轴突变性

电镜观察发现无髓纤维轴突变性及雪旺细胞里大量麻风杆菌聚集。

The electron microscopy observed marked axonal degeneration of unmyelinated nerve fibers with many leprosy bacillus in Schwann ' cells .

急性脊髓损伤主要导致轴突变性、神经元坏死、胶质瘢痕生成等，从而造成肢体麻痹、截瘫。

Acute SCI generally leads to axonal degeneration , neuronal necrosis , glial scar , etc. , and causes limb paralysis and paraplegina .

电镜下，辐照15s，髓鞘变形，分层；35s轴突变性，髓鞘脱失。

Myelin sheath deformation and delamination at 15 s , axonal degeneration and myelin sheath breakdown and loss at 35 s were observed under electron microscope .

周围神经损伤后，轴突变性、炎症反应等逐渐引起神经元变性、坏死；损伤处的雪旺细胞和成纤维细胞等互相作用，形成结缔组织瘢痕，对轴突再生并到达远端靶器官造成阻碍。

After peripheral nerve injury , axonal degeneration and inflammatory reactions gradually lead to neuronal degeneration and necrosis ; Schwann cells and fibroblasts act with each other and form connective tissue scar , obstructing axonal regeneration and arrival at remote target organs .

15s组神经传导抑制时间（46±12）d，大部分髓鞘重度板层间开离，轴突轻度变性，口轮匝肌纤维的Z带轻度变形。

Nerve conduction inhibition time of compression for 15s group was ( 46 ± 12 ) d. Severe lamina separation of most myelin sheath was observed . Axon mildly degenerated .

结论Ola鼠对ACR所致的类华勒氏变性反应是延迟的，而6J鼠中毒后出现轴突肿胀、变性，电镜下以神经微丝的聚集、线粒体堆积为特征；

Conclusion In Ola mice treated with ACR , the Wallerian like degeneration delayed . However , in 6J mice , neurofilaments and mitochondria accumulation could be observed within axons .

与脊髓损伤模型组比较，甲基强的松龙组脊髓组织肿胀较轻，出血较少，胞浆空泡化及核固缩现象减少；白质轴突水肿、空泡变性减轻。

Compared with the spinal cord injury group , there was the mild swelling of spinal cord tissues , slightly bleeding , reduction of vacuolization of endochylema and karyopycnosis , hydrosarca of white matter axiscylinder , abatement of vacuolar degeneration in the methylprednisolone in prophylaxis group .

有髓轴突横断损伤后钠通道聚集状态研究神经的病变先有轴突变性，继有髓鞘变性。

Dynamics of Sodium Channels Clustering in Myelinated Axons after Transection Nerval pathological changes has axial mutation sex first , afterwards has pith scabbard denaturation .