BACKGROUND: 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.
CONCLUSIONS: 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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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.

UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: 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.

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.

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.

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.

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.

UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: 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.

BACKGROUND: 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.
OBJECTIVE: 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.