The neuropathology of autism.
The neuropathology of autism.
复制标题
自闭症的神经病理学。
作者：
Blatt GJ
自闭症是一种行为上定义的神经发育障碍，在美国影响超过1%的新生儿和约2%的男孩。病因尚不清楚，而且遗传上很复杂。可能存在表观遗传效应、环境影响和其他因素，这些因素促成了机制和受影响的神经通路。在文献中，这种疾病的潜在神经病理学已经发展到包括小脑、边缘系统和皮质中的特定脑区。部分结构似乎受到影响最多，而不是整个结构，例如，杏仁核的选择核，梭状面区域等。改变的皮质组织的特点是更频繁和更窄的微柱和早期过度生长的额叶部分的大脑，影响连接。异常包括细胞结构层差异、过量的白色物质神经元、GABA能小脑浦肯野细胞数量减少，以及其他可追溯到发育并导致回路异常的事件。通过最近的受体和结合位点研究，神经传递的问题是明显的，特别是在抑制性GABA系统中，可能导致兴奋性/抑制性传递的不平衡。随着尸检结果与核心行为症状相关，以及技术的进步，研究人员正在更好地了解导致这种疾病的因素。
Autism is a behaviorally defined neurodevelopmental disorder that affects over 1% of new births in the United States and about 2% of boys. The etiologies are unknown and they are genetically complex. There may be epigenetic effects, environmental influences, and other factors that contribute to the mechanisms and affected neural pathway(s). The underlying neuropathology of the disorder has been evolving in the literature to include specific brain areas in the cerebellum, limbic system, and cortex. Part(s) of structures appear to be affected most rather than the entire structure, for example, select nuclei of the amygdala, the fusiform face area, and so forth. Altered cortical organization characterized by more frequent and narrower minicolumns and early overgrowth of the frontal portion of the brain, affects connectivity. Abnormalities include cytoarchitectonic laminar differences, excess white matter neurons, decreased numbers of GABAergic cerebellar Purkinje cells, and other events that can be traced developmentally and cause anomalies in circuitry. Problems with neurotransmission are evident by recent receptor and binding site studies especially in the inhibitory GABA system likely contributing to an imbalance of excitatory/inhibitory transmission. As postmortem findings are related to core behavior symptoms, and technology improves, researchers are gaining a much better perspective of contributing factors to the disorder.