Whiplash prognosis: what is the role of pathology?

Physiotherapist Chris Worsfold talks to Spinal Surgery News about identifying and managing risk factors for poor recovery following whiplash injury

There are scores of animal, human cadaver and computer simulation studies that have identified the cervical spine facet joints [1,2], intervertebral discs and ligaments [3–5], muscles [6–8], dorsal root ganglia [9,10] and vertebral artery [11,12] as being susceptible to injury during the whiplash mechanism, with the majority of the experimental evidence implicating the facet joint – and most probably the facet joint capsule – as a primary cause of symptoms following whiplash injury. Clinical studies demonstrating significant pain relief in chronic neck pain cohorts following nerve blocks or radiofrequency neurotomy lend support to this view [13]. The experimental evidence is compelling for facet joint injury following whiplash.

In vivo studies of pathology following whiplash injury are historically poorly represented in the literature [14], and they have not been without their critics [15]. In a high-quality study, Freeman and colleagues [16] demonstrated “substantial neuroradiographic differences” in the frequency of cerebellar tonsillar ectopia (CTE or Chiari malformation) between 1195 subjects with neck pain, with and without a recent history of motor vehicle-related crash trauma. Indeed, the authors concluded by criticising prior research on psychosocial causes of chronic pain following whiplash for failing to account for a possible neuropathologic basis for the symptoms. A recent investigation within 48 hours of the injury and using a turbo STIR sequence on a sample of subjects – a proportion demonstrating no objective signs (i.e. Quebec Grade I) – documented occult fractures and bone contusions of vertebral bodies and strains, tears, haematomas and perimuscular fluid in muscle [17] (see Table 1).

 

 

 

 

 

 

 

 

 

Muscle damage has also been demonstrated in the acute stage of injury using diagnostic ultrasound scanning [18] (Figure 1) and there has been anecdotal surgical evidence of muscle rupture, facet joint capsule rupture and ligament sprain [19].

 

 

 

 

 

 

 

 

 

 

 

In the absence of Chiari-type symptoms (a history of whiplash injury and persisting suboccipital headache in combination with headache worsened by cough or bilateral sensory or motor deficits in the upper extremities [16]), many people with high levels of pain and disability will have no precise injury identified that can be linked to the symptoms using currently available technology. Indeed, the majority of the injuries arising from cadaver and animal models cannot be identified by clinically available diagnostic modalities. The prospect of imaging devices with higher resolution may provide a link between tissue injury and outcome in the future; however, for the present time, we must rely on the clinical history and examination to provide a window onto prognosis.

Prognosis: history and clinical examination

Pre-injury status

The prognostic role of pre-injury neck pain remains unclear [20] and those reviews that have demonstrated an effect for the presence of pre-injury neck pain have described it as “small but significant” [21]. The effect size for history of headache suggests no significant risk of persistent problems [21]. Carroll and co-workers [20] found “no scientifically admissible” studies that addressed the impact of disc degeneration on recovery from whiplash injury, and a more recent one-year prospective study demonstrated that pre-existing degeneration on magnetic resonance imaging (MRI) was not associated with prognosis [22].

 

Demographic variables

The evidence varies on the role of age and gender as a prognostic factor for recovery following whiplash injury; however, in those reviews that have identified older age and gender as prognostic for poor recovery, the effects are negligible to modest [20,21] with the prognosis for females being slightly worse (female OR = 1.64) [21]. Having less than post-secondary education has also been associated with poor prognosis. [21]

 

Crash-related factors

Crash-related factors include collision direction, use and type of head restraints, speed of impact, awareness of collision, position in seat and whether the person’s head was turned at the time of the accident. Although experimental data has suggested that having a rotated neck position at the time of impact doubles the strain through the facet capsule [23,24], clinically orientated systematic reviews have identified few crash-related factors that have predictive utility.

