Widespread sensitization in patients with chronic pain after revision total knee arthroplasty

Pain and sensitization are major issues in patients with osteoarthritis both before and after total knee arthroplasty (TKA) and revision TKA (re-TKA). The aim of this study was to assess sensitization in patients with and without chronic pain after re-TKAs. Twenty patients with chronic knee pain and 20 patients without pain after re-TKA participated. Spreading of pain was evaluated as the number of pain sites using a region-divided body chart. The pressure pain threshold (PPT) and pressure pain tolerance (PTT) were assessed by cuff algometry at the lower leg. Temporal summation of pain was assessed by recordings of the pain intensity on a visual analog scale (VAS) during repeated cuff pressure stimulations. Conditioning pain modulation (CPM) was recorded by experimental tonic arm pain by cuff pressure stimulation and assessment of PPTs on the knee, leg, and forearm using handheld pressure algometry. Participants with pain after re-TKA compared to participants without pain demonstrated: (1) significantly more pain sites (P = .004), (2) decreased cuff PPTs and PTTs at the lower leg (P < .001), (3) facilitated temporal summation (P < .001), and (4) impaired CPM (P < .001). Additionally, significant correlations between knee pain intensity and cuff PPTs, temporal summation, and CPM and between total duration of knee pain and temporal summation were found (P < .05). This study demonstrated widespread sensitization in patients with pain after re-TKA and highlighted the importance of ongoing nociceptive input for the chronification process. This has important implications for future revisions, and precautions should be taken if patients have widespread sensitization.     

Cognitive manipulation targeted at decreasing the conditioning pain perception reduces the efficacy of conditioned pain modulation

Although painfulness of the conditioning stimulus (CS) is required for the activation of conditioned pain modulation (CPM), it is still unclear whether CPM expression depends on the objective physical intensity of the CS or the subjective perception of its pain. Accordingly, we cognitively manipulated the perceived CS pain, rendering the physical aspects of the CPM paradigm untouched. Baseline CPM was measured among 48 young healthy male subjects using the parallel paradigm with contact heat as test pain and hand immersion in hot water as CS. Subjects were then randomized into 4 groups, all of which were cognitively manipulated as to the CS-induced pain: group 1, placebo (CS less painful); group 2, nocebo (CS more painful); and groups 3 and 4, the informed control groups for groups 1 and 2, respectively. CPM was reassessed after the manipulation. Comparing the groups by MANCOVA (multivariate analysis of covariance) revealed that placebo exerted decreased CS pain and consequent attenuation of CPM magnitudes, while nocebo elicited increased CS pain, but without CPM elevation (P < .0001). Within the placebo group, the reduction in CS pain was associated with diminished CPM responses (r = 0.767; P = .001); however, no such relationship characterized the nocebo group. Pain inhibition under CPM seems to depend on the perceived level of the CS pain rather than solely its physical intensity. Cognitively decreasing the perceived CS pain attenuates CPM magnitude, although a ceiling effect may limit CPM enhancement after cognitively increased CS pain. These findings emphasize the relevance of cognitive mechanisms in determining endogenous analgesia processes in humans.     

Conditioned Pain Modulation and Pressure Pain Sensitivity in the Adult Danish General Population: The DanFunD Study

Increased pressure pain sensitivity and impaired descending pain control have been associated with chronic pain, but knowledge on the variability in the adult general population is lacking. Pressure pain thresholds (PPTs) and descending pain control assessed using conditioned pain modulation (CPM) were recorded in a randomly selected sample (n = 2,199, 53% female) of the Danish adult general population aged 18 to 70 years. PPTs were recorded over the tibialis anterior muscle and the upper trapezius muscle. CPM was defined as the difference between PPT assessments before and during conditioning with cold pressor pain (hand) for 2 minutes. Conditioning pain intensity was assessed using a visual analog scale and questionnaire data were collected. Female sex (P < .001) and younger age (P ≤ .02) was associated with lower PPTs at both body sites. For the trapezius muscle, high perceived stress was associated with lower PPTs (P < .02), whereas an interaction was found between body mass index and sex. CPM potency was lower in female compared with male participants (P ≤ .003), whereas no association with age was found. Higher level of education (P ≤ .05), premature withdrawal from the cold pressor test (P ≤ .02), and high visual analog scale score (P ≤ .02) were associated with a larger CPM response.

