It came as a surprise to me when I first started exploring the whiplash literature that there were only a handful of in vivo studies of acute injury following whiplash. Perhaps I was being naïve but I thought for a ‘condition’ that leads to such apparent widespread suffering and colossal expenditure – we are talking more than £3 billion per annum in the UK – that we would have a firm grasp on the ’pathology’ of whiplash. It seems this is not the case.

Whiplash appears to have been investigated ‘indirectly’ and mostly through animal, human cadaver and post mortem studies (fatal whiplash anyone?) in predominantly laboratory and computer based models of research. There is also some evidence of pathology that can be gleaned from clinical trials.

Compare this to the volume of work on in vivo pathology – often imaging – in tendinopathy or even muscle injury and our knowledge of in vivo pathology in whiplash is found clearly to be lacking.

But – and it is a big ‘BUT’ – how does this paucity of evidence impact our clinical practice? It is an interesting question. Do we really miss out by not having access to imaging ( e.g. MRI / x rays) or in vivo studies when it comes to whiplash?

Imaging in the clinical setting comes with considerable baggage, not least the risk of pathologising normal age-related changes and impacting negatively upon outcome (as we have seen here in the management of low back pain).

Let’s review four important findings from the whiplash literature and see if knowledge of pathology following whiplash injury can influence our practice.

Finding 1: The facet joint capsule is the most likely source of nociception in whiplash injury.

There exist scores of studies that have identified the cervical spine facet joints as a primary source of symptoms following whiplash injury (Dong et al. 2008, Quinn et al. 2010). Unfortunately the vast majority of these studies are experimental in nature.

The studies include mathematical / computer modelling approaches and also a bewildering array of whiplash simulation experiments: entire cadavers on sleds, isolated cervical spine specimens on mini-sleds termed ‘head-neck preparations’ (Ito et al. 2004) and even partial cadaveric cervical spine specimens, consisting of isolated facet joint specimens from just two cervical vertebrae (Quinn et al. 2007): extrapolating from these data to the living breathing human being in your clinic must take place with due caution!

Despite these shortcomings the latter experimental studies have demonstrated that the facet joint capsule undergoes forces greater than its physiological threshold for injury during the whiplash kinematic. Additionally, these forces appear to increase if the head is rotated at the time of injury (Siegmund et al. 2008, Winkelstein et al. 2000), presumably due to the ligament fibres being nearer to their limit due to this ‘pre-rotation’. ‘Reorganisation’ of the facet capsule fibres has also been demonstrated. It appears the collagen fibre bundles are re-arranged from a normal parallel organisation to a less strong and spaghetti-like appearance following whiplash-like distraction strains.

The experimental evidence is compelling for facet joint injury following whiplash and there may well be a spectrum of capsular disruption as there has been anecdotal surgical evidence of facet joint capsule rupture (Gunzburg and Szpalski 1998).

What about clinical studies? These have demonstrated significant pain relief in chronic neck pain cohorts following nerve blocks and radiofrequency neurotomy – where the facet joint nerves are ablated – and lend support to the view that facet joint nociception can occur following whiplash injury (Bogduk and McGuirk 2006).

Interestingly although there is convergent support through these many and varied experimental fields of study for the facet joint as a source of pain, MR imaging studies have failed to identify facet joint ‘fluid’ or ‘contusion’ in the acute stage following whiplash injury (Anderson et al. 2012). Likewise it is not possible to use MR or CT scanning in the clinical setting to diagnose the injuries described in the animal and cadaver studies discussed here: the pathology is currently undetectable.

So it’s an odd mix of experimental animal and cadaver studies and clinical evidence of pain relief following nerve blocks that points at the facet joint as a source of nociception following whiplash.

Finding 2: Occult fracture and bone contusion occurs in whiplash injury – but it’s rare.

A recent investigation within 48 hours of the injury and using an MRI turbo STIR sequence on a sample of subjects (note that a proportion of the subjects demonstrated no objective clinical signs ie Quebec Grade I) documented rare occurrences of occult fracture and bone contusions of vertebral bodies (Anderson et al. 2012). Occult fracture refers to a fracture that cannot be seen on standard radiographic examination i.e. x ray. Although occurrences of occult fracture of the vertebral body and facet joint were more prevalent in whiplash injured subjects compared to uninjured controls, they comprised only 0.5% of all whiplash injured MRI observations: rare!

Finding 3: Muscle injury occurs in whiplash injury – but it’s rare.

Muscle damage has been demonstrated in the acute stage of injury using diagnostic ultrasound scanning (Roshier 2005). Forty eight hours following whiplash injury perimuscular fluid, haematoma and muscle strain has also been found on MRI but it is exceptionally rare: 1% of post whiplash MRI observations (Anderson et al. 2012). Once again a spectrum of injury probably exists with some reports of surgical evidence of muscle rupture (Gunzburg and Szpalski 1998).

One very interesting study investigated creatine kinase levels following whiplash injury. This is a biochemical marker of muscle damage. Blood tests can reveal elevated creatine kinase levels after muscle trauma and this often correlates with the degree / severity of the muscle injury. The researchers could find no evidence of muscle damage following whiplash injury (Scott and Sanderson 2002); further evidence that frank muscle injury is rare.

Finding 4: Upper cervical ligament injury does not occur in whiplash injury.

A series of interesting early studies examined the extent of upper cervical ligament damage following whiplash injury. Both alar and transverse ligament changes were demonstrated using MRI scanning of whiplash injured subjects suffering persistent pain (Kaale et al 2005, Krakenes et al 2002, 2003). An increased incidence of alar ligament changes were found among those subjects who had their neck rotated at the time of injury. Unfortunately these studies did not have control groups – neither normal nor neck pain – for comparison and so it cannot be concluded that the observed changes were a valid indicator of ‘injury’.

Thus criticism of these early studies hinged upon the lack of control group but also referred to the problems around the validity of the MRI diagnosis of ligament damage.

More recent studies utilising higher resolution MRI scanning and atraumatic neck pain controls in the acute phase following injury appear to suggest that upper cervical ligament damage does not occur following whiplash injury. Findings at the acute and chronic stage following whiplash are comparable to findings in normal and atraumatic neck pain (See Vetti et al 2011b). Li et al’s (2013) meta-analysis of case-control studies also concludes that signal changes are not correlated with whiplash injury.

Does knowledge of whiplash pathology change clinical practice?

These studies demonstrate that there are MRI findings in the cervical spine that are associated with acute whiplash injury such as:

• bone abnormalities of vertebral bodies (occult fractures and bone contusions)
• muscle abnormalities (strains or tears and/or hematomas and perimuscular fluid).

But these findings are incredibly rare. Anderson et al. sum it up nicely (2012):

‘…in rare cases, traumatic cervical spine lesions do occur, but such lesions currently do not necessarily provide the cause of any symptoms or indicate specifically “more relevant” or “more severe” injury and whether they have any clinical relevance remains to be evaluated.’

Take home massages:

1. Imaging has no role in whiplash injury.
2. Nociception following whiplash is probably related to simple facet joint capsule strain. Think ‘ankle sprain of the neck’.
3. Management approaches should focus on reassurance (‘no serious pathology’), advice to remain active and individualised strengthening and sensorimotor exercise where appropriate – again ‘ankle sprain of the neck’ – strength and balance!
4. The lack of evidence (and this is not absence of evidence) for physical drivers for ongoing nociception strongly suggests continued emphasis upon psychosocial factors such as expectations for recovery, catastrophisation, fear of movement and screening for post-traumatic stress reactions (see here and here).

References

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