Carroll et al. [20] concluded there was no association between crash-related factors and outcome, except for a modest effect for those injured while driving a vehicle fitted with a tow bar having a poorer prognosis. Not wearing a seat belt at the time of the collision appears to lead to a two-fold increase in the risk of developing whiplash-related pain and disability at a 12-month follow up [25]. Sterling makes the interesting point that this factor (“I was not wearing my seatbelt”) is likely to be under-reported in jurisdictions where compulsory seat belt use is legislated, so the risk associated with this factor may be even higher [26]. More recently, Walton et al. [21], utilising rigorous inclusion criteria in a systematic review and meta-analysis, concluded that parameters of the collision show no predictive ability in identifying risk of poor outcome. Variables with strong evidence of no effect include: “unprepared for collision”, no head restraint in use and vehicle stationary when hit [25].

In an attempt to explain the lack of evidence, some authors have noted that crash-related factors rely heavily upon the self-report of the claimant – making them highly susceptible to both recall bias and desirability bias (secondary motive influencing reports) [21].

 

Presenting signs and symptoms

The history

Initial post-injury pain intensity, number and severity of injury-related symptoms and the presence of radicular signs or symptoms appear to be substantial predictors of recovery [20,21,25]. Walton et al. [21] found a six-fold increase in risk of persistent pain or disability at follow-up in those complaining of high neck pain intensity (defined as a score of 5.5/10 on a visual analogue scale or VAS). Self-reported headache at inception is associated with a significant increase in the risk of reporting persistent problems at follow-up, and reports of low back pain also demonstrate a small but significant risk for persistent problems [21]. In one cohort, 30 per cent of acute whiplash patients presented with a neuropathic pain component, as measured by the Leeds Assessment of Neuropathic Symptoms and Signs pain scale (S-LANSS) [27] – a score of ≥12 on this scale predicted poor recovery.

The most commonly used measure of disability in whiplash is the Neck Disability Index (NDI) [28]. The NDI is a ten-item questionnaire that allows scoring of activities of daily living pertaining to the neck region from 0 to 5. The scores are summed to give a total of 50 or multiplied by 2 to give a percentage score. Scores on this instrument are predictive of poor recovery: 30 per cent or higher in one meta-analysis [21]. In a more recent study designed to establish a clinical prediction rule for use following whiplash injury, a score of ≥40 per cent predicted chronic moderate/severe disability, while a score of ≤32 per cent predicted recovery [29]. The latter study also included age and a measure of post-traumatic stress response in the clinical prediction rule, and this is discussed below.

Dizziness appears to be a common yet overlooked symptom following whiplash injury. In one cohort of whiplash injuries, as many as 75 per cent of subjects complained of dizziness [30]. The unsteadiness that can occur after whiplash injury is hypothesised to arise from injury and disruption to the deep muscle spindles of the cervical spine and the mechanoreceptors of the facet joint capsule. One theory suggests that distortion of the afferent signals from the muscle spindles leads to a conflict of information in the dense anatomical reflex connections between the muscle spindles, the eyes (cervico-ocular reflex) and the vestibular system (vestibulo-ocular reflex) [31]. Indeed, there is increasing objective evidence of disturbances to smooth pursuit eye movement control, proprioception of the head and neck, and postural instability following whiplash injury [32–34]; however, these sensorimotor signs and symptoms, including smooth pursuit eye movement tests, do not appear to be useful as predictive factors after injury [35].

 

The physical examination

Cervical range of motion has been found to have no significant effect on recovery [36], with a recent meta-analysis confirming these findings [25] despite its continued use as one of the sole ‘objective’ prognostic measures in whiplash injury assessments.

Widespread sensory change has been identified in a sub-group of 20 per cent of whiplash injured subjects [37]. This manifests as reduced pressure pain thresholds (PPT – the threshold at which pressure becomes pain) at areas removed from the site of injury, and a heightened sensitivity to a cold stimulus, both indicative of augmented central pain processing that has also been identified in fibromyalgia.

In one systematic review, cold hyperalgesia was found to be associated with a poorer outcome [36]. Walton et al. [38] have demonstrated that PPTs at a site over the anterior shin (tibialis anterior muscle) significantly predicted the variance in short-term outcome in individuals with acute whiplash injury. The authors concluded that PPTs represent a promising addition to the clinical assessment of traumatic neck pain.

