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. 2023 Nov 15;8(6):e1110.
doi: 10.1097/PR9.0000000000001110. eCollection 2023 Dec.

Sensory phenotypes in complex regional pain syndrome and chronic low back pain-indication of common underlying pathomechanisms

Iara De Schoenmacker  1   2 , Laura Sirucek  2   3 , Paulina S Scheuren  1   4 , Robin Lütolf  1 , Lindsay M Gorrell  3 , Florian Brunner  5 , Armin Curt  1 , Jan Rosner  1   4   6 , Petra Schweinhardt  3   7 , Michèle Hubli  1
Affiliations

Sensory phenotypes in complex regional pain syndrome and chronic low back pain-indication of common underlying pathomechanisms

Iara De Schoenmacker et al. Pain Rep. .

Abstract

Introduction: First-line pain treatment is unsatisfactory in more than 50% of chronic pain patients, likely because of the heterogeneity of mechanisms underlying pain chronification.

Objectives: This cross-sectional study aimed to better understand pathomechanisms across different chronic pain cohorts, regardless of their diagnoses, by identifying distinct sensory phenotypes through a cluster analysis.

Methods: We recruited 81 chronic pain patients and 63 age-matched and sex-matched healthy controls (HC). Two distinct chronic pain cohorts were recruited, ie, complex regional pain syndrome (N = 20) and low back pain (N = 61). Quantitative sensory testing (QST) was performed in the most painful body area to investigate somatosensory changes related to clinical pain. Furthermore, QST was conducted in a pain-free area to identify remote sensory alterations, indicating more widespread changes in somatosensory processing.

Results: Two clusters were identified based on the QST measures in the painful area, which did not represent the 2 distinct pain diagnoses but contained patients from both cohorts. Cluster 1 showed increased pain sensitivities in the painful and control area, indicating central sensitization as a potential pathomechanism. Cluster 2 showed a similar sensory profile as HC in both tested areas. Hence, either QST was not sensitive enough and more objective measures are needed to detect sensitization within the nociceptive neuraxis or cluster 2 may not have pain primarily because of sensitization, but other factors such as psychosocial ones are involved.

Conclusion: These findings support the notion of shared pathomechanisms irrespective of the pain diagnosis. Conversely, different mechanisms might contribute to the pain of patients with the same diagnosis.

Keywords: Chronic pain; Cluster analysis; Pain phenotyping; Quantitative sensory testing; Sensory function.

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Conflict of interest statement

The authors have no conflict of interest to declare.Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Figures

Figure 1.
Figure 1.
Sensory profiles and proportional cohort distribution of the 2 patient clusters. (A) Sensory profiles measured in the painful area of the 2 clusters and healthy controls (HC). (B) Sensory profiles measured in the control area of the 2 clusters and HC. Illustrated are the averaged z-scores for each QST measurement domain (thermal detection, thermal pain, mechanical pain, mechanical detection). (C) Relative cohort distributions for each cluster. *P < 0.05, **P < 0.01, ***P < 0.001. CRPS, complex regional pain syndrome; LBP, low back pain; QST, quantitative sensory testing.
Figure 2.
Figure 2.
Relative number of participants with significant loss (blue) or gain (red) of function (based on the DFNS z-scores) for each cluster and healthy controls. (A) Cluster 1, (B) cluster 2, and (C) healthy controls are illustrated separately. CDT, cold detection threshold; CPT: cold pain threshold; DFNS, German research network on neuropathic pain; HPT, heat pain threshold; MDT, mechanical detection threshold; MPS, mechanical pain sensitivity; MPT, mechanical pain threshold; PPT, pressure pain threshold; TSL, thermal sensory limen; VDT, vibration detection threshold; WDT, warm detection threshold; WUR, wind-up ratio.
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