A significant proportion of people (up to 50%) who develop neck pain following a car accident continue to report neck pain at long term follow up. It’s not clear why these patients don’t recover and unfortunately current evidence seems to indicate that usual rehabilitative management is not very effective for patients with chronic whiplash. The development of post traumatic stress disorder (PTSD) symptoms and lowered pain thresholds (mechanical and cold hyperalgesia) soon after injury can help identify those most at risk of persistent symptoms following a whiplash injury. Although not present in every patient with chronic whiplash it seems these features are somehow related to persistent problems in this population. The presence of these complex clinical presentations suggest there may be a variety of causative factors underlying chronic whiplash. In order to achieve positive outcomes we may need to tailor specific treatment strategies to patients with chronic whiplash based on the factors underlying their pain. Identification of distinct clinical presentations in patients with chronic whiplash may give us clues as to the mechanisms driving continued pain and disability. This can help identify the treatment options with the best chance of success for patients with chronic whiplash.
We used cluster analysis in a large sample (n = 331) of patients with chronic whiplash in an attempt to identify groups of patients with a similar clinical presentation based on the presence or not of sensory hypersensitivity and PTSD symptoms. We identified 4 groups of patients: no PTSD symptoms or sensory hypersensitivity (nPnH); no PTSD symptoms with sensory hypersensitivity (nPH); moderate or severe PTSD symptoms with no sensory hypersensitivity (PnH); and moderate or severe PTSD symptoms with sensory hypersensitivity (PH).
The nPnH group accounted for 43.5% of the sample. We had expected to find some patients without sensory hypersensitivity or PTSD symptoms, just not this many. Unfortunately this analysis gives us little information about why this group have not recovered. There are a myriad of potential psychological and physical factors which may contribute to the continued pain and disability experienced by these patients. The presence and size of this group is helpful in reminding us to not forget about the patients with ‘less complex’ clinical presentations when pondering the causative factors in the maintenance of pain and disability in patients with chronic WAD.
Roughly 25% of the sample reported moderate to severe PTSD symptoms. These patients had significantly worse neck pain and disability than the other groups. This highlights the association between PTSD, pain and disability in patients with whiplash. Although no causal link between PTSD and pain has been definitively established in patients with whiplash, data from similar patient groups provides some insight. A large sample of patients experiencing pain following a traumatic injury were followed over the course of 12 months and the causal pathways between PTSD and pain were examined. In the first 6 months after injury a mutual maintenance between pain and PTSD was observed. After 6 months, pain no longer influenced the level of PTSD, while PTSD significantly influenced pain levels. It is possible that psychological intervention for patients showing moderate or severe levels of PTSD may ‘unlock’ the potential benefits of subsequent physical interventions through removing one of the drivers of pain. Encouragingly there is some evidence to suggest that treatment of PTSD can have a positive effect on neck symptoms, although further evidence is required to confirm this. This line of reasoning challenges the traditional practice of treating psychological and physical symptoms as dichotomous. Critically and empirically challenging this traditional paradigm may help us develop new approaches to the treatment of chronic pain conditions such as WAD.
We were also intrigued to find that two sub-groups of patients could be characterised as hyperalgesic: the PH group (14% of the sample) who reported moderate to severe levels of PTSD; and the nPH group (30% of the sample) who did not. These clinical features have been shown to be closely related and it has been hypothesised that they share a common neurobiological origin. Our findings do not refute this hypothesis they just indicate that moderate or severe PTSD is not a requirement for the presence of sensory hypersensitivity. The nPH group reported similar pain and disability levels as the nPnH group indicating that sensory hypersensitivity alone does not predicate a more severe clinical presentation in patients with chronic whiplash, even though it is an established risk factor for non-recovery in patients with acute whiplash.
Overall our findings highlight the variety of ways in which patients with chronic WAD may present clinically. This suggests to us that there are multiple mechanisms which may underlie the continuing pain in this population. Continued exploration of the drivers of pain and disability in this population will aid us in developing management strategies specifically targeted at these mechanisms.
About Ash Pedler
His research is focussed on identifying the mechanisms underlying pain and disability in patients with chronic whiplash and the development of effective treatments for this condition.
 Pedler A, & Sterling M (2013). Patients with chronic whiplash can be subgrouped on the basis of symptoms of sensory hypersensitivity and posttraumatic stress. Pain, 154 (9), 1640-8 PMID: 23707284
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