Research Paper
Presurgical assessment of temporal summation of pain predicts the development of chronic postoperative pain 12 months after total knee replacement Kristian Kjær Petersena, Lars Arendt-Nielsena,*, Ole Simonsenb, Oliver Wilder-Smitha,c, Mogens Berg Laursenb
Abstract Patients with knee osteoarthritis demonstrate decreased pressure pain thresholds (PPTs), facilitated temporal summation (TS) of pain, and decreased conditioned pain modulation (CPM) compared with healthy controls. This study aimed to correlate preoperative PPTs, TS, and CPM with the development of chronic postoperative pain after total knee replacement (TKR) surgery. Knee pain intensity (visual analog scale [VAS]: 0-10), PPTs, TS, and CPM were collected before, 2 months, and 12 months after TKR. Patients were divided into a low-pain (VAS , 3) and a high-pain (VAS $ 3) group based on their VAS 12 months after TKR. The high-pain group (N 5 17) had higher pain intensities compared with the low-pain group (N 5 61) before surgery (P 5 0.009) and 12 months after surgery (P , 0.001). The PPTs of the low-pain groups were normalized for all measurement sites comparing presurgery with 12 months postsurgery (P , 0.05, contralateral arm: P 5 0.059), which was not the case for the high-pain group. The low-pain group showed a functional inhibitory CPM preoperatively and 12 months postoperatively (P , 0.05), which was not found in the high-pain group. The high-pain group had higher facilitated TS preoperatively and 12 months postoperatively compared with the low-pain group (P , 0.05). Preoperative TS level correlated to 12-month postoperative VAS (R 5 0.240, P 5 0.037). Patients who developed moderate-to-severe pain had pronociceptive changes compared with patients who developed mild pain postsurgery. Preoperative TS level correlated with the postoperative pain intensity and may be a preoperative mechanistic predictor for the development of chronic postoperative pain in patients with osteoarthritis after TKR. Keywords: Osteoarthritis, Conditioning pain modulation, Hyperalgesia, Temporal summation, Chronic postoperative pain
1. Introduction Osteoarthritis (OA) is the most frequent painful musculoskeletal diagnosis in the elderly population and the most common cause of disability29 with 40% of women and 25% of men aged 60 to 70 years being diagnosed with OA.35 With an expected global growth in the elderly population, the incidence of OA is predicted to increase in the future.10,11,13 Nearly 500,000 total knee replacements (TKRs) were performed in the United States in 2011, which is estimated to increase to 3.5 million in 2030.27 Approximately 20% of these patients will suffer from chronic postoperative pain after TKR surgery.12 Pre- and post-TKR treatment with pregabalin seem to inhibit the development of chronic postoperative pain,14 indicating that preoperative sensitization of the nervous system may be connected with the development of postoperative chronic pain. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. a
Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark, b Orthopaedic Surgery Research Unit, Aalborg University Hospital, Aalborg, Denmark, c Department of Anaesthesiology, Pain and Palliative Medicine, Radboud University Medical Centre, Nijmegen, the Netherlands *Corresponding author. Address: Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Fredrik Bajers Vej 7, D3, DK-9220 Aalborg, Denmark. Tel.: 145 9940 8831; fax: 145 9815 4008. E-mail address: [email protected] (L. Arendt-Nielsen). PAIN 156 (2015) 55–61 © 2014 International Association for the Study of Pain http://dx.doi.org/10.1016/j.pain.0000000000000022
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Pressure pain thresholds (PPTs), temporal summation (TS) of pain, and conditioned pain modulation (CPM) are 3 types of quantitative sensory testing (QST) measurements that have been widely used to diagnose altered pain processing in patients with hip and knee OA.7,11,21,24,32 Widespread hyperalgesia, a sign of sensitized and facilitated pain processing, has been demonstrated in patients with knee OA,7 which has been normalized after TKR surgery.21 Patients with OA demonstrating more than 1 location of pain often express pain symptoms that are more diffuse and spread to larger areas,34 supporting the notion that spreading sensitization may be present in these patients.4 Recently, several studies have identified subgroups of patients with knee OA with different degrees of radiological joint damage, pain, inflammation levels, and sensitization of pain processing.7,17,18,21–23,31 Inhibition and facilitation of descending inhibitory modulation of the peripheral nociceptive inputs to the dorsal horn neurons are important mechanisms in the sensitization of pain processing.6 Conditioned pain modulation, a measure of potential descending modulatory capacity, is an estimate of the net effect of the facilitating and the inhibitory system,6 and it is induced by a painful conditioning stimulus, eg, a cold pressor test,8 ischemic7 or heat38 pain. Preoperative CPM deficiency has been shown to predict the risk of development of postoperative chronic pain in patients undergoing thoracotomy38 and abdominal surgery.37 In chronic musculoskeletal pain conditions such as OA and fibromyalgia, TS of pain has been demonstrated to be facilitated compared with healthy controls.7,33 Facilitated TS has been shown to predict the development of acute postoperative pain in www.painjournalonline.com
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patients undergoing thoracotomy,36 which is a precursor for the development of chronic postoperative pain.30 To date, no studies have linked a battery of preoperative QST parameters (including TS and CPM) to the development of chronic pain after TKR surgery in patients with knee OA. The aims of this study were (1) to compare preoperative pain intensity and QST parameters in patients with knee OA who develop different degrees of chronic pain after TKR surgery and (2) to identify preoperative parameters that possibly predict the development of chronic postoperative pain after TKR.
