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INTRODUCTION: Conditioned pain modulation (CPM) is a quantitative estimation of the capacity for endogenous pain modulation. Reduced CPM enables chronic painful event development or exacerbates pre-existing pain symptoms. Emerging reports indicate that patients with trigeminal neuralgia (TN) have dysregulated endogenous pain modulation. Transauricular vagus nerve stimulation (taVNS) is known to alleviate both acute and chronic pain symptoms. Its role in modulation or management of TN remains unknown. Here, we evaluated the taVNS efficacy in modulating CPM among TN patients. Conclusions from this investigation may facilitate establishment of novel non-invasive adjunctive approaches to treating TN patients. METHODS: All research work was conducted at the First Affiliated Hospital of the University of Science and Technology of China (Anhui Provincial Hospital). In all, we recruited 62 study participants, 31 TN patients and 31 healthy volunteers, for a 2-day experimental test. At the beginning of the experiment (Day 1), all subjects received 30 min of active taVNS. On Day 2, they received sham taVNS with the same duration and intensity. Meanwhile, technicians documented participant pressure pain thresholds (PPT) and CPM values at baseline, and at 15 and 30 min post-active or sham taVNS. RESULTS: A 30-min active taVNS exposure substantially elevated the PPT and CPM effect (P < 0.05) among TN patients, and we also observed a notable rise in the PPT and CPM effect (P < 0.05) among healthy controls. Additionally, there were no serious adverse events from the administered treatment. CONCLUSION: Exposure to 30 min of active taVNS strongly augmented the CPM effect and elevated the PPT among TN patients and healthy controls. These effects were not observed with sham stimulation. Despite the limitations inherent to survey studies, such as duration and compliance biases, we consider that taVNS is a promising, safe, and cost-effective therapy. In future investigations, we recommend assessment of long-term taVNS application and its effects on CPM and clinical pain. TRIAL REGISTRATION: ChiCTR2300078673 ( www.Chictr.org.cn ).

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The objectives of this study were to estimate the intra-rater and inter-rater reliability of the Pressure Pain Threshold (PPT) and Conditioned Pain Modulation (CPM) in healthy participants and patients with chronic shoulder pain. Additionally, the Standard Error of Measurement (SEM) and Smallest Detectable Change (SDC) were calculated. Thirty-one healthy volunteers and twenty patients with chronic shoulder pain were assessed using the PPT and CPM by two raters, with a 24 h interval between sessions. Excellent intra-rater reliability was demonstrated for PPT, with similar SEM and SDC when assessed by the same rater. The inter-rater reliability for PPTs in patients was moderate to good (ICC = 0.59-0.89) with higher SEM (73.83-121.98 kPa) and SDC (61.58-97.59) values than the asymptomatic group (ICC = 0.92-0.96, SEM = 49.61-103.12 kPa, SDC = 42.01-56.30) respectively. CPM's intra-rater reliability was good (ICC = 0.82) in the patients and moderate (ICC = 0.67) in the asymptomatic group, while inter-rater reliability was low for the asymptomatic group (ICC = 0.37) and extremely low (ICC = 0.074) for the patients, with comparable SEM and SDC outcomes in both groups. PPT and CPM measurements are highly reliable when conducted by the same rater on the same day. Patients had lower inter-rater PPT reliability but better intra-rater CPM reliability. Clinicians need to be mindful of potential variability when interpreting these test results.

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Conditioned pain modulation and exercise-induced hypoalgesia reflect inhibitory pain controls emanating from the brain. The aim of this study was to compare the extent of pain inhibition from exercise-induced hypoalgesia (isometric wall squat), conditioned pain modulation (cold-water immersion), and their combination (wall squat followed by cold water in fixed order) in healthy pain-free adults. Sixty-one participants (median age 21 years) completed three sessions (Wall-squat, Cold-water, Combined) in random order. Sessions were separated by at least a week. In each session, pressure-pain thresholds, single-pinprick-pain ratings, and pinprick-temporal summation of pain (the fifth minus the first) were obtained at quadriceps, forearms, and forehead, before and after wall squat and/or cold water. Each intervention inhibited pain to pressure (partial η2 =.26) and single pinprick (partial η2 =.16) to a similar extent; however, pressure-pain inhibition was negligible in the forehead. After adjusting for age and sex, single-pinprick-pain inhibition in the forehead induced by wall squat was associated with that induced by cold water (adjusted R2 =.15; p =.007), and stronger pain inhibition was predicted by a higher thigh-pain rating to wall squat (adjusted R2 =.10; p =.027). Neither intervention affected pinprick-temporal summation of pain. Together, the findings suggest that pain inhibitory effects of exercise-induced hypoalgesia and conditioned pain modulation may overlap when exercise is at least moderately painful (6/10 intensity). Pressure-pain in body regions remote from the exercised or conditioned sites may be weakly modulated. PERSPECTIVE: The current findings suggest that pain inhibitory effects induced by painful wall squat and by cold-water immersion may overlap. The magnitude of pain inhibition in the forehead remote from the exercised thigh or the conditioned foot appears smaller, which could be examined further in future research.

