Patients with non-specific neck pain often develop persistent or recurrent pain and associated disability. This review investigated which physical and psychological factors predict persistent and recurrent neck pain and disability.
Five databases were searched from inception to January 31, 2025. After data extraction, the Quality in Prognosis Studies tool (QUIPS) was used for risk of bias assessment and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) tool was used to assess the certainty of evidence for each factor's predictive capability for neck disability, pain intensity and incidence.
Six prospective cohort studies were selected. Three studies were rated with high overall risk of bias and three with moderate overall risk of bias. Consistent findings supported that high pain catastrophizing and psychological distress predict persistent and recurrent pain, disability and incidence with low to moderate certainty of evidence. There was inconsistency of results or limited studies reporting association between neck flexion strength, cold pain threshold tested over the tibialis anterior, pressure pain threshold tested over the neck or tibialis anterior, conditioned pain modulation, neck extensor endurance, and temporal summation with disability. In addition, there was low certainty of evidence which showed no relationship between cervical range of motion, cold pain threshold tested over the neck and neck extensor strength with disability.
Pain catastrophizing and psychological distress were identified as predictors of persistent and recurrent neck pain, disability and incidence. Further studies are needed to confirm findings of an association between physical factors with future neck pain and disability.
This review provides evidence to support the addition of early assessment of pain catastrophizing and psychological distress to identify patients that are more susceptible to persistent and recurrent neck pain. When warranted, psychological interventions targeting maladaptive beliefs, pain-related anxiety and catastrophizing may be required to minimize persistent and recurrent neck pain and disability.
Individuals with chronic pain are both more likely to have an insecure adult attachment style and impaired conditioned pain modulation (CPM) than pain-free individuals. This study investigated whether impaired CPM is seen in pain-free individuals and determined associations with attachment.
A CPM test paradigm was used to determine the differences in the measures of pain across attachment anxiety and avoidance dimensions in pain-free females in a neutral social context. First, static (heat pain threshold, heat pain tolerance, and cold pain intensity) and dynamic (cumulative pain load) measures of pain were explored.
One hundred and three females were recruited (median [IQR] age: 21 [20–23] years). We found no associations between attachment dimensions and static measures of pain (ps > 0.05). Higher attachment anxiety, but not avoidance, was associated with an increase in pain intensity over time (Estimate [95% CI] = 0.15 [0.06–0.25], p-value = 0.002), and increased average test stimulus pain intensity rating both before (Estimate [95% CI] = 0.15 [0.07–0.23], p-value < 0.001) and during (Estimate [95% CI] = 0.36 [0.23–0.48], p-value < 0.001) conditioning. In the 78% (80/103) who completed the full CPM procedure, there was no association between CPM effect and attachment anxiety (Estimate [95% CI] = −3.79 [−8.62 to 1.03], p = 0.122) or avoidance (Estimate [95% CI] = 0.25 [−4.88 to 5.38], p = 0.923). Effective CPM was seen in 90% (72/80).
Impaired CPM was not seen in pain-free individuals suggesting that impaired endogenous analgesia may develop from chronic pain, rather than cause chronic pain.
Individuals with chronic pain are both more likely to have an insecure adult attachment style and impaired conditioned pain modulation (CPM) than pain-free individuals. This is the first study to investigate a link between attachment and experimental pain using a conditioned pain modulation (CPM) paradigm in a neutral social context. Impaired CPM was not seen in pain-free individuals, suggesting that impaired endogenous analgesia may develop from chronic pain, rather than cause chronic pain.
The purpose of this systematic review was to identify and evaluate the quality of cross-cultural adaptations of the six core outcome measures (NRS, SF-12, PROMIS, ODI, RMDQ and VAS) for low back pain (LBP) and assess their psychometric properties.
Medline, EMBASE, Emcare and CINAHL databases were searched from inception to August 2024. Eligible studies included those assessing core LBP outcome measures in adults with LBP. The COSMIN checklist was used to assess the quality of cross-cultural adaptations and evaluate the psychometric properties. Additionally, the COSMIN risk of bias tool and GRADE approach were employed to assess study quality and provide levels of evidence.
A total of 82 studies were included. Among them, 35 studies examined the cross-cultural adaptations of the ODI, 25 for the RMDQ, 4 for PROMIS, 1 for SF-12 and 2 for NRS/VAS. The quality of cross-cultural adaptations was generally poor or fair due to inadequate reporting of pre-testing processes and small sample sizes. Most psychometric properties were rated as having an inadequate risk of bias, with evidence quality ranging from very low to low.