2. Methods 2.1. Protocol Patients from the North Denmark Region with severe knee OA scheduled for TKR surgery were invited to join the study. Clinical OA was defined following the American College of Rheumatology criteria,2 and OA progression was evaluated using the Ahlback ¨ score.1 Patients with previously diagnosed rheumatoid arthritis and fibromyalgia and patients with a fractured knee were excluded from the study. The peak pain intensity within the last 24 hours (visual analog scale [VAS]) from the assessment time point and QST recordings (PPT, TS, and CPM) were collected before, 2 months after, and 12 months after surgery. Patients were requested not to take any analgesic medication 24 hours before an examination. Exclusion criteria included the presence of other pain problems (eg, hip OA), sensory dysfunction (eg, fibromyalgia, neuropathic pain), or mental impairment. The study was approved by the local ethical committee (N-20100050) and conducted in accordance with the Helsinki Declaration. All patients read and signed the informed consent forms. 2.2. Subjects Seventy-eight patients with severe knee OA participated (Kellgren & Lawrence 3 and 4, at least moderate pain15 measured as maximal knee pain intensity within the last 24 hours; VAS . 3). The patients were divided into 2 groups according to the development of postoperative chronic pain. Thus, the maximal pain intensity within the previous 24 hours at the 12-month follow-up after surgery was used to define 2 groups: patients with mild pain (VAS , 3) were assigned to the low-pain group, whereas patients with moderate-tosevere pain (VAS $ 3) were assigned to the high-pain group.
the patient defined the pressure as pain and pressured a button. Pressure pain threshold was measured bilaterally at the 7 peripatellar sites, the TA, and the arm. An average of the 7 peripatellar sites was calculated to give general understanding of the sensitivity of the knee, and the data were used for further analysis. 2.5. Temporal summation A von Frey stimulator with a weighted load (Aalborg University, Aalborg, Denmark) was used to induce TS. A force of 25.6g was applied once on the patient’s knee (5 cm directly proximal to the center of patella), and the patient was asked to rate the pain intensity on the VAS (0-10). Then, 10 consecutive stimulations were applied (1second interval between stimulations) to the same site, and the patient was asked to rate the pain intensity of the last stimulation on the VAS. Temporal summation was calculated as the difference in pain intensity between the first and the last stimulation. 2.6. Conditioned pain modulation Conditioned pain modulation was calculated as the difference in PPT (pressure pain as test stimulus) at site 1 before and after the conditioning stimulation. The cold pressor test was used as the conditioning pain stimulus. The hand contralateral to the most affected knee was submerged in ice water (2˚C, water stirred in ice). The patients were instructed to keep their hand in the water until the sensory experience became “unbearable” with a cut-off time of 2 minutes. 2.7. Statistics The data are presented as means and SEs if not otherwise stated. An independent sample t test was used to compare preoperative data between the 2 groups. A mixed-model analysis of variance (ANOVA) was performed to compare QST parameters before surgery and 2 and 12 months after surgery using the factors: time (preoperatively and 2 and 12 months postoperatively) and group (low pain, high pain). For PPTs, another factor for side (affected, contralateral) was added. The Bonferroni post hoc test was used in case of significant factors. Pearson’s correlation was used for correlation analysis. Linear regression was used to categorize independent parameters. P , 0.05 was considered significant.
3. Results 2.3. Sites for quantitative sensory testing
3.1. Demographics
Patients were examined at the most affected knee joint using the following 3 QST measurements: PPTs, TS, and CPM. Seven sites in the peripatellar region, 1 control site on the tibialis anterior ([TA], 5 cm distal to the tibial tuberosity), and 1 control site at the extensor carpi radialis longus (arm, 5 cm distal to lateral epicondyle of humerus) were located and marked for both the knee osteoarthritis (KOA)-affected and contralateral sides. The 7 peripatellar sites were located with reference to the center of patella: site 1: 5 cm directly proximal, site 2: 5 cm proximal–medial, site 3: 7 cm proximal–medial, site 4: 5 cm distal–medial, site 5: 5 cm distal– lateral, site 6: 5 cm proximal–lateral, site 7: 7 cm proximal–lateral.
Of 78 patients with KOA, 61 patients (78%) had VAS , 3 (lowpain group) and 17 patients (22%) had VAS $ 3 (high-pain group) 12 months after surgery. Patient demographics are listed in Table 1. No differences were found between groups regarding patient demographics.
