Regional blood flow in the chronically compressed rat spinal cord

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。为了研究病理生理学，我们开发了一个简单的实验模型再现的过程。在大鼠中，通过显微外科手术在C5-C6椎板下植入一片膨胀聚合物薄片。在对照组中，立即移除聚合物片材。术后25周监测运动功能的变化，通过连接到旋转笼的里程计测量自愿运动活动，并通过在旋转跑步机上运动的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体视学计数。在压迫组中，强迫跑步能力在17周的潜伏期后恶化，此后逐渐恶化。在对照组中，它在25周内保持不变。两组志愿运动的过程是相似的。压迫组运动神经元密度在9周（-20.3%）和25周（-35.5%）明显下降，但在1周或3周内则无明显下降。这个实用的模型正确地再现了临床脊髓型颈椎病的特征，在潜伏期后进行性运动障碍和潜伏性神经元丢失之前的症状。这些变化可能是由放射自显影术测量的脊髓血流量减少引起的

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. These changes may be caused by decreased spinal cord blood flow measured by autoradiography