Background & Aims
Abnormalities in central pain processing have been implicated in various chronic pain conditions such as Fibromyalgia syndrome (FMS), migraines, and neuropathy. Two commonly used experimental methods for evaluating central pain modulation are conditioned pain modulation (CPM) and offset analgesia (OA). However, it is still uncertain how similar are the underlying processes they measure and whether they similarly or differentially relate to clinical pain symptomatology. Here, we applied CPM and OA in patients with FMS, a case study of central sensitization syndromes, to further explore these questions.
Methods
Fifty-four participants, twenty-seven female FMS patients, and twenty-seven age and sex-matched healthy controls, filled out questionnaires (Fibromyalgia Impact Questionnaire (FIQ), short-form McGill, State-Trait Anxiety Inventory (STAI), and pain catastrophizing scale) and underwent psychophysical pain testing (VAS60 determination test, CPM, and OA). CPM and OA were conducted in a randomized order.
Results
A significant positive correlation was found between CPM and OA in healthy controls (Rs=0.405, P=0.03), while a significant negative correlation was found between the two tests in FMS (R?= -0.478, P=0.01). Additionally, we divided FMS patients into good and bad CPM modulators (negative or positive CPM scores, respectively) and found that the significant negative correlation existed exclusively in bad modulators (R?=-0.57, P=0.03), while no correlation was found in good modulators. Furthermore, CPM in patients significantly and positively correlated with FIQ (R?=0.403, P=0.04) and McGill scores (R?=0.47, P=0.04), while OA negatively correlated with both (R?=-0.416, P=0.03) and (R?=-0.44, P=0.04), respectively.
Conclusions
This study is the first to link OA, and not just CPM with clinical features in FMS, and shows that these two experimental paradigms are differentially related to disease symptomatology. Accordingly, it suggests that different mechanisms seem to underlie CPM and OA, and that these can become dissociated in chronic pain such as FMS.
References
1.Clauw DJ. Fibromyalgia: An Overview. American Journal of Medicine. 2009;122(12 SUPPL.). doi:10.1016/j.amjmed.2009.09.006.
2.Staud R, Spaeth M. Psychophysical and neurochemical abnormalities of pain processing in fibromyalgia. CNS Spectrums. 2008;13(3 SUPPL. 5):12-17.
3.Defrin R, Pope G, Davis KD. Interactions between spatial sum-
mation, 2-point discrimination and habituation of heat pain. Eur
J Pain 2008;12(7):900–9.
4.Nahman-Averbuch, H., Martucci, K. T., Granovsky, Y., Weissman-Fogel, I., Yarnitsky, D., & Coghill, R. C. (2014). Distinct brain mechanisms support spatial vs temporal filtering of nociceptive information. PAIN®, 155(12), 2491-2501.
5. Petersel DL, Dror V, Cheung R. Central amplification and fibromyalgia: Disorder of pain processing. Journal of Neuroscience Research. 2011;89(1):29-34. doi:10.1002/jnr.22512.
6.Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition. Pain. 2005;114(1-2):295-302. doi:10.1016/j.pain.2004.12.032 .
7.Oudejans, L. C., Smit, J. M., van Velzen, M., Dahan, A., & Niesters, M. (2015). The influence of offset analgesia on the onset and offset of pain in patients with fibromyalgia. Pain, 156(12), 2521-2527.
8.Hubbard, C. S., Lazaridou, A., Cahalan, C. M., Kim, J., Edwards, R. R., Napadow, V., & Loggia, M. L. (2020). Aberrant salience? Brain hyperactivation in response to pain onset and offset in fibromyalgia. Arthritis & Rheumatology, 72(7), 1203-1213.
Presenting Author
Yara Agbaria
Poster Authors
Yara Agbaria
MSc
Tel Aviv University
Lead Author
Raz Preger
Tel Aviv University
Lead Author
Valerie Aloush MD
Tel Aviv Sourasky Medical Center
Lead Author
Jacob Ablin
Tel Aviv medical center
Lead Author
Giris Jacob MD PhD
Tel Aviv Sourasky Medical Center
Lead Author
Haggai Sharon MD PhD
Tel Aviv Sourasky Medical Center
Lead Author
Topics
- Assessment and Diagnosis