The mediating role of pain catastrophizing in the relationship between presurgical anxiety and acute postsurgical pain after hysterectomy

The aim of this study was to examine the joint role of demographic, clinical, and psychological variables as predictors of acute postsurgical pain in women undergoing hysterectomy due to benign disorders. A consecutive sample of 203 women was assessed 24 hours before (T1) and 48 hours after (T2) surgery. Baseline pain and predictors were assessed at T1 and postsurgical pain and analgesic consumption at T2. Several factors distinguished women who had no or mild pain after surgery from those who had moderate to severe pain, with the latter being younger, having more presurgical pain, and showing a less favorable psychological profile. Younger age (odds ratio [OR] = 0.90, P < .001), presurgical pain (OR = 2.50, P <.05), pain due to other causes (OR = 4.39, P = .001), and pain catastrophizing (OR = 3.37, P = .001) emerged as the main predictors of pain severity at T2 in multivariate logistic regression. This was confirmed in hierarchical linear regression (β = −0.187, P < .05; β = 0.146, P < .05; β = 0.136, P < .05; β = 0.245, P < .01, respectively). Presurgical anxiety also predicted pain intensity at T2. Findings revealed an integrative heuristic model that accounts for the joint influence of demographic, clinical, and psychological factors on postsurgical pain intensity and severity. In further mediation analysis, pain catastrophizing emerged as a full mediator between presurgical anxiety and postsurgical pain intensity. The potential clinical implications for understanding, evaluating, and intervening in postsurgical pain are discussed.     

Pronociceptive pain modulation in patients with painful chemotherapy-induced polyneuropathy

Context

Several chemotherapy agents induce polyneuropathy that is painful for some patients, but not for others. We assumed that these differences might be attributable to varying patterns of pain modulation.

Objectives

The aim of the present study was to evaluate pain modulation in such patients.

Methods

Twenty-seven patients with chemotherapy-induced polyneuropathy were tested for detection thresholds (cold, warm, and mechanical) in both the forearm and foot, as well as for heat pain threshold, mechanical temporal summation (TS), and conditioned pain modulation (CPM; also known as the diffuse noxious inhibitory control-like effect), which were tested in the upper limbs.

Results

Positive correlations were found between clinical pain levels and both TS (r = 0.52, P = 0.005) and CPM (r = 0.40, P = 0.050) for all patients. In addition, higher TS was associated with less efficient CPM (r = 0.56, P = 0.004). The group of patients with painful polyneuropathy (n = 12) showed a significantly higher warm detection threshold in the foot (P = 0.03), higher TS (P < 0.01), and less efficient CPM (P = 0.03) in comparison to the group with nonpainful polyneuropathy.

Conclusion

The painfulness of polyneuropathy is associated with a “pronociceptive” modulation pattern, which may be primary to the development of pain. The higher warm sensory thresholds in the painful polyneuropathy group suggest that the severity of polyneuropathy may be another factor in determining its painfulness.     

Parent behaviors moderate the relationship between neonatal pain and internalizing behaviors at 18 months corrected age in children born very prematurely

Children born very preterm (?32 weeks gestation) exhibit greater internalizing (anxious/depressed) behaviors compared to term-born peers as early as 2 years corrected age (CA); however, the role of early stress in the etiology of internalizing problems in preterm children remains unknown. Therefore, we examined the relationship between neonatal pain and internalizing behavior at 18 months CA in children born very preterm and examined whether parent behavior and stress moderated this relationship. Participants were 145 children (96 very preterm, 49 full term) assessed at 18 months CA. Neonatal data were obtained from medical and nursing chart review. Neonatal pain was defined as the number of skin-breaking procedures. Cognitive ability was measured with the Bayley Scales of Infant Development II. Parents completed the Parenting Stress Index III, Child Behavior Checklist 1.5–5, and participated in a videotaped play session with their child, which was coded using the Emotional Availability Scale IV. Very preterm children displayed greater Internalizing behaviors compared to full-term control children (P = .02). Parent Sensitivity and Nonhostility moderated the relationship between neonatal pain and Internalizing behavior (all P < .05); higher parent education (P < .03), lower Parenting Stress (P = .001), and fewer children in the home (P < .01) were associated with lower Internalizing behavior in very preterm children, after adjusting for neonatal medical confounders, gender, and child cognitive ability (all P > .05). Parent Emotional Availability and stress were not associated with Internalizing behaviors in full-term control children. Positive parent interaction and lower stress appears to ameliorate negative effects of neonatal pain on stress-sensitive behaviors in this vulnerable population.     

