A neurological model for childhood autism.
A neurological model for childhood autism.
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儿童自闭症的神经模型。
作者：
A. Damasio;R. Maurer
我们分析儿童自闭症的行为和运动障碍。基于与成人神经学的症状和条件的类比，我们提出该综合征是由双侧神经结构系统的功能障碍引起的，该系统包括位于额叶和颞叶内侧的中边缘皮层环、新纹状体以及丘脑的前核群和内侧核群。中脑边缘皮层在细胞结构、血管结构和神经化学上都是不同的，它与纹状体一起构成了多巴胺能中脑神经元的整个靶区。这就提出了自闭症与这些结构中的神经介质失衡有关的可能性。这种功能障碍可能是靶区或影响靶区功能的结构的宏观或微观变化的结果，这些变化是由各种原因引起的，如围产期病毒感染、心室周围分水岭区损伤或遗传决定的神经化学异常。
We analyze the behavioral and motor disturbances in childhood autism. On the basis of analogy to signs and conditions seen in adult neurology, we propose that the syndrome results from dysfunction in a system of bilateral neural structures that includes the ring of mesolimbic cortex located in the mesial frontal and temporal lobes, the neostriatum, and the anterior and medial nuclear groups of the thalamus. The mesolimbic cortex is cytoarchitectonically, angioarchitectonically, and neurochemically distinct and, along with the striatum, forms the entire target area of dopaminergic mesencephalic neurons. This raises the possibility that autism is related to neuromediator imbalance in those structures. Such dysfunction might be the result of macroscopic or microscopic changes in the target area or in structures functionally influencing them, consequent to a variety of causes such as perinatal viral infection, insult to the periventricular watershed area, or genetically determined neurochemical abnormalities.