慢性压迫性颈髓损伤体感诱发电位变化与神经丝磷酸化异常的病理机制

 【目的】 观察慢性压迫性颈脊髓损伤神经元和轴突中神经丝高度磷酸化和异常积聚的特征，探讨其介导体感诱发电位（SEP)变化的神经病理机制。【方法】 将20只SD大鼠随机分为实验组（n=15）和对照组（n=5），实验组采用聚氨酯胶片建立脊髓背侧慢性压迫模型；BBB评分法和SEP评估造模前、后6个月脊髓功能变化；Luxol Fast Blue（LFB）染色观察脱髓鞘变性、免疫组织化学法观察磷酸化（SMI-31）和非磷酸化（SMI-32）神经丝在脊髓灰质前角神经元、轴突中的表达，并探讨其与SEP变化的关系。【结果】 造模6个月后大鼠BBB评分均下降（p<0.001）、SEP潜伏期延长（p<0.05）、波幅下降（p<0.001）；LFB染色强度显著降低（p<0.001）;脊髓灰质前角SMI-32阳性神经元计数明显增多、染色强度增强，两组差异具有统计学意义（p<0.05）；脊髓白质SMI-31染色强度升高（p<0.05）。【结论】 神经丝在脊髓前角神经元的过度表达与高度磷酸化以及在轴突中异常聚积是导致轴突变性、神经元损伤和体感诱发电位异常的神经病理机制之一。

Pathological Mechanism of Neurofilament Hyperphosphorylation Mediated Somatosensory Evoked Potential Abnormality in Chronic Compressive Cervical Spinal Cord Injury

【Objective】 To investigate the mechanism of neurofilament phosphorylation which mediates somatosensory evoked potential(SEP) abnormal in chronic cervical spinal cord compressive injury in rat.【Methods】 20 rats were randomly divided into experiment group(n = 15) and control group(n = 5).Experiment group were operated with implantation of a polyurethane sheet into the cervical spinal cord canal to established dorsal cord compressive models.Functional integrity of the cord among the model rats were evaluated by BBB score and SEP monitoring 6 months postoperative.Luxol fast blue(LFB) staining was used to detected axonal degeneration in white matter.Phosphorylated and non-phosphorylated neurofilaments were immunohistochemistrically stained with SMI-32 and SMI-31 respectively in the ventral horn and white matter of the cord.The relationship between SEP latency,amplitude,and neurofilament staining were analyzed.【Results】 The BBB score(P < 0.001) and SEP amplitude(P < 0.05)were decreased 6 months postoperative.The SEP latency was delayed in experiment group(P < 0.001).LBF staining intensity was significant decreased in experiment group than that in the control group(P < 0.001).The number of SMI-32 positive neurons in the ventral horn of the cord and the staining intensity were significant increased in experiment group compared to the control group(P < 0.05).SMI-31 staining intensity was higher in experiment group than in the control group(P < 0.05).【Conclusion】 Over-expression and hyperphosphorylation of neurofilament in the neurons and accumulation in axons were possibly one of the mechanisms attributing to neurons injury and axonal degenerative,which leads to SEP abnormal in the chronic compressive cervical spinal cord injury in rats.