Altered experimental pain perception after cerebellar infarction

Animal studies have suggested that the cerebellum, in addition to its motor functions, also has a role in pain processing and modulation, possibly because of its extensive connections with the prefrontal cortex and with brainstem regions involved in descending pain control. Consistently, human imaging studies have shown cerebellar activation in response to painful stimulation. However, it is presently not clear whether cerebellar lesions affect pain perception in humans. In the present study, we used experimental pain testing to compare acute pain perception and endogenous pain inhibition in 30 patients 1 to 11 years after cerebellar infarction and in 30 sex- and age-matched healthy control subjects. Compared to controls, patients exhibited a significantly increased pain perception in response to acute heat stimuli (44°C–48°C, average pain intensity rating for patients 3.4 ± 2.8 and for controls 1.5 ± 1.7 [on a numeric rating scale of 0–10], P < .01) and to repeated 256 mN pinprick stimuli (1.3 ± 1.9 vs 0.6 ± 1.0 [0–10], P < .05). Heat hyperalgesia in patients was more pronounced on the body side ipsilateral to the infarction. In addition, patients showed reduced offset analgesia (change in pain intensity rating: 0.0% ± 15.8% vs −16.9% ± 36.3%, P < .05) and reduced placebo analgesia (change in pain intensity rating: −1.0 ± 1.1 vs −1.8 ± 1.3 [0–10], P < .05) compared to controls. In contrast, heat and pressure pain thresholds were not significantly different between groups. These results show that, after cerebellar infarction, patients perceive heat and repeated mechanical stimuli as more painful than do healthy control subjects and have deficient activation of endogenous pain inhibitory mechanisms (offset and placebo analgesia). This suggests that the cerebellum has a previously underestimated role in human pain perception and modulation.     

Increased wind-up to heat pain in women with a childhood history of functional abdominal pain

Idiopathic or functional abdominal pain (FAP) is common in school-age children and typically reflects a functional gastrointestinal disorder (FGID). FGIDs in adults have been distinguished by enhanced responses of the central nervous system to pain stimuli, known as central sensitization. This study investigated whether adolescents and young adults with a history of pediatric FAP (n = 144), compared with well control subjects (n = 78), showed enhanced central sensitization demonstrated by greater temporal summation (wind-up) to brief, repetitive heat pulses. We also assessed the role of gender and trait anxiety in wind-up to heat pain. Women with a history of FAP showed greater wind-up to heat pain than men with a history of FAP (P < .05) and well control subjects of both genders (P < .05). Results were similar for FAP participants whose abdominal pain was ongoing at follow-up and those whose pain had resolved. Although anxiety was significantly higher in the FAP group compared with control subjects (P < .01) and in women compared with men (P < .05), anxiety did not explain the increased wind-up observed in women with a childhood history of FAP. Results suggest that women with a pediatric history of FAP may have a long-term vulnerability to pain associated with enhanced central nervous system responses to pain stimuli.     

Higher Dispositional Optimism Predicts Lower Pain Reduction During Conditioned Pain Modulation

Optimism is associated with lower pain sensitivity, positive adjustment to chronic pain, and greater reduction of pain thresholds in a conditioned pain modulation (CPM) paradigm. We hypothesized that participants with higher levels of optimism would experience greater inhibition of suprathreshold pain during CPM. Seventy-seven healthy adults completed a test of optimism, the Life Orientation Test-Revised, as well as measures of depression, pain catastrophizing, and neuroticism. Participants also underwent psychophysical tests of heat pain tolerance, heat pain threshold, and CPM. CPM magnitude was calculated as the change in heat pain ratings when applied alone and simultaneously with painful pressure. Greater optimism was significantly correlated with reduced CPM magnitude (P = .013). Regression analysis was performed using optimism as a predictor of CPM magnitude while controlling for pain catastrophizing, neuroticism, depression, and age. The overall model was significant (P?=?.003). Significant positive coefficients were found for depression (P?=?.014) and optimism (P < .001) scores. These results suggest that greater optimism predicts less inhibition of suprathreshold pain, the opposite of our hypothesis. This unexpected finding may be due to factors such as perceived stress and coping differences, and suggests that modulation of threshold-level and suprathreshold pain involves different underlying mechanisms.

