Elsevier

Clinical Biomechanics

Volume 23, Issue 2, February 2008, Pages 159-165
Clinical Biomechanics

Whiplash causes increased laxity of cervical capsular ligament

https://doi.org/10.1016/j.clinbiomech.2007.09.003Get rights and content

Abstract

Background

Previous clinical studies have identified the cervical facet joint, including the capsular ligaments, as sources of pain in whiplash patients. The goal of this study was to determine whether whiplash caused increased capsular ligament laxity by applying quasi-static loading to whiplash-exposed and control capsular ligaments.

Methods

A total of 66 capsular ligament specimens (C2/3 to C7/T1) were prepared from 12 cervical spines (6 whiplash-exposed and 6 control). The whiplash-exposed spines had been previously rear impacted at a maximum peak T1 horizontal acceleration of 8 g. Capsular ligaments were elongated at 1 mm/s in increments of 0.05 mm until a tensile force of 5 N was achieved and subsequently returned to neutral position. Four pre-conditioning cycles were performed and data from the load phase of the fifth cycle were used for subsequent analyses. Ligament elongation was computed at tensile forces of 0, 0.25, 0.5, 0.75, 1.0, 2.5, and 5.0 N. Two factor, non-repeated measures ANOVA (P < 0.05) was performed to determine significant differences in the average ligament elongation at tensile forces of 0 and 5 N between the whiplash-exposed and control groups and between spinal levels.

Findings

Average elongation of the whiplash-exposed capsular ligaments was significantly greater than that of the control ligaments at tensile forces of 0 and 5 N. No significant differences between spinal levels were observed.

Interpretation

Capsular ligament injuries, in the form of increased laxity, may be one component perpetuating chronic pain and clinical instability in whiplash patients.

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.

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