Heat Pain Thresholds Research Articles

Spontaneous Pain and Pain Sensitivity in Response to Prolonged Experimental Sleep Disturbances-Potential Sex Differences.

Insomnia is a highly prevalent condition that predisposes individuals to many chronic pain disorders, with most of them showing pronounced sexual dimorphism. We investigated whether experimental insomnia-like sleep disturbances (ESD) affect spontaneous pain and pain sensitivity, and whether sex modulates pain responses. Twenty-four healthy participants (50% females, age 28.3 ± 5.9 years) participated in a study consisting of two 19-day in-laboratory protocols-an ESD protocol consisting of repeated nights of short and disrupted sleep with intermittent nights of undisturbed sleep and a control sleep (CS) protocol consisting of 18 nights with an undisturbed 8-h sleep opportunity. Spontaneous pain was assessed using electronic rating scales during daytime and night-time wake periods. Pain sensitivity was assessed through pressure and heat pain threshold measures every other day of the protocol. Females responded with higher daytime pain ratings in the ESD compared to the CS condition, while males responded with lower pain ratings (p < 0.05 for condition*sex). Spontaneous pain ratings were higher at night-time than during daytime and worsened across successive nights of sleep disturbances, independent of sex (p < 0.05 for condition*study day*daytime-night-time). Females developed greater pressure pain sensitivity, while males developed greater pain sensitivity to heat in the ESD compared to the CS condition (p < 0.05 for condition*sex). Pain responses to sleep disturbances strongly vary by sex and may contribute to sex differences in the prevalence and symptom burden of many chronic pain conditions. Because the study was not a priori powered on sex, findings are preliminary and require follow-up in larger samples. Findings further suggest to specifically target night-time pain in sleep disturbed individuals, for example, through optimised timing of analgesic-acting medications. Exploration of sex as a modulator suggest that sleep disturbances amplify spontaneous pain and pressure pain sensitivity to a greater extent in females than in males, and this may contribute to females' overrepresentation and disproportionate symptom burden observed for many pain-related disorders for which insomnia is comorbid or a risk factor.

Do Female and Male Chests Feel the Same? A Comprehensive Quantitative Sensory Analysis

There is growing interest in understanding chest sensory function due to the significant morbidity associated with impaired sensation following nerve injury. While the baseline quantitative sensory and pain thresholds in female and male patients have been studied in various other anatomic areas, there is little knowledge on quantitative sensation at the chest as well as the presence of possible gender differences. Therefore, this study aimed to conduct a comprehensive quantitative sensory analysis to determine if female and male chests feel the same. A total of 100 chests in 50 subjects (25 females and 25 males) were evaluated. Quantitative sensory testing (QST) was performed on the nipple areola complex (NAC) and surrounding chest skin and included mechanical detection using Semmes-Weinstein monofilaments, two-point discrimination, vibration detection, pin prick, cold detection, warm detection, heat pain and pressure pain thresholds. Male chests were significantly more sensitive to mechanical detection, two-point discrimination, vibration, pin prick as well as cold and warm detection at both the NAC and chest as compared to female chests (p<0.05). Females had significantly lower sensory thresholds to heat pain and pressure pain detection at both the NAC and chest as compared to males (p<0.05). The quantitative sensory functions of female and male chests are significantly different. This knowledge helps to better understand baseline sensory functions at the chest and the awareness of gender differences in this anatomic area.

Effects of Repetitive Transcranial Magnetic Stimulation Applied over the Primary Motor Cortex on the Offset Analgesia Phenomenon

In this study, we investigate the effects of high-frequency repetitive transcranial magnetic stimulation (rTMS) applied over the left upper limb primary motor cortex (M1) on the offset analgesia (OA) phenomenon, a measure of endogenous pain modulation. In particular, we aim to determine whether rTMS influences OA differently in the forearm region, corresponding to the stimulated cortical area, compared to the trigeminal region. Twenty-two healthy volunteers underwent three experimental sessions: a baseline session without stimulation, an active rTMS session, and a sham rTMS session. Quantitative sensory testing (QST) paradigms, including warm and cold detection thresholds, heat pain threshold corresponding to a visual analogue scale (VAS) score of approximately 50–60 out of 100 (Pain50–60), and constant and offset trials, were assessed in both the forearm and trigeminal regions. The results revealed that active rTMS significantly enhanced the OA phenomenon in the forearm during the late phase, while no significant effects were observed in the trigeminal region. These findings suggest that rTMS may modulate central pain mechanisms in a body region-specific manner, potentially linked to the somatotopic organization of M1. This study points to possible mechanisms of action of rTMS for pain relief, highlighting the importance of region-specific effects in chronic pain treatment. Further research is needed to investigate the underlying mechanisms and clinical applicability of rTMS in patients with chronic pain conditions, especially when OA is compromised.

