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Descriptors provided by patients with neuropathic low back pain (NLBP) with or without spinally referred leg pain are frequently used by clinicians to help to identify the predominant pain mechanisms. Indeed, many neuropathic screening tools are primarily based on subjective descriptors to determine the presence of neuropathic pain. There is a need to systematically review and analyse the existing evidence to determine the validity of such descriptors in this cohort. Ten databases were systematically searched. The review adhered to PRISMA and CRD guidelines and included a risk of bias assessment using QUADAS-2. Studies were included if they contained symptom descriptors from a group of NLBP patients +/-leg pain. Studies had to include a reference test to identity neuropathic pain from other pain mechanisms. Eight studies of 3,099 NLBP patients were included. Allodynia and numbness were found to discriminate between NLBP and nociceptive LBP in 4 studies. Autonomic dysfunction, (changes in the colour or appearance of the skin), was also found to discriminate between the groups in 2 studies. Dysesthesia identified NLBP in 5/7 respectively. Results from studies were equivocal regarding pain described as hot/burning cold and paroxysmal pain in people with NLBP. Subjectively reported allodynia and numbness would suggest a neuropathic pain mechanism in LBP. Dysesthesia would raise the suspicion of NLBP. More research is needed to determine if descriptors suggesting autonomic dysfunction can identify NLBP. There is poor consensus on whether other descriptors can identify NLBP.
Concerns about the adequacy of pain management among older adults are increasing, particularly with restrictions on opioid prescribing.
LPA is one of six known receptors (LPA) for lysophosphatidic acid (LPA). Constitutive Lpar1 null mutant mice have been instrumental in identifying roles for LPA-LPA signaling in neurobiological processes, brain development, and behavior, as well as modeling human neurological diseases like neuropathic pain. Constitutive Lpar1 null mutant mice are protected from partial sciatic nerve ligation (PSNL)-induced neuropathic pain, however, the cell types that are functionally responsible for mediating this protective effect are unknown. Here, we report the generation of an Lpar1 conditional null mutant mouse that allows for cre-mediated conditional deletion, combined with a PSNL pain model. Lpar1 mice were crossed with cre transgenic lines driven by neural gene promoters for nestin (all neural cells), synapsin (neurons), or P0 (Schwann cells). CD11b-cre transgenic mice were also used to delete Lpar1 in microglia. PSNL-initiated pain responses were reduced following cre-mediated Lpar1 deletion with all three neural promoters as well as the CD11b promoter, supporting involvement of Schwann cells, central and/or peripheral neurons, and microglia in mediating pain. Interestingly, rescue responses were nonidentical, implicating distinct roles for Lpar1-expressing cell types. Our results with a new Lpar1 conditional mouse mutant expand an understanding of LPA signaling in the PSNL model of neuropathic pain.
Adolescents with musculoskeletal disorders experience acute exacerbations in pain, colloquially called 'pain flares' in adult literature. This study aimed to explore adolescents' lived experience of pain flares, including what pain flares are, why they occur, how they are managed and what lasting effects they have on adolescents.
One-size-fits-all interventions reduce chronic low back pain (CLBP) a small amount. An individualised intervention called cognitive functional therapy (CFT) was superior for CLBP compared with manual therapy and exercise in one randomised controlled trial (RCT). However, systematic reviews show group interventions are as effective as one-to-one interventions for musculoskeletal pain. This RCT investigated whether a physiotherapist-delivered individualised intervention (CFT) was more effective than physiotherapist-delivered group-based exercise and education for individuals with CLBP.
To detect the involvement of immune cells in the pathogenesis of endometriosis in patients with stable status or pelvic pain.
Although nonlinear burst and tonic SCS are believed to treat neuropathic pain via distinct pain pathways, the effectiveness of these modalities on brain activity in vivo has not been investigated. This study compared neuronal firing patterns in the brain after nonlinear burst and tonic SCS in a rat model of painful radiculopathy.
Background and aims Women with chronic pelvic pain represent a heterogeneous group, and it is suggested that the existence of sub-groups can explain varying results and inconclusiveness in clinical trials. Some predictors of treatment outcome are suggested, but the evidence is limited. The primary aim of this study was to explore if selected pre-treatment characteristics of the participants in a recently conducted randomized controlled trial were associated with treatment outcome. Methods In this study secondary analysis of data collected in a randomized trial were conducted. The participants were women with chronic pelvic pain randomized to two different physical therapy treatments. Analyses in this study were performed for the whole group as a cohort. The primary outcome measure was change in pain intensity from baseline to 12 months, measured with the numeric rating scale (0-10). The women were asked to rate their mean pelvic pain intensity during the last 7 days. Based on previous research and on available variables from the randomized controlled trial four potential predictive factors were derived from the baseline data and assessed one by one in a linear regression model, adjusted for age and treatment group. The variables with strongest association (p < 0.10) with the primary outcome were further included in a multivariable linear regression model with backward selection, adjusted for age and treatment group. Results Fifty women (mean age 38.1, SD = 12.2) were included in the analysis. For these women the mean change in pain intensity was -1.2 points (95% CI -1.8 to -0.7) from baseline to 12 months. The multivariable regression model showed that pelvic pain duration of 6 years or more was associated with less decrease in pain intensity with a regression coefficient of 1.3 (95% CI 0.3-2.4). Baseline pain intensity was associated with higher pain reduction after PT treatment with a regression coefficient per SD increase in baseline pain of -0.6 (95% CI -1.1 to -0.1). None of the women with main pain site other places than in the pelvis reported any pain reduction after physical therapy treatment, but due to the small numbers the predictor was not included in the regression analysis. Conclusions We identified that pelvic pain duration of 6 years or more was associated with less pain reduction, and that higher baseline pain intensity was associated with higher pain reduction after physical therapy treatment in this sample of women with chronic pelvic pain. For the variable main pain site other places than the pelvis the results are unsure due to small numbers. Implications Based on our finding of long pain duration as a negative predictor for pain reduction, we emphasize that early intervention is important. Many of the participants in our RCT reported pelvic surgeries or other treatments prior to referral for PT, and we suggest that referral to a non-invasive intervention such as PT should be considered at an earlier stage. In order to tailor interventions to the individual women's needs, thorough baseline assessments, preferably in a multidisciplinary setting, should be performed.