November 16, 2016

The Complex World Of WAD: Prognosis

Author: Maggie Henjum

Lets pause the prognosis discussion and back up a bit to run over general characteristics of WAD. Anatomical lesion location has moderate supportive evidence of why the neck hurts after whiplash, with Jull et. al stating the largest body of evidence supporting lesions to zygapophysial joints.7 Some suggested evidence supports ligametous disruption, DRG/nerve roots, muscular injury, or disc injuries all being possibility of pain driver after WAD.2,5  A grading system can be clinically useful to differentiate between patients, but again seems to over-simplify the situation. Accepted grading system runs 0-4 with neck pain starting at grade 1 to grade 4, and differentiating factors between the other grades are: grade 1 having only reports of stiffness, grade 2 having palpable tenderness, and decreased ROM, and grades 3 and 4 becoming more drastic with neurological and sensory deficits (sensory disturbances, dizziness, hypo/hyperparesthesias, or hyporeflexia) with grade 4 defined as all of the above but with added fracture or dislocation.2,3 As previously stated, locating possible lesion area then grading the patient does not encompass the full story to drive prognosis.

Heterogeneity in presentation for patients with WAD creates difficulty for management and classification. Previously, I treated WAD by simplifying my approach to managing most obvious impairments, decreased ROM and weakness. This is moderately effective, but why not manage patients to the best of our ability? Patients with acute WAD demonstrate abnormal cervical and shoulder muscular recruitment patterns, balance loss, joint position error, local cervical mechanical hyperalgesia and psychological suffering.2,8Not all of these factors are appropriate to manage in a PT clinic, but all should be addressed. (Physical therapy treatments for WAD will be expanded on in a future post.)

Prognostic factors are important as drastic prevalence of persisting symptoms at 6 months (40-50%) and 2 years (10-25%).2 Identifying patients who are at higher liklihood to become chronic vs. acute, can be a challenge.2,4 Jull et. al article put it extremely well by stating that research has opened up and changed in the last decade to assessing how WAD injury mechanisms, attendant sensory, psychophysical, sensorimotor, and psychological responses can affect outcomes.4 The complexity of variables that play a role in recovery, alongside the heterogeneity of patients, may provide challenge when evaluating prognosis. Even though we may not understand the whole story, a few clinical factors are shown to correlate with persisting symptoms including: initial pain intensity (NDI > 30), age >45, and being a female. Also, the following are suggested: restricted neck ROM (combined right and left rotation of < 90 degrees: sp .95), cold hyperalgesia, catastrophizing symptoms, fear of movement, passive coping, lower pain self efficacy and distress (PTSS).2,5,6,8 How much do these affect outcomes?  We are not sure, but Interestingly enough, a study in 2007 by Jull et. al compared groups with or without cold hyperalgesia in chronic WAD patients. Both groups had 10 weeks of manual therapy, exercise, advice and assurance. Patients with the sensory presentation had no change on pain or disability, possibly indicating its importance.9

Disappointingly, even with the fun new pain science we have uncovered, it has made little affect on reducing progression from acute to chronic neck pain as reviews from 1983, and 2006 still report about 1/2 of patients have persistent symptoms past 1 month.6 Especially as most of these prognostic factors are not practical or challenging to identify in clinic. With as costly as this condition can be – 29 billion dollars/year – possibly more research is required for us to start managing outcomes a little better.5,6 Take home point here is this: we spend a lot of time with patients so take time to listen to their concerns, encourage them to actively cope, and when in doubt – ask for help.


Original post: August 26, 2013



1) Chien A, Eliav E, Sterling M. Whiplash (grade II) and cervical radiculopathy share a similar sensory presentation: an investigation us- ing quantitative sensory testing.Clin J Pain. 2008;24:595-603. AJP.0b013e31816ed4fc

2) Tim Noteboom. (2013, August). Whiplash Associated Disorders: Pain Control Category. Lecture conducted through EIM.

3) Sterling M. A Proposed New Classification System For Whiplash Associated Disorders — Implications For Assessment and Management. Manual Therapy. 2004; 9:60-79

4) Jull, G. a, Söderlund, A., Stemper, B. D., Kenardy, J., Gross, A. R., Côté, P., … Curatolo, M. (2011). Toward optimal early management after whiplash injury to lessen the rate of transition to chronicity: discussion paper 5. Spine, 36(25 Suppl), S335–42. doi:10.1097/BRS.0b013e3182388449

5) Elliott, J. M., Noteboom, J. T., Flynn, T. W., & Sterling, M. (2009). Characterization of acute and chronic whiplash-associated disorders. The Journal of Orthopaedic and Sports Physical Therapy, 39(5), 312–23. doi:10.2519/jospt.2009.2826

6) Carroll LJ. Holm LW, Guzman J. Course and Prognostic Factors For Neck Pain in Whiplash Associated Disorders. Eur Spine J. 2008; 17: 83-92.

7) Jull, G. a, Sterling, M., Curatolo, M., Carroll, L., & Hodges, P. (2011). Toward lessening the rate of transition of acute whiplash to a chronic disorder. Spine, 36(25 Suppl), S173–4. doi:10.1097/BRS.0b013e31823883e6

8) Sterling, M., & Kenardy, J. (2008). Physical and psychological aspects of whiplash: Important considerations for primary care assessment. Manual therapy, 13(2), 93–102. doi:10.1016/j.math.2007.11.003

9) Jull, G, Sterling, M, Kenardy J, Beller E. Does the presence of sensory hypersensitivity influence outcomes of physical rehabilitation for chronic whiplash? – A preliminary RCT. Pain. 2007: 129; 28-34.