The Effects of Noxious Electrical Stimulation and Eccentric Exercise on Mechanical and Thermal Pain Sensitivity in Recreational Runners with Achilles Tendinopathy.

Achilles tendinopathy is a common overuse condition that can become persistent despite conservative treatment. Sensitization of both the peripheral and central nervous systems may contribute to the persistent pain. Both exercise and electrical stimulation have the potential to modulate the nervous system's sensitivity to painful stimuli. The purpose of this study was to describe the changes in pain sensitivity and self-reported function in runners with chronic Achilles tendon pain following sequential treatment with noxious electrical stimulation (NxES) and eccentric plantarflexion exercise. Single group, repeated measures design. Sixteen participants with chronic Achilles tendinopathy completed the Lower Extremity Functional Scale (LEFS) and the Victorian Institute of Sport Assessment-Achilles scale (VISA-A) and quantitative sensory tests (pressure pain threshold, heat temporal summation, and heat pain threshold) at baseline, one week, seven weeks, and then at a one month post intervention follow-up. The NxES was applied for one week, then followed by plantarflexion eccentric exercise for six weeks. Changes across timepoints were assessed using repeated measures ANOVA and post hoc analysis to describe differences. Hedges g effect sizes were also calculated. There was a significant improvement in LEFS (p < 0.001) and VISA-A (p < 0.001) from baseline to one month follow-up, with a mean change of 9.6 ± 7.7 and 19.4 ± 17.7 points respectively. Pressure pain threshold of the involved Achilles tendon increased over time (p < 0.001) with significant improvements after NxES application (p = 0.002) and after six weeks of eccentric exercise (p < 0.001). There were significant improvements from baseline to one month follow-up for heat temporal summation (p = 0.001) and heat pain threshold ( p < 0.001). For individuals with chronic Achilles tendinopathy, a sequential treatment of NxES followed by eccentric exercise resulted in a clinically significant improvement in self-reported pain and function. During the first week of treatment there was a reduction in mechanical hyperalgesia during the NxES-only phase, while a large reduction in primary heat hyperalgesia and additional desensitization to mechanical pain occurred during the eccentric training phase of treatment. 2b.

Changes in spatial bodily pain distribution one year after benign hysterectomy with emphasis on prevalence and risk factors for de novo and persistent pelvic pain- a prospective longitudinal multicenter study

BackgroundThe objectives were to determine the prevalence of de novo and persistent pelvic pain after benign hysterectomy and to assess risk factors.MethodsA Swedish prospective multicenter study of 440 women undergoing benign hysterectomy was conducted between October 2011 and March 2017. Measures of pain, the spatial extent of bodily pain, and pain sensitivity were assessed using a self-reporting questionnaire, Margolis’s patient pain drawing, and quantitative sensory testing of pain thresholds for pressure, heat, and cold, respectively. Quality of life was evaluated by EQ-5D-3L and SF-36. Psychological distress was assessed by the Hospital Anxiety and Depression Scaleand the Stress-Coping Inventory. Logistic regression models were used to assess risk factors, and the outcome was presented as an adjusted odds ratio (aOR) and 95% confidence interval (CI).ResultsPreoperatively, 18.0% of the women reported no bodily pain, 41.5% had pelvic pain, either as the only location (7.0%) or along with pain in other locations (34.5%), and 40.5% had non-pelvic pain only. Postoperatively, 6.2% developed de novo pelvic pain and 16.4% had persistent pelvic pain. De novo pelvic pain developed exclusively in women who preoperatively had non-pelvic pain only. Risk factors for de novo pelvic pain were a long hospital stay (aOR 1.50 (95%CI) 1.02–2.21)), high preoperative pain intensity (aOR 1.25 (95%CI 1.01–1.62)) and a high number of pain areas (aOR 1.15 (95%CI 1.05–1.27)), along with anxiety (aOR 10.61 (95%CI 1.84–61.03)) and low EQ-5D-3L health index (aOR 0.02 (95%CI 0.00–0.31)). Risk factors for persistent pelvic pain were lower age (aOR 0.89 (95%CI 0.81–0.97)), higher number of pain areas (aOR 1.08 (95%CI 1.02–1.14)), and a higher frequency of preoperative pain (aOR 12.75 (95%CI 2.24–72.66)).ConclusionAlthough hysterectomy appeared to be reasonably effective in curing pelvic pain, a non-negligible proportion of women developed de novo pelvic pain or had persistent pelvic pain. De novo pelvic pain seemed to affect only those who preoperatively had widespread bodily pain. Women at risk for de novo and persistent pelvic pain after hysterectomy could be identified preoperatively.Trial registrationsThe study was retrospectively registered in ClinicalTrial.gov (NCT01526668) on 01/27//2012.