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CONTEXT: Patellofemoral pain (PFP) has poor long-term recovery outcomes. Central sensitization describes central nervous system changes altering pain modulation, which can complicate recovery (poorer prognosis, worse function). Signs of central sensitization include amplified pain facilitation, pain hypersensitivity, and impaired pain inhibition, which can be measured with temporal summation of pain (TSP), pressure pain thresholds (PPTs) and conditioned pain modulation (CPM), respectively. Sex differences exist for these test responses, but female-only PFP investigations of sensitization are uncommon. Understanding pain modulation in females with PFP could improve treatment protocols. OBJECTIVE: To determine whether females with PFP exhibit signs of central sensitization (greater TSP, lower PPTs, reduced CPM) compared to pain-free females. DESIGN: Cross-sectional Setting: Laboratory Patients or Other Participants: Thirty-three females [(20 PFP, 13 pain-free); Age: PFP 29.2 ± 7 years, pain-free 28 ± 7 years; Height: PFP 166.7 ± 5.9cm, pain-free 166 ± 9.5cm, Mass: PFP 66.7 ± 9.6kg, pain-free 69.3 ± 7.5kg). MAIN OUTCOME MEASURES: TSP was assessed with ten punctate stimuli applied to the knee and calculated by the difference in pain intensity between beginning and end responses. PPTs were tested at four sites [3 for local hypersensitivity (knee), 1 for widespread hypersensitivity (hand)]. CPM was conducted by comparing PPTs during two conditions (baseline, ice immersion). CPM response was defined as the percent difference between conditions. Between-group differences in TSP response were analyzed with a Welch's test. Separate Welch's tests analyzed group comparisons of PPTs and CPM responses at four sites. RESULTS: Females with PFP exhibited greater TSP response (P=0.019) and lower CPM response at patella center (P=0.010) and hand sites (P=0.007) than pain-free females. PPT group differences were not observed at any site (P>0.0125). CONCLUSIONS: Females with PFP modulate pain differently than pain-free females. Clinicians should recognize signs of central sensitization and their potential impact on treatment options.

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INTRODUCTION: Conditioned pain modulation (CPM) allows to investigate endogenous pain modulation and its clinical outcomes. Although co-activation of emotions has been shown to affect CPM, the impact of 'threat,' which may accompany CPM stimulation itself, has been mostly neglected. A critical factor for the threat level of the conditioning stimulus (CS) may be its predictability. METHODS: 38 healthy participants (18 female) took part in a CPM study with pressure stimulation on the leg (blood-pressure cuff) serving as CS and heat stimulation on the forearm (contact thermode; CHEPS) serving as test stimulus (TS). While CS varied in intensity and -as operationalisation of threat- in temporary predictability, TS was kept constant. CPM effects were studied by EEG parameters (N2P2) and pain ratings. RESULTS: We found a significant CPM effect when considering N2P2, with low CS predictability augmenting CPM inhibition; in contrast, a surprisingly facilitatory CPM effect occurred in pain ratings (in the high CS predictability condition). The threat manipulation was only partially successful because CS intensity increased the threat ratings but not -as intended- CS predictability. Correlations between subjective and psychophysiological CPM responses were low. DISCUSSION: The differing CPM effects in subjective and psychophysiological responses, with both inhibitory and facilitatory effects, is puzzling but has already been observed earlier. The consideration of the CPM stimulation as major threat that is emotionally active is theoretically clearly justifiable but the operationalisation by means of different levels of CS predictability as in the present study might not have been ideal. Thus, further attempts of experimental verification are warranted.