This review highlights that the cross-cultural adaptations of the five core LBP outcome measures have generally been conducted with low quality. To improve the adaptation process, studies should employ larger sample sizes and standardised pre-testing procedures. Additional research is needed to explore a broader range of psychometric properties of cross-cultural adaptations, ensuring better validity, reliability and comparability across adapted versions.
Improving the quality of cross-cultural adaptations of LBP outcome measures is crucial to ensuring that assessments are culturally relevant and accurate across diverse populations, leading to better-informed clinical decisions and equitable care for patients with LBP globally.
CRD42023413077
The weighting of somatosensory input and pain expectation during pain perception is promising for pain phenotyping, with good test–retest reliability. Yet, their concurrent validity with neural and psychological variables requires further investigation.
In this cross-sectional study, we investigated the concurrent validity of these weights with EEG source correlates of the somatosensory and expectation components during pain processing.
Participants completed a cued pain paradigm, with EEG recorded during pain expectation and perception. We used Bayesian inference to estimate the participant-specific weighting of somatosensory input, expectations and trait-like bias, and identified sources of brain activity at different stages of the cued pain task (early anticipation, late anticipation and post-stimulation). We correlated the estimated weights with EEG source activity across individuals.
As hypothesised, the weight placed on somatosensory input correlated with source activity in areas related to attention (middle frontal gyrus) and sensory processing (postcentral gyrus) during late anticipation. The expectation weight positively correlated with activity in areas related to attention (middle frontal gyrus) and semantic processing (medial temporal gyrus). We found no significant correlations between any of the weights and analgesic or hyperalgesic psychological variables (mindfulness, pain catastrophising and attachment).
Our findings support the concurrent validity of sensory and expectation weights with related EEG source activity in pain perception, reinforcing their utility in pain phenotyping and paving the way for more personalised pain management.
Our findings support the concurrent validity of sensory and expectation weights extracted through a Bayesian model. This finding supports the use of these weights for pain phenotyping.
Immunological pathophysiological mechanisms have been postulated in Complex Regional Pain Syndrome (CRPS).Clinical features suggest abnormal immune activation, supported in laboratory studies. The purpose of this review is to systematically review the effects of therapies that can modulate the immune system in persistent CRPS.
Articles were screened from PubMed, Embase, Scopus, clinicaltrials.gov, ISRCTN databases and Web of Science for articles, studies and conference abstracts in CRPS and immune therapies from inception up to April 2024. Titles and abstracts were screened, followed by reading the full text and reference lists to determine the final articles for analysis. Studies were restricted to adults and a duration of disease greater than 1 year. Randomised controlled trials were appraised using the Cochrane Risk of Bias (RoB2).
A total of 1404 studies were yielded, and 23 articles were retrieved for full-text analysis after reviewing the titles, texts and abstracts. A narrative synthesis was used due to the heterogeneity of studies. The immune therapies used were glucocorticoids, thalidomide/lenalidomide, immunoglobulin, plasmapheresis, mycophenolate, anti-TNF-alpha inhibitors and epidermal growth factor receptor inhibitors. There were 16 reports of beneficial effects from non-randomised trials, case series and case reports of treatment with immunomodulating drugs or interventions. Small randomised trials of low-dose immunoglobulin, epidermal growth factor receptor inhibitors and mycophenolate suggest possible treatment benefit, but larger randomised trials of immunoglobulin and lenalidomide demonstrated no effect.
The emergence of novel immune therapies for persistent CRPS shows promise, but evidence based on high-quality randomised trials remains limited and does not show a positive effect.
This work summarises the current use of immune-modulating therapies in managing patients with persistent Complex Regional Pain Syndrome (CRPS). It complements the current interest in immunological approaches to pain management with the increasing role of immune mechanisms in both pain and CRPS. While promise has been shown in small case reports and cohort studies, the need for high-quality clinical trials is highlighted by the few large randomised controlled trials.
The minimal important difference (MID) is established for pain intensity scores in acute pain management, but not for rescue opioid consumption. This scoping review aimed to estimate the MID in rescue opioid consumption for acute pain among adult patients in the postoperative and emergency settings.
We searched MEDLINE, Embase, CENTRAL, clinicaltrials.gov and clinicaltrialsregister.eu for studies published in English from inception to May 2024. We included studies investigating the MID of rescue opioid consumption in adults with acute pain in the postoperative and emergency settings. Because limited studies explicitly investigated the MID, we also included studies assessing the dose–response relationship between opioid consumption and relevant anchors (e.g., pain intensity scores). The primary outcome was MID for 0–24 h rescue opioid consumption; secondary outcomes included longer postoperative periods.
