Somatosensory Function and Pain: Associations Over 12 Months post-injury in Youth with Acute Musculoskeletal Pain.

Quantitative sensory testing: identifying pain characteristics in patients with osteoarthritis

Abnormalities in pain regulatory mechanisms are common in patients with rheumatoid arthritis (RA). We investigated whether pain sensitization changes after treatment with a disease-modifying antirheumatic drug (DMARD) and explored associations between changes in pain sensitization and disease activity. We included 182 participants with active RA initiating/switching DMARD therapy who were observed for 12 weeks. To assess pain sensitization, participants underwent quantitative sensory testing (QST), including pressure pain thresholds (PPTs) at multiple anatomic sites, temporal summation (TS) at the wrist and forearm, and conditioned pain modulation (CPM). RA disease activity was measured using the Disease Activity Score 28 with C-reactive protein (DAS28-CRP) and its components. Mean changes in QST measures were examined from baseline to 12 weeks, and associations between QST and disease activity measures were explored using Pearson correlation coefficients and adjusted linear regression analyses. PPTs significantly increased (improved) at multiple anatomic sites following 12 weeks of DMARD therapy. No significant changes were observed in TS or CPM. Increased PPTs at multiple anatomic sites were associated with reductions in DAS28-CRP, swollen joint count, tender joint count, and improvements in patient global assessment. No significant associations were observed between TS, CPM, and disease activity. Pain sensitivity improved after 12 weeks of DMARD therapy. These improvements were associated with reductions in disease activity.

Pain Catastrophizing Moderates the Relationship Between Pain Sensitivity and Clinical Pain in Adolescents With Functional Abdominal Pain

BackgroundWhether patient’s experience of fibromyalgia severity is related to measures of pain sensitisation assessed by quantitative sensory testing is not clear. How disease duration effects the relationship between disease severity...

Pain sensitization in knee osteoarthritis (OA) is associated with greater symptom severity and poorer clinical outcomes. Measures that identify pain sensitization and are accessible to use in clinical practice have been suggested to enable more targeted treatments. This merits further investigation. This study examines the relationship between quantitative sensory testing (QST) and clinical measures of pain sensitization in people with knee OA. A secondary analysis of data from 134 participants with knee OA was performed. Clinical measures included: manual tender point count (MTPC), the Central Sensitization Inventory (CSI) to capture centrally mediated comorbidities, number of painful sites on a body chart, and neuropathic pain-like symptoms assessed using the modified PainDetect Questionnaire. Relationships between clinical measures and QST measures of pressure pain thresholds (PPTs), temporal summation, and conditioned pain modulation were investigated using correlation and multivariable regression analyses. Fair to moderate correlations, ranging from -0.331 to -0.577 (P<0.05), were identified between MTPC, the CSI, number of painful sites, and PPTs. Fair correlations, ranging from 0.28 to 0.30 (P<0.01), were identified between MTPC, the CSI, number of painful sites, and conditioned pain modulation. Correlations between the clinical and self-reported measures and temporal summation were weak and inconsistent (0.09 to 0.25). In adjusted regression models, MTPC was the only clinical measure consistently associated with QST and accounted for 11% to 12% of the variance in PPTs. MTPC demonstrated the strongest associations with QST measures and may be the most promising proxy measure to detect pain sensitization clinically.