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Chronic spinal pain has negative effects on physical and mental well-being. Psychological factors can influence pain tolerance. However, whether these factors influence descending modulatory control mechanisms measured by conditioned pain modulation (CPM) in people with chronic spinal pain is unclear. This systematic review investigated the association between CPM response and psychological factors in people with chronic spinal pain. Published and unpublished literature databases were searched from inception to 23rd October 2023 included MEDLINE, EMBASE, CINAHL, and PubMed. Studies assessing the association between CPM response and psychological factors in people with chronic spinal pain were eligible. Data were pooled through meta-analysis. Methodological quality was assessed using the AXIS tool and the certainty of evidence measured through GRADE. From 2172 records, seven studies (n = 598) were eligible. Quality of included studies was moderate. There was very low certainty of evidence that depression (r = 0.01 [95% CI -0.10 to 0.12], I2 = 0%), and anxiety (r = -0.20 [95% CI -0.56 to 0.16], I2 = 84%), fear avoidance (r = -0.10 [95% CI -0.30 to 0.10], I2 = 70%) had no statistical associations with CPM responder status. Higher pain catastrophising was associated with CPM non-responder status (r = -0.19; 95% CI: -0.37 to -0.02; n = 545; I2: 76%) based on a very low certainty of evidence measured by GRADE. There is currently limited available evidence demonstrating an association between CPM response and psychological factors for people with chronic pain. Managing an individual's chronic pain symptoms irrespective of comorbid psychological distress, should continue until evidence offer insights that more targeted interventions are needed.

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INTRODUCTION: Chronic pain is a public health issue, leading to substantial healthcare costs and diminished quality of life for sufferers. While the role of anxiety in pain modulation has been extensively studied, the effects of other emotional states on the body's pain control mechanisms remain less understood. This study sought to explore how different emotions (happiness, anger, sadness, and interest) affect conditioned pain modulation (CPM) and the wind-up phenomenon in healthy adults. METHODS: This randomized controlled, cross-over trial involved 28 healthy participants aged 18-60. Participants watched video clips designed to induce specific emotions: happiness, anger, sadness, and interest. Emotional states were assessed using a 7-point Likert scale. Pain modulation was measured using CPM and the wind-up phenomenon. CPM was assessed with a hot water bath as the conditioning stimulus and pressure pain tolerance as the test stimulus. Wind-up was measured using pinprick needle stimulators and a visual analog scale. Data were analyzed using paired t tests to compare pre- and post-emotion induction values. RESULTS: Significant changes in emotional self-assessment values were observed for all emotions. Happiness increased CPM (4.6 ± 11.4, p = 0.04277), while sadness - 9.9 ± 23.1, p = 0.03211) and anger - 9.1 ± 23.3, p = 0.04804) decreased it. Interest did not significantly alter CPM (- 5.1 ± 25.8, p = 0.31042). No significant effects were found for the wind-up phenomenon across any emotional states. CONCLUSION: This study shows that emotional states significantly affect the body's ability to modulate pain. Positive emotions like happiness enhance pain inhibition, while negative emotions such as sadness and anger impair it. These findings suggest that emotional modulation techniques could be integrated into pain management strategies to improve patient outcomes. Further research should explore a broader range of emotions and include objective measures to validate these results.

Chronic pain is a widespread problem that affects millions of people and leads to high healthcare costs and decreased quality of life. Understanding how emotions impact pain can help us find better ways to manage it. This study looked at how different emotions (happiness, anger, sadness, and interest) affect the ability of the body to naturally control pain in healthy adults. Participants experienced different tests in a random order, like flipping a coin to decide the order. Each participant took part in all the tests to compare how different conditions affected them. We measured changes in their pain perception using two methods: conditioned pain modulation, which reflects how well the body can suppress pain after experiencing another painful stimulus, and the wind-up phenomenon, which measures how pain intensity increases with repeated stimulation. We found that emotions affected the body's ability to control pain. Sadness and anger reduced the efficacy of conditioned pain modulation, making it harder for the body to reduce pain. Happiness improved CPM, enhancing the body's natural ability to stop pain. Interest did not significantly change how pain was felt. We also did not find any significant changes in the wind-up phenomenon for any of the emotions tested. The results suggest that positive emotions like happiness can help reduce pain, while negative emotions like sadness and anger can make pain worse. This could lead to new pain management approaches that include methods to boost positive emotions and reduce negative ones.

