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Dysmenorrhea catastrophizing and functional impairment in female pelvic pain.

Dysmenorrhea is suggested to increase the risk of chronic pain by enhancing central sensitization. However, little is known about whether emotional and cognitive responses induced by dysmenorrhea contribute to chronic pain interference. This study examined the association between catastrophizing specific to dysmenorrhea and both dysmenorrhea and chronic pelvic pain (CPP)-associated pain interference.

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Efficacy of topical and systemic treatments for atopic dermatitis on pruritus: A systematic literature review and meta-analysis.

Pruritus is a major and burdensome symptom in atopic dermatitis (AD). The number of systemic treatments available for AD has increased recently, enabling improved patient relief.

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Distress as a mediator for pain and activities of daily living in older adults with fibromyalgia.

Pain, distress, and activities of daily living impact the lives of those with chronic pain. This study investigated distress (depressive symptoms, anxiety) on the relationship between pain (intensity and pain interference) and activities of daily living in individuals with fibromyalgia while controlling for age.

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Epidemiological trends of hand osteoarthritis from 1990 to 2019: Estimates from the 2019 Global Burden of Disease study.

Hand osteoarthritis (OA) is a chronic progressive disease characterized by disabling pain in the hand, with a high clinical burden. This study is designed to assess the epidemiological patterns of hand OA from 1990 to 2019 and analyze its secular trends based on sex, age, and socio-demographic index (SDI) at global, regional, and national levels.

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Modelling skeletal pain harnessing tissue engineering.

Bone pain typically occurs immediately following skeletal damage with mechanical distortion or rupture of nociceptive fibres. The pain mechanism is also associated with chronic pain conditions where the healing process is impaired. Any load impacting on the area of the fractured bone will stimulate the nociceptive response, necessitating rapid clinical intervention to relieve pain associated with the bone damage and appropriate mitigation of any processes involved with the loss of bone mass, muscle, and mobility and to prevent death. The following review has examined the mechanisms of pain associated with trauma or cancer-related skeletal damage focusing on new approaches for the development of innovative therapeutic interventions. In particular, the review highlights tissue engineering approaches that offer considerable promise in the application of functional biomimetic fabrication of bone and nerve tissues. The strategic combination of bone and nerve tissue engineered models provides significant potential to develop a new class of in vitro platforms, capable of replacing in vivo models and testing the safety and efficacy of novel drug treatments aimed at the resolution of bone-associated pain. To date, the field of bone pain research has centred on animal models, with a paucity of data correlating to the human physiological response. This review explores the evident gap in pain drug development research and suggests a step change in approach to harness tissue engineering technologies to recapitulate the complex pathophysiological environment of the damaged bone tissue enabling evaluation of the associated pain-mimicking mechanism with significant therapeutic potential therein for improved patient quality of life.

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The effect and mechanism of exercise for post-stroke pain.

One of the common negative effects of a stroke that seriously lowers patients' quality of life is post-stroke pain (PSP). Thus, exercise in PSP management has become a hot research topic. The main advantages of exercise therapy are affordability and ease of acceptance by patients compared to other treatment methods. Therefore, this article reviews the effectiveness and possible mechanisms of exercise interventions for PSP. Exercise training for patients with PSP not only improves physical function but also effectively reduces pain intensity and attenuates the behavioral response to pain. In addition, exercise therapy can improve brain function and modulate levels of pro-inflammatory and neurotrophic factors to exert specific analgesic effects. Potential mechanisms for exercise intervention include modulation of synaptic plasticity in the anterior cingulate gyrus, modulation of endogenous opioids , reversal of brain-derived neurotrophic factor overexpression, inhibition of purinergic receptor (P2X4R, P2X7R) expression, and inhibition of microglia activation. However, current research on exercise for PSP remains limited, and the sustainable benefits of exercise interventions for PSP need to be further investigated.

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Low-dose naloxone for prophylaxis of sufentanil-induced choking and postoperative nausea and vomiting.

