Is Preexisting Cervical Degeneration a Risk Factor for Poor Prognosis in Whiplash-Associated Disorder?

INTRODUCTION

The term whiplash is used to describe the acceleration-deceleration mechanism of injury to the cervical spine (c-spine), most frequently caused by rear-end or side impact in motor vehicle accidents (MVAs).¹ Patients with whiplash injuries present with a variety of clinical and psychological manifestations which may include neck pain and stiffness, paresthesia, dizziness, deafness, tinnitus, depression, sleep disturbance, and posttraumatic stress disorder. This group of symptoms was collectively termed as whiplash-associated disorders (WADs) by the Quebec Task Force in 1995.¹

WAD is associated with a substantial socioeconomic burden worldwide, with a significant increase in incidence reported over the last 4 decades.² The incidence of WAD in Western Europe and North America is approximately 300 per 100 000 inhabitants each year.³ The annual economic cost of WAD is estimated to be around £3.1 billion in the United Kingdom, US$3.9 billion in the United States and A$950 million in Australia.^4–6 Additionally, rehabilitation of patients with WAD is associated with the highest financial cost among all musculoskeletal injuries.⁷

It has been hypothesized that the sudden impact in whiplash injuries causes the c-spine to develop an abnormal S-shaped curve due to simultaneous extension in the lower c-spine (LCS) and relative flexion in the upper c-spine (UCS).^8,9 Under physiological conditions, movement in the neck is initiated from the UCS to the LCS in an antegrade fashion. This pattern of movement is reversed in whiplash injuries, as the c-spine is forced to initiate movement from the LCS upwards.¹⁰ Clinical studies have suggested that the mechanism of whiplash injuries may result in damage to the intervertebral discs in the LCS and injury to the facet joints in both the UCS and LCS.^11–15 Furthermore, injury to the muscles of the c-spine due to lengthening contraction has also been implicated in WAD.¹⁶ Although WAD is largely a self-limiting condition, some patients may experience long-lasting and occasionally disabling symptoms.¹⁷ The recovery rate among patient with WAD is variable, with over 60% reporting symptoms at 3 months following the initial injury and 50% experiencing neck pain at 12 months.^17–19 The etiology behind the persistence of symptoms in WAD remains largely unknown. Previous studies have identified the severity of initial symptoms, psychological factors, and medicolegal involvement as predictors for poor prognosis in WAD.^17,20–22

Cervical spondylosis is reported as the most frequent radiological finding in WAD, yet its role as a predictive factor for nonrecovery in WAD remains unclear.²³ The terms cervical spondylosis and cervical degeneration are often used interchangeably. Cervical spondylosis is the most common disorder of the c-spine caused by age-related degeneration of the intervertebral discs and facet joints.²⁴ Although cervical spondylosis is seen in 95% of the population by the age of 65 years, the majority of these individuals remain asymptomatic.²⁵ Symptomatic patients may present with neck pain, cervical radiculopathy, and very rarely with cervical myelopathy.²⁶ In this review, we aim to summarize the current literature regarding the predictive value of cervical degeneration in the prognosis of patients with WAD.

METHODS

A comprehensive search of PubMed, MEDLINE, and Embase was conducted using the terms whiplash, whiplash associated disorder, WAD, cervical spondylosis, cervical degeneration, disc degeneration, and facet degeneration. We included all studies published in the English literature that investigated the association between preexisting cervical spondylosis (intervertebral disc or facet joint degeneration) and outcomes following whiplash injuries.

RESULTS

Nine studies were identified: 6 prospective cohort and 3 retrospective comparative studies.^27–35 These studies included 894 patients, with an age range from 16 to 76 years. The characteristics of the included studies are summarized in the Table.