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Even in healthy populations, conditioned pain modulation (CPM) magnitude varies. This may be accounted for by (non-)modifiable factors, including physical activity (PA). Yet, little research has thoroughly examined PA and its relation with CPM magnitude in a representative sample. Therefore, the present study investigated the predictive effect of PA on CPM magnitude in 105 healthy adults. PA was assessed during 7 consecutive days by self-report using the International Physical Activity Questionnaire and by monitor-based accelerometry. CPM was examined using a heterotopic noxious-conditioning stimulation protocol during which the effect of a hot water-conditioning stimulus on pressure pain thresholds was evaluated. Comparative, correlation, and hierarchical linear regression analyses were performed. Report-based walking predicts 4.8% of variance in pain-modulatory capacity, moderate PA predicts 10.2% of variance in pain-modulatory capacity, and report-based time spent on total PA predicts 7.0% of variance in pain-modulatory capacity. More metabolic equivalent-minutes/week spent on total PA, including walking and moderate PA, is associated with greater pain-modulatory capacity. The findings of this study add to the limited evidence on the predictive effect of PA on CPM. It urges to consider PA a confounding factor when examining CPM. The current study provides evidence that a physically active lifestyle benefits endogenous pain modulation in healthy adults. Given its potential, walking and moderate-intensity PA might be achievable treatment strategies for pain patients known to have impaired CPM. PERSPECTIVE: The results of this article show that a physically active lifestyle, including larger amounts of walking and moderate activity, predicts greater pain-modulatory capacity. TRIAL REGISTRATION: This study has not been preregistered.

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Background and purpose: Fibromyalgia (FM) is associated with altered descending pain modulatory pathways, which can be assessed through Conditioned Pain Modulation (CPM). In this study, we aimed to explore the relationship between CPM and self-reported baseline characteristics in patients with fibromyalgia. We also performed a longitudinal analysis exploring CPM as a potential predictor of clinical improvement over time in individuals with FM. Methods: We performed cross-sectional univariable and multivariable analyses of the relationship between CPM and other variables in 41 FM patients. We then performed longitudinal analyses, building linear mixed effects models with pain in the Visual Analogue Scale (VAS) as the dependent variable, and testing for the interaction between time and CPM. We also tested the interaction between CPM and time in models using other outcomes, such as the revised Fibromyalgia Impact Questionnaire (FIQR) and Quality of Life Scale (QOLs). Results: We found no association between CPM and other demographic and clinical variables in the univariable analysis. We found a statistically significant association in the multivariable linear regression model between CPM and the QOLs at baseline, after controlling for age, sex, and duration of symptoms. In the longitudinal analyses, we found that CPM is an effect modifier for clinical improvement over time for the pain VAS, QOLs and FIQR: individuals with low-efficient CPM at baseline have a different (improved) pattern of response over time when compared to those with high-efficient CPM. Conclusions: Our findings suggest that CPM is not a reliable biomarker of clinical manifestations in chronic pain patients during cross-sectional assessments. However, our results are consistent with previous findings that CPM can be used to predict the evolution of clinical pain over time. We expect that our findings will help in the selection of patients with the best profile to respond to specific interventions and assist clinicians in tailoring pain treatments.

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Objective: The aim of this study is to assess whether pain-inducing manual pressure (PIMP) leads to effects on pressure pain threshold (PPT) mediated by conditioned pain modulation (CPM) and whether these effects are influenced by the intensity and repetition of the stimulus. Additionally, the influence of psychological factors and physical activity on the response to PIMP was explored. Methods: A total of 72 pain-free students were randomly assigned to three crossover trials. Trial 1 compared the effects of PIMP with the cold pressor task and pain-inducing electrostimulation. Trial 2 compared the effects of manual pressure that elicited moderate pain, mild pain, and no pain. Trial 3 compared a single PIMP stimulation with four stimuli applied at the same site or at different sites. Results: PIMP produced a lower increase in PPT than cold pressor task and no difference with electrostimulation. Manual pressure that caused moderate pain led to a greater increase in PPT compared to mild pain and pain-free application. Repetition of PIMP stimulus, whether at the same or different sites, did not significantly increase PPT compared to a single stimulation. No association with psychological factors or physical activity was found. Conclusions: PIMP produces an increase in PPT, suggesting the involvement of CPM-related mechanisms.

