Post-surgical contributors to persistent knee pain following knee replacement: The Multicenter Osteoarthritis Study (MOST).

Objective: Pain persistence following knee replacement (KR) occurs in ∼20-30% of patients. Although several studies have identified preoperative risk factors for persistent post-KR pain, few have focused on post-KR contributing factors. We sought to determine whether altered nociceptive signaling and other peripheral nociceptive drivers present post-operatively contribute to post-KR pain. Design: We included participants from the Multicenter Osteoarthritis Study who were evaluated ∼12 months after KR. We evaluated the relation of measures of pain sensitivity [pressure pain threshold (PPT), temporal summation (TS), and conditioned pain modulation (CPM)] and the number of painful body sites to post-KR WOMAC knee pain, and of the number of painful sites to altered nociceptive signaling using linear or logistic regression models, as appropriate. Results: 171 participants (mean age 69 years, 62% female) were included. TS was associated with worse WOMAC pain post-KR (ߠ​= â€‹0.77 95% CI:0.19-1.35) and reduced odds of achieving patient acceptable symptom state (aOR â€‹= â€‹0.54 95%CI:0.34-0.88). Inefficient CPM was also associated with worse WOMAC pain post-KR (ߠ​= â€‹1.43 95% CI:0.15-2.71). In contrast, PPT was not associated with these outcomes. The number of painful body sites present post-KR was associated with TS (ߠ​= â€‹0.05, 95% CI:0.01, 0.05). Conclusions: Post-KR presence of central sensitization and inefficient descending pain modulation was associated with post-KR pain. We also noted that presence of other painful body sites contributes to altered nociceptive signaling, and this may thus also contribute to the experience of knee pain post-KR. Our findings provide novel insights into central pain mechanisms and other peripheral pain sources contributing to post-KR persistent knee pain.

Patterns of movement-evoked pain during tendon loading and stretching tasks in Achilles tendinopathy: A secondary analysis of a randomized controlled trial.

BACKGROUND: This study aimed to characterize movement-evoked pain during tendon loading and stretching tasks in individuals with Achilles tendinopathy, and to examine the association between movement-evoked pain with the Achilles tendinopathy type (insertional and midportion), biomechanical, and psychological variables. METHODS: In this laboratory-based, cross-sectional study, 37 individuals with chronic Achilles tendinopathy participated. Movement-evoked pain intensity (Numeric Rating Scale: 0 to 10) and sagittal-plane ankle biomechanics were collected simultaneously during standing, fast walking, single-leg heel raises, and weight-bearing calf stretch. Description of symptoms, including location of Achilles tendon pain and duration of tendon morning stiffness, as well as pain-related psychological measures, including the Tampa Scale of Kinesiophobia were collected. Linear mixed effects models were built around two paradigms of movement-evoked pain (tendon loading and stretching tasks) with each model anchored with pain at rest. FINDINGS: Movement-evoked pain intensity increased as task demand increased in both models. Lower peak dorsiflexion with walking (ß = -0.187, 95% CI: -0.305, -0.069), higher fear of movement (ß = 0.082, 95% CI: 0.018, 0.145), and longer duration of tendon morning stiffness (ß = 0.183, 95% CI: 0.07, 0.296) were associated with greater pain across tendon loading tasks (R2 = 0.47). Lower peak dorsiflexion with walking (ß = -0.27, 95% CI: -0.41, -0.14), higher dorsiflexion with the calf stretch (ß = 0.095, 95% CI: 0.02, 0.16), and insertional Achilles tendinopathy (ß = -0.93, 95% CI: -1.65, -0.21) were associated with higher pain across tendon stretching tasks (R2 = 0.53). INTERPRETATION: In addition to exercise, the ideal management of Achilles tendinopathy may require adjunct treatments to address the multifactorial aspects of movement-evoked pain.

Association of Pain Sensitization and Conditioned Pain Modulation to Pain Patterns in Knee Osteoarthritis.

OBJECTIVE: To examine the cross-sectional association of ascending pain mechanisms, implicated in pain sensitization, and descending pain modulation with pain patterns and unpredictability of pain. METHODS: The Multicenter Osteoarthritis Study is a longitudinal cohort of older adults with or at risk of knee osteoarthritis. Peripheral and central ascending pain mechanisms were assessed using quantitative sensory tests, pressure pain thresholds using a handheld pressure algometer (knee/peripheral and wrist/central), and temporal summation using weighted probes (wrist/central). Descending modulation was assessed by conditioned pain modulation using pressure pain thresholds and a forearm ischemia test. Pain patterns were characterized based on responses to the Intermittent and Constant Osteoarthritis Pain questionnaire: 1) no intermittent or constant pain, 2) intermittent pain only, 3) constant pain only, and 4) combined constant and intermittent pain. A question regarding frequency assessed unpredictable pain. We assessed the association of quantitative sensory test measures to pain patterns using regression models with generalized estimating equations. RESULTS: There were 2,794 participants (mean age 63.9 years, body mass index 29.5 kg/m2 , and 57% female). Lower pain sensitization by wrist pressure pain threshold (odds ratio [OR] 0.80 [95% confidence interval (95% CI) 0.68, 0.93]) and adequate conditioned pain modulation (OR 1.45 [95% CI 1.10, 1.92]) were associated with having constant ± intermittent pain compared with intermittent pain only. Higher pain sensitization (by pressure pain thresholds and temporal summation) was associated with a higher likelihood of unpredictable pain. CONCLUSION: Knee pain patterns appear to be related to peripheral ± central facilitated ascending pain mechanisms and descending modulatory mechanisms. These findings highlight the need for a broader approach to understanding pain mechanisms by symptomatic disease progression.