 

The psychological

Carroll et al. found that psychological factors are prognostic of recovery in whiplash injury – with passive coping, helplessness, fear of movement, catastrophising and anxiety all predicting slower recovery [20]. Catastrophising appears to have a significant effect on recovery, while depressive symptoms appear to play no role in outcome [25]. Fear of movement appears to contribute to the relationship between pain and disability after whiplash injury [39]. Lower expectations of recovery have been shown to predict poor recovery [40].

Williamson et al.’s systematic review of psychological risk factors [41] concluded that decreased self-efficacy (“confidence to perform activities despite pain”) and a post-traumatic stress reaction are predictive of poor recovery but identified no other prognostic psychological factors. Sterling et al. have suggested that a score of ≥26 on the Impact of Event Scale questionnaire (IES), a measure of post-traumatic reaction, indicates risk of poor recovery [42]. In one study utilising a group-based trajectory model at three months post-whiplash, 22 per cent of participants met the criteria for a probable PTSD diagnosis, with this percentage decreasing to 17 per cent at 12 months [43]. Sterling has noted that these data are surprisingly similar to that documented for people with more severe traumatic injury that requires hospitalisation or admission to intensive care [26].

In a prospective cohort followed up for three years, age, NDI score, cold hyperalgesia and post-traumatic stress symptoms measured at 4 weeks had a classification rate of 60 per cent for this group of non-recovered ‘high pain and disability’ subjects at 3 years [37]. In the latter study, ‘at risk’ subjects presented with high levels of pain, high levels of disability, an unresolved post-traumatic stress response and increased sensitivity to both mechanical pressure at areas removed from the site of injury (reduced pressure pain threshold) and cold stimuli (cold hyperalgesia). This group has been described as having “complex whiplash” [42].

As discussed above, a recent study has derived a clinical prediction rule for identifying recovery and non-recovery that includes age, NDI score and the hyper-arousal subscale of the Post-traumatic Diagnostic Scale (PDS): an individual who meets the following three criteria is likely to develop moderate/severe disability: NDI >40 per cent, age >35 years and >6 on the hyper-arousal subscale of the PDS [29,44]. Hyper-arousal symptoms include having trouble falling asleep, feelings of irritability, difficulty concentrating, being overly alert and being easily startled. Conversely, an individual who meets the following two criteria is likely to recover fully: NDI <32 per cent and age <35 years.

 

Screening for risk of poor recovery in the clinic

Table 2 lists those factors that appear to be strongly predictive of poor recovery following whiplash injury.

 

 

 

 

 

 

 

 

 

 

 

 

 

The subjective self-report aspects (e.g. pain levels, sites of injury, etc.) are easily assessed in the clinic. Assessing disability levels and screening for neuropathic pain and a post-traumatic stress reaction requires the use of standardised, validated questionnaires (Table 3).

 

 

 

 

 

 

The infographic shown in Figure 2 uses the mnemonic C-SPINE to aid recall of the more important factors that appear to be prognostic of poor recovery. In the clinical setting it is useful to informally screen by probing with the items listed under ASK in the infographic. Basic management suggestions are also provided. If the clinician feels that the injured person requires more formal testing, the most commonly used screening tools are listed at the foot of each column.

 

 

 

 

 

 

 

 

 

 

 

 

 

An interactive NDI that sums the total automatically is available on-line at www.chrisworsfold.com/ndi and can be completed relatively quickly ‘in-house’ during the examination.

In terms of assessing PPTs, a relatively inexpensive hand-held device called an algometer, which reliably quantifies tenderness by measuring the precise force required to produce the first sensation of pain, can be utilised (see Figure 3).

There has been data published in acute and sub-acute neck pain patients, with lower scores (0–25th quartile range from <1.5kg/f in the upper trapezius and <2.5kg/f at the tibialis anterior site [47]) increasing the risk of ongoing disability at 1 to 3 months. Mechanical hyperalgesia is a common finding in the majority of neck pain patients but increased tenderness at a location removed from the area of trauma – the shin is commonly used in the research setting, as stated above – strongly suggests the presence of widespread mechanical hyperalgesia following whiplash injury.

