Sim E, Vaccaro A R, Berzlanovich A, Schwarz N, Sim B
Unfallkrankenhaus Klagenfurt, Klagenfurt, Austria.
Spine (Phila Pa 1976). 2001 Jun 15;26(12):1317-23. doi: 10.1097/00007632-200106150-00009.
In vitro anatomic study investigating the degree of soft tissue disruption required to produce a subaxial cervical unilateral facet dislocation.
To develop an understanding of the relative contributions to stability of the subaxial cervical soft tissues and to define an anatomic threshold of injury necessary to produce a unilateral cervical facet dislocation.
The literature at this time is unclear regarding the precise pathomechanics of a cervical unilateral facet dislocation and the required threshold of soft tissue injury necessary for its genesis. Published clinical reports do not make any specific reference to these factors or are unclear in their objectivity.
Two adjacent vertebra at a time in 10 fresh-frozen subaxial cervical spine specimens (C2-C3 to C6-C7) were transfixed in the coronal plane with 3.5-mm Schanz screws. A steady unilateral vertical distraction force resulting in lateral cervical flexion was applied to these screws as the surrounding cervical soft tissue structures were sequentially ablated. Four experimental models were developed, varying the order of soft tissue disruption.
The physiologic coupling of subaxial cervical unilateral distraction and rotation, because of the spatial orientation or inclination of the cervical facet joints, allowed the creation of a unilateral facet dislocation without an additional flexion moment. Disruption of the ipsilateral articular capsule, ligamentum flavum, and more than half of the anulus fibrosus was necessary for the genesis of a unilateral facet dislocation. Disruption of the supraspinous and interspinous ligaments was not necessary but appeared to facilitate or lessen the force required to dislocate a unilateral facet. Disruption of the anterior and posterior longitudinal ligaments and intertransverse ligaments was not necessary to create a unilateral facet dislocation.
This anatomic study further supports the theory that discontinuity of the anterior and posterior longitudinal ligaments is not necessary for a unilateral facet dislocation to occur. The ipsilateral facet capsule, anulus fibrosus, and ligamentum flavum appear to be the physical soft tissue restraints that need to be disrupted to produce a unilateral facet dislocation.
一项体外解剖学研究,旨在探究导致下颈椎单侧小关节脱位所需的软组织破坏程度。
了解下颈椎软组织对稳定性的相对贡献,并确定产生单侧颈椎小关节脱位所需的解剖学损伤阈值。
目前关于颈椎单侧小关节脱位的确切发病机制以及其发生所需的软组织损伤阈值,文献尚无定论。已发表的临床报告未对这些因素进行具体提及,或在客观性方面不明确。
在10个新鲜冷冻的下颈椎标本(C2 - C3至C6 - C7)中,每次用3.5毫米的斯氏针在冠状面固定相邻的两个椎体。在依次切除周围颈椎软组织结构时,对这些针施加稳定的单侧垂直牵张力,从而导致颈椎侧屈。建立了四种实验模型,改变软组织破坏的顺序。
由于颈椎小关节的空间取向或倾斜度,下颈椎单侧牵张和旋转的生理耦合使得在没有额外屈曲力矩的情况下产生单侧小关节脱位。同侧关节囊、黄韧带以及超过一半的纤维环破裂是产生单侧小关节脱位的必要条件。棘上韧带和棘间韧带破裂并非必要,但似乎有助于或减少单侧小关节脱位所需的力量。前纵韧带、后纵韧带和横突间韧带破裂并非产生单侧小关节脱位所必需。
这项解剖学研究进一步支持了以下理论,即前纵韧带和后纵韧带的连续性中断并非单侧小关节脱位发生的必要条件。同侧小关节囊、纤维环和黄韧带似乎是产生单侧小关节脱位时需要破坏的物理性软组织限制因素。