Delayed demyelination and macrophage invasion: a candidate for secondary cell damage in spinal cord injury.
Delayed demyelination and macrophage invasion: a candidate for secondary cell damage in spinal cord injury.
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DOI：
10.1089/cns.1985.2.299
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
A. Blight
中科院分区：
文献类型：
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作者：
A. Blight
本文综述了猫实验性脊髓损伤（SCI）的慢性形态学和生理学的最新研究，并概述了其结论。特别是，已发现病变的慢性髓鞘形成障碍的变化在很大程度上独立于损伤强度，这表明继发性病理起源。新的形态计量学研究的亚急性发展的挫伤病变的描述。使用电子显微镜和光学显微镜行取样的有髓鞘的轴突，它被发现，脱髓鞘的轴突，幸存的最初的损伤主要发生在挫伤后2和7天之间，并没有伴随着更快的溶解髓鞘从那些轴突，在前2天内退化。在2-7天的相同时间间隔内，病变中心明显完整的轴突数量下降了2倍或更多。这种继发性病理学与巨噬细胞对病变的密集浸润及其对最初出血性坏死残留的膜性碎片的吞噬作用一致。它的结论是，创伤后炎症在脊髓中应进行更详细的调查作为一个可能的贡献者慢性赤字。此外，这些数据强调了定义继发性损伤的性质、发生时间和比例意义的重要性，以便评价那些试图区分急性继发性病理生理学与原发性退行性过程的研究和假设。
Recent studies of the chronic morphology and physiology of experimental spinal cord injury (SCI) in the cat are reviewed and their conclusions outlined. In particular, variations in chronic dysmyelination of the lesion have been found to be largely independent of injury intensity, suggesting a secondary pathologic origin. New morphometric studies of the subacute development of contusion lesions are described. Using electron microscopy and light microscopic line-sampling of myelinated axons, it was found that demyelination of axons that survived the initial injury occurred largely between 2 and 7 days after contusion and did not accompany the much more rapid dissolution of myelin from those axons that degenerated within the first 2 days. The number of apparently intact axons at the center of the lesion declined by a factor of 2 or more in the same interval of 2-7 days. This secondary pathology was coincident with dense invasion of the lesion by macrophages and their phagocytosis of the membraneous debris remaining from the initial hemorrhagic necrosis. It is concluded that posttraumatic inflammation in the spinal cord should be investigated in more detail as a possible contributor to chronic deficits. In addition, these data emphasize the importance of defining the nature, time of occurrence, and proportional significance of secondary damage in order to evaluate those studies and hypotheses that attempt to differentiate acute secondary pathophysiology from primary degenerative processes.