Bachevalier J
Department of Neurobiology and Anatomy, University of Texas Health Sciences Center-Houston 77030.
Neuropsychologia. 1994 Jun;32(6):627-48. doi: 10.1016/0028-3932(94)90025-6.
Although substantive understanding of brain dysfunction in autism remains meager, clinical evidence as well as animal brain research on the effects of early damage to selective brain system have now yielded enough knowledge that some provisional hypotheses concerning the etiology of autism can be generated. Basically, the underlying premise of this review is that a major dysfunction of the autistic brain resides in neural mechanisms of the structures in the medial temporal lobe, and, perhaps, more specifically the amygdaloid complex. This review begins with a summary of clinical evidence of the involvement of the medial temporal lobe structures in autism. The major behavioral disturbances seen in monkeys that had received neonatal lesions of the medial temporal lobe structures are then described. From this survey it can be seen that distinct patterns of memory losses and socioemotional abnormalities emerge as a result of extent of damage to the medial temporal lobe structures. The potential value of the experimental findings for an understanding of neural dysfunction in autism as well as directions of future research are discussed in the final section of the review.
尽管目前对自闭症中大脑功能障碍的实质性理解仍然匮乏,但临床证据以及关于早期选择性脑系统损伤影响的动物脑研究,现已产生了足够的知识,从而能够提出一些关于自闭症病因的初步假设。基本上,本综述的基本前提是,自闭症大脑的主要功能障碍存在于内侧颞叶结构的神经机制中,或许更具体地说是杏仁核复合体。本综述首先总结了内侧颞叶结构与自闭症相关的临床证据。接着描述了接受内侧颞叶结构新生期损伤的猴子所出现的主要行为障碍。从这项调查中可以看出,由于内侧颞叶结构受损程度不同,出现了不同模式的记忆丧失和社会情感异常。综述的最后一部分讨论了这些实验结果对于理解自闭症神经功能障碍的潜在价值以及未来研究的方向。