Changes in Descending Pain Modulation During Anti-Tumor Necrosis Factor Therapy: A Prospective Study in Rheumatoid Arthritis and Spondyloarthritis.

In rheumatoid arthritis (RA) and spondyloarthritis (SpA), managing persistent pain remains challenging. Little is known regarding impaired pain pathways in these patients and the impact of biologic disease-modifying antirheumatic drugs (bDMARDs). The objective of the Rheumatism Pain Inhibitory Descending Pathways study was to assess pain thresholds and descending pain modulation in patients with active RA or SpA following introduction of a tumor necrosis factor inhibitor (TNFi). Patients with active disease (50 with RA and 50 with SpA) naive to bDMARDs or targeted synthetic DMARDs and starting a TNFi were included. Patients were observed for six months after TNFi initiation with clinical, psychological, and pain assessment. At all visits, participants underwent quantitative sensory testing with heat and cold pain thresholds and descending inhibition by conditioned pain modulation (CPM). Descending pain control (CPM effect) was assessed as the change in heat pain threshold (°C) following a conditioning stimulus. Of the 100 patients (59 women, mean ± SD age 45.8 ± 14.6 years), 74 completed the six-month follow-up. Thermal pain thresholds did not significantly change during follow-up. CPM effect improved significantly during follow-up (mean ± SD 0.25 ±2.57°C at baseline and 2.96 ± 2.50°C at six months; P < 0.001). At the end of follow-up, the mean CPM effect was significantly higher in patients without significant pain compared with patients with persistent pain (>3 of 10 on the Brief Pain Inventory) (mean ± SD 3.25 ± 2.68°C vs 2.47 ± 2.11°C; P = 0.04) and in patients achieving remission or low disease activity compared with patients with active rheumatism (mean ± SD 3.31 ± 2.68°C vs 2.18 ± 1.87°C; P = 0.01). In active inflammatory rheumatisms, impaired descending pain modulation, but not thermal pain thresholds, is improved after TNFi treatment, suggesting a possible effect of TNFi on central pain modulation.

Posterior-superior insula repetitive transcranial magnetic stimulation reduces experimental tonic pain and pain-related cortical inhibition in humans.

High frequency repetitive transcranial magnetic stimulation (rTMS) to the posterior-superior insula (PSI) may produce analgesic effects. However, the alterations in cortical activity during PSI-rTMS analgesia remain poorly understood. The present study aimed to determine whether tonic capsaicin-induced pain and cortical inhibition (indexed using TMS-electroencephalography) are modulated by PSI-rTMS. Twenty healthy volunteers (10 females) attended 2 sessions randomized to active or sham rTMS. Experimental pain was induced by capsaicin administered to the forearm for 90 minutes, with pain ratings collected every 5 minutes. Left PSI-rTMS was delivered (10 Hz, 100 pulses per train, 15 trains) ∼50 minutes postcapsaicin administration. Transcranial magnetic stimulation-evoked potentials (TEPs) and thermal sensitivity were assessed at baseline, during capsaicin pain prior to rTMS and after rTMS. Bayesian evidence of reduced pain scores and increased heat pain thresholds were found after active rTMS, with no changes occurring after sham rTMS. Pain (prior to active rTMS) led to an increase in the frontal negative peak ∼45 ms (N45) TEP relative to baseline. After active rTMS, there was a decrease in the N45 peak back to baseline levels. In contrast, after sham rTMS, the N45 peak was increased relative to baseline. We also found that the reduction in pain numerical rating scale scores after active vs sham rTMS was correlated with and partially mediated by decreases in the N45 peak. These findings provide evidence of the analgesic effects of PSI-rTMS and suggest that the TEP N45 peak is a potential marker and mediator of both pain and analgesia. This study demonstrates that high-frequency rTMS targeting the posterior-superior insula reduces capsaicin-induced pain and alters cortical activity, with changes in the N45 TMS-evoked potential peak mediating the analgesic effects.

