THE ASSOCIATION of PAINFUL and NON-PAINFUL COMORBIDITIES with CENTRAL MECHANISMS of KNEE PAIN.

Abstract

Background Central mechanisms of knee pain occur in the central nervous system and may intensify and prolong pain. Central pain mechanisms might be facilitated by ongoing nociceptive input. A link between multimorbidity and central mechanisms of knee pain is proposed; ongoing sensory inputs due to comorbidities may trigger changes in pain processing by the CNS. This might be particularly expected with painful comorbidities. Objectives To investigate potential relationships of painful and non-painful multimorbidity with central mechanisms of knee pain. Methods Cross-sectional analysis of self-report data from participants of the Investigating Musculoskeletal Health and Wellbeing cohort, who reported knee as their most bothersome site of joint pain over the previous month, with pain rated ≥1/10, and who had completed FRAIL and CAP-Knee (1) questionnaires. Two indirect measures suggesting central mechanisms involvement in knee pain were used as dependent variables; pain intensity (0-10 numerical rating scale) and CAP-Knee score (0-16 scale). Comorbidities were assigned either “painful comorbidity” or “non-painful comorbidity” status based on IASP classification of chronic pain criteria (2). Multivariable linear regression models, adjusted for age and sex, were employed to explore associations of comorbidity counts with pain intensity and CAP-Knee score. Results 736 participants satisfied inclusion criteria. 55% were female, mean age 71 (range 40 to 95). Painful comorbidity count and non-painful comorbidity count each had positive associations with pain intensity (β=0.42, 95% CI=0.29 to 0.54, p<0.001; and β=0.31, 95%CI=0.16 to 0.45, p<0.001, respectively). Painful and non-painful comorbidity counts each also were associated with CAP-Knee score (β=0.80, 95% CI=0.59 to 1.01, p<0.001; and β=0.52, 95% CI=0.27 to 0.77, p<0.001, respectively). Painful and non-painful comorbidity counts each remained significantly associated both with pain intensity and with CAP-Knee scores when both types of comorbidity count were included in the same multivariable model. Conclusion Both painful and non-painful comorbidities were positively associated with central mechanisms of knee pain, providing further insight into the interconnectedness of pain processing systems and the rest of the body. The explanation behind these relationships may depend on more than just ongoing nociceptive input. Future work should address possible contributions from genetic, pathophysiological, psychological, and pharmacological factors associated with comorbid diagnosis.