2.4. Pressure pain threshold A handheld pressure algometer (Somedic AB, Horby, ¨ Sweden) was used for measuring PPT. A 1-cm2 probe was used and placed perpendicularly to the skin. Pressure was applied at 30 kPa/s until
3.2. Pain intensities Pain intensities preoperatively and 2 and 12 months postoperatively for the low- and high-intensity pain groups are seen in Figure 1. Both groups had a significant decrease in pain comparing 2-month and 12-month postoperative pain with preoperative pain intensities (P , 0.001). The high-pain group had overall higher pain intensities (repeated-measures ANOVA: F 5 1.794, P , 0.001), higher preoperative pain intensities (P 5 0.009), and 12-month postoperative pain (P , 0.001) compared with the low-pain group.
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Table 1
Preoperative demographics of the low- and high-pain groups. Number (% of total) Age (range), y BMI (range), kg/m2 Sex (total 59% females) Ahlback ¨ score (range)
Low-pain group
High-pain group
61 (78) 68 (47-86) 30 (20-45) 64% females 2.49 (1-4)
17 (22) 72 (56-86) 30 (19-38) 41% females 2.41 (2-4)
BMI, body mass index.
3.3. Pressure pain thresholds Pressure pain thresholds for both groups are seen in Figure 2. Significant differences were found when comparing time points and PPTs (ANOVA: F 5 3.756, P 5 0.008). The lowpain group showed significantly decreased preoperative PPTs compared with increased PPTs 12 months postoperatively at the most affected side for the knee (P 5 0.008), the TA (P , 0.008), and the arm (P 5 0.014). Furthermore, the low-pain group showed significantly decreased preoperative PPTs for the contralateral side for the knee (P 5 0.001), the TA (P 5 0.020) and a trend toward significance for the arm (P 5 0.059) compared with 12 months postoperatively. The high-pain group showed a significant increase in PPTs from preoperatively to 12 months postoperatively at the contralateral arm (P 5 0.049). The factor “group” was nonsignificant, indicating no differences in PPTs when comparing the low- and high-pain group.
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with baseline PPTs for the low-intensity group, indicating functional pain inhibition. No significant difference was observed in the high-intensity group, but 12 months after surgery, the high-pain group had a higher difference (P 5 0.006) compared with the low-pain group (Fig. 4). 3.6. Correlations Pooling all patient data showed significant correlations between 12-month postoperative pain intensity, preoperative pain intensity (R 5 0.229, P 5 0.045), and preoperative TS (R 5 0.240, P 5 0.037), showing that patients with higher preoperative pain intensity and facilitated TS had a higher risk of developing chronic postoperative pain. No correlation was found between pain intensity 12 months postoperatively and preoperative PPTs (affected side: R 5 20.051, P 5 0.657; contralateral side: R 5 20.077, P 5 0.502) or preoperative CPM and (R 5 20.176, P 5 0.123). Furthermore, a linear regression analysis (Table 2) to predict the pain intensity level 12 months after surgery showed a trend toward independent parameters for preoperative pain intensity (P 5 0.080) and preoperative TS (P 5 0.052).
4. Discussion This study showed that using preoperative assessment of TS, it is possible to identify a group of patients with KOA with a high risk of developing long-term postoperative pain 12 months after TKR. No prognostic information could be gained from the preoperative PPT or CPM values.
3.4. Temporal summation The high-pain group had significantly higher (F 5 6.293, P 5 0.003) facilitated TS measured preoperatively (P 5 0.009) and 12 months postoperatively (P 5 0.012) compared with the low-pain group (Fig. 3). 3.5. Conditioned pain modulation A significant increase in PPTs after submerging the hand was found (ANOVA: F 5 4.046, P 5 0.029) preoperatively (P 5 0.019) and 12 months postoperatively (P 5 0.030) compared
4.1. Chronic pain after surgery This study found that 22% of patients who underwent KOA surgery had moderate-to-severe chronic postoperative pain, which is comparable with the previous literature citing an approximately 20% risk of developing severe chronic postoperative pain after TKR surgery.12 The variation across the studies could be due to the time point of assessment, which ranges from 12 months to 5 years, and also the cut-off pain intensity identifying postoperative pain. In this study, patients who developed chronic pain 12 months after surgery showed
Figure 1. Patients with mild (low-pain group: VAS , 3, N 5 61) and moderate-to-severe (high-pain group: VAS $ 3, N 5 17) pain 12 months after TKR surgery have different preoperative and 12-month postoperative pain intensities (*P , 0.05). Visual analog scale was measured as maximum pain within the last 24 hours. Error bars represent SE. VAS, visual analog scale; TKR, total knee replacement.
