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Differences in fibromyalgia impact on functioning exist and appear to be influenced by numerous factors, including symptomatology severity, as well as the cognitive profile of the individual. The contribution of these elements, however, tends to be explored in a fragmented manner. To address this issue, we tested a comprehensive structural equation model in which associations of cognitive fusion and pain catastrophizing with function limitations are investigated through fibromyalgia symptomatology (i.e., fatigue, pain severity, and depression) in 231 women with fibromyalgia. In the model, cognitive fusion and two catastrophizing components (magnification and helplessness) were associated with poorer functioning indirectly through fibromyalgia symptomatology. Only the rumination component of catastrophizing had a direct association with functional limitations. All fibromyalgia symptoms were linked to increased functional limitations. A parsimonious model with significant associations only obtained an excellent fit (S-B = 774.191, df = 543, < 0.001; CFI = 0.943; RMSEA = 0.043; CAIC = -2724.04) and accounted for 50% of the variance of functional limitations. These results suggest that the relationship between psychological cognitive processes, fibromyalgia symptomatology, and functional limitations is complex and support the need for comprehensive models such as the present. The findings are discussed in the context of personalized psychological treatments (i.e., the need to address certain cognitive processes according to the problematic symptomatology or outcome).
The purpose of this review is to provide a comprehensive update of the different known components of the endogenous cannabinoid system and the mechanisms of action, as it applies to analgesia.
Neurofeedback provides real-time feedback about neurophysiological signals to patients, thereby encouraging modulation of pain-associated brain activity. This review aims to evaluate the effectiveness and safety of neurofeedback in alleviating pain and pain-associated symptoms in chronic pain patients.
Chronic pain among adolescents is common but effective interventions applicable in a school setting are rare. Person-centred care (PCC) is a key factor in improving health by engaging people as partners in their own care.
An increasing number of studies are focusing on secondary hyperalgesia to better understand central sensitization, as this phenomenon may play an important role in persistent pain. Recent studies have shown that, compared to the classical high frequency stimulation protocol (HFS) at 100 Hz, a protocol using 42 Hz stimulation induces a more intense and a larger area of secondary hyperalgesia (SH).
No externally validated presurgical risk score for chronic postsurgical pain (CPSP) is currently available. We tested the generalizability of a six-factor risk model for CPSP developed from a prospective cohort of 2929 patients in four surgical settings. Seventeen centers enrolled 1225 patients scheduled for inguinal hernia repair, hysterectomy (vaginal or abdominal), or thoracotomy. The six clinical predictors were surgical procedure, younger age, physical health (Short Form Health Survey-12), mental health (Short Form Health Survey-12), preoperative pain in the surgical field, and preoperative pain in another area. CPSP was confirmed by physical examination at 4 months. The model's discrimination (c-statistic), calibration, and diagnostic accuracy (sensitivity, specificity and positive and negative likelihood ratios) were calculated to assess geographic and temporal transportability in the full cohort and two subsamples (historical and new centers). The full dataset after exclusions and losses included 1088 patients; 20.6% had developed CPSP at 4 months. The c-statistics (95% CI) were similar in the full validation sample and the two subsamples: 0.69 (0.65-0.73), 0.69 (0.63-0.74) and 0.68 (0.63-0.74), respectively. Calibration was good (slope b and intercept close to 1 and 0, respectively and nonsignificance in the Hosmer-Lemeshow goodness-of-fit test). The validated model based on six clinical factors reliably identifies risk for CPSP risk in about 70% of patients undergoing the surgeries studied, allowing surgeons and anesthesiologists to plan and initiate risk reduction strategies in routine practice and researchers to screen for risk when randomizing patients in trials.
Primary burning mouth syndrome (BMS) is an orofacial disease with neuropathic characteristics. Psychophysics, such as quantitative sensory testing (QST) are used to sub-classify neuropathic pain syndromes, but their usefulness in characterizing BMS is not yet clear.