A Thermoroller, cooled to 15°C (see Figure 4), can be used to examine for signs of cold hyperalgesia. More recent work has suggested a simpler method that involves applying an ice pack to the posterior aspect of the cervical spine for 10 seconds [48]: if the patient rates the resulting sensation as painful and scores >5/10 on the VAS, this strongly suggests the presence of cold hyperalgesia; if the patient scores <1/10 on the VAS, this strongly suggests the absence of cold hyperalgesia.

 

 

 

 

 

 

 

 

 

 

 

 

A logical, evidence-based pathway for screening for poor recovery would be: NDI >40%, screening for (a) post-traumatic stress response, (b) widespread hyperalgesia (PPTs at shin using an algometer) and (c) cold hyperalgesia at the neck (measured using Thermoroller or ice pack).

 

References 

1. Dong L, Odeleye A, Jordan-Sciutto K, Winkelstein B. Painful facet joint injury induces neuronal stress activation in the DRG: Implications for cellular mechanisms of pain. Neuroscience letters 2008;443(2):90-4.
2. Quinn K, Dong L, Golder F, Winkelstein B. Neuronal hyperexcitability in the dorsal horn after painful facet joint injury. Pain 2010.
3. Krakenes J, Kaale B, Moen G, Nordli H, Gilhus N, Rorvik J. MRI assessment of the alar ligaments in the late stage of whiplash injury-a study of structural abnormalities and observer agreement. Neuroradiology 2002;44(7):617-24.
4. Krakenes J, Kaale B, Nordli H, Moen G, Rorvik J, Gilhus N. MR analysis of the transverse ligament in the late stage of whiplash injury. Acta Radiologica 2003;44(6):637-44.
5. Vetti N, Kråkenes J, Eide G, Rørvik J, Gilhus N, Espeland A. MRI of the alar and transverse ligaments in whiplash-associated disorders (WAD) grades 1–2: high-signal changes by age, gender, event and time since trauma. Neuroradiology 2009;51(4):227-35.
6. Brault J, Siegmund G, Wheeler J. Cervical muscle response during whiplash: evidence of a lengthening muscle contraction. Clinical Biomechanics 2000;15(6):426-35.
7. McCully K, Faulkner J. Injury to skeletal muscle fibers of mice following lengthening contractions. Journal of Applied Physiology 1985;59(1):119.
8. Scott S, Sanderson P. Whiplash: a biochemical study of muscle injury. European Spine Journal 2002;11(4):389-92.
9. Svensson MY, Aldman B, Bostrom O, Davidsson J, Hansson HA, Lovsund P et al. Transient pressure gradients in the pig spinal canal during experimental whiplash motion causing membrane dysfunction in spinal ganglion nerve cells. [German]. Orthopade 1998;27(12):820-6.
10. Eichberger A, Darok M, Steffan H, Leinzinger P, Boström O, Svensson M. Pressure measurements in the spinal canal of post-mortem human subjects during rear-end impact and correlation of results to the neck injury criterion. Accident Analysis &amp; Prevention 2000;32(2):251-60.
11. Carlson E, Tominaga Y, Ivancic P, Panjabi M. Dynamic vertebral artery elongation during frontal and side impacts. The spine journal: official journal of the North American Spine Society 2007;7(2):222.
12. Ivancic P, Ito S, Tominaga Y, Carlson E, Rubin W, Panjabi M. Effect of rotated head posture on dynamic vertebral artery elongation during simulated rear impact. Clinical Biomechanics 2006;21(3):213-20.
13. Bogduk N, McGuirk B. Management of acute and chronic neck pain: an evidence-based approach. Elsevier Science Health Science div; 2006.
14. Kaale B, Krakenes J, Albrektsen G, Wester K. Whiplash- associated disorders impairment rating: neck disability index score according to severity of MRI findings of ligaments and membranes in the upper cervical spine. Journal of Neurotrauma 2005;22(4):466-75.
15. Ferrari R. Re: Myran R, Kvistad KA, Nygaard OP, et al. Magnetic resonance imaging assessment of the alar ligaments in whiplash injuries: a case-control study. Spine 2008;33:2012-6. Spine 2010;35(1):131-.