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Figure 2. Pressure pain thresholds (PPTs) measured at the knee, the TA, and extensor carpi radialis longus (arm). The low-pain group had significantly higher PPT 12 months after TKR surgery compared with preoperative measurements. The high-pain group showed significantly lower PPT at the contralateral arm comparing before and 12 months after TKR surgery (*P , 0.05). Error bars represent SE. TA, tibialis anterior; TKR, total knee replacement.
increased presurgical pain intensities compared with patients with low intensity or no chronic pain. In this study, preoperative pain intensities were significantly and positively correlated with pain intensities 12 months after surgery, which agrees with the current literature.25 This study shows that QST can help
provide a mechanistic understanding of surgical pain and its chronification20 and further supports the view that mechanism-based pharmaceutical targeting based on QST parameters may help preventing long-term postoperative pain.14,28
Figure 3. Temporal summation to repeated (10 stimuli, 1-second interstimulus interval) pinprick stimulation. The high-pain group had more facilitated temporal summation presurgically and 12 months after surgery compared with the low-pain group (*P , 0.05). Error bars represent SE.
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Figure 4. Pressure pain thresholds (PPTs) assessed at the knee before and after the cold pressor test (conditioning pain modulation). The low-pain group showed higher PPT comparing before and after the cold pressor test 12 months after TKR surgery. *P , 0.05 when PPTs are compared before and after the cold pressor test. #P , 0.05 when the low- and high-pain groups are compared. Error bars represent SE. TKR, total knee replacement.
4.2. Widespread deep tissue hyperalgesia
4.3. Conditioned pain modulation
Preoperative widespread deep tissue hyperalgesia is consistently present in patients with knee OA7,17,18,21–23 and normalizes after surgery in patients with no or low postoperative chronic pain.21 This trend was also found for patients with low postoperative pain in this study. Several recent studies have shown that the patient population with knee OA consists of several subgroups of patients with different patterns of altered sensory processing.3,19,31 This study reported that patients who had intense chronic pain 12 months after TKR surgery showed ongoing sensitization without a return of the pain processing to a normal state.5,20
A less-efficient CPM mechanism has been reported in patients with hip OA before total hip replacement, which was restored in patients with no postoperative chronic pain.26 A dysfunctional preoperative CPM has been suggested to predict which patients may develop chronic postoperative pain.37,38 This study reported that patients who had no or low postoperative pain had normal preoperative and 12-month postoperative CPM responses. The CPM response reflects the net sum of inhibitory and facilitatory descending modulation.20 Thus, a high CPM, as in the low-pain group 12 months after TKR surgery, may indicate high inhibition/low
Table 2
Univariate and multivariate logistic regression analysis. Crude coefficient Preoperative pain intensity Preoperative TS
0.297 0.311
SE
P
1.073 0.147
0.045 0.037
Adjusted coefficient 0.265 0.289
SE
P
0.149 0.146
0.080 0.052
Crude coefficient shows the result from the univariate logistic regression analysis between the pain intensity level 12 months after TKR surgery and either the preoperative TS or the pain intensity. Adjusted coefficient shows the results from the multivariate logistic regression analysis. TKR, total knee replacement; TS, temporal summation.
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facilitation, whereas a low CPM, as in the high-pain group 12 months after TKR surgery, may indicate low inhibition/high facilitation, which could be 1 of the reasons that patients in the high-pain group have higher pain intensities 12 months after TKR surgery. 4.4. Temporal summation Previous studies have shown that patients with knee OA have enhanced TS compared with healthy controls7 and that patients with pain after a revision of TKR have enhanced TS compared with patients without pain after a revision of TKR surgery.32 This study showed that patients who developed severe chronic postoperative pain had enhanced preoperative TS compared with patients without or with mild chronic postoperative pain. Furthermore, patients who developed severe chronic postoperative pain showed enhanced TS at the 12-month follow-up, indicating that these patients were more sensitized to this specific stimulus paradigm both before and after surgery.5 A positive correlation between preoperative TS and 12month postoperative pain intensity (ie, stronger presurgical TS correlated to higher postsurgical pain intensity) and a trend toward independent preoperative parameters were reported in this study. Preoperative QST has been shown to predict the treatment outcome of analgesic therapies in several chronic pain disorders,9,16,28,39 supporting the findings of this study. It also supports the possibility of preoperative prediction of patients at risk of developing postoperative chronic pain. 4.5. Limitations This study is limited by the small size of the patient group who developed chronic postoperative pain (the high-pain group). Thus, the results of this study should be interpreted with care, especially, the CPM comparisons and the predictions of pain intensity levels 12 months after TKR surgery. This study was conducted in a single hospital. A multicenter study should confirm the findings of this study.
5. Conclusions Preoperative pain intensity and TS correlated with 12-month postoperative pain intensity and showed a trend toward independence. TS of pain may be a mechanistic preoperative predictor of the development of chronic postoperative pain in patients with knee OA after TKR surgery.
Conflict of interest statement None of the authors have conflicts of interest to declare.