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Acute sleep deprivation in experimental studies has been shown to induce pain hypersensitivity in females. However, the impact of natural sleep deficiency and fluctuations across the week on pain perception remains unclear. A sleep-monitoring headband and self-reports were utilized to assess objective and subjective sleep in longer (> 6 hr) and short sleepers (< 6 hr). Pain sensitivity measures including heat, cold, pressure pain thresholds, pain inhibition (conditioned pain modulation) and facilitation (tonic pain summation) were assessed on Mondays and Fridays. Forty-one healthy young (23.9 ± 0.74 years) women participated. Short sleepers slept on average 2 hr less than longer sleepers (297.9 ± 8.2 min versus 418.5 ± 10.9 min) and experienced impaired pain inhibitory response (mean = -21.14 ± 7.9°C versus mean = 15.39 ± 9.5°C; p = 0.005). However, no effect was observed in pain thresholds and pain summation (p > 0.05). Furthermore, pain modulatory responses differed between Mondays and Fridays. Chronic sleep deficiency (< 6 hr) compromises pain responses, notably on Mondays. Maintaining a consistent sleep pattern with sufficient sleep (> 6 hr) throughout the week may protect against pain sensitization and the development of chronic pain in females. Further research is needed, especially in patients with chronic pain.

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Posttraumatic headache (PTH) is common following traumatic brain injury and impacts quality of life. We investigated descending pain modulation as one possible mechanism for PTH and correlated it to clinical measures. Pain-related evoked potentials (PREP) were recorded in 26 PTH-patients and 20 controls after electrical stimulation at the right hand and forehead with concentric surface electrodes. Conditioned pain modulation (CPM) was assessed using painful cutaneous electric stimulation (PCES) on the right hand as test stimulus and immersion of the left hand into 10 °C-cold water bath as conditioning stimulus based on changes in pain intensity and in amplitudes of PCES-evoked potentials. All participants completed questionnaires assessing depression, anxiety, and pain catastrophising. PTH-patients reported significantly higher pain ratings during PREP-recording in both areas despite similar stimulus intensity at pain threshold. N1P1-amplitudes during PREP and CPM-assessment were lower in patients in both areas, but statistically significant only on the hand. Both, PREP-N1-latencies and CPM-effects (based on the N1P1-amplitudes and pain ratings) were similar in both groups. Patients showed significantly higher ratings for anxiety and depression, which did not correlate with the CPM-effect. Our results indicate generalized hyperalgesia for electrical stimuli in both hand and face in PTH. The lacking correlation between pain ratings and EEG parameters indicates different mechanisms of pain perception and nociception.

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The variability of the Conditioned Pain Modulation (CPM) effect can be attributed to conditioning stimulus (CS) characteristics, such as intensity, duration, unpleasantness, or affinity. This study investigates the impact of affinity and unpleasantness variables on the CPM effect using two protocols (cold water and ischemia) in the same healthy individuals (n = 54). Additional variables were also examined for their potential influence on the CPM effect. The main results are as follows: (1) a higher level of affinity and a lower level of unpleasantness for the stimuli used resulted in a stronger CPM effect; (2) significant differences were observed in the extreme categories (high and low) of both variables, whereas the 'indifferent' group did not show a clear trend; (3) within-subject analysis demonstrated that affinity for the CS had a clear impact on the CPM effect; (4) no correlations were found between the CPM effect and the additional variables, except for the extraversion variable with the CPM effect of the ischemia protocol, and CS duration variable with CPM effect in the cold water protocol; and (5) only the affinity variable explained the CPM effect in both protocols in the multiple linear regression analysis. The affinity variable was found to influence the CPM effects significantly, indicating its important role in our perception and response to pain.

