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

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 cohor...

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Detalles Bibliográficos
Autores principales: De Schoenmacker, Iara, Sirucek, Laura, Scheuren, Paulina S., Lütolf, Robin, Gorrell, Lindsay M., Brunner, Florian, Curt, Armin, Rosner, Jan, Schweinhardt, Petra, Hubli, Michèle
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10653599/
https://www.ncbi.nlm.nih.gov/pubmed/38027464
http://dx.doi.org/10.1097/PR9.0000000000001110
Descripción
Sumario: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.