Ivancic Paul C, Pearson Adam M, Tominaga Yasuhiro, Simpson Andrew K, Yue James J, Panjabi Manohar M
Biomechanics Research Laboratory, Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, CT 06520-8071, USA.
Spine (Phila Pa 1976). 2007 Oct 15;32(22):2467-73. doi: 10.1097/BRS.0b013e3181573b67.
An in vitro biomechanical study.
The objectives were to: quantify dynamic canal pinch diameter (CPD) narrowing during simulated bilateral facet dislocation of a cervical functional spinal unit model with muscle force replication, determine if peak dynamic CPD narrowing exceeded that observed post-trauma, and evaluate dynamic cord compression.
Previous biomechanical models are limited to quasi-static loading or manual ligament transection. No studies have comprehensively analyzed dynamic CPD narrowing during simulated dislocation.
Bilateral facet dislocation was simulated using 10 cervical functional spinal units (C3-C4: n = 4; C5-C6: n = 3; C7-T1: n = 3) with muscle force replication by frontal impact of the lower vertebra. Rigid body transformation of kinematic data recorded optically was used to compute the CPD in neutral posture (before dislocation), during dynamic impact (peak during dislocation), and post-impact (flexion rotation = 0(0) degrees ). Peak dynamic impact and post-impact CPD narrowing were statistically compared.
Average peak dynamic impact CPD narrowing significantly exceeded (P < 0.05) post-impact narrowing and occurred as early as 71.0 ms following impact. The greatest dynamic impact narrowing of 7.2 mm was observed at C3-C4, followed by 6.4 mm at C5-C6, and 5.1 mm at C7-T1, with average occurrence times ranging between 71.0 ms at C7-T1 and 97.0 ms at C5-C6.
Extrapolation of the present results indicated dynamic spinal cord compression of up to 88% in those with stenotic canals and 35% in those with normal canal diameters. These results are consistent with the wide range of neurologic injury severity observed clinically due to bilateral facet dislocation.
一项体外生物力学研究。
目的是：在具有肌肉力复制功能的颈椎功能脊柱单元模型模拟双侧小关节脱位过程中，量化动态椎管夹捏直径（CPD）变窄情况；确定动态CPD变窄峰值是否超过创伤后观察到的值；并评估动态脊髓压迫情况。
先前的生物力学模型仅限于准静态加载或手动韧带切断。尚无研究全面分析模拟脱位过程中的动态CPD变窄情况。
使用10个颈椎功能脊柱单元（C3 - C4：n = 4；C5 - C6：n = 3；C7 - T1：n = 3）模拟双侧小关节脱位，通过下椎体的正面撞击来复制肌肉力。利用光学记录的运动学数据进行刚体变换，以计算中立姿势（脱位前）、动态撞击过程中（脱位峰值时）和撞击后（屈曲旋转 = 0（0）度）的CPD。对动态撞击峰值和撞击后CPD变窄情况进行统计学比较。
平均动态撞击峰值CPD变窄显著超过（P < 0.05）撞击后变窄，且最早在撞击后71.0毫秒出现。在C3 - C4观察到最大动态撞击变窄为7.2毫米，其次在C5 - C6为6.4毫米，在C7 - T1为5.1毫米，平均出现时间在C7 - T1为71.0毫秒至C5 - C6为97.0毫秒之间。
根据目前结果推断，狭窄椎管者动态脊髓压迫可达88%，正常椎管直径者为35%。这些结果与临床上因双侧小关节脱位观察到的广泛神经损伤严重程度一致。
