为下象限重度象限盲。这些差异表明，不太可能所有失读不伴失写症病例都由类似的病变解剖位置和单一机制所致。在我们的病例中，右侧视野视觉输入的持续性是部分存在的，但失读不伴偏盲确实存在。这些事实与Geschwind提出的“胼胝体-皮质”分离机制作为唯一解释相矛盾。也有人提出了“皮质”或失认机制，即优势侧舌回和梭状回病变，以及“角回下”机制，即位于视觉联合区和角回之间的病变导致半球内分离：在这后两种情况下，偏盲不一定与失读不伴失写症相关。