Selective nociceptive modulation using a novel prototype of transcutaneous kilohertz high-frequency alternating current stimulation: a crossover double-blind randomized sham-controlled trial

BackgroundKilohertz high-frequency alternating current (KHFAC) stimulation has demonstrated to induce rapid and reversible nerve blocks without causing nerve damage. Previous studies have explored frequency-dependent effects using a transcutaneous approach in humans from 5 to 20 kHz. Nevertheless, its application in humans is limited by the lack of stimulators approved for frequencies above 20 kHz. Therefore, this study aimed to assess the effects and safety of transcutaneous KHFAC stimulation using a novel prototype stimulator, comparing interventions at 30, 40, and 50 kHz to sham stimulation on experimental pain, sensory, motor, and neurophysiological outcomes.MethodsA randomized, double-blind, sham-controlled crossover study involving 34 healthy participants was conducted. Four interventions (30, 40, 50 kHz, and sham) were administered, and stimulation was applied for 20 min to the median nerve of the non-dominant hand. A prototype stimulator capable of delivering frequencies between 1 and 50 kHz, with a maximum peak-to-peak output current intensity of 400 mA was designed. The intensity applied during the stimulation was below motor threshold, evoking a ‘strong but comfortable’ tingling sensation. Primary outcomes included heat pain threshold (HPT), pressure pain threshold (PPT), and adverse effects. The secondary outcomes included static two-point discrimination sensitivity, isometric pinch strength, and median sensory nerve action potential (SNAP).ResultsCompared with the sham stimulation, all the active interventions exhibited a significantly greater increase in the PPT during and immediately after the stimulation, while only a significant increase was observed at 40 kHz (4.1 N/cm2; 95%CI 0.3 to 7.9) at 15 min post-intervention. Compared to sham stimulation, the 40 kHz intervention had a significantly greater effect on the HPT at all time points, with the greatest difference (1.4 °C; 0.6 to 2.1) occurring immediately post-intervention. Adverse effects during active interventions included petechiae, erythema, and itching, which resolved at 24 h post-intervention. For secondary outcomes, only a significant reduction in the median SNAP velocity was observed in the sham stimulation group compared to the 50 kHz group.ConclusionsActive KHFAC stimulation, particularly at 40 kHz, delivered through a novel stimulator, effectively increased the PPT and HPT without affecting tactile or motor outcomes, inducing mild skin-related adverse effects. These findings have potential implications for people with pain-related pathologies.Trial registrationNCT05230836.

Effect of Lingual Nerve Block and Localised Somatosensory Abnormalities in Patients With Burning Mouth Syndrome-A Randomised Crossover Double-Blind Trial.

To investigate the effect of a lingual nerve block on spontaneous pain in patients with burning mouth syndrome (BMS) and to estimate associated somatosensory abnormalities by quantitative sensory testing (QST). A standardised QST battery including cold detection threshold (CDT), warmth detection threshold (WDT), thermal sensory limen (TSL), paradoxical heat sensation (PHS), cold pain threshold (CPT), heat pain threshold (HPT), mechanical pain threshold (MPT), wind-up ratio (WUR) and pressure pain threshold (PPT) was performed at the oral mucosa of the most painful site and intraoral control site in 20 BMS patients, and at the tongue and cheek mucosa in 22 age- and gender-matched healthy controls. The effect of a lingual nerve block on spontaneous burning pain reported by the BMS patients on a 0-10 cm visual analogue scale (VAS) was investigated in a randomised double-blind crossover design using (1 mL) lidocaine (lido) or saline (sal) with an interval of 1 week. The BMS patients were grouped into 'central' and 'peripheral' mechanisms based on the effect of the lingual nerve injections. For each BMS patient, Z-scores and Loss/Gain scores were computed. Differences among groups and sites were analysed using a two-way ANOVA. Differences within group were assessed by paired t-test. The 20 BMS patients were characterised on the basis of VAS changes (ΔLido-ΔSal) as a peripheral BMS subgroup (n = 9) with pain relief more than 1 cm on the VAS and a central BMS subgroup (n = 11) with pain relief less than 1 cm. BMS patients (n = 20) had lower sensitivity to thermal stimuli (i.e., CDT, WDT, TSL, CPT, HPT and PPT) and higher sensitivity to mechanical stimuli (i.e., PPT) compared with controls (p ≤ 0.007). Based on Loss/Gain coding, L1G0 (loss of thermal somatosensory function with no somatosensory gain, 55.0%) was the most frequent coding in the BMS group, which was higher than 11.4% in the control group (p < 0.001). Surprisingly, there was no significant difference between the peripheral and central BMS subgroups with regard to the Z-scores of any of the nine QST parameters (p > 0.097). The results of the lingual nerve blocks demonstrated two distinct phenotypes with either peripheral or central mechanisms but no direct impact on somatosensory function. Overall, somatosensory function in BMS patients seems abnormal in the painful areas compared to matched controls with a conspicuous loss of thermosensory function.