As treatment for postsurgical pain (PSP) remains a major unmet medical need, the emergence of safe and innovative non-opioid drugs has been strongly coveted. Tetrahydrobiopterin (BH4) is an interesting molecule for gaining a better understanding the pathological mechanism of neuropathic pain. However, whether BH4 and its pathway are involved in the pathogenesis of PSP remains unclear. In this study, we found that early in a rat paw incision model, the gene expression of GTP cyclohydrolase 1 (GTPCH) and sepiapterin reductase (SPR), BH4-producing enzymes in the de novo pathway, were significantly increased in incised compared with naïve paw skin. Although a significant increase in GTPCH protein levels was observed in incised paw skin until only 1 day after incision, a significant increase in BH4 levels was observed until 7 days after incision. In vivo, Spr-knockout mice showed an antinociceptive phenotype in the hind paw incision compared with the wild-type and Spr heterozygote groups. Furthermore, QM385, the SPR inhibitor, showed a significant dose-dependent, antinociceptive effect, which was supported by a reduction in BH4 levels in incised skin tissues, with no apparent adverse effects. Immunohistochemical analysis demonstrated that macrophages expressing GTPCH protein were increased around the injury site in the rat paw incision model. These results indicate that BH4 is involved in the pathogenesis of PSP, and that inhibition of the BH4 pathway could provide a new strategy for the treatment of acute PSP.
Migraine is commonly reported among patients with temporomandibular disorders (TMDs), especially myogenic TMD. The pathophysiologic mechanisms related to the comorbidity of the two conditions remain elusive. In the present study, we combined masseter muscle tendon ligation (MMTL)-produced myogenic TMD with systemic injection of nitroglycerin (NTG)-induced migraine-like hypersensitivity in mice. Facial mechanical allodynia, functional allodynia, and light-aversive behavior were evaluated. Sumatriptan, an FDA-approved medication for migraine, was used to validate migraine-like hypersensitivity. Additionally, we examined the protein level of calcitonin gene-related peptide (CGRP) in the spinal trigeminal nucleus caudalis using immunohistochemistry. We observed that mice with MMTL pretreatment have a prolonged NTG-induced migraine-like hypersensitivity, and MMTL also enabled a non-sensitizing dose of NTG to trigger migraine-like hypersensitivity. Systemic injection of sumatriptan inhibited the MMTL-enhanced migraine-like hypersensitivity. MMTL pretreatment significantly upregulated the protein level of CGRP in the spinal trigeminal nucleus caudalis after NTG injection. Our results indicate that a pre-existing myogenic TMD can upregulate NTG-induced trigeminal CGRP and enhance migraine-like hypersensitivity.
Placebos can reduce pain by inducing beliefs in the effectiveness of an actually inert treatment. Such top-down effects on pain typically engage lateral and medial prefrontal regions, the insula, somatosensory cortex, as well as the thalamus and brainstem during pain anticipation or perception. Considering the level of large-scale brain networks, these regions spatially align with fronto-parietal/executive control, salience, and sensory-motor networks, but it is unclear if and how placebos alter interactions between them during rest. Here, we investigated how placebo analgesia affected intrinsic network coupling. Ninety-nine human participants were randomly assigned to a placebo or control group and underwent resting-state fMRI after pain processing. Results revealed inverse coupling between two resting-state networks in placebo but not control participants. Specifically, networks comprised the bilateral somatosensory cortex and posterior insula, as well as the brainstem, thalamus, striatal regions, dorsal and rostral anterior cingulate cortex, and the anterior insula, respectively. Across participants, more negative between-network coupling was associated with lower individual pain intensity as assessed during a preceding pain task, and there was no significant relation with expectations of medication effectiveness in the placebo group. Altogether, these findings provide initial evidence that placebo analgesia affects the intrinsic communication between large-scale brain networks, even in the absence of pain. We suggest a theoretical model where placebo analgesia might affect processing within a descending pain-modulatory network, potentially segregating it from somatosensory regions that may code for painful experiences.