Can cortisol levels predict the severity of acute whiplash-associated disorders?

  • Daniela Shaked
  • Gad ShakedEmail author
  • Gilbert Sebbag
  • David Czeiger
Original Article



The exact underlying mechanism of whiplash-associated disorders still remains obscure. Central sensitization of the brain to painful stimulus and disturbances in the hypothalamic–pituitary–adrenal axis has been suggested to contribute to the development of whiplash-associated disorders. Although cortisol is a well-known factor in the acute stress response and its effects on chronic pain sensation were studied, information is lacking regarding the relation between acute phase cortisol concentrations and the intensity of whiplash-associated disorders. The aim of this prospective observational study was to investigate the relationship between acute serum cortisol concentrations and the severity of whiplash-associated disorders.


55 patients enrolled in the study and they answered a pertinent questionnaire. A blood sample was drawn to determine serum cortisol concentration.


The mean cortisol concentration of the whiplash-associated disorder score 2–3 patients was significantly lower compared to the whiplash-associated disorder score 1 patients, 9.5 ± 6.9 vs. 13.22 ± 8.3 µg% (p = 0.02). The mean cortisol concentrations increased significantly from mild through moderate to serious grade of severity of accident as perceived by the patient, 9.64 ± 4.82, 11.59 ± 6.85, 17.39 ± 12.1 µg% (p = 0.02).


The study supports the possibility that cortisol plays a role in the development of whiplash-associated disorders. Low or relatively low cortisol concentrations might be associated with more severe forms of the disorder.


Neck injury Whiplash Cortisol Stress 


Compliance with ethical standards

Conflict of interest

All authors declare to have no conflict of interest in this research.

Ethical approval

The study was approved by the local Institutional Review Board committee (SOR-0237-13).

Informed consent

All patients enrolled into the study signed a consent form.


