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Catastrophising, pain self-efficacy and acceptance in patients with Burning Mouth Syndrome.

Little is known about pain catastrophising, pain self-efficacy and chronic pain acceptance in burning mouth syndrome (BMS) and their effect on health-related quality of life (HRQoL) and symptoms of anxiety and depressive disorders.

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The migraine signature study: Methods and baseline results.

To characterize patients who utilize services for migraine in a large integrated health care network, and describe patterns of care and utilization.

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Racial and Ethnic Disparities in the Treatment of Chronic Pain.

To summarize the current literature on disparities in the treatment of chronic pain.

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Nociceptive nerves regulate haematopoietic stem cell mobilization.

Haematopoietic stem cells (HSCs) reside in specialized microenvironments in the bone marrow-often referred to as 'niches'-that represent complex regulatory milieux influenced by multiple cellular constituents, including nerves. Although sympathetic nerves are known to regulate the HSC niche, the contribution of nociceptive neurons in the bone marrow remains unclear. Here we show that nociceptive nerves are required for enforced HSC mobilization and that they collaborate with sympathetic nerves to maintain HSCs in the bone marrow. Nociceptor neurons drive granulocyte colony-stimulating factor (G-CSF)-induced HSC mobilization via the secretion of calcitonin gene-related peptide (CGRP). Unlike sympathetic nerves, which regulate HSCs indirectly via the niche, CGRP acts directly on HSCs via receptor activity modifying protein 1 (RAMP1) and the calcitonin receptor-like receptor (CALCRL) to promote egress by activating the Gα/adenylyl cyclase/cAMP pathway. The ingestion of food containing capsaicin-a natural component of chili peppers that can trigger the activation of nociceptive neurons-significantly enhanced HSC mobilization in mice. Targeting the nociceptive nervous system could therefore represent a strategy to improve the yield of HSCs for stem cell-based therapeutic agents.

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Pain Characteristics, Psychosocial, and Sexual Wellbeing of Women Diagnosed with Provoked Vestibulodynia and a History of Sexual Abuse.

Provoked vestibulodynia (PVD) is a common chronic pain condition characterized by pain at the vulvar vestibule elicited by touch. Both PVD and sexual abuse lead to negative psychosocial and sexual consequences. However, little is known about the wellbeing of women with PVD and a history of sexual abuse. The aim of this study was to characterize a sample of women seeking treatment for PVD who have experienced sexual abuse.

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Characterisation of pragmatic postoperative PAin trajectories over seven days and their association with CHronicity after 3 months: a prospective, pilot cohort study (PATCH study).

Reliable outcome measurement providing information both on early and late postoperative pain outcomes are still lacking. The purpose of this study was: 1) to characterise postoperative pain trajectories according to an innovative pragmatic concept: ideal pain trajectory (rapid and sustained pain relief) vs non-ideal pain trajectories (late, transient, or no pain relief); and 2) to assess the incidence of persistent post-surgical pain (PPSP) and the potential association between non-ideal pain trajectories and PPSP.

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Enhanced Pronociceptive and Disrupted Antinociceptive Mechanisms in Nonspecific Chronic Neck Pain.

Evidence suggests altered pronociceptive and antinociceptive mechanisms in many chronic pain conditions. Knowledge about these mechanisms in nonspecific chronic neck pain (NSNP) would improve understanding of the causes and the design of more effective treatments. Pressure pain threshold (PPT) is often used to assess presence of altered nociceptive processing in NSNP; however, its usefulness to detect this is yet to be established. The purpose of this study was to determine the functional status of temporal summation of second pain (TSSP) and conditioned pain modulation (CPM) in NSNP and to characterize the association of both measures with PPT and clinical features of NSNP.

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Mobile Health-Collected Biophysical Markers in Children with Serious Illness-Related Pain.

There is an ongoing established need to develop engaging pain assessment strategies to provide more effective individualized care to pediatric patients with serious illnesses. This study explores the acceptability of wireless devices as one option. To evaluate the ability of wrist-wearable technology to collect physiological data from children with serious illnesses. Single-site prospective observational study conducted between September 2017 and September 2018 at Rady Children's Hospital, San Diego, California, inpatient wards. Pediatric patients with diagnoses of cancer and sickle cell disease admitted to the hospital for acute-on-chronic pain and taking opioid pain medications were asked to complete two 24-hour continuous monitoring periods with the Empatica E4 wristband. Data collected from the device correlated with manually obtained vital signs. Children responded favorably to wearing the device. Participants with reported subjective pain versus no pain had average heart rate increased by 16.4 bpm, skin temperature decreased by 3.5°C, and electrodermal activity decreased by 0.27. This study shows the possibility of collecting continuous biophysical data in a nonobtrusive manner in seriously ill children experiencing acute-on-chronic pain using wearable devices. It provides the framework for larger studies to explore the utility of such data in relation to metrics of pain and suffering in this patient population.

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Neuropathic Pain Related to Peripheral Neuropathies According to the IASP Grading System Criteria.

Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory system. Neuropathic pain represents a broad category of pain conditions, common complications of peripheral neuropathies, which are characterized by a combination of positive symptoms, including paresthesia and/or dysesthesia and sensory deficits in the painful area. In the present paper, we aimed to assess neuropathic pain frequency and clinical characteristics of peripheral neuropathies due to different aetiologies according to grading system criteria of the International Association for the Study of Pain for a definitive diagnosis of neuropathic pain. Epidemiological studies applying these criteria have been conducted in patients with diabetes, brachial plexus injury, and other traumatic nerve injuries. Neuropathic pain was diagnosed in 37-42% of patients with diabetic peripheral neuropathy, 56% of patients with brachial plexus injury, and 22% of patients with intercostobrachial neuropathy. The most frequent neuropathic pain type was ongoing pain (described as burning or pressing), followed by paroxysmal pain (electric shock-like sensations) and allodynia (pain evoked by brushing and pressure). By providing information on the frequency, clinical signs, and variables associated with neuropathic pain due to different aetiologies, these studies contribute to improving the clinical management of this condition.

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Phosphorylation of a chronic pain mutation in the voltage-gated sodium channel Nav1.7 increases voltage sensitivity.

Mutations in voltage-gated sodium channels (Navs) can cause alterations in pain sensation, such as chronic pain diseases like inherited erythromelalgia (IEM). The IEM-causing mutation Nav1.7 p.I848T is known to induce a hyperpolarized shift in the voltage dependence of activation in Nav1.7. So far, however, the mechanism to explain this increase in voltage sensitivity remains unknown. In the present study, we show that phosphorylation of the newly introduced Thr residue explains the functional change. We expressed either wild type human Nav1.7, the I848T mutant, or other mutations in HEK293T cells and performed whole-cell patch-clamp electrophysiology. As the insertion of a Thr residue potentially creates a novel phosphorylation site for Ser/Thr kinases and because Nav1.7 had been shown in Xenopus oocytes to be affected by protein kinases C (PKC) and A (PKA), we used different non-selective and selective kinase inhibitors and activators to test the effect of phosphorylation on Nav1.7 in a human system. We identify PKC, but not PKA, to be responsible for the phosphorylation of T848 and thereby for the shift in voltage sensitivity. Introducing a negatively charged amino acid instead of the putative phosphorylation site mimics the effect on voltage gating to a lesser extent. 3D modelling using the published cryo-EM structure of human Nav1.7 showed that introduction of this negatively charged site seems to alter the interaction of this residue with surrounding amino acids and thus to influence channel function. These results could provide new opportunities for the development of novel treatment options for chronic pain patients.

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