Pain
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Peripheral nerve injury leads to structural and functional changes in the spinal dorsal horn, and these are thought to be involved in the development of neuropathic pain. In the chronic constriction injury (CCI) model, abnormal 'dark' neurons and apoptotic nuclei have been observed in laminae I-III of the dorsal horn in the territory innervated by the injured sciatic nerve. These findings have been taken as evidence that there is significant neuronal death in this model, and it has been suggested that loss of inhibition resulting from death of GABAergic inhibitory interneurons contributes to the neuropathic pain. ⋯ All of the CCI animals showed clear signs of thermal hyperalgesia. However, the numbers of neurons in laminae I-III of the ipsilateral dorsal horn in these animals did not differ significantly from those on the contralateral side, nor from those of sham-operated or naïve animals. These results do not, therefore, support the suggestion that there is significant neuronal death in the dorsal horn in this model.
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N-methyl-D-aspartate (NMDA) receptors serve prominent roles in vast physio-pathological conditions including hyperalgesia (defined as augmented pain intensity in response to painful stimuli) associated with central sensitization. Using M40403 a synthetic low molecular weight superoxide dismutase mimetic that removes superoxide we show for the first time that this radical plays a key role in NMDA-mediated hyperalgesia. Intrathecal administration of NMDA in rats led to a time-dependent development of thermal hyperalgesia. ⋯ M40403 by preventing MnSOD nitration restored its activity and inhibited the hyperalgesic response to intrathecal NMDA. Thus, superoxide-mediated nitration and deactivation of spinal MnSOD is a novel pathway of NMDA-mediated spinal hyperalgesia and hence central sensitization since it helps to maintain high levels of superoxide that in turn maintains nociceptive signaling. The broader implication of our findings is that superoxide may contribute to various forms of pain events that are driven by NMDA-receptor activation.
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Clinical Trial Controlled Clinical Trial
Manipulating presence influences the magnitude of virtual reality analgesia.
Excessive pain during medical procedures performed in unanesthetized patients is frequently reported, but can be reduced with virtual reality (VR) distraction. Increasing the person's illusion of going into the virtual world may increase how effectively VR distracts pain. Healthy volunteers aged 18-20 years participated in a double-blind between-groups design. ⋯ Each subject provided subjective 0-10 ratings of cognitive, sensory and affective components of pain, and rated their illusion of going inside the virtual world. Subjects in the High Tech VR group reported a stronger illusion of going into the virtual world (VR presence) than subjects in the Low Tech VR group, (4.2 vs. 2.5, respectively, P = 0.009) and more pain reduction (reduction of worst pain is 3.1 for High Tech VR vs. 0.7 for Low Tech VR, P < 0.001). Across groups, the amount of pain reduction was positively and significantly correlated with VR presence levels reported by subjects ( r = 0.48 for 'worst pain', P < 0.005).
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Randomized Controlled Trial Clinical Trial
Effects of exposure on perception of pain expression.
The present study evaluated the effects of exposure to facial expression of pain, on observers' perceptions of pain expression. Thirty-one male and 49 female observers judged 1-s video excerpts in a signal detection paradigm. The excerpts showed facial expressions of shoulder-pain patients displaying no pain or moderate pain. ⋯ There was a linear relationship between the density of exposure to strong pain and observers' response criteria: greater exposure was associated with more conservative decisions. On average, participants showed very high levels of sensitivity to pain expression, with women significantly outperforming men. Results are discussed in terms of their implications for pain judgments of health care professionals, adaptation-level theory, and the psychophysical method of selective adaptation.
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Recent research has implicated anxiety sensitivity (AS), the fear of anxiety-related sensations, as a mitigating factor involved in fear and avoidance in patients with chronic back pain [Understanding and treating fear of pain (2004) 3]. Given reported similarities between individuals experiencing chronic pain and those experiencing recurrent headaches, it is theoretically plausible that AS plays a role in influencing fear of pain and avoidance behavior in people with recurrent headache. This has not been studied to date. ⋯ Results also revealed that AS and headache severity had indirect relationships to pain-related escape and avoidance via their direct loadings on fear of pain. Headache severity also had a small direct loading on escape and avoidance behavior. These results provide compelling evidence that AS may play an important role in pain-related fear and escape and avoidance behavior in patients with recurrent headaches.