Spine: Volume 29(4) 15 February 2004 pp 390-397 Facet Joint Kinematics and Injury Mechanisms During Simulated Whiplash Pearson, Adam M. BA; Ivancic, Paul C. MPhil; Ito, Shigeki MD; Panjabi, Manohar M. PhD Abstract Study Design. Facet joint kinematics and capsular ligament strains were evaluated during simulated whiplash of whole cervical spine specimens with muscle force replication. Objectives. To describe facet joint kinematics, including facet joint compression and facet joint sliding, and quantify peak capsular ligament strain during simulated whiplash. Summary of Background Data. Clinical studies have implicated the facet joint as a source of chronic neck pain in whiplash patients. Prior in vivo and in vitro biomechanical studies have evaluated facet joint compression and excessive capsular ligament strain as potential injury mechanisms. No study has comprehensively evaluated facet joint compression, facet joint sliding, and capsular ligament strain at all cervical levels during multiple whiplash simulation accelerations. Methods. The whole cervical spine specimens with muscle force replication model and a bench-top trauma sled were used in an incremental trauma protocol to simulate whiplash of increasing severity. Peak facet joint compression (displacement of the upper facet surface towards the lower facet surface), facet joint sliding (displacement of the upper facet surface along the lower facet surface), and capsular ligament strains were calculated and compared to the physiologic limits determined during intact flexibility testing. Results. Peak facet joint compression was greatest at C4-C5, reaching a maximum of 2.6 mm during the 5 g simulation. Increases over physiologic limits (P < 0.05) were initially observed during the 3.5 g simulation. In general, peak facet joint sliding and capsular ligament strains were largest in the lower cervical spine and increased with impact acceleration. Capsular ligament strain reached a maximum of 39.9% at C6-C7 during the 8 g simulation. Conclusions. Facet joint components may be at risk for injury due to facet joint compression during rear-impact accelerations of 3.5 g and above. Capsular ligaments are at risk for injury at higher accelerations. Despite clinical and biomechanical research efforts, the underlying mechanisms causing whiplash-associated disorders remain unknown. 1 A variety of anatomic structures have been identified as potential injury sites without the necessary supporting clinical or biomechanical evidence. 2 Establishing the specific anatomic injury sites and acceleration thresholds would allow for improved diagnosis, treatment, and prevention of whiplash-associated disorders. Clinical and pathologic investigations have targeted the facet joints (FJs) as possible sources of pain in whiplash patients. The only clinical evidence comes from a series of studies that used nerve block and radiofrequency ablation of FJ afferents to successfully relieve pain. 3-6 Autopsy studies of subjects with soft tissue neck injuries have revealed FJ hemarthroses, articular cartilage damage, synovial fold displacement, and capsular ligament (CL) tears. 7,8 In a whiplash simulation using cadavers, FJ diastases and CL tears were found in two of four specimens subjected to low-speed rear impacts. 9 Thus, sufficient clinical and pathologic evidence exists to support the hypothesis of possible FJ injury during whiplash. To explain the clinical observation of facet pain, two distinct FJ injury mechanisms have been hypothesized: excessive compression of the FJ articulation and CL strain beyond the physiologic limit. An in vivo study demonstrated that the C5-C6 intervertebral center of rotation was dynamically shifted superiorly during simulated whiplash impacts, implying that the facet articular surfaces were forcefully compressed during intervertebral extension. 10 Facet joint compression was also demonstrated directly in two cadaver studies, giving further support to the impingement injury mechanism hypothesis. 11,12 These investigators hypothesized that FJ compression could damage synovial folds that contain nociceptive nerve endings and potentially lead to facet pain. 13,14 Thus, both in vivo and in vitro work support the FJ compression injury mechanism hypothesis. In vitro biomechanical studies have also identified excessive CL strain during whiplash as a potential injury mechanism. Two studies using quasistatic loading of cervical FJs to simulate whiplash-type loading demonstrated that mean CL strains were below the subfailure thresholds, though isolated cases of CL strain in excess of the subfailure threshold were observed. 15,16 Direct measurement of CL elongation during simulated whiplash, using specialized transducers placed across the FJ in a whole cervical spine (WCS) model, showed maximum strains of less than 40% in a CL fiber. 17 During simulated whiplash of one cadaver, hypothetical CLs were constructed and tracked throughout the simulation, and a maximum strain of 51% at C5-C6 was reported. 18 Although prior studies have evaluated the two FJ injury mechanism hypotheses separately, none have comprehensively analyzed complete cervical spine FJ kinematics at various impact accelerations. In order to develop a more thorough understanding of FJ injury mechanisms in whiplash, the goals of this study were to: 1) quantify peak FJ compression, FJ sliding, and CL strain; 2) determine the acceleration thresholds at which these parameters exceed the physiologic limits; and 3) evaluate the two injury mechanisms hypotheses.