DISCUSSION

This review highlights the presence of significant variability in the existing literature concerning WAD in terms of study methodology, the definition of cervical degeneration, and outcome measures. Disc degeneration was assessed with MRI in 3 studies, whereas only 1 study used CT scanning to assess facet joint arthrosis and disc degeneration.^27–30 All included studies published before 1995 used plain radiographs and did not explicitly define cervical spondylosis, using the terms degeneration, spondylosis, and osteoarthritis synonymously.^31–35 Furthermore, there was significant heterogeneity among the included studies in accounting for confounders such as smoking history, body mass index, occupation, level of education, and variables relating to MVAs.

The process of cervical degeneration begins with desiccation of the nucleus pulposus.³⁶ With increasing age, the nucleus pulposus loses its intradiscal pressure and hence its elasticity.³⁷ As the nucleus pulposus becomes more fibrous and smaller in size, more of the mechanical load is transferred to the annulus fibrosus leading to the development of clefts and fissures, resulting in disc bulging and loss of intervertebral height.³⁸ A kyphotic deformity of the c-spine may occur due to the initial loss of intervertebral height ventrally, which creates a positive-feedback cycle as more forces are applied to the ventral aspect of the vertebral bodies under physiological load.²⁴ These changes cause the posterior longitudinal ligaments and peripheral fibers of the annulus fibrosus to be dissected away from the vertebral endplates leading to degenerative intervertebral instability (degenerative spondylolisthesis).²⁴

Loss of intervertebral disc height leads to a greater load transfer to the uncovertebral and facet joints leading to facet joint hypertrophy and osteophyte formation. Facet joints (also known as zygapophyseal joints) are true synovial joints. Although facet joint degeneration is typically considered as a secondary process associated with disc degeneration, it may also occur independently.³⁹ Additionally, disc degeneration and intervertebral instability may also cause the ligamentum flavum to become hypertrophic.⁴⁰ The combination of these degenerative changes may result in the narrowing of the central spinal canal, lateral recess, and intervertebral foramina. Neck pain in cervical spondylosis is thought to arise from ligamentous laxity, disc herniation, and degenerative changes of the synovial facet joints.²⁴

Several cadaveric, biomechanical, and clinical studies have demonstrated facet joints as a source of pain in patients with chronic WAD.^10,12,41,42 During the pathological movement of the c-spine in the whiplash mechanism, the forceful impact of the inferior articular process of the upper vertebra against the superior articular process of the inferior vertebra may lead to damage to the articular cartilage, intra-articular hemorrhage, and rupture of the intra-articular meniscoids.¹⁰ During whiplash, the facet joints undergo compression that exceeds physiological limits followed by abnormally high strains in the facet capsule.¹² Simulated whiplash in animal studies has demonstrated that activation of the nociceptive pathway occurs secondary to stretch of the facet joint capsule.^41,42 Clinical studies using medial branch blocks as a diagnostic test found that the prevalence of pain originating from the zygapophysial joint in chronic WAD was about 50%.^13,43 Similarly, percutaneous radiofrequency neurotomy of the cervical zygapophyseal joints in symptomatic patients following whiplash injury showed successful outcome in 70% and pain relief (greater than 50%) lasting for a median of 263 days following treatment.⁴⁴ Furthermore, repeat neurotomy procedures are also proven to provide pain relief in recurrent cases.^45,46

Only 1 study (Rydman et al²⁷) evaluated both the intervertebral discs and facet joints in the context of cervical degeneration. The same study used CT scanning for the radiological assessment of the c-spine, which is shown to be superior to MRI and plain radiography in detecting facet joint degeneration and has relatively higher levels of interrater agreement in the assessment of facet joint degeneration.⁴⁷ This well-executed study demonstrated that moderate facet joint arthrosis was an independent risk factor for nonrecovery in WAD.²⁷ Additionally, 4 x-ray based studies also found that a significantly higher proportion of patients with preexisting cervical degeneration remained symptomatic following whiplash injuries, though these studies did not explicitly define cervical degeneration or spondylosis and did not differentiate between degenerative disc disease and facet joint degeneration.^31,33–35

