• 作者： 劉克明
• 作者服務機構： 高雄醫學院解剖學科
• 中文摘要： 根據以往的研究報告，麻瘋桿菌經由體表面溫度較低部位感染，主要侵犯末稍神經系統的無髓神經纖維及其舒旺氏細胞。本研究，應用光學及電子顯微鏡研究經由血管種入之麻瘋桿菌對於神經系統的有髓神經纖維的影響。 CBA/J鼠的脊髓神經組織中，神經細胞與神經膠細胞的數目與分布無特殊變化。神經細胞細胞體與細胞突起、神經膠細胞、室管膜細胞及髓鞘等形態學上的構造皆完整。在神經組織內、未發現麻瘋桿菌及炎性細胞。麻瘋桿菌僅見於血管內。 脊髓根與坐骨神經內的有髓神經纖維呈變性病變。髓鞘進行指紋狀突起、分解、破裂、或形成空泡而分解。髓鞘破裂的碎屑被巨噬細胞吞噬而形成蜂巢狀或海棉狀小體。於巨噬細胞的細胞體內發現有大量的麻瘋桿菌。 於神經髓鞘變性時，舒旺氏細胞顯示有絲分裂及增殖的情形。每一新增殖的舒旺氏細胞伸出數個突起以環繞數條已失去髓鞘的軸突，代替了正常情況下；一個舒旺氏細胞僅環繞一個結間節的關係。此種數個結間節被髓鞘環繞，可能是一種補充那些已變性的舒旺氏細胞的一種補償作用。 有髓神經纖維的脫髓現象係舒旺氏細胞受到麻瘋桿菌侵入加上末稍髓燐脂蛋白的自體免疫反應所導致的結果。髓稍的再生可能係受到已失去髓鞘的軸突刺激以及增殖的舒旺氏細胞重新形成髓鞘環繞所引起。
• 英文摘要： The effects of Mycobacterium leprae (M. leprae) via bloodstream on the myelinated nerve fibers inboth the central and the peripheral nervous systems were investigated by means of light and electron micro-scopy. In the spinal cord of CBA/J mice, the population of neurons and neuroglial cells was unremarkable;the morphological structures of neurons (cell bodies and processes), neuroglial cells, ependymal cells andmyelin sheaths appeared to be intact. There were neither M. leprae nor inflammatory cells in the nervoustissue. The M. leprae were found only in the lumen of blood vessels. In contrast, the myelinated nerve fibers in the roots of the spinal nerves and the sciatic nerve showeddegenerative changes. Myelin sheaths splitted with fingerprint-like droplets, and showed dying back disinte-gration, fragmentation and vacuolation. The debris and fragments of degenerated sheaths were engulfedwithin macrophages and formed honey-comb like or spongiform corpuscles. Many M. leprae were foundwithin the cytoplasm of macrophages. During the nerve demyelination, mitosis and proliferation of Schwann cells were also observed. Eachproliferating Schwann cell extended several cytoplasmic processes and spirally ensheathed several inter-nodes of demyelinating axons, replacing the normal relationship of one Schwann cell to one internode. Themultiple remyelination might be a reactive compensation for the degenerating Schwann cells. The demyelination of myelinated nerve fibers was caused by the Schwann cells affected by M. lepraeand the autoimmune response of Schwann cells to the peripheral myelin protein. The stimulation of de-myelinating axons and proliferating Schwann cells might contribute to the process of remyelination.
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