Pain
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Comparative Study
Assessing fear in patients with cervical pain: development and validation of the Pictorial Fear of Activity Scale-Cervical (PFActS-C).
The fear avoidance model (FAM) postulates that fear of pain or reinjury is a risk factor for persistent pain and disability, because it leads to the avoidance of physical activity. Research on the FAM has not yielded consistent results, which may be attributed to the model itself, but could also be a product of the way fear of movement is assessed. Studies of the FAM have measured fear using verbal scales consisting of items that are often vague and have only an indirect relationship with fear. ⋯ Internal consistency (alpha=.98), stability over time (n=44, IntraClass Correlation=.72), and construct validity were all good to excellent. The results indicate that the PFActS-C may be a useful tool for assessing fear of movement in patients with cervical pain. Research is needed to confirm the factor structure of the PFActS-C and to assess the generalizability of the results to other samples with neck pain.
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Comparative Study
Cholinergic mechanisms involved in the pain relieving effect of spinal cord stimulation in a model of neuropathy.
The mechanisms underlying the pain relieving effect of spinal cord stimulation (SCS) on neuropathic pain remain unclear. We have previously demonstrated that suppression of tactile hypersensitivity produced by SCS may be potentiated by i.t. clonidine in a rat model of mononeuropathy. Since the analgesic effect of this drug is mediated mainly via cholinergic mechanisms, a study exploring the possible involvement of the spinal cholinergic system in SCS was undertaken. ⋯ In another group of rats it was found that the response to SCS was completely eliminated by i.t. atropine and a muscarinic M(4) receptor antagonist while a partial attenuation was produced by M(1) and M(2) antagonists. Blocking of nicotinic receptors did not influence the SCS effect. In conclusion, the attenuating effect of SCS on pain related behavior is associated with the activation of the cholinergic system in the dorsal horn and mediated via muscarinic receptors, particularly M(4,) while nicotinic receptors appear not to be involved.
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Comparative Study
Oxidative stress in the spinal cord is an important contributor in capsaicin-induced mechanical secondary hyperalgesia in mice.
Recent studies indicate that reactive oxygen species (ROS) are critically involved in persistent pain primarily through spinal mechanisms, thus suggesting ROS involvement in central sensitization. To investigate ROS involvement in central sensitization, the effects of ROS scavengers and donors on pain behaviors were examined in mice. Capsaicin- induced hyperalgesia was used as a pain model since it has 2 distinctive pain components, primary and secondary hyperalgesia representing peripheral and central sensitization, respectively. ⋯ On the other hand, intrathecal injection of tert-butylhydroperoxide (t-BOOH, 5 microl), a ROS donor, produced a transient hyperalgesia in a dose-dependent manner. The number of MitoSox positive dorsal horn neurons was increased significantly after capsaicin treatment. This study suggests that ROS mediates the development and maintenance of capsaicin-induced hyperalgesia in mice, mainly through central sensitization and that the elevation of spinal ROS is most likely due to increased production of mitochondrial superoxides in the dorsal horn neurons.
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Comparative Study
Glycinergic mediation of tactile allodynia induced by platelet-activating factor (PAF) through glutamate-NO-cyclic GMP signalling in spinal cord in mice.
Our previous study showed that intrathecal (i.t.) injection of platelet-activating factor (PAF) induced tactile allodynia, suggesting that spinal PAF is a mediator of neuropathic pain. The present study further examined the spinal molecules participating in PAF-induced tactile allodynia in mice. I.t. injection of L-arginine, NO donor (5-amino-3-morpholinyl-1,2,3-oxadiazolium (SIN-1) or 3,3-bis(aminoethyl)-1-hydroxy-2-oxo-1-triazene (NOC-18)) or cGMP analog (8-(4-chlorophenylthio)-guanosine 3',5'-cyclic monophosphate; pCPT-cGMP) induced tactile allodynia. ⋯ A significant reduction of GlyR alpha3 expression in the spinal superficial layers of mice treated with GlyR alpha3 siRNA was confirmed by immunohistochemical and Western blotting analyses. Functional targeting of GlyR alpha3 was suggested by the loss of PGE(2)-induced thermal hyperalgesia and the enhancement of allodynia induced by bicuculline, a GABA(A) receptor antagonist in mice after GlyR alpha3 siRNA treatment. pCPT-cGMP, PAF, glutamate and SIN-1 all failed to induce allodynia after the knockdown of GlyR alpha3. These results suggest that the glutamate-NO-cGMP-PKG pathway in the spinal cord may be involved in the mechanism of PAF-induced tactile allodynia, and GlyR alpha3 could be a target molecule through which PKG induces allodynia.
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Comparative Study
The spatial characteristics of the painful thermal grill illusion.
Interlaced cold and warm stimuli may induce a paradoxical burning sensation termed the "thermal grill illusion". Studies on the grill illusion have yielded contradictory results regarding its quality and intensity, which in turn led to controversies concerning the underlying mechanism. Some controversies may result from testing the illusion with absolute temperatures thereby disregarding inter-subjects' variation in temperature sensitivity. ⋯ Gender did not affect the PGI. In conclusion, innocuous cold and warm stimuli can spatially summate, both within and between dermatomes and evoke a PGI. Possibly, non-nociceptive channels integrate onto 2nd or 3rd order nociceptive neurons which in turn induce a unique painful burning resulting from the blend of cold and warm sensations.