Degenerative changes of the facet joint lead to alterations in its biomechanics. Thinning of the articular cartilage and hypermobility of the spinal segments result in increased laxity of the facet joint capsule.⁴⁸ The collagen fibers of the facet joint capsule may rupture while resisting the higher tensile stress due to hypermobility of the diseased spinal segment. These ruptured fibers are replaced by scar tissue, hence resulting in loss of their mechanical properties.⁴⁹ It is plausible that whiplash injuries to a c-spine with preexisting degenerative changes may result in increased axial and rotational movement, resulting in a more severe articular and capsular injury compared to a normal c-spine. The existing literature suggests that whiplash trauma in the degenerative c-spine may represent a catalyst for clinical manifestations of WAD, potentially leading to a higher risk of nonrecovery. Although Rydman et al²⁷ showed a significant association between moderate facet joint degeneration and nonrecovery in WAD, no such association was demonstrated for severe facet joint degeneration. This may be explained by the fact that in advanced degeneration, the vertebral bodies may undergo ankylosis, resulting in a paradoxical increase in c-spine stability. This phenomenon may also explain why some patients with moderate myelopathy experience improvement in symptoms during the advanced stages of cervical spondylosis.^24,50

Although cervical disc degeneration is considered to be an important source of neck pain, it affects 80% of the population over the age of 60 without causing any symptoms.⁵¹ Cervical discs are innervated by sinuvertebral nerves posteriorly, the vertebral nerve laterally, and sympathetic trunks anteriorly.^52,53 In disc degeneration, annular tears may stimulate nociceptors in the disc tissue. Disc degeneration also leads to elevated levels of proinflammatory cytokines secreted by the intervertebral discs that facilitate matrix degradation, chemokine production, and changes in cell phenotype.⁵⁴ These cytokines promote nerve growth factor expression, resulting in nerve fiber ingrowth into an otherwise aneural tissue.⁵⁴ Loss of structural integrity due to matrix degradation in the degenerative disc may also cause mechanical stimulation, which in turn could generate an exaggerated response to innocuous stimuli, resulting in peripheral sensitization.⁵⁵

It has been previously hypothesized that preexisting cervical disc degeneration may be associated with increased severity and duration of symptoms in WAD due to sensitization of nociceptors in the cervical disc.⁵⁶ In the present review, all 4 studies that investigated the impact of disc degeneration on prognosis in WAD failed to show a significant correlation between preexisting cervical disc degeneration and chronicity of WAD symptoms.^27–30 In another cross-sectional study conducted by Fujimura and Matsumoto⁵⁷ between 1993 and 1996, MRI of the c-spine was performed in 506 patients after whiplash injury. The authors found no statistically significant difference in disc space narrowing, reduced signal of the intervertebral disc, and posterior disc protrusion between WAD patients and healthy volunteers.⁵⁷ Their 10- and 20-year follow-up study showed that although progression of the cervical disc degeneration was seen on MRI in over 95% of patients, it was not associated with clinical symptoms of WAD. Fujimura and Matsumoto concluded that following whiplash injuries, the progression of cervical disc degeneration on MRI was attributable to physiological ageing, rather than posttraumatic sequelae.^58,59

CONCLUSION

This review highlights the paucity of good-quality studies on this topic and significant heterogeneity in the definition of cervical degeneration and study methodology. The importance of the facet joint in the pathogenesis of WAD is well established. We present moderate evidence to suggest that preexisting facet joint degeneration is a negative prognostic indicator for long-lasting symptoms in WAD. Conversely, preexisting disc degeneration is not associated with chronicity of WAD symptoms. We propose axial and rotational facet joint instability due to facet joint capsule rupture as a potential mechanism for nonrecovery in WAD in diseased spinal segments. The traumatic nature of this injury makes prospective study design problematic. Further longitudinal studies are needed to inform our knowledge of the long-term sequelae of WAD among patients with preexisting c-spine degeneration.