Association of Joint Inflammation With Pain Sensitization in Knee Osteoarthritis: The Multicenter Osteoarthritis Study.

OBJECTIVE: Pain sensitization is associated with pain severity in knee osteoarthritis (OA), but its cause in humans is not well understood. We examined whether inflammation, assessed as synovitis and effusion on magnetic resonance imaging (MRI), or mechanical load, assessed as bone marrow lesions (BMLs), was associated with sensitization in knee OA. METHODS: Subjects in the Multicenter Osteoarthritis Study, a National Institutes of Health-funded cohort of persons with or at risk of knee OA, underwent radiography and MRI of the knee, and standardized quantitative sensory testing (temporal summation and pressure pain threshold [PPT]) of the wrist and patellae at baseline and 2 years later. We examined the relation of synovitis, effusion, and BMLs to temporal summation and PPT cross-sectionally and longitudinally. RESULTS: There were 1,111 subjects in the study sample (mean age 67 years, mean body mass index 30 kg/m(2) , 62% female). Synovitis was associated with a significant decrease in PPT at the patella (i.e., more sensitized) over 2 years (adjusted ß -0.30 [95% confidence interval (95% CI) -0.52, -0.08]). Effusion was similarly associated with a decrease in PPT at the wrist (adjusted ß -0.24 [95% CI -0.41, -0.08]) and with risk of incident temporal summation at the patella (adjusted OR 1.54 [95% CI 1.01, 2.36]). BMLs were not associated with either quantitative sensory testing measure. CONCLUSION: Inflammation, as evidenced by synovitis or effusion, is associated with pain sensitization in knee OA. In contrast, BMLs do not appear to contribute to sensitization in knee OA. Early targeting of inflammation is a reasonable strategy to test for prevention of sensitization and through this, reduction of pain severity, in knee OA.

The influence of the contralateral knee prior to knee arthroplasty on post-arthroplasty function: the multicenter osteoarthritis study.

BACKGROUND: Some of the poor functional outcomes of knee arthroplasty may be due to pain in the contralateral, unreplaced knee. We investigated the relationship between the preoperative pain status of the contralateral knee and the risk of a poor postoperative functional outcome in patients who underwent knee arthroplasty. METHODS: We analyzed data on 271 patients in the Multicenter Osteoarthritis Study who had undergone knee arthroplasty since the time of enrollment. Eighty-six percent of these patients were white, 72% were female, and the mean age was sixty-seven years. The severity of pain in the knee contralateral to the one that was replaced was measured before the knee arthroplasty with use of the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain scale, with the scores being grouped into four categories (0, 1 to 4, 5 to 9, and 10 to 20). Poor post-arthroplasty function six months or more after surgery was determined with use of the Patient Acceptable Symptom State (PASS) outcome tool and a clinical performance measure of walking speed. We evaluated the relationship between contralateral pain severity and the functional outcomes with use of Poisson regression. RESULTS: Seventy-two (27%) of 264 patients demonstrated poor post-arthroplasty function by failing to attain the threshold PASS score, and seventy-six (30%) of 250 subjects had a slow walking speed. As the pre-arthroplasty pain in the contralateral knee increased, there was a steady increase in the proportion with poor post-arthroplasty function (p < 0.0001 for PASS and p = 0.04 for slow walking speed). Compared with patients who had no pre-arthroplasty pain in the contralateral knee, those in the highest category of contralateral pain severity had 4.1 times the risk (95% confidence interval, 1.5 to 11.5) of having poor self-reported post-arthroplasty function. Patients in whom both knees had been replaced at the time of outcome collection were less likely to have poor self-reported function than those in whom only one knee had been replaced. CONCLUSIONS: Preoperative pain in the contralateral knee is strongly associated with self-reported post-arthroplasty functional outcome and may therefore be a useful indicator of prognosis or a potential target of perioperative intervention. LEVEL OF EVIDENCE: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

Modeling nonlinear errors in surface electromyography due to baseline noise: a new methodology.

The surface electromyographic (EMG) signal is often contaminated by some degree of baseline noise. It is customary for scientists to subtract baseline noise from the measured EMG signal prior to further analyses based on the assumption that baseline noise adds linearly to the observed EMG signal. The stochastic nature of both the baseline and EMG signal, however, may invalidate this assumption. Alternately, "true" EMG signals may be either minimally or nonlinearly affected by baseline noise. This information is particularly relevant at low contraction intensities when signal-to-noise ratios (SNR) may be lowest. Thus, the purpose of this simulation study was to investigate the influence of varying levels of baseline noise (approximately 2-40% maximum EMG amplitude) on mean EMG burst amplitude and to assess the best means to account for signal noise. The simulations indicated baseline noise had minimal effects on mean EMG activity for maximum contractions, but increased nonlinearly with increasing noise levels and decreasing signal amplitudes. Thus, the simple baseline noise subtraction resulted in substantial error when estimating mean activity during low intensity EMG bursts. Conversely, correcting EMG signal as a nonlinear function of both baseline and measured signal amplitude provided highly accurate estimates of EMG amplitude. This novel nonlinear error modeling approach has potential implications for EMG signal processing, particularly when assessing co-activation of antagonist muscles or small amplitude contractions where the SNR can be low.