Saida K, Sumner A J, Saida T, Brown M J, Silberberg D H
Ann Neurol. 1980 Jul;8(1):12-24. doi: 10.1002/ana.410080103.
A focal demyelinative lesion of peripheral nerve was produced by intraneural injection of either antiserum from rabbits with experimental allergic neuritis or experimental allergic encephalomyelitis or antiserum to galactocerebroside. We studied the relationship between clinical and electrophysiological recovery from this lesion and the morphological pattern of remyelination. Foot muscles on the the injected side weakened within an hour of injection and remained paralyzed for 7 days; strength gradually returned to normal by 16 days after injection. Electrophysiological conduction block, apparent within a few hours of injection, persisted for about 7 days. At 8 days we detected dispersed, very low amplitude muscle action potentials with long latency. Morphologically, demyelinated axons were surrounded by Schwann cells at 7 days after injection, but compacted myelin was not present. After 8 days, remyelinating axons became surrounded by thickening compacted myelin. The time of onset of remyelination and the rate of remyelination up to 14 days following the injection were independent of axon size. The onset of clinical and electrophysiological recovery from the lesion corresponded to the appearance of 2 to 8 myelin lamellae around each remyelinating axon. At 37 days after injection, when conduction velocities had returned to preinjection values, myelin thickness of remyelinating fibers had increased to approximately one-third that of control nerves.
通过向神经内注射来自患有实验性变应性神经炎或实验性变应性脑脊髓炎的兔子的抗血清或半乳糖脑苷脂抗血清,造成周围神经的局灶性脱髓鞘病变。我们研究了该病变临床和电生理恢复与髓鞘再生形态模式之间的关系。注射侧足部肌肉在注射后1小时内减弱,并在7天内保持麻痹状态;注射后16天力量逐渐恢复正常。电生理传导阻滞在注射后数小时内出现,持续约7天。在第8天,我们检测到离散的、极低振幅且潜伏期长的肌肉动作电位。形态学上,注射后第7天脱髓鞘轴突被施万细胞包围,但不存在致密髓鞘。8天后,正在进行髓鞘再生的轴突被增厚的致密髓鞘包围。注射后髓鞘再生的起始时间和直至14天的髓鞘再生速率与轴突大小无关。病变临床和电生理恢复的起始与每个正在进行髓鞘再生的轴突周围出现2至8个髓鞘板层相对应。注射后37天,当传导速度恢复到注射前值时,正在进行髓鞘再生的纤维的髓鞘厚度增加到对照神经的约三分之一。