The role of fear of movement in subacute whiplash-associated disorders grades I and II

Fear and avoidance of activity may play a role in fostering disability in whiplash-associated disorders (WAD). This study examined the role of fear after WAD and assessed the effectiveness of 3 treatments targeting fear. People still symptomatic from WAD grade I-II injuries approximately 3 months previously (n = 191) completed questionnaires (eg, Neck Disability Index [NDI]) and were randomized to 1 of the treatments: (1) informational booklet (IB) describing WAD and the importance of resuming activities, (2) IB + didactic discussions (DD) with clinicians reinforcing the booklet, and (3) IB + imaginal and direct exposure desensitization (ET) to feared activities. DD and ET participants received three 2-hour treatment sessions. Absolute improvements in NDI were in predicted direction (ET = 14.7, DD = 11.9, IB = 9.9). ETs reported significantly less posttreatment pain severity compared with the IB (Mean = 1.5 vs 2.3, P < .001, d = 0.6) and DD (M = 1.5 vs 2.0, P = .039, d = 0.6) groups. Reduction in fear was the most important predictor of improvement in NDI (β = 0.30, P < .001), followed by reductions in pain (β = 0.20, P = .003) and depression (β = 0.18, P = .004). The mediational analysis confirmed that fear reduction significantly mediated the effect of treatment group on outcome. Results highlight the importance of fear in individuals with subacute WAD and suggest the importance of addressing fear via exposure therapy and/or educational interventions to improve function.     

Hypertension prevalence and diminished blood pressure–related hypoalgesia in individuals reporting chronic pain in a general population: The Tromsø Study

Resting blood pressure (BP) is inversely related to pain sensitivity in individuals free of chronic pain, reflecting homeostatic interactions between cardiovascular and pain modulatory systems. Several laboratory studies indicate that BP-related hypoalgesia is diminished in chronic pain patients, suggesting dysfunction in these interacting systems. Separate epidemiological findings reveal elevated hypertension prevalence in the chronic pain population. This study for the first time simultaneously evaluated both hypertension prevalence and BP-related hypoalgesia as they relate to chronic pain in the same sample. Resting BP and pain sensitivity were evaluated in a large general population sample (n = 10,135, aged 30–87 years). Subjects participated in a standardized 106 s cold pressor test, providing pain ratings at 9 s intervals. Self-reported presence of chronic pain and history of hypertension and use of antihypertensive medication were assessed. Significant interactions between chronic pain status and resting systolic (P < .001) and diastolic BP (P < .001) on mean pain ratings were observed. These interactions were due to significant (P < .001) BP-related hypoalgesia in individuals free of chronic pain that was twice the magnitude of the hypoalgesia observed in the group reporting chronic pain. Presence of chronic pain was associated with significantly increased odds of comorbid hypertension (P < .001). Within the chronic pain group, higher chronic pain intensity was a significant predictor of positive hypertension status beyond the effects of traditional demographic risk factors (P < .05). Results are consistent with the hypothesis that increased hypertension risk in the chronic pain population might be linked in part to chronic pain–related dysfunction in interacting cardiovascular–pain modulatory systems.     

Pain referral and regional deep tissue hyperalgesia in experimental human hip pain models

