Pain
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The goals of this study were to compare whether emergency department (ED) patients' pain intensity (PI) is measured differently by male and female nurses and to determine whether PI, heart rate (HR), and respiratory rate (RR) were used to prioritize patient urgency differently by male and female nurses. The associations between patients' PI|HR|RR and the Emergency Severity Index (ESI) scores they were assigned by attending nurses were analyzed using a national database of electronic medical records of US Veterans Affairs ED patients from 2008 to 2012. A total of 129,991 patients presenting for emergency care (Mage = 59.5, 92% males) and their triage nurses (n = 774, Mage = 47.5, 18% males) were analyzed, resulting in a total of 359,642 patient-provider interactions. ⋯ Higher PI levels were associated with more urgent (higher priority) ESI levels by female nurses, yet less urgent ESI levels by male nurses. In contrast, male patients with high RR received more urgent ESI levels by male nurses, whereas the nurse gender did not influence ESI assignments for female patients. These findings show that ED patients receive disparate treatment based on inherent characteristics of their triage nurses, and more standardized (eg, automated) protocols that can account for implicit social factors on health care practice for reliably assessing and prioritizing ED patients may be currently warranted.
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We aimed to develop a questionnaire that assesses the impact of pelvic pain on women, regardless of diagnosis, that has high utility, sound psychometric performance, easy scoring, and high reliability. Two studies, with 3 separate cohorts, were undertaken. Both studies were completed online. ⋯ Test-retest reliability was high (intraclass correlation coefficient 0.91, P < 0.001). The resultant Pelvic Pain Impact Questionnaire assesses the life impact of pelvic pain. It uses patient-generated language, is easily administered and scored, has very strong psychometric properties, and it is suitable for research and clinical settings across primary, secondary, and tertiary care.
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Here, it is shown that paclitaxel-induced neuropathy is associated with the development of spontaneous activity (SA) and hyperexcitability in dorsal root ganglion (DRG) neurons that is paralleled by increased expression of low-voltage-activated calcium channels (T-type; Cav3.2). The percentage of DRG neurons showing SA and the overall mean rate of SA were significantly higher at day 7 in rats receiving paclitaxel treatment than in rats receiving vehicle. Cav3.2 expression was increased in L4-L6 DRG and spinal cord segments in paclitaxel-treated rats, localized to small calcitonin gene-related peptide and isolectin B4 expressing DRG neurons and to glial fibrillary acidic protein-positive spinal cord cells. ⋯ Paclitaxel induced inward current and action potential discharges in cultured human DRG neurons, and this was blocked by ML218 hydrochloride pretreatment. Furthermore, ML218 hydrochloride decreased firing frequency in human DRG, where spontaneous action potentials were present. In summary, Cav3.2 in concert with TLR4 in DRG neurons appears to contribute to paclitaxel-induced neuropathy.
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Drugs able to treat both nociceptive and neuropathic pain effectively without major side effects are lacking. We developed a bifunctional peptide-based hybrid (KGNOP1) that structurally combines a mu-opioid receptor agonist (KGOP1) with antinociceptive activity and a weak nociceptin receptor antagonist (KGNOP3) with anti-neuropathic pain activity. We investigated KGNOP1-related behavioral effects after intravenous administration in rats by assessing thermal nociception, cold hyperalgesia in a model of neuropathic pain induced by chronic constriction injury of the sciatic nerve, and plethysmography parameters including inspiratory time (TI) and minute ventilation (VM) in comparison to the well-known opioid analgesics, tramadol and morphine. ⋯ KGNOP1 and KGOP1 produced a larger increase in TI and deleterious decrease in VM in comparison to morphine and tramadol (ED50(TI): 0.63, 0.52, 12.2, and 50.9 μmol/kg; ED50(VM): 0.57, 0.66, 10.6, and 50.0 μmol/kg, respectively). Interestingly, the calculated ratios of anti-neuropathic pain/antinociceptive to respiratory effects revealed that KGNOP1 was safer than tramadol (ED50 ratio: 5.44 × 10 vs 0.24) and morphine (ED50 ratio: 0.72 vs 1.39). We conclude that KGNOP1 is able to treat both experimental neuropathic and nociceptive pain, more efficiently and safely than tramadol and morphine, respectively, and thus should be a candidate for future clinical developments.