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Background: Pain leads to activation of the autonomic nervous system and thus, among other things, to pupillary reflex dilation (PRD). Previous studies have already confirmed a correlation between the perception of pain and the pupillary reaction, measured using pupillometry. However, the previous study populations were under the influence of medication for analgesia in perioperative setting or suffered from pain. This study examines the relationship between pupillary reaction and pain perception in healthy controls and addresses the question of whether endogenous pain inhibition, clinically tested by conditioned pain modulation (CPM), can be quantified using pupillometry. Methods: Forty-two healthy volunteers (21 females, 21 males, mean age 27.9 ± 5.8 years, range 20-39 years) were included in this study. The PRD, as a measure of the pupillary reaction (variance from the base diameter in percent), was investigated during baseline, heat application and during CPM testing and results compared to the reported pain intensity on the numerical rating scale (NRS). Results: The volunteers showed higher variances under painful conditions compared to the measurement at rest corresponding to higher sympathetic activity during pain. Volunteers with a higher variance, ie a stronger pupillary reaction, gave higher pain ratings than subjects with a lower pupil variance. However, there was no correlation between the NRS and PRD. PRD and pain ratings during CPM were significantly lower compared to heat pain application alone. However, there was no correlation between the calculated CPM effect and the PRD. Conclusion: Pupillometry is capable of objectively reflecting the pain response, eg pain relief through CPM testing. However, the CPM effect calculated from the subjective pain ratings and the objective PRD measurements is not associated suggesting that both measure different aspects of pain perception. It must be discussed whether the CPM effect can be the correct measure for the functionality of the pain system.

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INTRODUCTION: Myofascial trigger point therapy (MTrP) is a widely used therapeutic approach, although the underlying mechanisms remain unclear. Mechanisms discussed include peripheral involvement of muscles as well as central pain modulating processes such as the conditioned pain modulation (CPM). The aim of this study was to investigate whether the analgesic response of MTrP and the analgesic response of CPM correlate in asymptomatic participants in order to identify shared underlying mechanisms of MTrP and CPM. METHOD: Both, CPM and MTrP protocols consisted of heat-based test stimuli (heat pain thresholds before and after the intervention) and pressure-based (conditioning) stimuli. Asymptomatic participants (n = 94) were randomly assigned to receive either mild, intense or no pressure stimuli (between-group design) to both the fingernail and the MTrP of the infraspinatus muscle (within-group design). Pressure stimuli at both locations (fingernail, MTrP) were applied with a pressure algometer for 120 s and continuously adjusted to maintain a constant pain intensity of mild or intense pain. All thermal stimuli were applied on the lower leg with a thermal stimulator. RESULTS: A significant correlation was shown between the analgesic effect of CPM and MTrP therapy for mild (r = 0.53, p = 0.002) and intensive stimuli (r = 0.73, p < 0.001). 17.3% of the variance of the MTrP effect were explained by CPM after mild stimulation, and 47.1% after intense stimulation. Pain-related characteristics did not explain the variance within the analgesic response using a regression analysis. CONCLUSIONS: Between the analgesic responses following MTrP and CPM paradigms, a moderate to strong correlation was observed, suggesting shared underlying mechanisms.

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INTRODUCTION: Chronic neck pain (CNP) is a global public health problem, with high prevalence and absenteeism rates. Central sensitization (CS) as a basis for chronic pain may play an essential role in its development and progression. It is often comorbid with low conditioned pain modulation (CPM) effects, cognitions, and psychological problems. OBJECTIVES: The purposes of this study were to (1) explore the relationship between pain-related cognitions and psychological factors, CPM effects, and the central sensitization inventory (CSI) scores; and (2) determine whether cognitions and psychological factors can predict CSI scores and CPM effects in individuals with CNP. METHODS: Fifty-four individuals with CNP were recruited for this cross-sectional study. The following outcome measures were evaluated: The CSI (screening tool) was compared with the cold pressor test (CPT), which was the psychophysical test used to assess the CPM; neck pain intensity using the visual analogue scale (VAS), as well as pain-related cognitions (including kinesiophobia and pain catastrophization) and psychological states (including anxiety and depression) using self-report questionnaires. RESULTS: CSI score was not associated with the CPM effect (r = 0.257, p > 0.05), and no cognitions or psychological factors were associated with CPM (p > 0.05), but CSI score was moderately positively correlated with kinesiophobia (r = 0.554, p < 0.01), lowly positively correlated with pain catastrophization (r = 0.332, p = 0.017) and anxiety (r = 0.492, p < 0.01), but not depression (r = 0.207, p = 0.132). Multiple linear regression analysis showed that kinesiophobia (B = 1.308, p < 0.01) and anxiety (B = 1.806, p = 0.02) were significant positive predictors of CSI score. CONCLUSIONS: The findings confirm some of our hypotheses. Accordingly, the findings inferred that the CSI does not seem to respond to CPM effect in patients with CNP effectively. In addition, CSI score was associated with cognitions and psychological factors, of which kinesiophobia and anxiety were effective predictors. In clinical practice, pain-related cognitions and psychological factors should be fully considered to manage neck pain efficiently.

