Galaburda A M, Aboitiz F
Neurological Unit, Beth Israel Hospital, Harvard University, Boston, Mass. 02215.
Arch Biol Med Exp. 1986 Jan;19(1):57-65.
This is a review that summarizes the work done in our laboratory during the last three years. We have studied four dyslexic brains. They all bear a symmetric anatomical pattern in a structure closely related to the language areas (planum temporale), which is more commonly asymmetric in normal brains. In addition, their microscopic examination shows numerous ectopias and dysplasias in the cerebral cortex. The high incidence of immune disease in dyslexics and their families suggests a more general developmental problem in developmental dyslexia. The hypothesis is raised that fetal effects of testosterone are involved in regulating neurological as well as immunological development, whereby abnormally high testosterone activity would produce a twofold deficit. Finally, strains of immune-defective mice have been found that bear the same cortical abnormalities as seen in the dyslexic brains previously studied. The immune-defective mouse may prove to be an excellent model for the study of the neuropathological basis of developmental dyslexia.
这是一篇综述，总结了我们实验室在过去三年所做的工作。我们研究了四个诵读困难者的大脑。它们在与语言区域（颞平面）密切相关的结构中都呈现出对称的解剖模式，而在正常大脑中该结构通常是不对称的。此外，对它们的显微镜检查显示大脑皮层中有大量的异位和发育异常。诵读困难者及其家族中免疫疾病的高发病率表明发育性诵读困难存在更普遍的发育问题。有人提出一种假说，即睾酮的胎儿效应参与调节神经以及免疫发育，异常高的睾酮活性会导致双重缺陷。最后，已发现免疫缺陷小鼠品系具有与先前研究的诵读困难者大脑中所见相同的皮层异常。免疫缺陷小鼠可能被证明是研究发育性诵读困难神经病理学基础的优秀模型。
