The debate over whiplash injuries over the past 20 years is reminiscent of incandescent globes, generating more heat than light and using important energy. We know that the overwhelming majority of patients with neck pain after motor vehicle crashes recover completely over a few weeks. The problem is the cohort with ongoing symptoms, which often extend beyond the neck and are not associated with clinical or radiological abnormalities. This group of patients are often inextricably involved with insurance claims, and this in itself attracts pejorative views from some practitioners.

Studies into the proportion of patients with chronic symptoms and the determinants of these symptoms have varied in design and execution. Counting insurance claims is fraught with behavioural, motivational, and jurisdictional confounders. Identifying patients as they present to hospital risks including only those with more severe initial symptoms. Police records depend on accurate reporting. Mindful of these limitations, the cohort followed robustly by Gargan and colleagues over 30 years shows that more than a third of patients still have symptoms, but that these symptoms may diminish after 15 years.^₁ Although this may be biased towards an overestimate, it still indicates an important burden of illness. Systematic reviews have identified a range of predictors of chronicity. These include non-use of seatbelts, more severe pain at presentation, headache, back pain, immediate neck pain, previous neck pain and more clinical signs. 

Psychosocial factors include no education beyond school, female sex and tendency to catastrophise. However, it is unclear how much of the variability these factors explain. Other studies have suggested that even the expectation of recovery itself affects prognosis, so that those not expecting to recover are less likely to. Of note, settlement of compensation has not been shown to result in recovery. The common ground in the whiplash debate is that the prevalence of chronic neck pain is higher in patients who have been exposed to whiplash injuries. Accepting this, then something happens in a motor vehicle crash that facilitates a change in neuronal activity that causes the perception of neck pain.

Of particular interest in the context of a chronic painful condition is the demonstration of an association in early whiplash between stress response genes and symptoms. Catechol-O-methyltransferase (COMT) is the main enzyme that degrades catecholamines. Different enzyme activities are encoded by common genetic variations, with people having a less active haplotype being more vulnerable to pain. A study of whiplash patients in the ED found that those with pain-vulnerable COMT genotypes had more severe neck pain, headaches, dizziness and dissociative symptoms than those with a more pain-resistant haplotype. This finding may underpin the somatic and psychological responses to whiplash, and – given the observation that the severity of headache and neck pain predict chronicity – may have a role in determining long-term symptoms. 

Further research is needed into this and other genetic, phenotypic and psychological predispositions to pain, but it seems likely that there are innate and assessable predictors for chronic whiplash pain. The treatment of early whiplash has the potential for harm. Adverse effects have been reported for prolonged use of collars, and also the high use of healthcare can delay recovery. The best approach is that applied to acute low back pain: education, exercise and return to usual activities.

Reference

1. Rooker J, Bannister M, Amirfeyz R et al. Whiplash injury: 30-year follow-up of a single series. J Bone Joint Surg (Br) 2010; 92: 853-835