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Chronic whiplash-associated disorders: to exercise or not?

Two recent trials published in The Lancet1,2 have provided important information about the management of patients with whiplash-associated disorders. In a new study, Zoe Michale and colleagues2 recorded that a comprehensive exercise programme is not better than one physiotherapy advice session supplemented with telephone support in people with whiplash-associated disorders.2 The results serve as a reminder that chronic whiplash-associated disorder is an underestimated condition that needs specic treatment, and that more studies are needed to establish eective interventions. We focus here on the chronic whiplash-associated disorder group and address clinical implications of, and possible explanations for, the study ndings, and opportunities for further investigation. The comprehensive exercise programme employed by Michale and coworkers consisted of 20 sessions (lasting 1 hour) of specic motor relearning exercises and graded activity, with cognitive behavioural treatment rules.2 The researchers randomised 172 patients to either exercise or advice and, in terms of the trials primary endpoint of pain intensity, the dierences between groups were 00 (95% CI 07 to 07) at 14 weeks, 02 (05 to 10) at 6 months, and 01 (08 to 06) at 12 months. On the basis of current understanding of whiplash-associated disorders, the method used is a state-of-the-art approach to exercise in people with chronic whiplash-associated disorders. The investigators used high-quality research methods, which suggests a low risk of bias. The ndings could be explained by several factors. First, but of little clinical importance, dysfunctional cervical neuromuscular control is an established feature in patients with chronic whiplash-associated disorders,3 because people move dierently when they are in pain.4 The brain does not need nociception to change control of body movementanticipation of pain suces.5 This point could be addressed by a reduction in the threat of paineg, therapeutic pain neuroscience education6 before exercise is started. This is a crucial issue in whiplash because many patients continue their search for objective evidence of structural (cervical) damage. One of the main goals of therapeutic pain neuroscience education is to change patients pain beliefs through reconceptualisation of painie, that pain does not result from tissue damage. In view of the established presence of hypersensitivity of the CNS (ie, central sensitisation) in patients with chronic whiplash-associated disorders,7 this step is likely to be a crucial prerequisite for exercise interventions. Michale and colleagues aimed to change patients understanding of pain through education and by use of cognitive behavioural therapy. Therapeutic pain neuroscience education might address this point more thoroughly, by allowing patients to understand their pain, including the absence of objective biomarkers or imaging ndings. Compared with pain education in cognitive behavioural therapy, pain neuroscience education focuses on the neurophysiology of pain to change beliefs about pain so that even patients with a focus on biomedical mechanisms, who are reluctant to adopt psychological explanations for their pain, become likely to change their pain beliefs. Some argue that patients with chronic whiplashassociated disorders not only need exercise treatment and graded activity, but stress management, counselling, and activity management. Indeed, people with chronic whiplash-associated disorders show a dysfunctional stress response,8 and many have post-traumatic stress symptoms that can be treated successfully with trauma-focused cognitive behavioural therapy.9 Additionally, not all patients need grading of activity from the early treatment phase; patients can show persistence behaviour rather than avoidance behaviour, which makes the application of activity pacing and acceptance-based interventions appropriate.10 Still, these are hypothetical solutions for the
Central sensitisation (ie, hypersensitivity of the nervous system) Published Online April 4, 2014 S0140-6736(14)60130-6 See Online/Articles S0140-6736(14)60457-8

Dysfunctional endogenous analgesia in response to exercise

Post-traumatic stress

Cognitive-emotional factors, including maladaptive pain cognitions

Whiplash-associated disorders

Dysfunctional stress response systems

Impaired cervical neuromuscular control

Figure: Various aspects of whiplash-associated disorders Several of the factors are partly overlapping (eg, dysfunctional endogenous analgesia in response to exercise can be seen as one aspect of central sensitisation) or interconnected (eg, cognitive-emotional factors contribute to both central sensitisation and the dysfunctional stress response). Published online April 4, 2014


