Kim Phyo, Haisa Toshihiko, Kawamoto Toshiki, Kirino Takaaki, Wakai Susumu
Department of Neurosurgery Dokkyo University School of Medicine, Tochighi, Japan.
Ann Neurol. 2004 Apr;55(4):503-11. doi: 10.1002/ana.20018.
Cervical myelopathy is a common cause of neurological disability among the elderly; however, the exact mechanism for the insidious and progressive deterioration remains to be elucidated. To study the pathophysiology, we developed a simple experimental model reproducing the course. In rats, a thin sheet of expanding polymer was implanted microsurgically underneath the C5-C6 laminae. In the control group, the polymer sheet was removed immediately. Changes in motor functions were monitored for 25 weeks after the operation, with voluntary exercise activity measured by odometer attached to revolving cages, and forced running capability measured by duration of exercise on a rotating treadmill. Motor neurons were counted stereologically in continuous sections. In the compression group, the forced running capability deteriorated after a latent period of 17 weeks and progressively thereafter. In the control group, it stayed unchanged throughout 25 weeks. Course of the voluntary exercise was comparable between the groups. Motor neuron density in the compression group decreased significantly in 9 weeks (-20.3%) and 25 weeks (-35.5%), but not in 1 or 3 weeks. This practical model properly reproduces characteristic features of the clinical cervical myelopathy, with progressive motor disturbance after a latency and insidious neuronal loss preceding the symptoms.
脊髓型颈椎病是老年人神经功能障碍的常见原因；然而，其隐匿性和进行性恶化的确切机制仍有待阐明。为了研究其病理生理学，我们建立了一个简单的实验模型来重现这一过程。在大鼠中，通过显微手术在C5 - C6椎板下方植入一片可膨胀的聚合物薄片。在对照组中，聚合物薄片在植入后立即取出。术后25周监测运动功能的变化，通过安装在旋转笼上的里程表测量自主运动活动，通过在旋转跑步机上的运动持续时间测量强迫跑步能力。在连续切片中对运动神经元进行立体计数。在压迫组中，强迫跑步能力在17周的潜伏期后恶化，并在之后逐渐恶化。在对照组中，其在25周内保持不变。两组之间自主运动的过程相似。压迫组的运动神经元密度在9周时显著降低（-20.3%），在25周时显著降低（-35.5%），但在1周或3周时没有降低。这个实用的模型恰当地重现了临床脊髓型颈椎病的特征，即在潜伏期后出现进行性运动障碍，且在症状出现之前存在隐匿性神经元丢失。
