Pain
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Comparative Study
Analysis of ultrasonic vocalisation does not allow chronic pain to be evaluated in rats.
Most pain tests used for the assessment of drug analgesic activity in animal chronic pain models are based on the measurement of the response to an external acute stimulation (thermal, mechanical or electrical). But these stimuli are not related to the chronic pain experienced by the animal. Quantitative analysis of the spontaneous behaviour induced by the chronic pain state is needed. ⋯ In a third study, the influence of three parameters, degree of confrontation between the rats, age of the conspecific and housing conditions (isolated or collective) was studied in the arthritic rat model. Arthritic rats did not emit more USVs than controls in any of our experimental conditions. A fourth study showed that Aspirin (200 mg/kg) had no effect on the USVs, this data confirms the lack of direct relationship between USVs and experimental chronic pain in rats in our conditions.
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A variety of second messenger systems have been implicated in the intracellular mechanisms of tolerance development to the analgesic actions of morphine, a mu opioid, and clonidine, an alpha-2 adrenergic receptor agonist. Here, we studied mice that carry a null mutation in the gene encoding a neuronal specific isoform of protein kinase C (PKC), namely, PKC gamma. We used the tail-flick test to construct dose-response curves before and 4 days after chronic morphine (75-mg pellets, subcutaneously (s.c.)) or clonidine treatment (0.3mg/kg, s.c., twice daily). ⋯ Chronic morphine treatment can also result in sensitization of spinal cord neurons and increased pain behaviors following a noxious insult. To assess the contribution of PKC gamma to this process, we studied the responses of wild-type and mutant mice to an intraplantar injection of formalin (a model of persistent pain) following chronic morphine treatment. Although morphine tolerance increased formalin-evoked persistent pain behavior and Fos-LI in wild-type mice, there was no difference between placebo- and morphine-treated mutant mice, suggesting that PKC gamma also contributes to chronic morphine-induced changes in nociceptive processing.
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Randomized Controlled Trial Multicenter Study Clinical Trial
Intra-articular morphine as analgesic in temporomandibular joint arthralgia/osteoarthritis.
The aim of this study was to determine the analgesic efficacy of a single dose intra-articular injection (i.a.) of morphine in 53 patients with unilateral arthralgia/osteoarthritis of the temporomandibular joint (TMJ). This randomized, double-blind, parallel group, multicenter study included a screening visit, a treatment visit, and a follow-up visit 1 week after treatment. Recordings of visual analog scales (VAS) pain intensity scores at maximum mouth opening (main efficacy variable) and at jaw rest were made directly before a 1-ml i.a. injection into one TMJ of either 1.0mg morphine-HCl, 0.1mg morphine-HCl, or saline (placebo). ⋯ In conclusion, one i.a. injection of 0.1mg morphine significantly increased the pain pressure threshold and mouth opening ability, but evidence for the analgesic property of the locally applied opioid was inconclusive. No dose-effect relation and no significant short-term analgesic property were seen. Although statistically significant, the magnitude of the reduced VAS pain intensity score was not clinically relevant at the 1-week follow-up.
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Many therapists treat the spine as a 'functional unit', but suitable condition-specific outcome measures for the whole spine are not available. One of the most rigorously tested measures for back pain related health status is the Aberdeen Back Pain Scale, but it is only suitable for the lower back. The Aberdeen Back Pain Scale was extended to create a set of interlocking outcome measures for the neck, upper and lower back. ⋯ The Extended Aberdeen Spine Pain Scales for neck, upper and lower back pain, showed evidence of reliability, validity, responsiveness and acceptability. They can be used for single regions of the spine or combined as clinically necessary. They are particularly recommended for primary care patients.
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Paclitaxel, an effective anti-neoplastic agent in the treatment of solid tumors, produces a dose-limiting painful peripheral neuropathy in a clinically significant number of cancer patients. Prior work has demonstrated paclitaxel-induced neurodegeneration and sensory loss in laboratory rodents. We describe here an experimental paclitaxel-induced painful peripheral neuropathy. ⋯ Light-microscopic inspection of the sciatic nerve (mid-thigh level), L4-L5 dorsal root ganglia, and dorsal and ventral roots, and the gray and white matter of the L4-L5 spinal cord, showed no structural abnormalities. Electron microscopic examination of the sciatic nerve (mid-thigh level) and the L4-L5 dorsal root ganglia and dorsal horns demonstrated no degeneration of myelinated and unmyelinated axons in the sciatic nerve and roots, but revealed endoneurial edema. This model may be useful in understanding a significant source of pain in cancer patients, and in finding ways to avoid the neurotoxicity that limits paclitaxel therapy.