In many patients with axial spondyloarthritis (axSpA), pain persists despite anti-inflammatory medication. Quantitative sensory testing (QST) indirectly assesses altered somatosensory function, though its clinical practicality is limited. The Central Sensitisation Inventory (CSI) could be an alternative in the initial assessment of central sensitisation (CS). This study aimed to investigate the value of the CSI in evaluating CS in patients with axSpA by (1) assessing somatosensory function related to CS with QST and (2) exploring associations between CSI, QST, patient and disease characteristics and pain-related psychosocial factors. Consecutive outpatients from the Groningen Leeuwarden AxSpA cohort underwent QST, including pressure pain threshold (PPT), temporal summation (TS) and conditioned pain modulation (CPM). Participants completed questionnaires assessing CS (CSI), illness perception (Revised Illness Perception Questionnaire, IPQ-R), pain-related worrying (Pain Catastrophising Scale, PCS), fatigue (Modified Fatigue Impact Scale, MFIS), anxiety/depression (Hospital Anxiety and Depression Scale, HADS) and coping. QST measurements were stratified for CSI≥40. 201 patients with axSpA were included; 63% male, 64% radiographic axSpA, median symptom duration 12 years (IQR 5-24), mean Axial Spondyloarthritis Disease Activity Score 2.1±1.0. Patients with CSI≥40 had significantly lower PPTs and higher TS than CSI<40 (p<0.004). No significant differences in CPM were observed. In multivariable linear regression, sex, PCS, IPQ-R Identity, MFIS and HADS anxiety were independently associated with CSI (78% explained variance). In this large cross-sectional study in patients with axSpA, the CSI appears as a useful initial CS assessment questionnaire. When CSI scores indicate CS, considering pain-related psychosocial factors is important. These results emphasise the need for a biopsychosocial approach to manage chronic pain in patients with axSpA.

BackgroundThis study described a sensory profile of participants with chronic pain (CP) in a previously reported feasibility RCT, in terms of quantitative sensory testing (QST) measures and the Central Sensitisation Inventory (CSI).AimsThe study aimed to explore the changes in QST measures and the CSI in this sample following participation in a mindfulness and physical activity intervention compared to an online self-management guide.MethodsParticipants were randomised into (i) a combined mindfulness and exercise online interactive group or (ii) an online self-management group. Pressure pain thresholds (PPT), temporal summation (TS), conditioned pain modulation (CPM) measures, and the CSI were completed with participants at baseline and post-intervention.ResultsBaseline (n = 33) and post-intervention (n = 22) measurements were completed. High mean CSI scores (54.69, SD 23.85) were noted at baseline in participants, indicating the presence of central sensitisation [n = 33; 70% (n = 23) score > 40]. Mean baseline scores for TS were high (2.64, SD 1.60), indicating the presence of pain facilitation, and variable results were observed for baseline PPT and CPM measures. The combined intervention was not found to be superior to a self-management guide in this cohort in terms of changes in PPT, TS, and CPM measures and the CSI.ConclusionsHigh baseline CSI and TS scores were identified in the cohort at baseline, with no notable trends identifiable with regard to changes in QST scores or the CSI post-intervention. Further studies are recommended with larger sample sizes in order to understand changes in QST measures following participation in interventions of this nature.Supplementary InformationThe online version contains supplementary material available at 10.1007/s11845-025-03947-y.

The relationship of pain sensitivity with pain and disability in low back pain (LBP) is complicated. It has been suggested increased understanding of dynamic quantitative sensory testing (QST) might be useful in increasing understanding of these relationships. This study aimed to create subgroups based on participant responses to dynamic QST, profile these subgroups based on multidimensional variables (including clinical measures of pain and disability, psychological and lifestyle variables and static QST), and investigate the association of subgroup membership with levels of pain intensity, LBP-related disability and disability risk at 12-month follow up. Participants (n=273) with dominant axial chronic non-specific LBP with duration of pain >3months were included in this study. At baseline, eligible participants completed a self-report questionnaire to collect demographic, clinical, psychological and lifestyle data prior to dynamic and static QST. Dynamic QST measures were conditioned pain modulation (CPM) and temporal summation (TS). At 12-months follow up, clinical data were collected, including pain intensity and LBP-related disability. Sub-groups were formed by cross-tabulation. Analysis was undertaken to profile dynamic QST subgroup on demographic, clinical, psychological, lifestyle and static QST measures. Associations between dynamic QST subgroups and follow-up clinical variables were examined. Based on dynamic QST, participants were allocated into four subgroups; normal CPM and normal TS (n=34, 12.5%); normal CPM and facilitated TS (n=6, 2.2%); impaired CPM and normal TS (n=186, 68.1%); impaired CPM and facilitated TS (n=47, 17.2%). At baseline no differences were demonstrated between subgroups across most clinical variables, or any psychological or lifestyle measures. The two subgroups with impaired CPM were more likely to have a higher number of painful body areas. Cold pain sensitivity was heightened in both the subgroups with facilitated TS. Subgroups did not differ across pain intensity, LBP-related disability and disability risk stratification at follow-up. The profiles of people with axial LBP did not vary significantly across dynamic QST subgroups, save forthose in groups with impaired CPM being more likely tohave more widespread symptoms and those with facilitated TS having heightened cold pain sensitivity. Further, subgroup membership was not related to future pain and disability. The role of dynamic QST profiles in LBP remains unclear. Further work is required to understand the role of pain sensitivity in LBP. The utility of dynamic QST subgrouping might not be in determining of future disability. Future research might focus on treatment modifying effects of dynamic QST subgroups.