Neuropathic Pain and Clinical Sensory Testing in Young Patients with Sickle Cell Disease

Abstract Background The pathophysiology of pain in sickle cell disease (SCD) is complex and not fully understood. Neuropathic pain (NP) is an emerging theory of chronic pain in SCD. Nevertheless, assessment of NP is not a part of standard care of patients with SCD. Aim and Objectives To study the frequency of neuropathic pain among young patients with SCD by ID-P questionnaire and Clinical Sensory Testing (CST). Patients and Methods In this cross-sectional study Patients with SCD were recruited and data were collected on sociodemographic and clinical criteria of the disease. ID Pain (ID-P) questionnaire was used as a screening tool for NP. We performed a bedside clinical sensory testing (CST) including cold, warm, and pressure detection, cold, heat, mechanical and pressure pain threshold. Results Fifty-six participants were screened for eligibility and twelve of them were excluded; ten had stroke and two patients were diabetic. A total of 44 participants (25 males and 19 females) were included, their mean age was 12.4 years (SD 4.8; range 5.9-25 years). Screening of NP using the ID-P questionnaire revealed that 22.7% of the study cohort likely had NP. On the other hand, 34% of the participants had abnormal CST; 10 patients (22.7%) had abnormal mechanical pain threshold, 6 (13.6%) showed abnormal cold pain threshold, 2 (4.5%) had abnormal heat pain threshold and 2 (4.5%) with abnormal pressure threshold, while only one patient had delayed cold detection. Conclusion Neuropathic pain, as assessed by ID-P questionnaire and CST, is not uncommon in young patients with SCD.

Resistance Training Demonstrates Acute Local Muscular Increases In Heat Pain Threshold

Resistance Training Demonstrates Acute Local Muscular Increases In Heat Pain Threshold

Sustained nerve growth factor-induced C-nociceptor sensitization to electrical sinusoidal stimulation in humans.

Injection of recombinant human nerve growth factor (rhNGF) evokes acute heat and prolonged "polymodal" (mechanosensitive [CM]) and "silent" (mechanoinsensitive [CMi]) C-nociceptor sensitization. Both nociceptor classes can be activated differentially using slowly depolarizing electrical sinusoidal stimuli. To explore the temporal profile of nociceptor sensitization to heat and mechanical and electrical stimuli in humans after rhNGF. Recombinant human nerve growth factor (1 µg) and NaCl (0.9%) was injected into human forearm skin (n = 9, 50 µL/injection). Pain ratings (numeric rating scale) to transcutaneous electrical stimuli (1 ms 20 Hz rectangular pulses, 500-ms half-period sine wave [1 Hz] and 4 Hz sine wave pulses [2.5 and 60 seconds]) were assessed at days 3, 21, and 49 after injection, in addition to heat pain thresholds (HPTs, 9 × 9 mm thermode) and mechanical impact pain (4 and 8 m/second). Suprathreshold sinusoidal stimulation for specific CM (1 Hz) and combined CM and CMi (4 Hz) activation resulted in enhanced pain from day 3 post rhNGF and lasted throughout 7 weeks. These temporal dynamics contrasted minimum HPTs at day 3 (normalized by day 49) or mechanical impact pain (developing slowly until day 21 before declining depending on stimulus intensity). Correlation analyses of electrical pain indicated diverging kinetics when assessed for CM with or without concomitant CMi activation at days 3 and 21, which converged 7 weeks post rhNGF. Exceptionally long sensitization of CM and CMi nociceptors by rhNGF, uncovered by suprathreshold electrical sinusoidal stimulation, indicates a signal transduction-independent long-lasting hyperexcitability of C-nociceptors that clinically may contribute to rhNGF-maintained chronic inflammatory pain.

