Articles: hyperalgesia.
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Crohn's disease (CD) is a painful chronic inflammatory bowel disease. It primarily affects terminal ileum, but the involvement of large and small intestines or extraintestinal manifestations is very common. CD may go along with neurogenic inflammation, mediated by substance P and CGRP, which are also key players in pain transmission. This may in turn contribute to hyperalgesia and altered somatosensory function in CD. ⋯ Our findings are consistent with the presence of a subclinical small fiber neuropathy. The group of CD patients with pronounced neuropathy findings were predominantly males, had a higher incidence of extraintestinal manifestations, and tended to have a longer history of disease duration.
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Lumbopelvic pain is common in pregnancy but the sensitization factors underlying the condition are largely unknown. This study characterized the somatosensory profile of pregnant and nonpregnant women and the relationship between pain, hypersensitivity, and commonly used manual clinical tests. Thirty-nine pregnant and 22 nonpregnant women were included. Although lumbopelvic pain was not an inclusion criterion, the pregnant women were divided into low- and high-pain groups following data collection. The sensitivity to light brush, pin-prick, and pressure pain was assessed bilaterally at 3 sites in the lumbopelvic region, at the shoulder, and in the lower leg. Responses to the active straight leg raise test and pain provocation tests of the sacroiliac joint were recorded. Participants completed questionnaires addressing emotional and physical well-being and rated disability using the Pelvic Girdle Questionnaire. Compared with controls, the high-pain group rated the active straight leg raise test as more difficult (P < .05), and both pain groups had more positive pain provocation tests (P < .05). The pregnant groups demonstrated significantly lower pressure pain thresholds at most assessment sites compared with controls (P < .05), but self-reported disability and pain were not correlated with pressure pain thresholds within pregnant participants. The high-pain group reported worse emotional health and poorer sleep quality than controls (P < .05). ⋯ This article presents the somatosensory profile of a healthy pregnant cohort. The results indicate that pain sensitivity increases during pregnancy possibly owing to the physical changes the body undergoes during pregnancy but also owing to changes in emotional health. This should be accounted for in clinical management of pregnant women with lumbopelvic pain.
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Hormone replacement remains one of the common therapies for menopause-related pain but is associated with risk of orofacial or back pain. Spinal endomorphin-2 (EM-2) is involved in varied pain and its release is steroid-dependent, but whether increasing spinal EM-2 can inhibit thermal hyperalgesia and inflammatory pain in ovariectomized (OVX) female rats, an animal model mimicking menopause, is not clear, nor is the potential involvement of spinal mu-opioid receptor (MOR). In the current study, we revealed that the temporal decrease of spinal EM-2 is accompanied with OVX-induced thermal hyperalgesia that was dose-dependently attenuated by intrathecal (IT) delivery of EM-2. ⋯ Furthermore, IT delivery of EM-2 did not affect the animals' locomotion or anxiety status. Our findings suggested that IT EM-2 might be a safer analgesia strategy than hormone replacement therapy in reducing risk of orofacial or back pain. However, a long-lasting form of EM-2 with less tolerance is needed to induce sustained analgesia.
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Primary and metastatic cancers that affect bones are frequently associated with severe and intractable pain. The mechanisms underlying the development of bone cancer pain are largely unknown. In the present study, we investigated whether inhibition of KCNQ/M (Kv7) potassium channels in the spinal cord contributes to the development of bone cancer pain via sensitization of dorsal horn wide dynamic range (WDR) neurons. ⋯ Furthermore, we discovered that blockade of KCNQ/M channels in the spinal cord by local administration of XE-991, a specific KCNQ/M channel blocker, caused a robust increase in excitability of dorsal horn WDR neurons, while, producing obvious pain hypersensitivity in normal rats. On the contrary, activation of spinal KCNQ/M channels by retigabine, a selective KCNQ/M channel opener, not only inhibited the bone cancer‑induced hyperexcitability of dorsal horn WDR neurons, but also alleviated mechanical allodynia and thermal hyperalgesia in the bone cancer rats, while all of these effects of retigabine could be blocked by KCNQ/M-channel antagonist XE-991. All things considered, these results suggest that suppression of KCNQ/M channels in the spinal cord likely contributes to the development of bone cancer pain via sensitization of dorsal horn WDR neurons in rats following tumor cell inoculation.
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Chronic widespread pain is a serious medical problem, yet the mechanisms of nociception and pain are poorly understood. Using a reserpine-induced pain model originally reported as a putative animal model for fibromyalgia, this study was undertaken to examine the following: (1) expression of several ion channels responsible for pain, mechanotransduction, and generation/propagation of action potentials in the dorsal root ganglion (DRG), (2) activities of peripheral nociceptive afferents, and (3) alterations in spinal microglial cells. A significant increase in mRNA expression of the acid-sensing ion channel (ASIC)-3 was detected in the DRG, and the behavioral mechanical hyperalgesia was significantly reversed by subcutaneous injection of APETx2, a selective blocker of ASIC3. ⋯ The activated microglia and behavioral hyperalgesia were significantly tranquilized by intraperitoneal injection of minocycline. These results suggest that the increase in ASIC3 in the DRG facilitated mechanical response of the remaining C-nociceptors and that activated spinal microglia may direct to intensify pain in this model. Pain may be further amplified by reserpine-induced dysfunction of the descending pain inhibitory system and by the decrease in peripheral drive to this system resulting from a reduced proportion of mechanoresponsive C-nociceptors.