improvement of physiotherapy management for patients with chronic whiplash-associated disorders. We propose each of the issues contributing to the symptoms and disability are addressed in a comprehensive rehabilitation programme for patients with chronic whiplash-associated disorders (gure). Further high-quality randomised controlled trials are needed to assess whether such a comprehensive rehabilitation programme is eective. Central sensitisation in patients with chronic whiplash-associated disorders7 warrants treatment of cognitive emotional factors like pain catastrophising, hypervigilance, and maladaptive beliefs about illness. Michale and coworkers addressed this point by use of cognitive behavioural therapy rules. The treating physiotherapists were experienced clinicians who were familiar with and trained to apply cognitive behavioural therapy rules, a dicult process.11 Physiotherapy curricula are only starting to integrate cognitive behavioural therapy as part of pain management modules. Future physiotherapists might have the necessary attitudes, beliefs, and skills to apply specic cognitive behavioural therapy rules during exercise therapy for chronic pain patients, including those with whiplash-associated disorders. Michale and colleagues results are surprising in view of the established eects of education for patients with chronic whiplash-associated disorders12 and the dysfunctional response of these patients to exercise.13 A normal response to exercise or physical activity entails activation of brain-orchestrated analgesia, a mechanism referred to as exercise-induced endogenous analgesia. However, patients with chronic whiplashassociated disorders do not activate endogenous analgesia in response to exercise.13 We are investigating the role of brain neurotransmitters like serotonin and noradrenaline in the dysfunctional endogenous analgesia in response to exercise in people with chronic whiplash-associated disorders. The study by Michale and colleagues2 advances our understanding of whiplash-associated disorders and provides physiotherapists with clear information about how to treat patients with chronic whiplash-associated

disorders. These ndings should not be interpreted as encouragement to abandon exercise therapy in these patients: the question is how and when to exercise people with chronic whiplash-associated disorders. *Jo Nijs, Kelly Ickmans
Pain in Motion research group, Departments of Human Physiology and Physiotherapy, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, BE-1090 Brussels, Belgium (JN, KI); and Pain in Motion research group, Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Belgium (JN)
We declare that we have no competing interests. 1 Lamb SE, Gates S, Williams MA, et al. Emergency department treatments and physiotherapy for acute whiplash: a pragmatic, two-step, randomised controlled trial. Lancet 2013; 381: 54656. Michale Z, Maher CG, Lin C-WC, et al. Comprehensive physiotherapy exercise programme or advice for chronic whiplash (PROMISE): a pragmatic randomised controlled trial. Lancet 2014; published online April 4. Daenen L, Nijs J, Raadsen B, Roussel N, Cras P, Dankaerts W. Cervical motor dysfunction and its predictive value for long-term recovery in patients with acute whiplash-associated disorders: a systematic review. J Rehabil Med 2013; 45: 11322. Hodges PW, Tucker K. Moving dierently in pain: a new theory to explain the adaptation to pain. Pain 2011; 152 (suppl 3): 18. Tucker K, Larsson AK, Oknelid S, Hodges P. Similar alteration of motor unit recruitment strategies during the anticipation and experience of pain. Pain 2012; 153: 63643. Van Oosterwijck J, Nijs J, Meeus M, et al. Pain neurophysiology education improves cognitions, pain thresholds and movement performance in people with chronic whiplash: a pilot study. J Rehabil Res Dev 2011; 48: 4358. Van Oosterwijck J, Nijs J, Meeus M, Paul L. Evidence for central sensitization in chronic whiplash: a systematic literature review. Eur J Pain 2013; 17: 299312. Gaab J, Baumann S, Budnoik A, Gmunder H, Hottinger N, Ehlert U. Reduced reactivity and enhanced negative feedback sensitivity of the hypothalamus-pituitary-adrenal axis in chronic whiplash-associated disorder. Pain 2005; 119: 21924. Dunne RL, Kenardy J, Sterling M. A randomized controlled trial of cognitivebehavioral therapy for the treatment of PTSD in the context of chronic whiplash. Clin J Pain 2012; 28: 75565. Huijnen IP, Verbunt JA, Peters ML, et al. Dierences in activity-related behaviour among patients with chronic low back pain. Eur J Pain 2011; 15: 74855. Brunner E, De Herdt A, Minguet P, Baldew SS, Probst M. Can cognitive behavioural therapy based strategies be integrated into physiotherapy for the prevention of chronic low back pain? A systematic review. Disabil Rehabil 2013; 35: 110. Meeus M, Nijs J, Hamers V, Ickmans K, Oosterwijck JV. The ecacy of patient education in whiplash associated disorders: a systematic review. Pain Physician 2012; 15: 35161. Van Oosterwijck J, Nijs J, Meeus M, Van Loo M, Paul L. Lack of endogenous pain inhibition during exercise in people with chronic whiplash associated disorders: an experimental study. J Pain 2012; 13: 24254.

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13 Published online April 4, 2014