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Fibromyalgia (FM) is a widespread chronic pain syndrome, possibly associated with the presence of central dysfunction in descending pain inhibition pathways. Conditioned Pain Modulation (CPM) has been proposed as a biomarker of FM. Nonetheless, the wide variety of methods used to measure CPM has hampered robust conclusions being reached. To clarify the validity of CPM as a biomarker of FM, we tested two CPM paradigms (parallel and sequential) in a sample of 23 female patients and 23 healthy women by applying test (mechanical) stimuli and conditioning (pressure cuff) stimuli. We evaluated whether CPM indices could correctly classify patients and controls, and we also determined the correlations between the indices and clinical variables such as symptomatology, disease impact, depression, quality of life, pain intensity, pain interference, fatigue and numbness. In addition, we compared the clinical status of CPM responders (efficient pain inhibitory mechanism) and non-responders. We observed that only parallel CPM testing correctly classified about 70% of patients with FM. In addition, more than 80% of healthy participants were found to be responders, while the rate was about 50% in the FM patients. The sequential CPM test was not as sensitive, with a decrease of up to 40% in the response rate for both groups. On the other hand, we did not observe any correlation between CPM measures and clinical symptoms. In summary, our findings demonstrate the influence of the CPM paradigm used and confirm that CPM may be a useful marker to complement FM diagnosis. However, the findings also cast doubts on the sensitivity of CPM as a marker of pain severity in FM.

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Pain catastrophizing has been linked to amplified pain sensitivity assessed using quantitative sensory testing (QST) in adults; pediatric data are limited, particularly in youth with functional abdominal pain (FAP). With increasing use of QST to evaluate somatosensory function and predict pain outcomes, we examined the associations between QST and clinical pain in adolescents with FAP and tested the moderating effects of pain catastrophizing. Seventy-seven adolescents (mean age 16.6 years, 85.7% female, 72.7% White, 90.8% non-Hispanic) who fulfilled diagnostic criteria for FAP completed QST assessment (pressure pain threshold and tolerance, heat pain threshold, conditioned pain modulation) and measures of abdominal pain intensity, pain interference, and pain catastrophizing. Adjusting for age and sex, only higher heat pain threshold was associated with higher abdominal pain intensity (Beta per 1-standard deviation = .54, P = .026). Contrary to hypothesis, for youth with higher pain catastrophizing, higher pressure pain tolerance was associated with greater abdominal pain intensity, but associations were not significant for youth with lower catastrophizing (P = .049). Similarly, for those with higher pain catastrophizing (in contrast to lower pain catastrophizing), higher pressure pain thresholds and tolerance were associated with higher pain interference (P = .039, .004, respectively). Results highlight the need to investigate the influence of pain catastrophizing on QST. PERSPECTIVE: This study demonstrated unexpected findings of pain catastrophizing moderating the relationships between pressure pain threshold and tolerance, and clinical pain in adolescents with FAP. This raised questions regarding our understanding of psychological contributions to QST findings in pediatric populations with chronic pain.

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Unilateral nociceptive stimulation is associated with subtle signs of pupil asymmetry that may reflect lateralized activity in the locus coeruleus. To explore drivers of this pupil asymmetry, electrical stimuli, delivered alone or 200 ms before or after an acoustic startle stimulus, were administered to one ankle under four experimental conditions: with or without a 1.6 s anticipatory period, or while the forearm ipsilateral or contralateral to the electrical stimulus was heated tonically to induce moderate pain (15 healthy participants in each condition). Pupil diameter was measured at the start of each trial, at stimulus delivery, and each second for 5 s after stimulus delivery. At the start of the first trial, the pupil ipsilateral to the side on which electric shocks were later delivered was larger than the contralateral pupil. Both pupils dilated robustly during the anticipatory period and dilated further during single- and dual-stimulus trials. However, pupil asymmetry persisted throughout the experiment. Tonically-applied forearm heat-pain modulated the pupillary response to phasic electrical stimuli, with a slight trend for dilatation to be greater contralateral to the forearm being heated. Together, these findings suggest that focusing anxiously on the expected site of noxious stimulation was associated with dilatation of the ipsilateral pupil whereas phasic nociceptive stimuli and psychological arousal triggered bilateral pupillary dilatation. It was concluded that preparatory cognitive activity rather than phasic afferent nociceptive input is associated with pupillary signs of lateralized activity in the locus coeruleus.

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