Understanding inter-individual variability of experimental pain habituation and conditioned pain modulation in healthy individuals

Although reduced experimental pain habituation is proposed as a proxy of diminished endogenous pain modulatory capacity in chronic pain, prior studies show contradictory findings. Even across healthy participants, pain habituation varies substantially, which may relate to another measure of endogenous pain modulation, i.e., conditioned pain modulation (CPM). Hence, this study investigated the relationship between pain habituation and CPM. Pain habituation was assessed in 45 healthy participants between two blocks of 15–20 contact-heat stimuli applied to the hand. Habituation of subjective pain ratings and objective neurophysiological readouts (contact-heat evoked potential (CHEP) and palmar sympathetic skin response (SSR)) was investigated. CPM was assessed by comparing heat pain thresholds before and after hand immersion in a noxious cold (9 °C) and lukewarm water bath (32 °C, to control for repeated measures effects). Pain habituation showed a large variability, with subjective but not objective pain habituation correlating with cold-induced CPM effects (r = 0.50; p = 0.025). This correlation was not observed for ‘true’ CPM effects (corrected for repeated measures effects) nor for CPM effects induced by a lukewarm water bath. These findings suggest that the observed variability in subjective pain habituation may be influenced by both descending endogenous pain modulation and peripheral adaptation processes associated with repeated measures. Objective pain habituation readouts, i.e., CHEPs and SSRs, capture different, complementary aspects of endogenous pain modulation.

Slow depolarizing electrical stimuli reveal differential time courses of nociceptor recovery after prolonged topical capsaicin in human skin.

We examined de-functionalization and temporal functional recovery of C-nociceptor evoked pain after topical 8% capsaicin applied for 4 consecutive days. Capsaicin and placebo patches were applied to human forearm skin (n = 14). Cold, warmth and heat pain thresholds, pain NRS to electrical and thermal (48°C, 5 s) stimuli and axon reflex flare were recorded weekly for 49 days. Mechanical and heat sensitive ('polymodal') nociceptors were activated by single electrical half-period sinusoidal pulses (0.5 s, 1 Hz). Mechanical and heat insensitive ('silent') nociceptors were activated by 4 Hz sinusoidal stimuli. Capsaicin abolished heat pain. Sensation to electrical sinusoidal stimulation was reduced but never abolished during the treatment. Pain to electrical 1 Hz 'polymodal' nociceptor stimulation took longer to recover than pain ratings to 4 Hz 2.5 s sinusoidal stimulation activating 'polymodal' and 'silent' nociceptors (35 vs. 21 days). Heat pain was indifferent to placebo from day 21-49. Axon reflex flare was abolished during capsaicin and only recovered to ~50% even after 49 days. Capsaicin abolishes heat transduction at terminal nociceptive endings, whereas small-diameter axons sensitive to sinusoidal electrical stimulation can still be activated. 1 Hz depolarizing stimuli evoke burst discharges, as demonstrated before, and recover slower after capsaicin than single pulses induced by 4 Hz. The difference in recovery suggests differential time course of functional regeneration for C-nociceptor sub-types after capsaicin. All sensations recovered completely within 7 weeks in healthy subjects. Our findings contrast analgesia lasting for months in spontaneous neuropathic pain patients treated with 8% capsaicin. Sinusoidal electrical stimulation can still activate small diameter axons desensitized to heat after 4 consecutive days of topical 8% capsaicin application and reveals differential temporal functional regeneration of C-nociceptor sub-types. Electrical sinusoidal stimulation may detect such axons that no longer respond to heat stimuli in neuropathic skin.

Can assessment of human assumed central sensitisation improve the predictive accuracy of the STarT Back screening tool in acute low back pain?

BackgroundThe STarT Back Screening Tool (SBT) is recommended to provide risk-stratified care in low back pain (LBP), yet its predictive value is moderate for disability and low for pain severity. Assessment of human assumed central sensitisation (HACS) in conjunction with the SBT may improve its predictive accuracy. ObjectivesTo examine whether assessment of HACS in acute LBP improves the predictive accuracy of the SBT for LBP recovery at six months in people with acute non-specific LBP. DesignA prospective longitudinal study. MethodData were drawn from the UPWaRD study. One hundred and twenty people with acute non-specific LBP were recruited from the community. Baseline measures included SBT risk status, nociceptive flexor withdrawal reflex, pressure and heat pain thresholds and conditioned pain modulation. Primary outcome was the presence of LBP (pain numeric rating scale ≥1 and Roland Morris Disability Questionnaire score ≥3) at six-month follow-up. Regression coefficients were penalised using the least absolute shrinkage and selection operator technique to select predictor variables. Internal validation was performed using ten-fold cross-validation. Results/findingsSBT risk status alone did not predict the presence of LBP at six months (area under receiver operating characteristic curve [AUC] = 0.58). Adding measures of HACS to the SBT did not improve discrimination for whether LBP was present at six months (AUC = 0.59). ConclusionsThis study confirmed the suboptimal predictive accuracy of the SBT, administered during acute LBP, for LBP recovery at six months. Assessment of HACS in acute LBP does not improve the predictive accuracy of the SBT.

