EXPERIMENTAL CHRONIC COMPRESSIVE CERVICAL MYELOPATHY
EXPERIMENTAL CHRONIC COMPRESSIVE CERVICAL MYELOPATHY
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DOI：
10.3171/jns.1993.79.4.0550
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发表时间：
1993-10-01
影响因子：
4.1
通讯作者：
MIDDLETON, TH
中科院分区：
文献类型：
--
作者：
ALMEFTY, O;HARKEY, HL;MIDDLETON, TH
提出了模拟颈椎病及其迟发性进行性脊髓病结果的犬模型。该模型可以控制压迫、持续评估神经缺陷，并使用诊断图像、频繁的电生理测试、局部血流测量和死后组织学检查进行评估。通过在后面放置聚四氟乙烯垫圈和在前面放置聚四氟乙烯螺钉，在 14 只狗身上实现了亚临床颈髓压迫，产生平均 29% 的椎管狭窄。四只接受假手术的狗被指定为对照。 12 只接受压迫的动物出现了迟发性和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。使用氢气清除法进行的脊髓血流研究表明，压迫后血流量立即显着短暂增加，而处死前则减少。体感诱发电位研究表明在压缩期间逐渐恶化。磁共振图像显示髓内变化。组织学研究显示灰质内绝大多数存在异常，包括血管形态的变化、大运动神经元的丧失、坏死和空洞。轴突变性和明显脱髓鞘很少见。最深刻的形态变化发生在受压最大的部位。有人提出，由于受损椎管内储备空间的丧失，在颈部伸展期间会发生微循环的暂时停止。这种微循环障碍主要发生在脊髓的分水岭区域，主要影响高度脆弱的前角细胞，导致神经元死亡、坏死，并最终在背角和前角交界处形成空洞。该假设的其他支持证据来自文献。
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.