Acknowledgements The authors thank The Danish Rheumatism Association, The Bevica foundation, the Danish Advanced Technology Foundation, and the Danish Council for Technology and Innovation (09-052174) for providing the opportunity to conduct this study. Article history: Received 15 August 2014 Received in revised form 18 September 2014 Accepted 30 October 2014
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Presurgical assessment of temporal summation of pain predicts the development of chronic postoperative pain 12 months after total knee replacement Kristian Kjær Petersena, Lars Arendt-Nielsena,*, Ole Simonsenb, Oliver Wilder-Smitha,c, Mogens Berg Laursenb
Abstract Patients with knee osteoarthritis demonstrate decreased pressure pain thresholds (PPTs), facilitated temporal summation (TS) of pain, and decreased conditioned pain modulation (CPM) compared with healthy controls. This study aimed to correlate preoperative PPTs, TS, and CPM with the development of chronic postoperative pain after total knee replacement (TKR) surgery. Knee pain intensity (visual analog scale [VAS]: 0-10), PPTs, TS, and CPM were collected before, 2 months, and 12 months after TKR. Patients were divided into a low-pain (VAS , 3) and a high-pain (VAS $ 3) group based on their VAS 12 months after TKR. The high-pain group (N 5 17) had higher pain intensities compared with the low-pain group (N 5 61) before surgery (P 5 0.009) and 12 months after surgery (P , 0.001). The PPTs of the low-pain groups were normalized for all measurement sites comparing presurgery with 12 months postsurgery (P , 0.05, contralateral arm: P 5 0.059), which was not the case for the high-pain group. The low-pain group showed a functional inhibitory CPM preoperatively and 12 months postoperatively (P , 0.05), which was not found in the high-pain group. The high-pain group had higher facilitated TS preoperatively and 12 months postoperatively compared with the low-pain group (P , 0.05). Preoperative TS level correlated to 12-month postoperative VAS (R 5 0.240, P 5 0.037). Patients who developed moderate-to-severe pain had pronociceptive changes compared with patients who developed mild pain postsurgery. Preoperative TS level correlated with the postoperative pain intensity and may be a preoperative mechanistic predictor for the development of chronic postoperative pain in patients with osteoarthritis after TKR. Keywords: Osteoarthritis, Conditioning pain modulation, Hyperalgesia, Temporal summation, Chronic postoperative pain
1. Introduction Osteoarthritis (OA) is the most frequent painful musculoskeletal diagnosis in the elderly population and the most common cause of disability29 with 40% of women and 25% of men aged 60 to 70 years being diagnosed with OA.35 With an expected global growth in the elderly population, the incidence of OA is predicted to increase in the future.10,11,13 Nearly 500,000 total knee replacements (TKRs) were performed in the United States in 2011, which is estimated to increase to 3.5 million in 2030.27 Approximately 20% of these patients will suffer from chronic postoperative pain after TKR surgery.12 Pre- and post-TKR treatment with pregabalin seem to inhibit the development of chronic postoperative pain,14 indicating that preoperative sensitization of the nervous system may be connected with the development of postoperative chronic pain. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. a
Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark, b Orthopaedic Surgery Research Unit, Aalborg University Hospital, Aalborg, Denmark, c Department of Anaesthesiology, Pain and Palliative Medicine, Radboud University Medical Centre, Nijmegen, the Netherlands *Corresponding author. Address: Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Fredrik Bajers Vej 7, D3, DK-9220 Aalborg, Denmark. Tel.: 145 9940 8831; fax: 145 9815 4008. E-mail address: [email protected] (L. Arendt-Nielsen). PAIN 156 (2015) 55–61 © 2014 International Association for the Study of Pain http://dx.doi.org/10.1016/j.pain.0000000000000022
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Pressure pain thresholds (PPTs), temporal summation (TS) of pain, and conditioned pain modulation (CPM) are 3 types of quantitative sensory testing (QST) measurements that have been widely used to diagnose altered pain processing in patients with hip and knee OA.7,11,21,24,32 Widespread hyperalgesia, a sign of sensitized and facilitated pain processing, has been demonstrated in patients with knee OA,7 which has been normalized after TKR surgery.21 Patients with OA demonstrating more than 1 location of pain often express pain symptoms that are more diffuse and spread to larger areas,34 supporting the notion that spreading sensitization may be present in these patients.4 Recently, several studies have identified subgroups of patients with knee OA with different degrees of radiological joint damage, pain, inflammation levels, and sensitization of pain processing.7,17,18,21–23,31 Inhibition and facilitation of descending inhibitory modulation of the peripheral nociceptive inputs to the dorsal horn neurons are important mechanisms in the sensitization of pain processing.6 Conditioned pain modulation, a measure of potential descending modulatory capacity, is an estimate of the net effect of the facilitating and the inhibitory system,6 and it is induced by a painful conditioning stimulus, eg, a cold pressor test,8 ischemic7 or heat38 pain. Preoperative CPM deficiency has been shown to predict the risk of development of postoperative chronic pain in patients undergoing thoracotomy38 and abdominal surgery.37 In chronic musculoskeletal pain conditions such as OA and fibromyalgia, TS of pain has been demonstrated to be facilitated compared with healthy controls.7,33 Facilitated TS has been shown to predict the development of acute postoperative pain in www.painjournalonline.com
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patients undergoing thoracotomy,36 which is a precursor for the development of chronic postoperative pain.30 To date, no studies have linked a battery of preoperative QST parameters (including TS and CPM) to the development of chronic pain after TKR surgery in patients with knee OA. The aims of this study were (1) to compare preoperative pain intensity and QST parameters in patients with knee OA who develop different degrees of chronic pain after TKR surgery and (2) to identify preoperative parameters that possibly predict the development of chronic postoperative pain after TKR.
