Intervention trials

There seem to be several obvious areas where trials of intervention are urgently required. The first of these would be the clear lack of trials investigating pharmacotherapy for patients with whiplash at both the acute and chronic stages. There is now convincing evidence of augmented central nociceptive processing that is present from soon after injury,¹ persists in and predicts those individuals with poor functional recovery,² and is associated with non-responsiveness to standard physical rehabilitation approaches.³ Other conditions showing similar phenomena (e.g. fibromyalgia) have undergone extensive investigation as to the effects of various pharmacotherapies to the extent that some medications are now approved by the US Food and Drug Administration for use in this condition.⁴ There are also a far greater number of trials investigating pharmacotherapy for low back pain⁵ than whiplash. Furthermore, initially higher levels of pain and/or disability are the most consistent predictors of poor health outcomes following whiplash injury.^6–8 Guidelines for acute pain management advocate the importance of early pain relief following injury,⁹ yet whiplash guidelines do not make this a priority of treatment as there are no high-quality trials available on which to base recommendations.^{10, 11}

In addition to pain, post-traumatic stress is also common in people with whiplash.¹² There is emerging evidence that administration of an opiate¹³ and beta blockers¹⁴ administered very soon after a traumatic injury can prevent the development of post-traumatic stress disorder (PTSD), and these may also be novel approaches in the management of patients with acute whiplash and symptoms of post-traumatic stress. Thus, trials of pharmacotherapy for whiplash should be a research priority.

There is now available a large volume of research on the psychological sequelae of whiplash injury, as can be seen from the discussions of Chapters 8 and 13. In contrast, there are few treatment trials of psychological interventions or combined psychological and physical management approaches for WAD. Again, this is in contrast to the data available in other musculoskeletal conditions, such as low back pain. Some whiplash studies have combined a cognitive behavioural type of approach delivered by a physiotherapist in conjunction with an exercise program,^{15, 16} making it difficult to tease out the relative efficacy of both components. Few studies have investigated the effects of a psychological-based intervention delivered by a clinical psychologist. In view of recent findings of the presence of PTSD symptoms and depression in some patients with whiplash (Chapters 8 and 13), it would seem important that future studies investigate the effectiveness of treatments targeted at PTSD and depression. As outlined in Chapter 13, effective treatments, such as trauma-focused cognitive behaviour therapy, exist for the management of PTSD, and preliminary data indicate that PTSD treatment may potentially have an effect not only on PTSD symptoms but also on pain and disability.¹⁷ This would also seem to be an area ripe for research, where there is much supporting evidence on which to base a case for such trials.

Most clinical guidelines recommend the provision of education and advice as part of the management of WAD.^{10, 11, 18} Individual studies have investigated various educational approaches, such as the provision of information pamphlets¹⁹ or educational videos,²⁰ but when taken together in a systematic review, the results are disappointing in that there was moderate evidence of no difference on pain and disability for various forms of advice focusing on return to activity.²¹ Thus, it would seem that we are no closer in understanding the most effective education to provide to whiplash-injured people and the most effective way to deliver that advice. Since the provision of education and advice forms the mainstay of most management approaches, albeit physical or psychological, then it would seem a priority that further investigation of this area is required.

Most exercise approaches to both acute and chronic whiplash have delivered only modest effects.^{3, 16, 22} Some studies have investigated approaches that, while efficacious for non-traumatic neck pain, have provided disappointing results when translation to the whiplash condition is attempted.³ In the study by Jull et al.,³ it was shown that those participants with higher levels of pain and disability and sensory hypersensitivity indicative of augmented central nociceptive processing responded poorly to an intensive 10-week program of specific exercise. It may be that more creative approaches to physical rehabilitation are required for whiplash, particularly for those with a more complex clinical presentation.

The whiplash subgroup with sensory hypersensitivity also shows sympathetic nervous system and motor disturbances^{1, 23} that are similar to features of complex regional pain syndrome (CRPS) type 1.²⁴ Altered central representation of perceptual, motor and autonomic systems has been implicated as possible mechanisms underlying the pain of CRPS.²⁵ Treatment approaches that broadly aim to restore altered cortical representation, such as graded motor imagery and mirror visual feedback, have been shown to decrease pain and disability associated with CRPS,²⁶ and sensory discrimination training can also decrease the pain and disability of CRPS.²⁷ The similarities of the manifestations of CRPS and complex whiplash suggest that investigation of such approaches is warranted.

Do some patients have a pre-existing risk of developing chronic pain after whiplash injury?

The co-occurrence of disturbed nociceptive processing, stress responses—both physiological and psychological, marked motor changes and moderate-to-high levels of pain and disability in some patients with whiplash may not be coincidental. It has been argued that these responses are interrelated and develop in response to a common stressor—the motor vehicle crash (MVC).^{28, 29} It may also be the case that some individuals have a pre-existing risk of developing chronic pain following a given injury or stressor. Animal studies have shown that an identical induced injury (chronic constriction injury of the sciatic nerve) evokes both pain and disability, including sleep disruption and disrupted social behaviours, in only a subgroup (approximately 30%) of rats.³⁰ The authors suggest that disabilities evoked by the injury reflect a specific and select neurobiological response to injury that may be related to genetic differences in neural and glial adaptations in the periaqueductal grey regions of the brain.³⁰ Preliminary evidence in whiplash-injured humans suggests that genetic variations in the function of catechol-O-methyltransferase (COMT, an enzyme involved in the degradation of catecholamines) may influence vulnerability to acute and chronic WAD symptoms after an MVC (Chapter 9).³¹ Additionally, population-based studies have demonstrated that pre-collision factors of perceived health and health-seeking behaviour are predictive of the development of widespread bodily pain (not specifically whiplash) following an MVC.³²

Taken together, these studies indicate that some people, for possibly genetic reasons, are more predisposed to tip into a hyperexcitable systemic-type state following an injury. These hypotheses require further evaluation, although it is not clear what should be done for individuals who may fit this scenario. It may be that they require earlier and targeted interventions towards settling the hyper-responsiveness, via decreasing either the stress responses or levels of pain, as outlined earlier.