Hip disorder patients typically present with extensive pain referral and hyperalgesia. To better understand underlying mechanisms, an experimental hip pain model was established in which pain referrals and hyperalgesia could be studied under standardized conditions. In 16 healthy subjects, pain was induced by hypertonic saline injection into the gluteus medius tendon (GMT), adductor longus tendon (ALT), or gluteus medius muscle (GMM). Isotonic saline was injected contralaterally as control. Pain intensity was assessed on a visual analogue scale (VAS), and subjects mapped the pain distribution. Before, during, and after injections, passive hip joint pain provocation tests were completed, together with quantitative sensory testing as follows: pressure pain thresholds (PPTs), cuff algometry pain thresholds (cuff PPTs), cutaneous pin-prick sensitivity, and thermal pain thresholds. Hypertonic saline injected into the GMT resulted in higher VAS scores than hypertonic injections into the ALT and GMM (P < .05). Referred pain areas spread to larger parts of the leg after GMT and GMM injections compared with more regionalized pain pattern after ALT injections (P < .05). PPTs at the injection site were decreased after hypertonic saline injections into GMT and GMM compared with baseline, ALT injections, and isotonic saline. Cuff PPTs from the thigh were decreased after hypertonic saline injections into the ALT compared with baseline, GMT injections, and isotonic saline (P < .05). More subjects had positive joint pain provocation tests after hypertonic compared with isotonic saline injections (P < .05), indicating that this provocation test also assessed hyperalgesia in extra-articular soft tissues. The experimental models may open for better understanding of pain mechanisms associated with painful hip disorders.     

Hyperalgesia and functional sensory loss in restless legs syndrome

Pain and other sensory signs in patients with restless legs syndrome (RLS) are still poorly understood, as most investigations focus on motor system dysfunctions. This study aimed to investigate somatosensory changes in patients with primary RLS and the restoration of somatosensory function by guideline-based treatment. Forty previously untreated RLS patients were investigated unilaterally over hand and foot using quantitative sensory testing (QST) and were compared with 40 age- and gender-matched healthy subjects. The predominant finding in RLS patients was 3- to 4-fold increase of sensitivity to pinprick stimuli in both extremities (hand: P < .05; foot: P < .001), a sensory pathway involved in withdrawal reflexes. Pinprick hyperalgesia was not paralleled by dynamic mechanical allodynia. Additional significant sensory changes were tactile hypoesthesia in both extremities (hand: P < .05; foot P < .01) and dysesthesia to non-noxious cold stimuli (paradoxical heat sensation), which was present in the foot in an unusually high proportion (14 of 40 patients; P < .01). In 8 patients, follow-up QST 2 to 20 months after treatment with l-DOPA (L-3,4-dihydroxyphenylalanine) revealed a significant reduction of pinprick hyperalgesia (−60%, P < .001), improved tactile detection (+50%, P < .05), and disappearance of paradoxical heat sensation in half of the patients. QST suggested a type of spinal or supraspinal central sensitization differing from neuropathic pain or human experimental models of central sensitization by the absence of dynamic mechanical allodynia. Reversal of pinprick hyperalgesia by l-DOPA may be explained by impaired descending inhibitory dopaminergic control on spinal nociceptive neurons. Restoration of tactile sensitivity and paradoxical heat sensations suggest that they were functional disturbances resulting from central disinhibition.     

Exposure to an Immersive Virtual Reality Environment can Modulate Perceptual Correlates of Endogenous Analgesia and Central Sensitization in Healthy Volunteers

Virtual reality (VR) has been shown to produce analgesic effects during different experimental and clinical pain states. Despite this, the top-down mechanisms are still poorly understood. In this study, we examined the influence of both a real and sham (ie, the same images in 2D) immersive arctic VR environment on conditioned pain modulation (CPM) and in a human surrogate model of central sensitization in 38 healthy volunteers. CPM and acute heat pain thresholds were assessed before and during VR/sham exposure in the absence of any sensitization. In a follow-on study, we used the cutaneous high frequency stimulation model of central sensitization and measured changes in mechanical pain sensitivity in an area of heterotopic sensitization before and during VR/sham exposure. There was an increase in CPM efficiency during the VR condition compared to baseline (P < .01). In the sham condition, there was a decrease in CPM efficiency compared to baseline (P < .01) and the real VR condition (P < .001). Neither real nor sham VR had any effect on pain ratings reported during the conditioning period or on heat pain threshold. There was also an attenuation of mechanical pain sensitivity during the VR condition indicating a lower sensitivity compared to sham (P < .05). We conclude that exposure to an immersive VR environment has no effect over acute pain thresholds but can modulate dynamic CPM responses and mechanical hypersensitivity in healthy volunteers.PerspectiveThis study has demonstrated that exposure to an immersive virtual reality environment can modulate perceptual correlates of endogenous pain modulation and secondary hyperalgesia in a human surrogate pain model. These results suggest that virtual reality could provide a novel mechanism-driven analgesic strategy in patients with altered central pain processing.     