16. Freeman MD, Rosa S, Harshfield D, Smith F, Bennett R, Centeno CJ et al. A case-control study of cerebellar tonsillar ectopia (Chiari) and head/neck trauma (whiplash). Brain Injury 2010;24(7-8):988- 94.
17. Anderson SE, Boesch C, Zimmermann H, Busato A, Hodler J, Bingisser R et al. Are There Cervical Spine Findings at MR Imaging That Are Specific to Acute Symptomatic Whiplash Injury? A Prospective Controlled Study with Four Experienced Blinded Readers. Radiology 2012;262(2):567-75.
18. Roshier, Amanda, Louise. Observation and quantification of pathological lesions in the musculoskeletal structures of the cervical spine. University of Nottingham.; 2005.
19. M GRaS. Whiplash injuries: Current concepts in prevention, diagnosis, and treatment of the cervical whiplash syndrome. Whiplash injuries: Current concepts in prevention, diagnosis, and treatment of the cervical whiplash syndrome 1998.
20. Carroll LJ, Holm LW, Hogg-Johnson S, Cote P, Cassidy JD, Haldeman S et al. Course and prognostic factors for neck pain in whiplash-associated disorders (WAD) – Results of the bone and joint decade 2000-2010 task force on neck pain and its associated disorders. Spine 2008;33(4):S83-S92.
21. Walton DM, MacDermid JC, Giorgianni AA, Mascarenhas JC, West SC, Zammit CA. Risk Factors for Persistent Problems Following Acute Whiplash Injury: Update of a Systematic Review and Meta-analysis. Journal of Orthopaedic &amp; Sports Physical Therapy 2013;43(2):31-43.
22. Kongsted A, Sorensen JS, Andersen H, Keseler B, Jensen TS, Bendix T. Are early MRI findings correlated with long-lasting symptoms following whiplash injury? A prospective trial with 1-year follow-up. European Spine Journal 2008;17(8):996-1005.
23. Siegmund GP, Davis MB, Quinn KP, Hines E, Myers BS, Ejima S et al. Head-turned postures increase the risk of cervical facet capsule injury during whiplash. Spine 2008;33(15).
24. Winkelstein BA, Nightingale RW, Richardson WJ, Myers BS. The cervical facet capsule and its role in whiplash injury – A biomechanical investigation. Spine 2000;25(10).
25. Walton DM, Pretty J, MacDermid JC, Teasell RW. Risk factors for persistent problems following whiplash injury: results of a systematic review and meta-analysis. J Orthop Sports Phys Ther 2009;39(5):334-50.
26. Sterling M, Kenardy J. Whiplash: Evidence base for clinical practice. Elsevier Australia; 2011.
27. Sterling M, Pedler A. A neuropathic pain component is common in acute whiplash and associated with a more complex clinical presentation. Manual Therapy 2009;14(2):173-9.
28. Vernon H, Mior S. The Neck Disability Index: a study of reliability and validity. Journal of Manipulative and Physiological Therapeutics 1991;14(7):409.
29. Ritchie C, Hendrikz J, Kenardy J, Sterling M. Derivation of a clinical prediction rule to identify both chronic moderate/severe disability and full recovery following whiplash injury. Pain 2013;154(10):2198-206.
30. Treleaven J, Jull G, Sterling M. Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. Journal of Rehabilitation Medicine 2003;35(1):36-43.
31. Treleaven J, LowChoy N, Darnell R, Panizza B, Brown-Rothwell D, Jull G. Comparison of sensorimotor disturbance between subjects with persistent whiplash-associated disorder and subjects with vestibular pathology associated with acoustic neuroma. Archives of Physical Medicine &amp; Rehabilitation 2008;89(3):522-30.
32. Treleaven J, Jull G, LowChoy N. Smooth pursuit neck torsion test in whiplash-associated disorders: relationship to self-reports of neck pain and disability, dizziness and anxiety. Journal of Rehabilitation Medicine 2005;37(4):219-23.
33. Treleaven J, Jull G, LowChoy N. The relationship of cervical joint position error to balance and eye movement disturbances in persistent whiplash. Manual Therapy 2006;11(2):99-106.
