Pain Research and Treatment

Pain Research and Treatment / 2016 / Article

Comment on “Cost-Saving Early Diagnosis of Functional Pain in Nonmalignant Pain: A Noninferiority Study of Diagnostic Accuracy”

  • Katsuhiro Toda |
  •  Article ID 8542491 |
  •  Published 14 Sep 2016
  • | View Article

Response to: Comment on “Cost-Saving Early Diagnosis of Functional Pain in Nonmalignant Pain: A Noninferiority Study of Diagnostic Accuracy”

  • N. Egloff | R. J. Cámara | ... | R. von Känel |
  •  Article ID 4657102 |
  •  Published 29 Nov 2016

Letter to the Editor | Open Access

Volume 2016 |Article ID 4657102 | 2 pages | https://doi.org/10.1155/2016/4657102

Response to: Comment on “Cost-Saving Early Diagnosis of Functional Pain in Nonmalignant Pain: A Noninferiority Study of Diagnostic Accuracy”

Academic Editor: Donald A. Simone
Received19 Sep 2016
Accepted28 Sep 2016
Published29 Nov 2016

It is with great interest that we have read the comment by Toda [1], who refers to our publication “Cost-Saving Early Diagnosis of Functional Pain in Nonmalignant Pain: A Noninferiority Study of Diagnostic Accuracy” [2]. Toda proposes abandoning the differentiation between functional pain and neuropathic pain.

We agree with the author in that we believe that both types of pain are related to the nervous system in an equally tangible way and that both types of pain differ from classic nociceptive pain.

Undeniably, there are also fluent transitions between the two categories of pain [3] and syndromes with combinations of these two pain categories [4].

However, we wish to emphasize that the main difference lies in the pathogenetic causality. By definition, neuropathic pain arises through localized damage or diseases of nerves [5]. According to this definition, neuropathic pain corresponds to a bottom-up dysfunction of the “neural hardware.”

In somatoform-functional pain, however, the functionality of the nervous system is altered as a result of higher order information processes that influence central pain perception. These processes have no structural correlate and can often only be depicted by functional imaging techniques [6].

Information processes, such as biographical imprints, conditioning, and stress can all lead to pain sensitization of the central nervous system on the one hand [7] and to sensitization of the periphery via neuroendocrine top-down mechanisms on the other hand [8]. As our study shows, a resulting generalized hyperalgesia can be used as a core criterion to identify, with high diagnostic accuracy, such hyperperceptive functional pain disorders [2].

Interestingly, patients with functional pain and patients with neuropathic pain do not qualitatively describe their pain with the same words (e.g., agonizing versus burning). Lastly, the causal context of concomitant psychological symptoms is also not quite the same: a neuropathic pain may induce dysphoria and depression as secondary reactions. In contrast, the concept of stress-induced hyperalgesia relies on the evidence that concomitant psychological symptoms (depression, anxiety) accompanying functional pain are a consequence of the same triggering circumstances, that is, long-lasting distress [7]. In our opinion, functional and neuropathic pain should be differentiated. The distinction in pathogenesis implies different therapeutic approaches and also different preventive measures for these two types of pain.

Competing Interests

The authors declare no competing interests regarding the publication of this paper.

References

  1. K. Toda, “Comment on ‘cost-saving early diagnosis of functional pain in nonmalignant pain: a noninferiority study of diagnostic accuracy’,” Pain Research and Treatment, vol. 2016, Article ID 8542491, 1 pages, 2016. View at: Publisher Site | Google Scholar
  2. R. J. Cámara, C. Merz, B. Wegmann, S. Stauber, R. von Känel, and N. Egloff, “Cost-saving early diagnosis of functional pain in nonmalignant pain: a noninferiority study of diagnostic accuracy,” Pain Research and Treatment, vol. 2016, Article ID 5964250, 7 pages, 2016. View at: Publisher Site | Google Scholar
  3. N. Egloff, M. E. Sabbioni, C. Salathé, R. Wiest, and F. D. Juengling, “Nondermatomal somatosensory deficits in patients with chronic pain disorder: clinical findings and hypometabolic pattern in FDG-PET,” Pain, vol. 145, no. 1-2, pp. 252–258, 2009. View at: Publisher Site | Google Scholar
  4. N. Üçeyler and C. Sommer, “Fibromyalgia syndrome: a disease of the small nerve fibers?” Zeitschrift für Rheumatologie, vol. 74, no. 6, pp. 490–495, 2015. View at: Publisher Site | Google Scholar
  5. R.-D. Treede, T. S. Jensen, J. N. Campbell et al., “Neuropathic pain: redefinition and a grading system for clinical and research purposes,” Neurology, vol. 70, no. 18, pp. 1630–1635, 2008. View at: Publisher Site | Google Scholar
  6. B. Walitt, M. Ceko, J. Gracely, and R. Gracely, “Neuroimaging of central sensitivity syndromes: key insights from the scientific literature,” Current Rheumatology Reviews, vol. 12, no. 1, pp. 55–87, 2016. View at: Publisher Site | Google Scholar
  7. E. M. Jennings, B. N. Okine, M. Roche, and D. P. Finn, “Stress-induced hyperalgesia,” Progress in Neurobiology, vol. 121, pp. 1–18, 2014. View at: Publisher Site | Google Scholar
  8. S. G. Khasar, J. Burkham, O. A. Dina et al., “Stress induces a switch of intracellular signaling in sensory neurons in a model of generalized pain,” Journal of Neuroscience, vol. 28, no. 22, pp. 5721–5730, 2008. View at: Publisher Site | Google Scholar

Copyright © 2016 N. Egloff et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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