‘Pain inhibits pain’ mechanisms: Is pain modulation simply due to distraction?

‘Diffuse noxious inhibitory controls’ (DNIC), a form of supraspinal descending endogenous analgesia, requires a noxious conditioning stimulus for pain attenuation. This may be partly dependent on a distraction effect. The term “conditioned pain modulation” (CPM) has recently been introduced to describe the psychophysical paradigm to test DNIC. The present study aimed to determine whether distraction and tonic heat stimulation inhibit pain through the same or different mechanisms by looking at whether there is a similar or even an additive effect on pain attenuation. Test pain was brief heat stimulation applied to the left volar of 34 healthy volunteers. For conditioning, the right hand was immersed in 46.5 °C water. Distraction was provided by three different difficulty levels of continuous cognitive visual tasks. Experimental blocks consisted of test pain: (1) alone; ‘baseline’, (2) with conditioning pain; ‘CPM’, (3) with distraction; ‘distraction’ and (4) with conditioning pain and distraction; ‘combined’. They were randomized and repeated three times and pain intensity and unpleasantness rated. Results showed an overall effect of experimental block on test pain intensity (P = 0.0125). Post-hoc tests revealed a significant reduction in pain intensity ratings under Combined (21.2 ± 2.3; mean ± SEM) compared to CPM alone (16.0 ± 2.3) (P < 0.05). Furthermore, at all levels of distraction there were always a few subjects who were not distracted despite expressing CPM. Based on the additive effect of CPM and distraction on pain inhibition, and the cases of no distraction despite CPM, we suggest that CPM acts independently from distraction.     

Effect of conditioned pain modulation on trigeminal somatosensory function evaluated by quantitative sensory testing

The aim of the study was to systematically investigate the effect of craniofacially evoked conditioned pain modulation on somatosensory function using a quantitative sensory testing (QST) protocol applied to the trigeminal area in healthy humans. Pressure pain evoked by a mechanical compressive device was applied as conditioning stimulus (CS) in the craniofacial region, with a pain intensity of 5 on a visual analogue scale (VAS: 0–10 cm) (painful session) or with VAS score of 0 (control session). A full QST battery of 13 parameters was performed as test stimuli on the dominant-side cheek. The individual QST data from 11 men and 12 women were transformed into z scores, and the QST data and z scores were tested using analyses of variance. Analyses of variance of pressure pain threshold (PPT) data (log-transformed values and z scores) indicated significant session (P ? .003) and time (P < .001) effects with a session–time interaction (P < .001), but no main effect of sex (P ? .053, effect size ? .166). The session–time interaction showed that the PPTs in the painful session were associated with significantly higher log-transformed PPT values and significantly lower z scores compared with the control session at the time point during CS (hypoalgesia) (P < .001). No other QST parameters were significantly modulated by the CS. Sex differences were not detected in this study; a larger sample size may be needed to further explore this possibility. However, the findings indicate that when extensive QST protocols are applied, PPT may be the most sensitive measure to detect endogenous pain inhibitory mechanisms.     

Associations between KCNJ6 (GIRK2) gene polymorphisms and pain-related phenotypes

G-protein coupled inwardly rectifying potassium (GIRK) channels are effectors determining degree of analgesia experienced upon opioid receptor activation by endogenous and exogenous opioids. The impact of GIRK-related genetic variation on human pain responses has received little research attention. We used a tag single nucleotide polymorphism (SNP) approach to comprehensively examine pain-related effects of KCNJ3 (GIRK1) and KCNJ6 (GIRK2) gene variation. Forty-one KCNJ3 and 69 KCNJ6 tag SNPs were selected, capturing the known variability in each gene. The primary sample included 311 white patients undergoing total knee arthroplasty in whom postsurgical oral opioid analgesic medication order data were available. Primary sample findings were then replicated in an independent white sample of 63 healthy pain-free individuals and 75 individuals with chronic low back pain (CLBP) who provided data regarding laboratory acute pain responsiveness (ischemic task) and chronic pain intensity and unpleasantness (CLBP only). Univariate quantitative trait analyses in the primary sample revealed that 8 KCNJ6 SNPs were significantly associated with the medication order phenotype (P < .05); overall effects of the KCNJ6 gene (gene set-based analysis) just failed to reach significance (P = .054). No significant KCNJ3 effects were observed. A continuous GIRK Related Risk Score (GRRS) was derived in the primary sample to summarize each individual’s number of KCNJ6 “pain risk” alleles. This GRRS was applied to the replication sample, which revealed significant associations (P < .05) between higher GRRS values and lower acute pain tolerance and higher CLBP intensity and unpleasantness. Results suggest further exploration of the impact of KCNJ6 genetic variation on pain outcomes is warranted.     

