al-Mefty O, Harkey H L, Marawi I, Haines D E, Peeler D F, Wilner H I, Smith R R, Holaday H R, Haining J L, Russell W F
Department of Neurosurgery, Loyola University Medical Center, Maywood, Illinois.
J Neurosurg. 1993 Oct;79(4):550-61. doi: 10.3171/jns.1993.79.4.0550.
A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months. Spinal cord blood flow studies using the hydrogen clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature.
本文介绍了一种模拟颈椎病及其导致的迟发性进行性脊髓病的犬类模型。该模型能够控制压迫程度，持续评估神经功能缺损，并通过诊断性影像、频繁的电生理测试、局部血流测量以及死后组织学检查进行评估。通过在14只犬的后方放置一个聚四氟乙烯垫圈、前方放置一个聚四氟乙烯螺钉，实现了亚临床型颈髓压迫，平均造成椎管狭窄29%。4只接受假手术的犬被指定为对照组。12只接受压迫的动物出现了迟发性进行性脊髓病的临床症状，脊髓病发病的平均潜伏期为7个月。采用氢清除法进行的脊髓血流研究显示，压迫后立即出现血流显著短暂增加，处死前血流减少。体感诱发电位研究表明，在压迫期间病情逐渐恶化。磁共振成像显示脊髓内有变化。组织学研究显示，绝大多数异常出现在灰质内，包括血管形态改变、大型运动神经元丧失、坏死和空洞形成。很少见到轴突退变和明显的脱髓鞘。最严重的形态学变化发生在压迫最严重的部位。有人提出，由于受损椎管内储备空间丧失，颈部伸展时会发生微循环瞬间停滞。这种微循环障碍在脊髓的分水岭区域最为明显，主要影响极易受损的前角细胞，导致神经元死亡、坏死，最终在背角和前角交界处形成空洞。该假说的其他支持性证据来自文献。
