Whiplash causes increased laxity of cervical capsular ligament
Introduction
Whiplash injuries of the neck, caused by relative acceleration between the head and thorax during motor vehicle collisions, produce acute and chronic neck pain, headache, dizziness, vertigo, and parasthesias in the upper extremities (Barnsley et al., 1994, Spitzer et al., 1995, Sterner and Gerdle, 2004). MRI and autopsy studies have correlated chronic symptoms with injuries to the cervical discs, ligaments, and facet joints in whiplash patients (Jonsson et al., 1991, Kaale et al., 2005a, Kaale et al., 2005b, Krakenes and Kaale, 2006, Pettersson et al., 1997). Previous clinical studies have targeted the cervical facet joint and capsule, including the capsular ligament (CL), as sources of chronic pain in whiplash patients (Barnsley et al., 1995, Lord et al., 1996a). These studies administered blockage of the facet joint afferents, including the CL nerves, in whiplash patients. Results demonstrated pain relief in up to 60% of the patients. Single or cumulative micro-trauma due to overstretching of CLs causing subfailure injuries and increased ligament laxity have been hypothesized to injure embedded ligament mechanoreceptors (Panjabi, 2006). The effect of injured ligament mechanoreceptors on spine stability has not been studied. However, in vivo animal models have demonstrated that stimulation of spinal ligaments initiated activity of spinal musculature (Indahl et al., 1997, Solomonow et al., 2002, Solomonow et al., 1998). Corrupted signals from the injured mechanoreceptors may potentially elicit abnormal muscle response patterns causing excessive facet loading and CL strains, further increasing the CL laxity and injury and preventing or delaying ligament healing.
Previous in vitro biomechanical studies have investigated potential neck ligament injuries due to whiplash (Panjabi et al., 2006, Pearson et al., 2004, Stemper et al., 2005, Tominaga et al., 2006). Tominaga et al. (2006) compared the high-speed mechanical properties of cervical bone-ligament-bone preparations between whiplash-exposed and control cervical spines. They found that the average failure force and average energy absorption capacity of the whiplash-exposed ligaments were significantly less than those of the control ligaments. The effect of whiplash on ligament laxity was not investigated. Others have documented potentially injurious CL strains and abnormal facet kinematics due to simulated whiplash loading (Pearson et al., 2004, Stemper et al., 2005). Although implied, neither study documented actual injury or increased laxity of CLs due to whiplash. Lastly, Panjabi et al. (2006) applied quasi-static physiological loading to cervical spine specimens prior to and following simulated rear impacts and documented injuries at the middle and lower cervical spine and increased injury risk due to rotated head posture at the time of impact, as compared to forward facing. Injuries to specific ligaments were not identified.
In vivo animal studies have investigated the relation between painful chronic symptoms and injurious CL strains (Lee et al., 2004, Lee et al., 2006). Using a rat model, Lee et al. (2004) determined the CL strain threshold for behavioral hypersensitivity as measured by mechanical allodynia up to 2 weeks following application of injurious CL strain. This CL strain injury threshold was used to demonstrate that the CL mechanical properties at failure differed significantly from those at the onset of subfailure strain injury (Lee et al., 2006). Others have used a goat model to measure and correlate CL nerve root activity, load, and strain during CL elongation (Chen et al., 2005, Lu et al., 2005a, Lu et al., 2005b). Nonetheless, these aforementioned animal studies have limitations. The tensile loading used to produce the CL strain does not fully represent the complex neck loading experienced by those involved in automobile collisions (Ivancic et al., 2006). Behavioral hypersensitivity was measured for up to only 2 weeks and these animal results have yet to be correlated with chronic symptoms in whiplash patients.
To our knowledge, no previous clinical or biomechanical studies have identified CL injuries due to whiplash as determined by increased ligament laxity. These data may aid understanding of the mechanism causing painful chronic symptoms in whiplash patients. Our goal was to determine whether whiplash caused increased CL laxity by applying quasi-static loading to whiplash-exposed and control facet-CL-facet preparations.
Section snippets
Specimen preparation
Facet-CL-facet specimens were prepared from 12 osteoligamentous whole cervical spines (6 whiplash-exposed: average age of 70.8 years, range, 52–84 years; 6 control: average age of 80.6 years, range, 71–92 years) (Tominaga et al., 2006). There were four male and two female donors in each group. The whiplash-exposed spines had been previously rear impacted using experimental methodology described in detail elsewhere (Ivancic et al., 2005). Briefly, this protocol entailed mounting of the occiput
Results
The force–elongation curve is shown for each whiplash-exposed CL (Fig. 2a) and control CL (Fig. 2b) along with the average curves with standard deviations (Fig. 2c). As expected, the average force–elongation curves were nonlinear, with greater flexibility at low forces and increasing stiffness at higher forces. Greater flexibility was generally observed in the whiplash-exposed CLs, as compared to the control CLs, particularly at low forces. The difference between the average elongation of the
Discussion
Whiplash causes soft tissue neck injuries that result in substantial societal costs (Spitzer et al., 1995). There is controversy as to which anatomical components are injured during whiplash and even greater debate regarding the specific cause and source of the chronic symptoms reported by whiplash patients. These chronic symptoms include neck pain, headache, dizziness, vertigo, and parasthesias in the upper extremities. Previous clinical and biomechanical studies have identified the cervical
Conclusions
This well-controlled biomechanical study, utilizing quasi-static, non-destructive tensile loading of whiplash-exposed and control facet-CL-facet specimens, documented injury in the form of significant increases in the laxity of whiplash-exposed CLs, as compared to controls. Our results are consistent with several clinical studies that have reported pain relief in whiplash patients following nerve block and radiofrequency ablation of facet joint afferents (Lord et al., 1995, Lord et al., 1996b).
Conflict of Interest Statement
We declare no conflicts of interest.
Acknowledgement
This research was supported by NIH Grant 1 RO1 AR45452 1A2.
References (46)
- et al.
Whiplash injury
Pain
(1994) - et al.
Tensile cervical facet capsule ligament mechanics: failure and subfailure responses in the rat
J. Biomech.
(2006) - et al.
Neurophysiological and biomechanical characterization of goat cervical facet joint capsules
J. Orthop. Res.
(2005) - et al.
Quantitative posturography in altered sensory conditions: a way to assess balance instability in patients with chronic whiplash injury
Arch. Phys. Med. Rehabil.
(2004) - et al.
Neuromuscular disorders associated with static lumbar flexion: a feline model
J. Electromyogr. Kinesiol.
(2002) - et al.
Biomechanical analyses of whiplash injuries using an experimental model
Accid. Anal. Prev.
(2002) - et al.
3D kinematic analysis and clinical evaluation of neck movements in patients with whiplash injury
Cephalalgia
(2002) - et al.
The prevalence of chronic cervical zygapophysial joint pain after whiplash
Spine
(1995) - et al.
Neck motion evaluation after whiplash: a radiographic and kinematic protocol
Ital. J. Anat. Embryol.
(2000) - et al.
Recording of neural activity from goat cervical facet joint capsule using custom-designed miniature electrodes
Spine
(2005)