2. Methods 2.1. Protocol Patients from the North Denmark Region with severe knee OA scheduled for TKR surgery were invited to join the study. Clinical OA was defined following the American College of Rheumatology criteria,2 and OA progression was evaluated using the Ahlback ¨ score.1 Patients with previously diagnosed rheumatoid arthritis and fibromyalgia and patients with a fractured knee were excluded from the study. The peak pain intensity within the last 24 hours (visual analog scale [VAS]) from the assessment time point and QST recordings (PPT, TS, and CPM) were collected before, 2 months after, and 12 months after surgery. Patients were requested not to take any analgesic medication 24 hours before an examination. Exclusion criteria included the presence of other pain problems (eg, hip OA), sensory dysfunction (eg, fibromyalgia, neuropathic pain), or mental impairment. The study was approved by the local ethical committee (N-20100050) and conducted in accordance with the Helsinki Declaration. All patients read and signed the informed consent forms. 2.2. Subjects Seventy-eight patients with severe knee OA participated (Kellgren & Lawrence 3 and 4, at least moderate pain15 measured as maximal knee pain intensity within the last 24 hours; VAS . 3). The patients were divided into 2 groups according to the development of postoperative chronic pain. Thus, the maximal pain intensity within the previous 24 hours at the 12-month follow-up after surgery was used to define 2 groups: patients with mild pain (VAS , 3) were assigned to the low-pain group, whereas patients with moderate-tosevere pain (VAS $ 3) were assigned to the high-pain group.
the patient defined the pressure as pain and pressured a button. Pressure pain threshold was measured bilaterally at the 7 peripatellar sites, the TA, and the arm. An average of the 7 peripatellar sites was calculated to give general understanding of the sensitivity of the knee, and the data were used for further analysis. 2.5. Temporal summation A von Frey stimulator with a weighted load (Aalborg University, Aalborg, Denmark) was used to induce TS. A force of 25.6g was applied once on the patient’s knee (5 cm directly proximal to the center of patella), and the patient was asked to rate the pain intensity on the VAS (0-10). Then, 10 consecutive stimulations were applied (1second interval between stimulations) to the same site, and the patient was asked to rate the pain intensity of the last stimulation on the VAS. Temporal summation was calculated as the difference in pain intensity between the first and the last stimulation. 2.6. Conditioned pain modulation Conditioned pain modulation was calculated as the difference in PPT (pressure pain as test stimulus) at site 1 before and after the conditioning stimulation. The cold pressor test was used as the conditioning pain stimulus. The hand contralateral to the most affected knee was submerged in ice water (2˚C, water stirred in ice). The patients were instructed to keep their hand in the water until the sensory experience became “unbearable” with a cut-off time of 2 minutes. 2.7. Statistics The data are presented as means and SEs if not otherwise stated. An independent sample t test was used to compare preoperative data between the 2 groups. A mixed-model analysis of variance (ANOVA) was performed to compare QST parameters before surgery and 2 and 12 months after surgery using the factors: time (preoperatively and 2 and 12 months postoperatively) and group (low pain, high pain). For PPTs, another factor for side (affected, contralateral) was added. The Bonferroni post hoc test was used in case of significant factors. Pearson’s correlation was used for correlation analysis. Linear regression was used to categorize independent parameters. P , 0.05 was considered significant.
3. Results 2.3. Sites for quantitative sensory testing
3.1. Demographics
Patients were examined at the most affected knee joint using the following 3 QST measurements: PPTs, TS, and CPM. Seven sites in the peripatellar region, 1 control site on the tibialis anterior ([TA], 5 cm distal to the tibial tuberosity), and 1 control site at the extensor carpi radialis longus (arm, 5 cm distal to lateral epicondyle of humerus) were located and marked for both the knee osteoarthritis (KOA)-affected and contralateral sides. The 7 peripatellar sites were located with reference to the center of patella: site 1: 5 cm directly proximal, site 2: 5 cm proximal–medial, site 3: 7 cm proximal–medial, site 4: 5 cm distal–medial, site 5: 5 cm distal– lateral, site 6: 5 cm proximal–lateral, site 7: 7 cm proximal–lateral.
Of 78 patients with KOA, 61 patients (78%) had VAS , 3 (lowpain group) and 17 patients (22%) had VAS $ 3 (high-pain group) 12 months after surgery. Patient demographics are listed in Table 1. No differences were found between groups regarding patient demographics.