Sufentanil, a potent opioid, serves as the first option for perioperative analgesia owing to its analgesic effect, long duration and stable hemodynamics, whereas its side effects frequently blunt its application. The intravenous (IV) injection of sufentanil during anesthesia induction has high incidence of choking or bucking reaction, which is defined as sufentanil-induced cough (SIC). Moreover, postoperative nausea and vomiting (PONV) is a common and stressful complication, which is also related to the usage of opioid. High incidence of PONV is reported in the patients with SIC. Hence, we sought to determine whether naloxone, an opioid antagonist, at low dose would decrease the incidences of SIC and PONV. 216 female patients undergoing gynecological laparoscopic operation (<2 h) under general anesthesia were recruited in this study, and randomly assigned into two groups: Group N (patients receiving naloxone and Group C (patients receiving vehicle). Sufentanil (0.5 μg/kg within 5 s) was given in anesthesia induction, and low-dose naloxone (1.25 μg/kg) or identical vehicle was initially injected 5 min prior to induction, with the incidence and severity of SIC estimated. Subsequently, naloxone or vehicle was continuously infused at the rate of 0.5 μg/kg/h in the initiation of operation until the end of the operation, and the transverse abdominal fascia block (TAP) was performed for postoperative analgesia. The PONV profiles such as incidence and the severity, grading, and the frequencies of antiemetic usage within 24 h were evaluated, with VAS scores and remedial measures for analgesia during the first 24 h postoperatively were recorded. Our results revealed that one bolus of low-dose naloxone prior to the induction significantly mitigated the incidence of SIC, and intraoperative continuous infusion of low-dose naloxone reduced the incidence and the severity of PONV, so that the postoperative VAS scores and further remedial analgesia were not altered. These results not only provide clinical solutions for prophylaxis of SIC and PONV, but also suggests that opioids may act as a key role in both SIC and PONV, whereas opioid antagonist may hit two tasks with one stone. Moreover, further investigations are required to address the underlying mechanism of SIC and PONV. : [www.chictr.org.cn], identifier [ChiCTR2200064865].

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Altered Structural and Functional Abnormalities of Hippocampus in Classical Trigeminal Neuralgia: A Combination of DTI and fMRI Study.

Diffusion tensor imaging (DTI) and resting-state functional magnetic resonance imaging (rs-fMRI) were applied to speculate the altered structural and functional abnormalities within the hippocampus in classical trigeminal neuralgia (CTN) patients by detecting the alteration of apparent diffusion coefficient (ADC), fractional anisotropy (FA), and regional homogeneity (ReHo). . Multimodal MRI dataset (DTI and fMRI) and clinical indices (pain and neuropsychological scores) were collected in 27 CTN patients and 27 age- and gender-matched healthy controls (HC). Two independent-sample -tests were performed to compare the ADC, FA, and ReHo values in hippocampus areas between CTN patients and HC. Correlation analyses were applied between all the DTI and fMRI parameters within the hippocampus and the VAS (visual analog scale), MoCA (Montreal cognitive assessment), and CDR (clinical dementia rating) scores.

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Assessment of the anti-nociceptive effects of fetal ventral mesencephalic tissue allografts in a rat model of hemi-Parkinson’s disease using fMRI.

Extensive studies showed increased subjective pain sensitivity in Parkinson's disease (PD), which appeared to be partially reversed by dopaminergic (DA) treatment. Although cell replacement represents an attractive therapeutic strategy, its potential for PD-related hyperalgesia remains unclear. We investigated re-establishment of DA function allografting exogenic DA cells on pain hypersensitivity in a rat model of PD. We evaluated the anti-nociceptive effects of fetal ventral mesencephalic (rVM) tissue allografts in PD rats after unilateral 6-OHDA-induced toxicity in the medial forebrain bundle. The drug -induced rotation test was used to validate the severity of the nigrostriatal lesion; von Frey and thermal pain tests were employed to evaluate nociceptive function. Nociception-induced cerebral blood volume (CBV) response was measured using a 4.7-T MR system. Finally, the immunohistochemical (IHC) studies were performed and the results were compared with the imaging findings from functional magnetic resonance imaging (fMRI). The grafts significantly improved drug-induced rotation behavior and increased mechanical and thermal nociceptive thresholds in PD rats. The elevation of CBV signals significantly recovered on the grafted striatum, whereas this effect was inhibited by the D2R antagonist eticlopride in each striatum. Quantitative IHC analysis revealed the transplantation markedly increased the numbers of tyrosine hydroxylase immunoreactive cells. Therefore, we concluded transplantation of rVM tissue results in anti-nociceptive effects and improves motor function. Moreover, CBV response confirmed the key role of D2R-mediated pain modulation. Therefore, we demonstrate fMRI as a reliable imaging index in evaluating the anti-nociceptive therapeutic effects of fetal rVM transplantation in the rat model of PD.

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Peripheral role of glutamate in orofacial pain.

Glutamate is the principal excitatory neurotransmitter in the central nervous system. In the periphery, glutamate acts as a transmitter and involves in the signaling and processing of sensory input. Glutamate acts at several types of receptors and also interacts with other transmitters/mediators under various physiological and pathophysiological conditions including chronic pain. The increasing amount of evidence suggests that glutamate may play a role through multiple mechanisms in orofacial pain processing. In this study, we reviewed the current understanding of how peripheral glutamate mediates orofacial pain, how glutamate is regulated in the periphery, and how these findings are translated into therapies for pain conditions.

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