European journal of pain : EJP
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Autonomic neuropathy seems to play a central role in the development of gastrointestinal symptoms in diabetes. In order to explore the neuronal mechanisms behind the symptoms we evaluated the brain processing of painful visceral stimuli. ⋯ There is evidence of altered central processing to visceral stimulation, and both peripheral and central mechanisms seem involved. Central neuronal reorganisation may contribute to our understanding of the gastrointestinal symptoms in patients with diabetic autonomic neuropathy and this may guide development and evaluation of new treatment modalities.
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Persistent postsurgical pain has been reported following cosmetic breast augmentation, but little is known about the underlying mechanisms. ⋯ Sensory changes and persistent pain are common following cosmetic breast augmentation and may have a negative impact on daily activities and satisfaction after surgery. Findings suggest that neuropathic pain should be considered in these patients. Preoperative information about the risk of developing sensory changes and chronic pain after breast augmentation is important.
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Motor cortex stimulation (MCS) has been used to treat patients with neuropathic pain resistant to other therapeutic approaches; however, the mechanisms of pain control by MCS are still not clearly understood. We have demonstrated that MCS increases the nociceptive threshold of naive conscious rats, with opioid participation. In the present study, the effect of transdural MCS on neuropathic pain in rats subjected to chronic constriction injury of the sciatic nerve was investigated. ⋯ Zif268 results were similar to those obtained for Fos, although no changes were observed for Zif268 in the anterior cingulate cortex and the central amygdaloid nucleus after MCS. The present findings suggest that MCS reverts neuropathic pain phenomena in rats, mimicking the effect observed in humans, through activation of the limbic and descending pain inhibitory systems. Further investigation of the mechanisms involved in this effect may contribute to the improvement of the clinical treatment of persistent pain.
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This study examines the changes in self-perception during resolution of an acutely painful neck injury sustained in a motor vehicle accident. We tested predictions from self-discrepancy theory and a model of self-pain enmeshment. Measures of discrepancy between the current (actual) self and both the ideal and feared-for self were predicted to remain stable over a 21-day recovery period whereas a measure of enmeshment was predicted to decrease as pain resolved. ⋯ Resolution of pain was associated with a reduction in enmeshment but not to change in self-discrepancy. Multilevel analyses of the diary data showed that concordance between actual and ideal performance increased over the 21 days of data collection. These data provide preliminary support for aspects of self-discrepancy theory and the self-pain enmeshment model.
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Neuropathic pain is a chronic pain state resulting from peripheral nerve injury, characterized by hyperalgesia and allodynia. We have reported that mice with genetic impairment of IL-1 signaling display attenuated neuropathic pain behavior and ectopic neuronal activity. In order to substantiate the role of IL-1 in neuropathic pain, WT mice were implanted subcutaneously with osmotic micropumps containing either IL-1ra or vehicle. ⋯ To test whether IL-1 is involved in maintenance of mechanical allodynia, a separate group of WT mice was treated with a single injection of either saline or IL-1ra four days following SNT, after the allodynic response was already manifested. Whereas saline-treated mice displayed robust allodynia, acute IL-1ra treatment induced long-lasting attenuation of the allodynic response. The results support our hypothesis that IL-1 signaling plays an important role in neuropathic pain and in the ectopic neuronal activity that underling its development.