We screened 11,748 citations and included 14 studies (8190 patients). Three studies explicitly evaluated MID for rescue opioid consumption. In the remaining 11 studies, we estimated the MID using a 10-point difference (0–100 scale) in pain intensity score as an anchor. The anchor-based estimates ranged from 2 to 5 mg IV morphine equivalents, varying by population, method and context.
Based on the currently available evidence, we propose a provisional MID of 5 mg IV morphine equivalent in rescue opioid consumption for acute pain. This is lower than the value used in most sample size calculations.
These results can guide sample size calculations and support patient-centered approaches in acute pain settings.
PROSPERO identifier: CRD42024547409
Central modulatory pain mechanisms may influence improvements after exercise in low back pain (LBP). This observational study explored whether temporal summation of pain (TSP) and exercise-induced hypoalgesia (EIH) are associated with improvements in resting pain and movement-evoked pain, as it may improve the understanding of variation in effectiveness after an exercise program in individuals with LBP.
At baseline and after an 8-week exercise program, ratings of resting pain and movement-evoked pain on a 0–10 numerical rating scale (NRS) were assessed in 69 individuals with LBP. Cuff algometry at the lower leg (recording of the pain intensity to 10 repeated painful cuff stimulation) and pressure pain thresholds at the low back and leg immediately before and after a 6-min walking test were used to assess baseline TSP and EIH, respectively. Linear regression analyses adjusted for age and gender were used to assess the strength and direction of associations between baseline TSP and EIH with pain improvements (baseline minus Week 8).
Resting-pain NRS scores were reduced by 0.9 (0.5–1.3) and movement-evoked pain by 0.9 (0.4–1.5) after 8 weeks of exercise. Higher baseline TSP was associated with improvement in resting pain (B = 0.29, p = 0.014), but not significantly with improvement in movement-evoked pain. Baseline EIH, regardless of the site point, was not significantly associated with resting or movement-evoked pain improvements.
This study suggests that higher TSP at baseline is weakly but significantly associated with larger improvement in resting-pain intensity after an 8-week exercise program in people with LBP but this should be confirmed in larger studies.
Assessing central pain mechanisms may help identify individuals more likely to benefit from therapy, guiding personalised exercise-based treatments. Thus, this exploratory study provides preliminary evidence that higher baseline TSP is associated with greater improvements in resting pain following an exercise intervention. However, neither TSP nor EIH were associated with movement-evoked pain changes. These findings highlight the potential clinical relevance of evaluating central pain mechanisms when designing rehabilitation strategies for pain relief in LBP.
Endometriosis is a chronic, inflammatory disease with considerable symptom load in affected female patients. Cyclic pain (associated with menstruation) dominates in most patients, but few patients suffer from persistent non-cyclic pain. This study aims to investigate whether the somatosensory profile in endometriosis differs from healthy controls or between cyclic and non-cyclic subtypes. Moreover, we aimed at potential identifiers of peripheral or central nervous sensitization underpinnings of endometriosis in the QST profile.
The standardised investigation protocol for quantitative sensory testing (QST) of the German research network of neuropathic pain was used to find possible differences compared to healthy controls or between cyclic and non-cyclic subtypes of endometriosis potentially providing hints for altered peripheral and central nociceptive processing.
Endometriosis patients showed significant hyperalgesia to cold and blunt pressure in the affected body area (non-cyclic>cyclic, all p < 0.05), but not pinprick hyperalgesia, dynamic mechanical allodynia or facilitated pain summation (all p > 0.30). Exaggerated pressure hyperalgesia was most pronounced, regionally restricted and present in every patient (p << 0.0001). Higher thermal and tactile detection thresholds indicated non-nociceptive somatosensory loss, which differed only marginally between subgroups. Thermal loss and hyperalgesia to cold, heat and blunt pressure were also identified to a lesser extent in a remote test site (hand dorsum).
Endometriosis patients exhibited a pattern of somatosensory changes that is consistent with peripheral rather than central sensitization. Primary afferent sensitization facilitating spinal transmission of convergent input from the affected and suprapubic referred pain area is the most likely mechanism of hyperalgesia in endometriosis.
Pain and hyperalgesia are amongst the most burdensome features in endometriosis. This QST case–control study in endometriosis patients identifies massive pressure hyperalgesia as the most significant somatosensory alteration in the viscerotome of the lower abdomen, which is easily accessible for testing in patients. This finding highlights the role of peripheral sensitization as the dominant mechanism of endometriosis-related hyperalgesia, which
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