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颈椎后路减压术后 C5 瘫痪的实验大鼠模型。

An Experimental Rat Model of C5 Palsy Following Posterior Decompression Surgery of the Cervical Spine.

机构信息

Department of Orthopedic Surgery, Osaka Medical and Pharmaceutical University, Osaka, Japan.

出版信息

Spine (Phila Pa 1976). 2022 Feb 1;47(3):E124-E131. doi: 10.1097/BRS.0000000000004195.

Abstract

STUDY DESIGN

Basic in vivo research.

OBJECTIVES

The aim of this study was to establish an animal model that is appropriate for analyzing the mechanisms of C5 palsy (C5P) and to clarify the structural and functional alterations of cervical roots following posterior decompression.

SUMMARY OF BACKGROUND DATA

Although C5P is one of the major complications of cervical surgery, the exact pathogenesis of C5P remains unclear partly because of the lack of an appropriate animal model. Tethering of the cervical roots due to posterior cord shift following posterior decompression is thought to be one of the possible factors that cause C5P.

METHODS

Twenty-eight Sprague-Dawley rats were divided into Group L (cervical laminectomy, N = 18) or Group S (sham surgery, N = 10) and examined up to postoperative day 14 (PO14). Posterior cord shift and the length of the anterior rootlets were quantified by computed tomography-myelogram images. Motor evoked potential (MEP) of the deltoid (C5, 6 innervated) and triceps brachii (C7-T1 innervated), mechanical allodynia, and grip strength of the forepaw (C7-T1 regulated) were measured.

RESULTS

All anterior rootlets were elongated as the cord gradually shifted posteriorly postoperatively. The elongation rate of the C6 anterior rootlets was the highest (142% at PO14). The MEP latency of the deltoid was significantly delayed throughout all postoperative time points. However, significant delay in the latency of the triceps brachii was observed only on postoperative day 10. The withdrawal threshold of the forepaw did not change; grip strength of the forelimb decreased at PO14.

CONCLUSION

This model was thought to be appropriate for analyzing the pathogenesis of C5P since our findings were comparable to the clinical course of C5P subsequent to posterior cervical decompression. Although a future study for clarifying histological and molecular alterations will be needed, tethering of the anterior rootlets due to posterior cord shift was suggested to be a probable mechanism causing C5P.Level of Evidence: 5.

摘要

研究设计

基础体内研究。

目的

本研究旨在建立一种适合分析 C5 麻痹(C5P)机制的动物模型,并阐明颈椎后路减压后神经根的结构和功能变化。

背景资料概要

尽管 C5P 是颈椎手术的主要并发症之一,但由于缺乏合适的动物模型,C5P 的确切发病机制仍不清楚。颈椎后路减压后脊髓后移导致神经根被牵拉,被认为是导致 C5P 的可能因素之一。

方法

28 只 Sprague-Dawley 大鼠分为 L 组(颈椎椎板切除术,N=18)或 S 组(假手术,N=10),并在术后 14 天(PO14)前进行检查。通过 CT 脊髓造影图像定量测量脊髓后移和前根长度。测量三角肌(C5、6 支配)和肱三头肌(C7-T1 支配)的运动诱发电位(MEP)、机械性痛觉过敏和前肢握力(C7-T1 调节)。

结果

所有前根均随脊髓逐渐向后移位而延长。C6 前根的伸长率最高(术后 14 天为 142%)。三角肌的 MEP 潜伏期在所有术后时间点均显著延迟。然而,肱三头肌的潜伏期仅在术后第 10 天出现显著延迟。前肢的退缩阈值没有变化;术后第 14 天前肢握力下降。

结论

由于我们的发现与颈椎后路减压后 C5P 的临床过程相当,因此认为该模型适合分析 C5P 的发病机制。尽管需要进一步研究以阐明组织学和分子改变,但脊髓后移导致前根的牵拉被认为是导致 C5P 的可能机制。

证据水平

5 级。

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