Effects of step length on patellofemoral joint stress in female runners with and without patellofemoral pain

Background

Patellofemoral pain is common among runners and is frequently attributed to increased patellofemoral joint stress. The purpose of our study was to examine the effects of changing step length during running on patellofemoral joint stress per step and stress per mile in females with and without patellofemoral pain.

Methods

Ten female runners with patellofemoral pain and 13 healthy female runners performed running trials at 3.7 m/s in three conditions: preferred step length, at least + 10% step length, and at least − 10% step length. Knee flexion angles and internal knee extension moments served as inputs for a biomechanical model to estimate patellofemoral joint stress per step. We also estimated total patellofemoral joint stress per mile based on the number of steps necessary to run a mile during each condition.

Findings

Patellofemoral joint stress per step increased 31% in the long step length condition (P < .001) and decreased 22.2% in the short step length condition (P < .001). Despite the inverse relationship between step length and number of steps required to run a mile, patellofemoral joint stress per mile increased 14% in the long step length condition (P < .001) and decreased 7.5% in the short step length condition (P < .001).

Interpretation

These results suggest a direct relationship between step length and patellofemoral joint loads. Total stress per mile experienced at the patellofemoral joint decreased with a short step length despite the greater number of steps necessary to cover this distance. These findings may have relevance with respect to both prevention and treatment of patellofemoral joint pain.     

Inability to self-report pain after a stroke: A population-based study

The frequency of not being able to self-report pain after a stroke has not been previously assessed in a population-based sample. We studied the epidemiology of this problem using a cohort of patients hospitalized after a stroke in Olmsted County, Minnesota, from June 1, 2008, to June 1, 2012. Overall, 52 of 388 (13.4%) individuals were unable to provide a meaningful response to either a Faces Pain Scale or Numerical Rating Scale on admission. Inability to self-report pain was associated with measures of stroke severity (P < .0001), aphasia severity (P < .0001), and level of consciousness (P < .0001). Inability to self-report pain on admission was further associated with either subsequent death during the hospitalization (P < .0001) or an inability to provide self-report on dismissal (P < .0001). Our study further defines the epidemiology of the inability to self-report pain after a stroke as being less common than previously thought. Attempts to validate observational pain scales for poststroke patients should focus on those individuals with aphasia and/or depressed levels of consciousness.     

Five-factor personality traits and pain sensitivity: A twin study

Factors underlying individual differences in pain responding are incompletely understood, but are likely to include genetic influences on basal pain sensitivity in addition to demographic characteristics such as age, sex, and ethnicity, and psychological factors including personality. This study sought to explore the relationship between personality traits and experimental pain sensitivity, and to determine to what extent the covariances between these phenotypes are mediated by common genetic and environmental factors. A sample composed of 188 twins, aged 23 to 35 years, was included in the study. Heat pain intensity (HPI) and cold-pressor pain intensity (CPI) ratings were obtained using standardized pain testing procedures, and personality traits were assessed with the NEO Personality Inventory, Revised. Associations between personality and the pain sensitivity indices were examined using zero-order correlations and generalized estimating equations. Bivariate Cholesky models were used in the biometric analyses. The most robust finding was a significant phenotypic association between CPI and the personality facets Impulsiveness (a facet of Neuroticism) and Excitement-Seeking (a facet of Extraversion), and estimates of the genetic correlation were .37 (P < .05) and .43 (P < .05), respectively. In contrast, associations between HPI and personality seemed weak and unstable, but a significant effect of Angry Hostility (a facet of Neuroticism) emerged in generalized estimating equations analysis. Although the genetic correlation between these phenotypes was essentially zero, a weak but significant individual-specific environmental correlation emerged (r_e = .21, P < .05). Taken together, these findings suggest that CPI is more consistently related to personality dispositions than HPI, both phenotypically and genetically.