2.4. Pressure pain threshold A handheld pressure algometer (Somedic AB, Horby, ¨ Sweden) was used for measuring PPT. A 1-cm2 probe was used and placed perpendicularly to the skin. Pressure was applied at 30 kPa/s until
3.2. Pain intensities Pain intensities preoperatively and 2 and 12 months postoperatively for the low- and high-intensity pain groups are seen in Figure 1. Both groups had a significant decrease in pain comparing 2-month and 12-month postoperative pain with preoperative pain intensities (P , 0.001). The high-pain group had overall higher pain intensities (repeated-measures ANOVA: F 5 1.794, P , 0.001), higher preoperative pain intensities (P 5 0.009), and 12-month postoperative pain (P , 0.001) compared with the low-pain group.
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Table 1
Preoperative demographics of the low- and high-pain groups. Number (% of total) Age (range), y BMI (range), kg/m2 Sex (total 59% females) Ahlback ¨ score (range)
Low-pain group
High-pain group
61 (78) 68 (47-86) 30 (20-45) 64% females 2.49 (1-4)
17 (22) 72 (56-86) 30 (19-38) 41% females 2.41 (2-4)
BMI, body mass index.
3.3. Pressure pain thresholds Pressure pain thresholds for both groups are seen in Figure 2. Significant differences were found when comparing time points and PPTs (ANOVA: F 5 3.756, P 5 0.008). The lowpain group showed significantly decreased preoperative PPTs compared with increased PPTs 12 months postoperatively at the most affected side for the knee (P 5 0.008), the TA (P , 0.008), and the arm (P 5 0.014). Furthermore, the low-pain group showed significantly decreased preoperative PPTs for the contralateral side for the knee (P 5 0.001), the TA (P 5 0.020) and a trend toward significance for the arm (P 5 0.059) compared with 12 months postoperatively. The high-pain group showed a significant increase in PPTs from preoperatively to 12 months postoperatively at the contralateral arm (P 5 0.049). The factor “group” was nonsignificant, indicating no differences in PPTs when comparing the low- and high-pain group.
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with baseline PPTs for the low-intensity group, indicating functional pain inhibition. No significant difference was observed in the high-intensity group, but 12 months after surgery, the high-pain group had a higher difference (P 5 0.006) compared with the low-pain group (Fig. 4). 3.6. Correlations Pooling all patient data showed significant correlations between 12-month postoperative pain intensity, preoperative pain intensity (R 5 0.229, P 5 0.045), and preoperative TS (R 5 0.240, P 5 0.037), showing that patients with higher preoperative pain intensity and facilitated TS had a higher risk of developing chronic postoperative pain. No correlation was found between pain intensity 12 months postoperatively and preoperative PPTs (affected side: R 5 20.051, P 5 0.657; contralateral side: R 5 20.077, P 5 0.502) or preoperative CPM and (R 5 20.176, P 5 0.123). Furthermore, a linear regression analysis (Table 2) to predict the pain intensity level 12 months after surgery showed a trend toward independent parameters for preoperative pain intensity (P 5 0.080) and preoperative TS (P 5 0.052).
4. Discussion This study showed that using preoperative assessment of TS, it is possible to identify a group of patients with KOA with a high risk of developing long-term postoperative pain 12 months after TKR. No prognostic information could be gained from the preoperative PPT or CPM values.
3.4. Temporal summation The high-pain group had significantly higher (F 5 6.293, P 5 0.003) facilitated TS measured preoperatively (P 5 0.009) and 12 months postoperatively (P 5 0.012) compared with the low-pain group (Fig. 3). 3.5. Conditioned pain modulation A significant increase in PPTs after submerging the hand was found (ANOVA: F 5 4.046, P 5 0.029) preoperatively (P 5 0.019) and 12 months postoperatively (P 5 0.030) compared
4.1. Chronic pain after surgery This study found that 22% of patients who underwent KOA surgery had moderate-to-severe chronic postoperative pain, which is comparable with the previous literature citing an approximately 20% risk of developing severe chronic postoperative pain after TKR surgery.12 The variation across the studies could be due to the time point of assessment, which ranges from 12 months to 5 years, and also the cut-off pain intensity identifying postoperative pain. In this study, patients who developed chronic pain 12 months after surgery showed
Figure 1. Patients with mild (low-pain group: VAS , 3, N 5 61) and moderate-to-severe (high-pain group: VAS $ 3, N 5 17) pain 12 months after TKR surgery have different preoperative and 12-month postoperative pain intensities (*P , 0.05). Visual analog scale was measured as maximum pain within the last 24 hours. Error bars represent SE. VAS, visual analog scale; TKR, total knee replacement.