Quantitative Sensory Testing of Spinal Cord and Dorsal Root Ganglion Stimulation in Chronic Pain Patients

The burden of chronic lower back pain with neuropathic components: a healthcare resource perspective

The prevalence of persistent pain among breast cancer survivors (BCS) is high, and it is unclear what distinguishes those with persistent pain from those without. Research suggests that differences in somatosensory function evaluated by quantitative sensory testing (QST) may be responsible. This study aimed to describe somatosensory profiles in terms of hyper- and hypoesthesia in BCS with and without persistent pain using reference data from healthy controls. Second, QST parameters of BCS with and without pain were compared with those of healthy controls (i.e., a negative control group) and patients with fibromyalgia (i.e., a positive control group). Participants (n = 128) were divided into four equal groups: healthy controls, BCS with persistent pain, BCS without persistent pain, and patients with fibromyalgia. Nine QST parameters were evaluated at the trunk and at a remote location. Somatosensory profiles were determined by Z-score transformation of QST data using normative data from healthy controls. At the trunk, compared to healthy controls, BCS with persistent pain exhibited sensory aberrations across five out of seven QST parameters: pressure pain threshold, mechanical detection, and thermal thresholds. Pain-free BCS showed similar sensory aberrations across the four QST parameters compared to healthy controls: mechanical detection and thermal thresholds. Temporal summation and conditioned pain modulation were not significantly different between groups. BCS with persistent pain exert aberrations in peripheral processing of nociceptive signals, heightened facilitation of nociceptive signals, and higher psychosocial burden when compared to pain-free BCS, healthy controls, and patients with fibromyalgia. This study investigates the somatosensory function of breast cancer survivors with and without persistent pain using quantitative sensory testing and two control group (i.e., patients with fibromyalgia and healthy controls). Our results indicate somatosensory aberrations within the peripheral, but not central pathways in breast cancer survivors with persistent pain. Our findings contribute to a better understanding of the somatosensory mechanisms underlying persistent pain, which may inform future interventions to prevent the development of persistent pain, and improve treatment modalities.

PurposeA major limitation in treatment outcomes for chronic pain is the heterogeneity of the population. Therefore, a personalized approach to the assessment and treatment of children and adolescents with chronic pain conditions is needed. The objective of the study was to subgroup pediatric patients with chronic MSK pain that will be phenotypically different from each other based on their psychosocial profile, somatosensory function, and pain modulation.Patients and MethodsThis observational cohort study recruited 302 adolescents (10–18 years) with chronic musculoskeletal pain and 80 age-matched controls. After validated self-report questionnaires on psychosocial factors were completed, quantitative sensory tests (QST) and conditioned pain modulation (CPM) were performed.ResultsThree psychosocial subgroups were identified: adaptive pain (n=125), high pain dysfunctional (n=115), high somatic symptoms (n=62). Based on QST, four somatosensory profiles were observed: normal QST (n=155), thermal hyperalgesia (n=98), mechanical hyperalgesia (n=34) and sensory loss (n=15). Based on CPM and temporal summation of pain (TSP), four distinct groups were formed, dysfunctional central processing group (n=27) had suboptimal CPM and present TSP, dysfunctional inhibition group (n=136) had suboptimal CPM and absent TSP, facilitation group (n=18) had optimal CPM and present TSP, and functional central processing (n=112) had optimal CPM and absent TSP. A significant association between the psychosocial and somatosensory profiles. However, no association was observed between the psychosocial or somatosensory profiles and pain modulatory profiles.ConclusionOur results provide evidence that adolescents with chronic musculoskeletal pain are a heterogenous population comprising subgroups that may reflect distinct mechanisms and may benefit from different treatment approaches. The combination of screening self-reported questionnaires, QST, and CPM facilitate subgrouping of adolescents with chronic MSK pain in the clinical context and may ultimately contribute to personalized therapy.

