TY - JOUR
T1 - Levels of preoperative cerebrospinal fluid pro-inflammatory mediators and chronic pain after total knee arthroplasty surgery
AU - Kato, Jungo
AU - Murase, Reiko
AU - Minoshima, Rie
AU - Lu, Fanglin
AU - Toramaru, Tomoko
AU - Niki, Yasuo
AU - Kosugi, Shizuko
AU - Morisaki, Hiroshi
N1 - Publisher Copyright:
© 2023 The Authors. Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.
PY - 2023/9
Y1 - 2023/9
N2 - Background: Patients undergoing total knee arthroplasty (TKA) surgery are at high risk of chronic postsurgical pain (CPSP). Accumulating evidence suggests an active role of neuroinflammation in chronic pain. However, its role in the progression to CPSP following TKA surgery remains unanswered. Here, we examined the associations between preoperative neuroinflammatory states and pre- and postsurgical chronic pain in TKA surgery. Methods: The data of 42 patients undergoing elective TKA surgery for chronic knee arthralgia at our hospital were analyzed in this prospective study. Patients completed the following questionnaires: brief pain inventory (BPI), hospital anxiety and depression scale, painDETECT, and pain catastrophizing scale (PCS). Cerebrospinal fluid (CSF) samples were collected preoperatively and concentrations of IL-6, IL-8, TNF, fractalkine, and CSF-1 were measured by electrochemiluminescence multiplex immunoassay. CPSP severity was ascertained, using the BPI, 6 months postsurgery. Results: While no significant correlation was observed between the preoperative CSF mediator levels and preoperative pain profiles, the preoperative fractalkine level in the CSF showed a significant correlation with CPSP severity (Spearman's rho = −0.525; p =.002). Furthermore, multivariate linear regression analysis revealed that the preoperative PCS score (standardized β coefficient [β]:.11; 95% confidence interval [CI]: 0.06–0.16; p <.001) and CSF fractalkine level (β: −.62; 95% CI: −1.10 to −0.15; p =.012) were independent predictors of CPSP severity 6 months after TKA surgery. Conclusions: We identified the CSF fractalkine level as a potential predictor for CPSP severity following TKA surgery. In addition, our study provided novel insights into the potential role of neuroinflammatory mediators in the pathogenesis of CPSP.
AB - Background: Patients undergoing total knee arthroplasty (TKA) surgery are at high risk of chronic postsurgical pain (CPSP). Accumulating evidence suggests an active role of neuroinflammation in chronic pain. However, its role in the progression to CPSP following TKA surgery remains unanswered. Here, we examined the associations between preoperative neuroinflammatory states and pre- and postsurgical chronic pain in TKA surgery. Methods: The data of 42 patients undergoing elective TKA surgery for chronic knee arthralgia at our hospital were analyzed in this prospective study. Patients completed the following questionnaires: brief pain inventory (BPI), hospital anxiety and depression scale, painDETECT, and pain catastrophizing scale (PCS). Cerebrospinal fluid (CSF) samples were collected preoperatively and concentrations of IL-6, IL-8, TNF, fractalkine, and CSF-1 were measured by electrochemiluminescence multiplex immunoassay. CPSP severity was ascertained, using the BPI, 6 months postsurgery. Results: While no significant correlation was observed between the preoperative CSF mediator levels and preoperative pain profiles, the preoperative fractalkine level in the CSF showed a significant correlation with CPSP severity (Spearman's rho = −0.525; p =.002). Furthermore, multivariate linear regression analysis revealed that the preoperative PCS score (standardized β coefficient [β]:.11; 95% confidence interval [CI]: 0.06–0.16; p <.001) and CSF fractalkine level (β: −.62; 95% CI: −1.10 to −0.15; p =.012) were independent predictors of CPSP severity 6 months after TKA surgery. Conclusions: We identified the CSF fractalkine level as a potential predictor for CPSP severity following TKA surgery. In addition, our study provided novel insights into the potential role of neuroinflammatory mediators in the pathogenesis of CPSP.
UR - http://www.scopus.com/inward/record.url?scp=85159359981&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85159359981&partnerID=8YFLogxK
U2 - 10.1111/aas.14278
DO - 10.1111/aas.14278
M3 - Article
C2 - 37193632
AN - SCOPUS:85159359981
SN - 0001-5172
VL - 67
SP - 1091
EP - 1101
JO - Acta Anaesthesiologica Scandinavica
JF - Acta Anaesthesiologica Scandinavica
IS - 8
ER -