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Figure 2. Pressure pain thresholds (PPTs) measured at the knee, the TA, and extensor carpi radialis longus (arm). The low-pain group had significantly higher PPT 12 months after TKR surgery compared with preoperative measurements. The high-pain group showed significantly lower PPT at the contralateral arm comparing before and 12 months after TKR surgery (*P , 0.05). Error bars represent SE. TA, tibialis anterior; TKR, total knee replacement.
increased presurgical pain intensities compared with patients with low intensity or no chronic pain. In this study, preoperative pain intensities were significantly and positively correlated with pain intensities 12 months after surgery, which agrees with the current literature.25 This study shows that QST can help
provide a mechanistic understanding of surgical pain and its chronification20 and further supports the view that mechanism-based pharmaceutical targeting based on QST parameters may help preventing long-term postoperative pain.14,28
Figure 3. Temporal summation to repeated (10 stimuli, 1-second interstimulus interval) pinprick stimulation. The high-pain group had more facilitated temporal summation presurgically and 12 months after surgery compared with the low-pain group (*P , 0.05). Error bars represent SE.
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Figure 4. Pressure pain thresholds (PPTs) assessed at the knee before and after the cold pressor test (conditioning pain modulation). The low-pain group showed higher PPT comparing before and after the cold pressor test 12 months after TKR surgery. *P , 0.05 when PPTs are compared before and after the cold pressor test. #P , 0.05 when the low- and high-pain groups are compared. Error bars represent SE. TKR, total knee replacement.
4.2. Widespread deep tissue hyperalgesia
4.3. Conditioned pain modulation
Preoperative widespread deep tissue hyperalgesia is consistently present in patients with knee OA7,17,18,21–23 and normalizes after surgery in patients with no or low postoperative chronic pain.21 This trend was also found for patients with low postoperative pain in this study. Several recent studies have shown that the patient population with knee OA consists of several subgroups of patients with different patterns of altered sensory processing.3,19,31 This study reported that patients who had intense chronic pain 12 months after TKR surgery showed ongoing sensitization without a return of the pain processing to a normal state.5,20
A less-efficient CPM mechanism has been reported in patients with hip OA before total hip replacement, which was restored in patients with no postoperative chronic pain.26 A dysfunctional preoperative CPM has been suggested to predict which patients may develop chronic postoperative pain.37,38 This study reported that patients who had no or low postoperative pain had normal preoperative and 12-month postoperative CPM responses. The CPM response reflects the net sum of inhibitory and facilitatory descending modulation.20 Thus, a high CPM, as in the low-pain group 12 months after TKR surgery, may indicate high inhibition/low
Table 2
Univariate and multivariate logistic regression analysis. Crude coefficient Preoperative pain intensity Preoperative TS
0.297 0.311
SE
P
1.073 0.147
0.045 0.037
Adjusted coefficient 0.265 0.289
SE
P
0.149 0.146
0.080 0.052
Crude coefficient shows the result from the univariate logistic regression analysis between the pain intensity level 12 months after TKR surgery and either the preoperative TS or the pain intensity. Adjusted coefficient shows the results from the multivariate logistic regression analysis. TKR, total knee replacement; TS, temporal summation.
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facilitation, whereas a low CPM, as in the high-pain group 12 months after TKR surgery, may indicate low inhibition/high facilitation, which could be 1 of the reasons that patients in the high-pain group have higher pain intensities 12 months after TKR surgery. 4.4. Temporal summation Previous studies have shown that patients with knee OA have enhanced TS compared with healthy controls7 and that patients with pain after a revision of TKR have enhanced TS compared with patients without pain after a revision of TKR surgery.32 This study showed that patients who developed severe chronic postoperative pain had enhanced preoperative TS compared with patients without or with mild chronic postoperative pain. Furthermore, patients who developed severe chronic postoperative pain showed enhanced TS at the 12-month follow-up, indicating that these patients were more sensitized to this specific stimulus paradigm both before and after surgery.5 A positive correlation between preoperative TS and 12month postoperative pain intensity (ie, stronger presurgical TS correlated to higher postsurgical pain intensity) and a trend toward independent preoperative parameters were reported in this study. Preoperative QST has been shown to predict the treatment outcome of analgesic therapies in several chronic pain disorders,9,16,28,39 supporting the findings of this study. It also supports the possibility of preoperative prediction of patients at risk of developing postoperative chronic pain. 4.5. Limitations This study is limited by the small size of the patient group who developed chronic postoperative pain (the high-pain group). Thus, the results of this study should be interpreted with care, especially, the CPM comparisons and the predictions of pain intensity levels 12 months after TKR surgery. This study was conducted in a single hospital. A multicenter study should confirm the findings of this study.
5. Conclusions Preoperative pain intensity and TS correlated with 12-month postoperative pain intensity and showed a trend toward independence. TS of pain may be a mechanistic preoperative predictor of the development of chronic postoperative pain in patients with knee OA after TKR surgery.
Conflict of interest statement None of the authors have conflicts of interest to declare.
Acknowledgements The authors thank The Danish Rheumatism Association, The Bevica foundation, the Danish Advanced Technology Foundation, and the Danish Council for Technology and Innovation (09-052174) for providing the opportunity to conduct this study. Article history: Received 15 August 2014 Received in revised form 18 September 2014 Accepted 30 October 2014
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