Patients with rheumatoid arthritis (RA) commonly demonstrate disordered pain processing associated with high pain sensitization. Pain sensitization is often assessed using quantitative sensory testing (QST), which is burdensome to patients. The self-administered Fibromyalgia Survey Questionnaire (FSQ) has been proposed as a low-burden, surrogate measure of central pain sensitization. We examined the correlation between FSQ and QST in patients with active RA. Participants in the Central Pain in Rheumatoid Arthritis (CPIRA) cohort underwent FSQ and QST evaluation at enrollment. QST measures included pressure pain threshold (PPT) at the thumb, trapezius, wrist, and knee; temporal summation (TS) at the wrist and arm; and conditioned pain modulation (CPM). Partial Spearman correlation between FSQ and each QST measure was assessed, adjusted for demographic factors, study site, disease characteristics, and pain catastrophizing. Sensitivity analyses included (1) stratified analysis by sex and (2) evaluation of how each component of FSQ associates with the QST measures. Among 285 participants with active RA, FSQ was weakly but statistically significantly correlated with PPT (r range = -0.31 to -0.21), and TS (r range = 0.13-0.15) at all sites in unadjusted analyses. After adjustment, statistically significant correlations persisted for TS at the wrist and PPT at all sites (except the thumb). Sensitivity analyses did not identify differences in association based on sex or with individual FSQ components. FSQ and QST were correlated among participants with active RA, but the strength of association was weak. QST and FSQ are not interchangeable measures of pain sensitization.

Does weight-bearing versus non-weight-bearing pain reflect different pain mechanisms in knee osteoarthritis?: the Multicenter Osteoarthritis Study (MOST)

Many patients with rheumatoid arthritis (RA) experience sleep disturbances, commonly attributed to joint pain. Sleep disturbances could also influence pain. One mechanism may be through dysregulated pain processing, manifested by enhanced pain sensitivity. The present study was undertaken to examine the role of pain sensitization, measured by quantitative sensory testing (QST), as a mediator in the pathway of sleep disturbance leading to subsequent pain. We used longitudinal data from 221 patients with active RA who were followed for 12 weeks after initiating a disease-modifying antirheumatic drug. Baseline QST included pressure pain thresholds at articular (wrists, knees) and nonarticular (trapezius, thumbnails) sites, temporal summation (TS) at the wrist and forearm, and conditioned pain modulation (CPM). Baseline sleep disturbance and subsequent pain intensity were assessed using the Patient-Reported Outcomes Measurement Information System (PROMIS). We evaluated correlations between sleep disturbance, QSTs, and subsequent pain intensity. Mediation analyses separately assessed each QST as a mediator, adjusting for baseline confounding factors. Sleep disturbance was correlated with all QST measures except wrist TS and CPM. Sleep disturbance significantly predicted subsequent pain (coefficient for a meaningful increase of 5 units in sleep disturbance=0.32 (95% confidence interval 0.11, 0.50) in multiple regression. QST mediated 10-19% of this effect. Pain sensitization may be one mechanism through which sleep disturbance contributes to pain. The small magnitude of association indicates that unmeasured pathways may contribute to this relationship. Intervention studies are needed to establish causality and determine whether improving sleep can improve pain in patients with RA.