Subgrouping patients with chronic whiplash on the basis of symptoms of sensory hypersensitivity and PTSD

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[1]. 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[2]. 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[3]. 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[4] 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

Ash PedlerAsh Pedler is a Postdoctoral Research fellow at the Centre of National Research on Disability and Rehabilitation Medicine (CONROD), The University of Queensland.

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.

References

[1] 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

[2] Jenewein J, Wittmann L, Moergeli H, Creutzig J, & Schnyder U (2009). Mutual influence of posttraumatic stress disorder symptoms and chronic pain among injured accident survivors: a longitudinal study. Journal of Traumatic Stress, 22 (6), 540-8 PMID: 19924822

[3] Dunne RL, Kenardy J, & Sterling M (2012). A randomized controlled trial of cognitive-behavioral therapy for the treatment of PTSD in the context of chronic whiplash. The Clinical Journal of Pain, 28 (9), 755-65 PMID: 22209798

[4] Sterling M, Hendrikz J, & Kenardy J (2011). Similar factors predict disability and posttraumatic stress disorder trajectories after whiplash injury. Pain, 152 (6), 1272-8 PMID: 21396780

Comments

  1. Ash Pedler says

    Hi Eric,
    Thanks for your comment/question.
    I would say that although it is definitely possible that patients move between clusters over time (especially those who are at the edges of the clusters), I don’t think that movement from the PH to the nPnH cluster would account for a very large portion of the nPnH cluster. From longitudinal studies it would seem that both cold hyperalgesia and symptoms of PTSD are fairly stable over time in patients with whiplash and they seem to follow the trajectory of pain and disability fairly closely as well (see http://www.ncbi.nlm.nih.gov/pubmed/16139185, http://www.ncbi.nlm.nih.gov/pubmed/21396780). In particular we see very little change after 12 weeks post-injury in all of these factors.
    Using these clusters to group patients early after injury and looking at the stability of cluster membership over time would be an interesting study though and might help us unravel some of the relationships between these symptoms.
    Cheers
    Ash

  2. Hi Ash, trying to find a reason why the NPnH is so huge… One important thing to consider is the time post-whiplash you evaluated those patients. Because i guess some might have been PH in the beginning but resolved, contrary to their pain. So it could be a bias where some PH patients are shifting toward the nPnH group over time. What do you think?

  3. Hi John,

    Thanks for your comments. You are certainly not alone in being confused it is definitely a new area and focus of research and the waters are still a bit muddy.

    With respect to the differing findings on the association between PTSD and pain, I think that there are a couple of things to bear in mind. Firstly in our recent paper we performed a cross-sectional, observational analysis on patients with chronic whiplash. This is in contrast to the longitudinal studies which Esther and Michele have previously conducted which provide the capacity to predict long term outcome from baseline variables. As I think Esther highlighted in her comments on her post, variable results are possible when performing predictive analyses based on the outcome which you are trying to predict, the statistical method you are using and the variables you include in your model. I would also note that Esther’s results are based on a clinical trial. It is possible that one or both interventions provided some beneficial effect to those patients who had or were at risk of developing a posttraumatic stress reaction. The difference in results between Michele and Esther’s work are likely reflective of these methodological differences.

    In regard to our recent paper in Pain, we observed that the clusters of patients who could be identified on the basis of moderate to severe levels of PTSD symptoms also reported significantly higher pain and disability than the clusters characterised by lower levels of PTSD symptoms. This link between more severe pain and the presence of PTSD symptoms has been widely reported in other patient populations as well as in whiplash cohorts (for a recent review see http://www.ncbi.nlm.nih.gov/pubmed/24336429). So the weight of evidence suggests that there is an association between PTSD and chronic pain.

    I think that my take home message from all of this would be that in the clinical situation we should be aware of the potential for the development of a posttraumatic stress reaction in patients with whiplash. It certainly is not going to be present in every patient or even in the majority of patients but for those who do develop this type of psychological reaction it is important that they are provided with appropriate care. Hopefully this will help both the psychological and physical recovery of these patients, although more work is needed to prove that physical recovery is aided by psychological intervention in this group.

    Cheers
    Ash

  4. Lesley singer says

    I remember literature on how whiplash patients who saw a video on what to expect post whiplash did better and less patients went on to chronicy. This was done in the er before patients were going home developing all this fear. I still think we spend a lot more time on the treatment of chronic pain when I think we could spend a little more on prevention. I know we would still have many who go on to chronicity but we may prevent a few as well. maybe we have done the education per so much in the past

  5. Ash,
    Thank you for adding to the growing body of work in this confusing- at least to me- area of delayed recovery following whiplash. A couple of years ago Esther Williamson summarized here at BiM (http://www.bodyinmind.org/chronic-neck-pain-beliefs/) her findings from the MINT trial on WAD. She described using the “Impact of Events” scale for identifying PTSD, which in the MINT trial failed to show that the early presence of PTSD following whiplash predicted delayed recovery at 8 and 12 months post-injury. She mentioned in the comments that her results differed from a previous trial by your co-author Michele Sterling on this same risk factor.

    Can you shed some light on why we’re seeing this variability in the research on the relationship between PTSD and chronic whiplash?