A multi-modal evaluation of experimental pain and psychological function in women with carpometacarpal osteoarthritis

ObjectiveThumb carpometacarpal osteoarthritis (CMC1 OA) is a prevalent and debilitating condition that lacks effective treatments. Understanding the multidimensional pain experience across CMC1 OA disease stages is crucial to improving treatment outcomes. This study examined how radiographic CMC1 OA severity is associated with physical, psychological, and somatosensory function. MethodThirty-one women with early-stage (Eaton-Littler 1–2) or end-stage (Eaton-Littler 3–4) radiographic CMC1 OA completed validated questionnaires to assess pain, disability, and psychological function. Additionally, experimental pain was measured in each participant using quantitative sensory testing (QST) (mechanical, pressure, vibratory, thermal) at seven body sites (thenar, hypothenar, brachioradialis bi-laterally; quadriceps on affected side). Cohort differences (early-vs. end-stage) across all variables were analyzed using a multivariable modeling approach that included fixed effects and interactions; notably, age was controlled as a confounder. ResultsEnd-stage CMC1 OA participants had higher scores in the pain (p ​= ​0.01) and function (p ​= ​0.02) portions of the AUSCAN assessment, self-reported disability of the DASH questionnaire (p ​= ​0.04), and painDETECT scores (p ​= ​0.03), indicating greater pain and disability compared to early-stage participants. Additionally, end-stage CMC1 OA participants demonstrated reduced vibratory detection and heat pain thresholds at multiple body sites (p's ​< ​0.05), with significant interactions observed across the mechanical and cold stimuli. ConclusionFindings revealed women with end-stage CMC1 OA exhibited increased neuropathic pain characteristics and somatosensory loss compared to those with early-stage CMC1 OA. These results underscore the importance of addressing both peripheral and centralized pain mechanisms and the need for multimodal approaches in the treatment of CMC1 OA.

Recovery of the Infraorbital Nerve Following Open Reduction and Fixation Surgery of Zygomaticomaxillary Complex Fractures-A Prospective Cohort Study Based on Quantitative Sensory Testing.

This study aimed to assess the sensory function of the infraorbital nerve in patients with fractures of the zygomatic complex who underwent open reduction and internal fixation at different time points using quantitative sensory testing, which was established by the German Neuropathic Pain Research Network, comprising a 7-item mechanical and thermal sensory test. A total of 21 patients (age range 17-46y, 14 males) with unilateral zygomatic complex fractures were included. Quantitative sensory testing was conducted before the operation and at 1 week, 3 months, and 6 months operatively, with cold detection threshold, warmth detection threshold, cold pain threshold, heat pain threshold, mechanical detection threshold, mechanical pain threshold, pressure pain threshold, and vibration detection threshold being measured in bilateral infraorbital regions. Notable changes in sensitivity were observed in all values except for the mechanical pain threshold. In the majority of patients with zygomaticomaxillary complex fractures, infraorbital hypoesthesia was significantly improved within 3 months postoperatively, and almost complete recovery could be achieved by 6 months postoperatively.

The combined effect of transcutaneous electrical nerve stimulation and transcutaneous auricular vagus nerve stimulation on pressure and heat pain thresholds in pain-free subjects: a randomized cross-over trial