34. Field S, Treleaven J, Jull G. Standing balance: a comparison between idiopathic and whiplash-induced neck pain. Manual Therapy 2008;13(3):183-91.
35. Kongsted A, Jorgensen LV, Leboeuf-Yde C, Qerama E, Korsholm L, Bendix T. Are altered smooth pursuit eye movements related to chronic pain and disability following whiplash injuries? A prospective trial with one-year follow-up. Clinical Rehabilitation 2008;22(5):469-79.
36. Williams M, Williamson E, Gates S, Lamb S, Cooke M. A systematic literature review of physical prognostic factors for the development of late whiplash syndrome. Spine 2007;32(25):E764.
37. Sterling M, Jull G, Kenardy J. Physical and psychological factors maintain long-term predictive capacity post-whiplash injury. Pain 2006;122(1-2):102- 8.
38. Walton D, MacDermid J, Nielson W, Teasell R, Reese H, Levesque L. Pressure Pain Threshold Testing Demonstrates Predictive Ability in People With Acute Whiplash. Journal of Orthopaedic & Sports Physical Therapy 2011;41(9):658-65.
39. Kamper SJ, Maher CG, Costa LdCM, McAuley JH, Hush JM, Sterling M. Does fear of movement mediate the relationship between pain intensity and disability in patients following whiplash injury? A prospective longitudinal study. Pain 2012;153(1).
40. Holm LW, Carroll LJ, Cassidy JD, Skillgate E, Ahlbom A. Expectations for recovery important in the prognosis of whiplash injuries. PLoS Med 2008;5(5):e105.
41. Williamson E, Williams M, Gates S, Lamb S. A systematic literature review of psychological factors and the development of late whiplash syndrome. Pain 2008;135(1-2):20- 30.
42. Sterling M, Kenardy J. Physical and psychological aspects of whiplash: Important considerations for primary care assessment. Manual Therapy 2008;13(2):93-102.
43. Sterling M, Hendrikz J, Kenardy J. Compensation claim lodgement and health outcome developmental trajectories following whiplash injury: A prospective study. Pain 2010;150(1):22-8.
44. Foa EB, Cashman L, Jaycox L, Perry K. The validation of a self-report measure of posttraumatic stress disorder: The Posttraumatic Diagnostic Scale. Psychological Assessment 1997;9(4):445-51.
45. Bennett M, Smith B, Torrance N, Potter J. The S-LANSS score for identifying pain of predominantly neuropathic origin: validation for use in clinical and postal research. The Journal of Pain 2005;6(3):149-58.
46. Horowitz M, Wilner N, Alvarez W. Impact of event scale. Psychosomatic Medicine 1979;41:209-18.
47. Walton D, MacDermid J, Nielson W, Teasell R, Nailer T, Maheu P. A Descriptive Study of Pressure Pain Threshold at 2 Standardized Sites in People With Acute or Subacute Neck Pain. Journal of Orthopaedic &amp; Sports Physical Therapy 2011;41(9):651-7.
48. Maxwell S, Sterling M. An investigation of the use of a numeric pain rating scale with ice application to the neck to determine cold hyperalgesia. Manual Therapy 2013;18(2):172-4.
49. Sterling M. Physiotherapy management of whiplash-associated disorders (WAD). J Physiother 2014;60(1):5-12.
50. Jull G, Kenardy J, Hendrikz J, Cohen M, Sterling M. Management of acute whiplash: a randomized controlled trial of multidisciplinary stratified treatments. Pain 2013;154(9):1798-806.
51. Sullivan MJ et al Catastrophizing and perceived injustice: risk factors for the transition to chronicity after whiplash injury. Spine 2011 Dec 1;36(25 Suppl):S244-9.
52. Dunne RL, Kenardy J, Sterling M. A Randomized Controlled Trial of Cognitive-behavioral Therapy for the Treatment of PTSD in the Context of Chronic Whiplash. Clinical Journal of Pain 2012;28(9):755-65.

 

Chris Worsfold has 30 years of experience as a physio-therapist and is a full-time clinician in Tonbridge, Kent, specialising in neck pain. He is also a visiting university lecturer. Read Chris’s neck pain blog at www.chrisworsfold.com. Chris is one of the faculty members speaking at NSpine 2017’s Whiplash Injury session in June.