Articles: hyperalgesia.
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Local sensitization to noxious stimuli has been previously described in acute whiplash injury and has been suggested to be a risk factor for chronic sequelae following acute whiplash injury. In this study, we prospectively examined the development of tender points and mechano-sensitivity in 157 acute whiplash injured patients, who fulfilled criteria for WAD grade 2 (n=153) or grade 3 (n=4) seen about 5 days after injury (4.8+/-2.3) and who subsequently had or had not recovered 1 year after a cervical sprain. Tender point scores and stimulus-response function for mechanical pressure were determined in injured and non-injured body regions at specific time-points after injury. ⋯ Tenderness was found in the neck region and in remote areas in non-recovered patients. The stimulus-response curves for recovered and non-recovered patients were similar after 12 days and 107 days after the injury, but non-recovered patients had steeper stimulus-response curves for the masseter (p<0.02) and trapezius muscles (p<0.04) after 384 days. This study shows early mechano-sensitization after an acute whiplash injury and the development of further sensitization in patients with long-term disability.
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Operant conditioning mechanisms have been demonstrated to be important in the development of chronic pain. Most experimental studies have investigated the operant modulation of verbal pain reports with extrinsic reinforcement, such as verbal reinforcement. Whether this reflects actual changes in the subjective experience of the nociceptive stimulus remained unclear. ⋯ Results demonstrated that sensitization to prolonged heat-pain stimulation was enhanced by operant learning within 1h. The extent of sensitization was directly dependent on the received magnitude of reinforcement. Thus, operant learning mechanisms based on intrinsic reinforcement may provide an explanation for the gradual development of sustained hypersensitivity during pain that is becoming chronic.
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Peripheral nerve injury produces a persistent neuropathic pain state characterized by spontaneous pain, allodynia and hyperalgesia. In this study, we evaluated the possible involvement of A 2ARs in the development of neuropathic pain and the expression of microglia and astrocytes in the spinal cord after sciatic nerve injury. For this purpose, partial ligation of the sciatic nerve was performed in A 2A knockout mice and wild-type littermates. ⋯ However, a significant decrease of the mechanical allodynia and a suppression of thermal hyperalgesia and allodynia were observed in A 2AR deficient mice. The expression of microglia and astrocytes was enhanced in wild-type mice exposed to sciatic nerve injury and this response was attenuated in knockout animals. Taken together, our results demonstrate the involvement of A 2ARs in the control of neuropathic pain and propose this receptor as an interesting target for the development of new drugs for the management of this clinical syndrome.
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Neuroscience letters · Nov 2008
Up-regulation of tumor necrosis factor-alpha in spinal cord contributes to vincristine-induced mechanical allodynia in mice.
Chronic treatment with vincristine (VCR) causes mechanical allodynia as an adverse effect. We previously reported that peripheral macrophage-derived interleukin-6 played a critical role in VCR-induced allodynia. However, the involvement of glial cell activation and central sensitization in VCR-induced allodynia is still unclear. ⋯ The immunoreactivity of TNF-alpha was co-localized in some of the activated microglia and astrocytes. In behavioral analysis, a neutralizing antibody of TNF-alpha, which was injected intrathecally on days 0, 3, and 6, significantly attenuated VCR-induced mechanical allodynia on days 4 and 7. These results suggest that VCR treatments elicited the activation of glial cells in spinal cord, and up-regulated TNF-alpha in these cells may play an important role in VCR-induced mechanical allodynia.
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Interruption of a continuous noxious heat by a relatively greater noxious heat evokes reductions in pain experience when the original noxious heat returns. The reduction is greater than that evoked by continuous delivery of noxious heat. This disproportionate reduction in pain experience, known as offset analgesia, is presumably mediated by a mechanism different to adaptation or habituation. ⋯ There was no attenuation effect for the unchanging stimuli delivered across the 3 days of testing but attenuation effects enhanced the offset analgesia resulting in a larger offset analgesia effect on days 2 and 3. It is possible that offset analgesia and attenuation are mediated by inter-related mechanisms. Further studies might investigate whether offset analgesia involves inhibitory structures such as the PAG-RVM.