BackgroundTranscutaneous electrical nerve stimulation (TENS) is a non-invasive modality that utilizes electrical currents to modulate pain in populations with acute and chronic pain. TENS has been demonstrated to produce hypoalgesic effects in postoperative pain, fibromyalgia, knee osteoarthritis, and healthy subjects. Transcutaneous auricular vagus nerve stimulation (TaVNS) is a non-invasive modality that modulates the vagus nerve by stimulating its auricular branches. The effects of the combination of TENS and TaVNS on producing an analgesic response have not been studied. Considering that TENS and TaVNS both stimulate similar analgesic pathways but through different means of activation, we can hypothesize that a combination of both methods can produce a more pronounced analgesic response. Therefore, the objective of this study is to assess the hypoalgesic effect of a combination of TENS and TaVNS in pain-free subjects.Methods/designThe study will be a simple crossover design conducted at the University of Hartford. Subjects will be recruited from the University of Hartford population via oral communication, digital flyers, and posters on campus. Thirty participants will undergo two sessions in a crossover manner with one week in between. During one session, the participants will receive TENS with active TaVNS and the other session will be a placebo procedure (TENS with placebo TaVNS). The order of these sessions will be randomized. Importantly, the pressure pain threshold (PPT) and heat pain threshold (HPT) assessors will be blinded to the treatment category. For active TaVNS, a frequency of 25 Hz will be applied with a pulse duration of 200 µs. For placebo TaVNS, the intensity will be increased to a sensory level and then decreased to 0 mA. High-frequency TENS of 100 Hz will be applied in both sessions, with a pulse duration of 200 µsec, asymmetrical biphasic square waveform, and intensity of maximal tolerance without pain. TENS and TaVNS will be turned on for 30 min after a baseline measurement of outcomes. TENS and TaVNS will then be turned off, but the electrodes will remain on until completion of post-treatment assessment. Pressure pain threshold, heat pain threshold, blood pressure, oxygen saturation, and heart rate will be tested 4 times: Once pre-intervention, once during intervention, once immediately after the intervention, and once 15 min post-intervention. Statistical analysis of the data obtained will consider a significance level of p < 0.05.DiscussionThis study will provide evidence concerning the combined effects of TENS and TaVNS on pain threshold in pain-free participants. Based on the outcomes, a greater understanding of how TENS and TaVNS, when used in conjunction, can modulate pain pathways.Trial registrationClinicalTrials.gov NCT06361381. Registered on 09 April 2024.

Exploring the role of viscosity-vaso-occlusion and haemolysis-endothelial dysfunction in pain sensitization among Jamaicans with sickle cell disease.

Viscosity-vaso-occlusion (VVO) and haemolysis-endothelial dysfunction (HED) are pathophysiological mechanisms and clinical subphenotypes of sickle cell disease (SCD). Recurrent vaso-occlusive crises (VOC) may lead to neuroplastic changes and pain sensitization. Among 257 SCD participants, we assessed the relationship of subphenotypes with pain sensitivity using quantitative sensory testing to identify heat pain thresholds (HPT) and pressure pain thresholds (PPT). VOC history and sleep, social and emotional functioning were assessed using the Adult Sickle Cell Quality of Life Measurement Information System. The 'elbow method' determined the optimal number of clusters as three. Clustering was performed using K-prototypes. Among clusters 2 and 3, VOC frequency and severity were higher. Clusters 1 and 3 had lower haemoglobin, higher reticulocytes and lactate dehydrogenase and more leg ulcers. In multivariate regression, cluster 3 was associated with approximately 13.6% lower PPT compared to cluster 1, and female sex was associated with decreases in PPT and HPT at the hands and feet (p < 0.001). Hydroxyurea use and unit increases in sleep functioning and age were associated with approximately 20.1% higher foot-PPT, 6.8% higher hand-PPT and 2.5% higher hand-HPT and foot-HPT respectively. Findings suggest that a third subphenotype with mixed VVO and HED features and worse pain sensitization may exist.

The effect of resistance exercise on multimodal pain thresholds in local and systemic muscle sites.

Dynamic resistance exercise may produce reductions in pain locally at the exercising muscle and systemically at non-exercising sites. However, limited research has examined these changes with multiple noxious stimuli. This study examined changes in heat pain threshold (HPT) and pressure pain threshold (PPT) on different musculature after an upper and lower body exercise to compare local and systemic effects. A crossover design with 28 participants (mean age: 21 ± 4 years, 21 female) completed three sessions. Visit one included baseline quantitative sensory testing and 5-repetition maximum (RM) testing for upper (shoulder press) and lower (leg extension) body. In subsequent sessions, participants performed upper or lower body exercises using an estimated 75% 1-RM with pre/post assessment of HPT and PPT at three sites: deltoid, quadriceps, and low back. A significant three-way interaction was observed for HPT (F (1.71, 3.80) = 2.19, p = 0.036, η2p = 0.12) with significant increases in HPT over the quadriceps (p = 0.043) after leg extension and over the deltoid (p = 0.02) after shoulder press. Significant systemic changes were not observed for HPT or PPT. Local but not systemic effects were demonstrated after an acute bout of exercise. Peripheral pain sensitivity may be more responsive to heat stimuli after resistance exercise.