Articles: function.
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The TRP channel ankyrin type 1 (TRPA1) is a nonselective cation channel known to be activated by environmental irritants, cold and endogenous mediators of inflammation. Activation of TRPA1 in trigeminal afferents innervating meningeal structures has recently been suggested to be involved in the generation of headaches. ⋯ Sole activation of TRPA1 receptor channels increases the activation threshold but does not cause propagated action potentials in meningeal afferents. TRPA1 agonists cause CGRP release from rodent dura mater. Peripheral TRPA1 receptors may have a pronociceptive function in trigeminal nociception only in combination with TRPV1.
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Protocols of temporal summation (TS) of pain typically involve the delivery of brief repetitive noxious pulses of a constant intensity while measuring the perceived intensity of pain after each pulse. The size percept of noxious repetitive stimulation has been poorly characterized. Furthermore, no studies have investigated age differences in TS of cold pain. ⋯ Additionally, older women experienced greater TS of the size percept of heat stimuli compared with older men and all younger participants. No overall age or sex differences were found in the TS of pain intensity for cold or heat trials. These results suggest dysfunctional modulation of the spatial percept of the painful stimuli by older adults, and in particular older women, during repetitive noxious thermal pulses.
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Although reducing pain catastrophizing has been shown to contribute to functional improvement in patients receiving interdisciplinary pain care, little is known about how changes in the different dimensions of pain catastrophizing uniquely contribute to improvement in outcome. The study examined the unique relationship between changes in the 3 distinct factors of pain catastrophizing-helplessness, rumination, and magnification-and changes in pain outcomes. ⋯ Results suggest that changes in the 3 dimensions of pain catastrophizing differentially mediate improvement in pain outcome. Treatment approaches that specifically target helplessness and rumination may be particularly useful in improving the outcomes of patients with refractory pain conditions enrolled in interdisciplinary pain rehabilitation program.
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Improved intrathecal (IT) pump technology is increasing the accuracy of IT opioid bolus dosing and promising advances in pain therapy. Opioid bolus dosing can be used with a minimal continuous infusion or it can function as the sole therapy. Bolus-only dosing is characterized by minimal use of opioid (often less than 1 mg of IT morphine). ⋯ With new bolus dosing possibilities, IT pumps can be used earlier in the treatment algorithm instead of being a late-stage treatment for patients who responded poorly to conservative treatments. We hypothesize that morphine bolus-only IT dosing will have comparable adverse effect rates, and possibly increased safety as compared to the more conservative continuous delivery method. We further predict that bolus-only delivery will provide better therapy satisfaction, improved functional scores, lower 24 hour opioid dose, and less dose escalation.
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Itch is a sensation that promotes the desire to scratch, which can be evoked by mechanical and chemical stimuli. In the spinal cord, neurons expressing the gastrin-releasing peptide receptor (GRPR) have been identified as specific mediators of itch. However, our understanding of the GRPR population in the spinal cord, and thus how these neurons exercise their functions, is limited. ⋯ Additionally, our analysis showed that the Grpr-Cre population expresses Vglut2 mRNA, and mice ablated of Vglut2 in Grpr-Cre cells (Vglut2-lox;Grpr-Cre mice) displayed less spontaneous itch and attenuated responses to both histaminergic and nonhistaminergic agents. We could also show that application of the itch-inducing peptide, natriuretic polypeptide B, induces calcium influx in a subpopulation of Grpr-Cre neurons. To summarize, our data indicate that the Grpr-Cre spinal cord neural population is composed of interneurons that use VGLUT2-mediated signaling for transmitting chemical and spontaneous itch stimuli to the next, currently unknown, neurons in the labeled line of itch.