Home Medicine High prevalence of posttraumatic stress disorder (PTSD) and pain sensitization in two Scandinavian samples of patients referred for pain rehabilitation
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High prevalence of posttraumatic stress disorder (PTSD) and pain sensitization in two Scandinavian samples of patients referred for pain rehabilitation

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Published/Copyright: January 1, 2012
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Scandinavian Journal of Pain
From the journal Scandinavian Journal of Pain Volume 3 Issue 1

In the study by Andersen et al. published in the present issue of the Scandinavian Journal of Pain [1] the authors report on posttraumatic distress disorder (PTSD) as seen in two pain rehabilitation units in Scandinavia and show a rather high proportion of patients having PTSD in these pain clinics. PTSD is a syndrome characterized by the presence of a specific traumatic event – physical or psychological – together with a series of different symptoms. These symptoms are related to the re-experience of symptoms during the traumatic event, avoidance and hypervigilance. The criteria have now been emphasized in the DSM IV criteria for PTSD. According to the DSM IV classification of PTSD, serious illness and traffic accident now qualify for one of the A criteria of PTSD. Given the fact that events such as traffic accidents now represent a qualifying condition for PTSD, it is not surprising that PTSD is seen in pain clinics and pain centers in high numbers. For example, pain in the neck and head following forced flexion-extension injury to the neck after traffic accidents as part of the so-called whiplash syndrome is a well known pain disorders referred to pain clinics for rehabilitation. In the present study by Andersen et al., pain was assessed indirectly and retrospectively by the referral of patients to a pain clinic so the exact contribution of pain per se cannot be determined. Further studies are necessary to determine more precisely the role of, for example, pain intensity and the role of pain among possible causes of the PTSD syndrome.

In this study [1], the authors looked specifically on sensitization phenomena in both PTSD and pain. It is a well-known fact that chronic pain often is associated with hypersensitivity [2]. Here hypersensitivity to cold, but not to mechanical modalities, was apparently more frequent among those pain patients who had PTSD than in those without PTSD. The reason for this selective hyper-sensitivity is not clear and calls for further examination. It is of interest to speculate on the neuronal mechanism that apparently gives rise to more hypersensitivity in the PTSD group. The proposal that both PTSD and chronic pain conditions such as fibromyalgia and whiplash-associated disorders (WAD) may have hyperalgesia [2, 3, 4, 5] raises the possibility that these conditions share common neuronal mechanisms. It is now well-known that the hypersensitivity in patients with fibromyalgia and WAD is associated with facilitation of descending control with a pronociceptive output from the brainstem to the spinal cord [6,7].

A puzzling feature in the study by Andersen et al. [1] is the combination of hyposensitivity and hypersensitivity in patients with PTSD. The combination of increased and decreased sensibility in the same patient is a characteristic albeit not pathognomonic feature of neuropathic pain. This observation should not lead to the conclusion that the present samples of patients with PTSD and pain have a neuropathic pain condition. Without a demonstrable lesion or disease of the normal somatosensory system, a neuropathic pain condition cannot be inferred [4]. Therefore, the exact underlying mechanisms for the present sensory abnormality are unclear. However, the study does suggest that the normal subtle balance regulating the somatosensory processing is disturbed in patients who have been exposed to a traumatic external event such as a traffic accident or a severe stressful psychological experience.

DOI of refers to article: 10.1016/j.sjpain.2011.10.001.

