A NOVEL OF EXPERIMENTAL MODEL FOR CENTRAL CORD INJURY ON CHRONIC SPINAL CORD COMPRESSION MODEL OF RAT. RESEARCH FOR THE TIME OF DECOMPRESSION AND CLINICAL STUDY

在动物模型中，没有建立一种新的中央脊髓损伤的实验模型。颈椎椎板下植入一种薄的膨胀性聚合物，无脊髓损伤。我们对大鼠慢性脊髓压迫模型进行了研究。我们采用了大鼠的模型，试图研究中央脊髓损伤的机制。在我们的模型中，运动神经元数量在9周和25周时显著减少。加压后25周仅为对照组的66%。然后，给出过伸过屈损伤；是否会发生上肢运动无力。我们的一些模特，出现了像个人一样的中央脊髓损伤。这一事实为建立大鼠中央脊髓损伤模型提供了可能。我们还研究了受压脊髓减压的时机。压迫后8~12周(运动神经元数量减少)，如不减压，运动能力无改善。在临床上，这一事实提示了减压手术的时机。我们将继续利用该模型和临床资料对中央脊髓损伤进行研究。我们认为，该模型有助于进一步研究中枢脊髓损伤的神经病理学和神经生理学机制。

A novel experimental model for central cord injury was not developed in the animal model. A thin expanding polymer was inserted under the cervical laminae without cord injury. We have studied the chronic spinal compression model of rat. We use the model of the rat; we tried studying the mechanism of central cord injury. In our model, the motor neuron count decreased in 9 weeks and 25 weeks significantly. The count of 25 weeks after compression was only 66% compared with control group. Then, the hyperextension of hyperflexion injury was given; a motor weakness of upper extremity will happen or not. Some of our model, there were the individual like a central cord injury. The fact will give us the possibility of central cord injury model of the rat. We also investigated the timing of decompression of the compressed spinal cord. At 8 to 12 weeks after compression (the time was the motor neuron count were decreased), if the decompression was not achieved, the capability of locomotion was not improved. In clinical, the fact suggested the timing of decompression surgery. We will continue the study of central cord injury using the model and clinical material. We believe the present model is to help advancement of the neuropathological and neurophysiological studies of the mechanism of central cord injury.