  1. 1.
    Bylund PO, Bjornstig U. Sick leave and disability pension among passenger car occupants injured in urban traffic. Spine (Phila Pa1976). 1998;23(9):1023–8.CrossRefGoogle Scholar
  2. 2.
    Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, et al. Scientific monograph of the Quebec Task Force on whiplash-associated disorders: redefining “whiplash” and its management. Spine (Phila Pa1976). 1995;20(8 Suppl):1S–73S.Google Scholar
  3. 3.
    Panjabi MM, Cholewicki J, Nibu K, Grauer JN, Babat LB, Dvorak J. Mechanism of whiplash injury. Clin Biomech (Bristol, Avon) 1998;(4–5):239–49.CrossRefGoogle Scholar
  4. 4.
    Croft AC, Herring P, Freeman MD, Haneline MT. The neck injury criterion: future considerations. Accid Anal Prev. 2002;34(2):247–55.CrossRefGoogle Scholar
  5. 5.
    Brault JR, Siegmund GP, Wheeler JB. Cervical muscle response during whiplash: evidence of a lengthening muscle contraction. Clin Biomech (Bristol Avon). 2000;15(6):426–35.CrossRefGoogle Scholar
  6. 6.
    Giannoudis PV, Mehta SS, Tsiridis E. Incidence and outcome of whiplash injury after multiple trauma. Spine (Phila Pa1976). 2007;32(7):776–81.CrossRefGoogle Scholar
  7. 7.
    Ferrari R, Schrader H. The late whiplash syndrome: a biopsychosocial approach. J Neurol Neurosurg Psychiatry. 2001;70(6):722–6.CrossRefGoogle Scholar
  8. 8.
    McLean SA, Clauw DJ, Abelson JL, Liberzon I. The development of persistent pain and psychological morbidity after motor vehicle collision: integrating the potential role of stress response systems into a biopsychosocial model. Psychosom Med. 2005;67(5):783–90.CrossRefGoogle Scholar
  9. 9.
    Rang HP, Bevan S, Dray A. Chemical activation of nociceptive peripheral neurones. Br Med Bull. 1991;47(3):534–48.CrossRefGoogle Scholar
  10. 10.
    Wand BM, O’Connell N, Parkitny L. Depression may contribute to the sensory changes in whiplash patients? Re: Chien, A, Sterling, M. Sensory hypoaesthesia is a feature of chronic whiplash but not chronic idiopathic neck pain. Man Ther. 2010;15:48–53 (Man. Ther. 2010; 15(3):e1; author reply e2).CrossRefGoogle Scholar
  11. 11.
    Wynne-Jones G, Jones GT, Wiles NJ, Silman AJ, Macfarlane GJ. Predicting new onset of widespread pain following a motor vehicle collision. J Rheumatol. 2006;33(5):968–74.PubMedGoogle Scholar
  12. 12.
    Hocking LJ, Smith BH, Jones GT, Reid DM, Strachan DP, Macfarlane GJ. Genetic variation in the beta2-adrenergic receptor but not catecholamine-O-methyltransferase predisposes to chronic pain: results from the 1958 British Birth Cohort Study. Pain. 2010;149(1):143–51.CrossRefGoogle Scholar
  13. 13.
    McLean SA. The potential contribution of stress systems to the transition to chronic whiplash-associated disorders. Spine (Phila Pa1976). 2011;36(25 Suppl):226–32.CrossRefGoogle Scholar
  14. 14.
    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(1–3):219–24.CrossRefGoogle Scholar
  15. 15.
    Galasko CSB, Murray P, Stephenson W. Incidence of whiplash-associated disorder. BCM J. 2002;44(5):237–40.Google Scholar
  16. 16.
    Quinlan KP, Annest JL, Myers B, Ryan G, Hill H. Neck strains and sprains among motor vehicle occupants-United States, 2000. Accid Anal Prev. 2004;36(1):21–7.CrossRefGoogle Scholar
  17. 17.
    Walton DM, Elliott JM. An integrated model of chronic whiplash-associated disorder. J Orthop Sports Phys Ther. 2017;47(7):462–71.CrossRefGoogle Scholar
  18. 18.
    Nijs J, Meeus M, Cagnie B, Roussel NA, Dolphens M, Van Oosterwijck J, et al. A modern neuroscience approach to chronic spinal pain: combining pain neuroscience education with cognition-targeted motor control training. Phys Ther. 2014;94(5):730–8.CrossRefGoogle Scholar
  19. 19.
    Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Giani C, Zbinden AM, Radanov BP. Central hypersensitivity in chronic pain after whiplash injury. Clin J Pain. 2001;17(4):306–15.CrossRefGoogle Scholar
  20. 20.
    Sterling M, Treleaven J, Edwards S, Jull G. Pressure pain thresholds in chronic whiplash associated disorder: further evidence of altered central pain processing. J Musculoskelet Pain. 2002;10(3):69–81.CrossRefGoogle Scholar
  21. 21.
    Sterling M, Jull G, Vicenzino B, Kenardy J. Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Pain. 2003;104(3):509–17.CrossRefGoogle Scholar
  22. 22.
    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(1–2):28–34.CrossRefGoogle Scholar
  23. 23.
    Jovanovic T, Phifer JE, Sicking K, Weiss T, Norrholm SD, Bradley B, et al. Cortisol suppression by dexamethasone reduces exaggerated fear responses in posttraumatic stress disorder. Psychoneuroendocrinology. 2011;36(10):1540–52.CrossRefGoogle Scholar
  24. 24.
    Paananen M, O’Sullivan P, Straker L, Beales D, Coenen P, Karppinen J, et al. A low cortisol response to stress is associated with musculoskeletal pain combined with increased pain sensitivity in young adults: a longitudinal cohort study. Arthritis Res Ther. 2015;17:355.CrossRefGoogle Scholar
  25. 25.
    Carstensen TB. The influence of psychosocial factors on recovery following acute whiplash trauma. Dan Med J. 2012;59(12):B4560.PubMedGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  • Daniela Shaked
    • 1
  • Gad Shaked
    • 2
    Email author
  • Gilbert Sebbag
    • 2
  • David Czeiger
    • 2
  1. 1.Physical Therapy Department, Recanati School for Community Health Professions, Faculty of Health SciencesBen-Gurion UniversityBeer ShevaIsrael
  2. 2.Department of General Surgery and Trauma UnitSoroka University Medical Center, Ben-Gurion UniversityBeer ShevaIsrael

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