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大鼠慢性颈脊髓压迫模型的建立:神经行为学及影像学和病理学改变。

Development of a chronic cervical cord compression model in rat: changes in the neurological behaviors and radiological and pathological findings.

机构信息

Faculty of Medical Sciences, The University of Fukui , Department of Orthopaedics and Rehabilitation Medicine, Fukui, Japan.

出版信息

J Neurotrauma. 2011 Mar;28(3):459-67. doi: 10.1089/neu.2010.1610.

DOI:10.1089/neu.2010.1610
PMID:21294701
Abstract

Cervical myelopathy is caused by chronic segmental compression of the spinal cord because of degenerative changes of the spine. However, the exact mechanisms of chronic cervical cord compression are not fully understood. The purpose of this study was to validate a new animal model of chronic cervical cord compression capable of reproducing the clinical course without laminectomy in rats. A polyethylene line attached to a plastic plate was fastened with three turns around the vertebral body of C4 in 1-month-old rats. After surgery, the polyethylene line grows deeper into the dorsal wall of the spinal canal along with the growth of the spinal canal and vertebral body, producing a gradual compression of the spinal cord. The results show that this cervical canal stenosis (CCS) model in rats caused motor deficits and sensory disturbances 9 months after initiating CCS; however, no clinical manifestations took place until 6 months. The intramedullary high-intensity area on T2-weighted images was observed in 70% of the CCS model rats at 12 months after initiating CCS. In histological sections, the spinal cord was compressed along the entire circumference at 12 months after initiating CCS. The number of ventral neurons was decreased, and the white matter showed wallerian degeneration. This model might reproduce characteristic features of clinical chronic cervical cord compression, including progressive motor and sensory disturbances after a latency period and insidious neuronal loss, and represents chronic compression of the cervical spinal cord in humans.

摘要

脊髓型颈椎病是由于脊柱退行性改变导致的脊髓慢性节段性压迫引起的。然而,慢性颈髓压迫的确切机制尚未完全明了。本研究旨在验证一种新的慢性颈髓压迫动物模型,该模型能够在不进行椎板切除术的情况下在大鼠中重现临床病程。在 1 月龄大鼠的 C4 椎体上,用聚乙烯线将塑料板固定 3 圈。手术后,聚乙烯线随着椎管和椎体的生长而深入椎管背侧壁,逐渐压迫脊髓。结果表明,该大鼠颈椎管狭窄(CCS)模型在引发 CCS 后 9 个月引起运动功能障碍和感觉障碍;然而,直到 6 个月后才出现临床症状。在引发 CCS 后 12 个月,70%的 CCS 模型大鼠的 T2 加权图像上出现了高信号强度区。在组织学切片中,在引发 CCS 后 12 个月,脊髓沿整个圆周受到压迫。腹侧神经元数量减少,白质出现沃勒变性。该模型可能复制出临床慢性颈髓压迫的特征性表现,包括潜伏期后进行性运动和感觉障碍以及隐匿性神经元丢失,并代表了人类慢性颈脊髓压迫。

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