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References

[1] Andersen TE, Andersen PG, Vakkala MA, Elklit A. The traumatized chronic pain patient – prevalence of PTSD and pain sensitization in two Scandinavian samples referred for pain rehabilitation. Scand J Pain 2012;3:39–43.Search in Google Scholar

[2] Mayer EA, Bushnell MC. Functional pain syndromes. Seattle: IASP Press; 2009. p. 1–580.Search in Google Scholar

[3] Clauw DJ. Fibromyalgia: an overview. Am J Med 2009;122 (12 Suppl.):S3–13.Search in Google Scholar

[4] Jensen TS, Baron R, Haanpaa M, Kalso E, Loeser JD, Rice ASC, Treede R-D. A new definition of neuropathic pain. Pain 2011;152:2204–5.Search in Google Scholar

[5] Kasch H, Qerama E, Kongsted A, Bach FW, Bendix T, Jensen TS. Deep muscle pain, tender points and recovery in acute whiplash patients: a 1-year follow-up study. Pain 2008;140:65–73.Search in Google Scholar

[6] Gebhart GF. Descending modulation of pain. Neurosci Biobehav Rev 2004;27:729–37.Search in Google Scholar

[7] Bannister K, Bee LA, Dickenson AH. Preclinical and early clinical investigations related to monoaminergic pain modulation. Neurotherapeutics 2009;4:703–12.Search in Google Scholar
Published Online: 2012-01-01
Published in Print: 2012-01-01

© 2011 Scandinavian Association for the Study of Pain

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  18. High prevalence of posttraumatic stress disorder (PTSD) and pain sensitization in two Scandinavian samples of patients referred for pain rehabilitation
  19. Clinical pain research
  20. The traumatised chronic pain patient—Prevalence of posttraumatic stress disorder - PTSD and pain sensitisation in two Scandinavian samples referred for pain rehabilitation
  21. Editorial comment
  22. Local infiltration analgesia (LIA) and repeated bolus or continuous infusion peripheral nerve blocks for acute postoperative pain: Be ware of local anaesthetic toxicity, especially in elderly patients with cardiac co-morbidities!
  23. Clinical pain research
  24. A randomized study comparing plasma concentration of ropivacaine after local infiltration analgesia and femoral block in primary total knee arthroplasty
  25. Editorial comment
  26. Computer work can cause deep tissue hyperalgesia: Implications for prevention and treatment
  27. Original experimental
  28. Deep tissue hyperalgesia after computer work
https://doi.org/10.1016/j.sjpain.2011.11.011

Articles in the same Issue

  1. Editorial comment
  2. Keeping an open mind: Achieving balance between too liberal and too restrictive prescription of opioids for chronic non-cancer pain: Using a two-edged sword
  3. Educational case report
  4. Chronic non-cancer pain and the long-term efficacy and safety of opioids: Some blind men and an elephant?
  5. Editorial comment
  6. National versions of fibromyalgia questionnaire: Translated protocols or validated instruments?
  7. Original experimental
  8. Validation of a Finnish version of the Fibromyalgia Impact Questionnaire (Finn-FIQ)
  9. Editorial comment
  10. The impact of chronic pain—European patients’ perspective over 12 months
  11. Original experimental
  12. The impact of chronic pain—European patients’ perspective over 12 months
  13. Editorial comment
  14. Pressure pain algometry — A call for standardisation of methods
  15. Original experimental
  16. Experimental pressure-pain assessments: Test-retest reliability, convergence and dimensionality
  17. Editorial comment
  18. High prevalence of posttraumatic stress disorder (PTSD) and pain sensitization in two Scandinavian samples of patients referred for pain rehabilitation
  19. Clinical pain research
  20. The traumatised chronic pain patient—Prevalence of posttraumatic stress disorder - PTSD and pain sensitisation in two Scandinavian samples referred for pain rehabilitation
  21. Editorial comment
  22. Local infiltration analgesia (LIA) and repeated bolus or continuous infusion peripheral nerve blocks for acute postoperative pain: Be ware of local anaesthetic toxicity, especially in elderly patients with cardiac co-morbidities!
  23. Clinical pain research
  24. A randomized study comparing plasma concentration of ropivacaine after local infiltration analgesia and femoral block in primary total knee arthroplasty
  25. Editorial comment
  26. Computer work can cause deep tissue hyperalgesia: Implications for prevention and treatment
  27. Original experimental
  28. Deep tissue hyperalgesia after computer work
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