European journal of pain : EJP
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Nitric oxide, which has been implicated in the development of hyperalgesia in the spinal system, has not been systematically studied in the trigeminal system, especially in the context of inflammatory muscle pain condition. In this study, we investigated the functional role of centrally released nitric oxide in the pathogenesis of orofacial muscle pain. Specifically, we examined the contribution of neuronal, inducible and endothelial nitric oxide synthases, nNOS, iNOS and eNOS, respectively, in mediating masseter hypersensitivity under acute inflammatory condition. ⋯ The expression of all three nitric oxide synthases was significantly up-regulated 30-60 min following capsaicin stimulation, which paralleled the time course of the development of capsaicin-induced masseter hypersensitivity. Pretreatment with each NOS inhibitor significantly attenuated the masseter hypersensitivity. These data showed that all three NOS in the Vc are functionally important for the development of craniofacial muscle hyperalgesia and suggest that the three NOS are closely orchestrated to regulate the level of nitric oxide under normal and pathologic conditions.
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This study investigated the relative contribution of individual, workplace, psychosocial and physiological features associated with neck pain in female office workers towards developing appropriate intervention programs. Workers without disability (Neck Disability Index (NDI) score < or = 8, n=33); workers with neck pain and disability (NDI > or = 9/100, n=52) and 22 controls (women who did not work and without neck pain) participated in this study. Two logistic regression models were constructed to test the association between various measures in (1) workers with and without disability, and (2) workers without disability and controls. ⋯ Workers without disability and controls could only be differentiated by greater muscle activity in the cervical flexors and extensors during a typing task. No psychosocial domains remained in either regression model. These results suggest that impairments in the sensory and motor system should be considered in any assessment of the office worker with neck pain and may have stronger influences on the presenting symptoms than workplace and psychosocial features.
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Recent research suggests that changes in cortical structures can contribute to the pathophysiology of Complex Regional Pain Syndrome (CRPS). This review provides an overview of studies showing cortical involvement in CRPS, including mislocalizations of tactile stimuli, changes in size and organization of the somatosensory map, changes in motor cortex representation and body perception disturbances. In addition, we review experimental treatment approaches, such as mirror therapy and motor imagery programs, aimed at restoring the integrity of neural processing in the sensory-motor cortex in individuals with CRPS. The intervention effects are promising and can be theoretically motivated on the basis of established principles of neural organization, although important questions concerning the precise neural mechanisms of action remain unanswered.
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Clinical Trial
Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain.
Allodynia is a common, troublesome feature of neuropathic pain conditions. In a previous study of postherpetic neuralgia we observed that repeated tactile stimulation appeared to reduce the size of the area of allodynia in some patients. We have undertaken a pragmatic clinical study to characterise this phenomenon in neuropathic pain patients with a range of different aetiologies. ⋯ There was no change in heat pain threshold at a distant site following allodynic stimulation, suggesting no activation of diffuse noxious inhibitory control. Repeated thermal noxious stimulation (median NRS 7) could also elicit changes (>30%) in the area of allodynia in some patients (reductions in 7/20, increases in 3/20). Thus, we have found that a brief period of homotopic painful stimulation can reduce the area of allodynia in around half of patients with established neuropathic pains.
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Comparative Study
Stress and thermoregulation: different sympathetic responses and different effects on experimental pain.
Stress and thermoregulation both activate the sympathetic nervous system (SNS) but might differently affect pain. Studies investigating possible interactions in patients are problematic because of the high prevalence of SNS disturbances in patients. We therefore analyzed the influence of these different sympathetic challenges on experimentally-induced pain in healthy subjects. ⋯ The control tasks neither activated the SNS nor altered pain perception. Our results suggest that (1) different patterns of sympathetic activation can be recorded after stress and thermoregulatory challenges and (2) that only stress is able to interfere with sensation of experimental pain. Whether SNS activation is causally responsible for analgesia needs to be further investigated.