Articles: hyperalgesia.
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Opioids are the cornerstone therapy for the treatment of moderate to severe pain. Although common concerns regarding the use of opioids include the potential for detrimental side effects, physical dependence, and addiction, accumulating evidence suggests that opioids may yet cause another problem, often referred to as opioid-induced hyperalgesia. Somewhat paradoxically, opioid therapy aiming at alleviating pain may render patients more sensitive to pain and potentially may aggravate their preexisting pain. This review provides a comprehensive summary of basic and clinical research concerning opioid-induced hyperalgesia, suggests a framework for organizing pertinent information, delineates the status quo of our knowledge, identifies potential clinical implications, and discusses future research directions.
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A reduced rectal perceptual threshold has been reported in patients with irritable bowel syndrome (IBS), but this phenomenon may be induced by a comorbid psychological state. We evaluated the rectal pain threshold at baseline and after conditioning (repetitive rectal painful distention: RRD) in patients with IBS or functional abdominal pain syndrome (FAPS), which is an abdominal pain disorder, and in healthy controls, and determined whether rectal hypersensitivity is a reliable marker for IBS. ⋯ Rectal hypersensitivity induced by RRD may be a reliable marker for IBS. Conditioning-induced visceral hypersensitivity may play a pathophysiologic role in IBS.
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Although peripheral nerve function is strongly dependent on energy stores, the role of the mitochondrial electron transport chain, which drives ATP synthesis, in peripheral pain mechanisms, has not been examined. In models of HIV/AIDS therapy (dideoxycytidine), cancer chemotherapy (vincristine), and diabetes (streptozotocin)-induced neuropathy, inhibitors of mitochondrial electron transport chain complexes I, II, III, IV, and V significantly attenuated neuropathic pain-related behavior in rats. While inhibitors of all five complexes also attenuated tumor necrosis factor alpha-induced hyperalgesia, they had no effect on hyperalgesia induced by prostaglandin E2 and epinephrine. ⋯ Neither of these inhibitors, however, affected tumor necrosis factor alpha, prostaglandin E2 or epinephrine hyperalgesia. These experiments demonstrate a role of the mitochondrial electron transport chain in neuropathic and some forms of inflammatory pain. The contribution of the mitochondrial electron transport chain in neuropathic pain is ATP dependent.
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Little is known about the sensory characteristics and underlying mechanisms behind secondary hyperalgesia (HA) (2 degrees HA). The aim of the present study was to investigate the relationships between two different noxious stimuli, mechanical and cold on capsaicin-induced 2 degrees HA. Fourteen healthy volunteers were exposed to three different cold stimuli (20, 10, 0 degrees C) 30 s each, on both forearms. ⋯ Further, 8 min after the injection, the cold stimulation led to an expansion of 2 degrees HA area (from 5.1+/-1.38 to 11.4+/-1.72 cm(2)) to punctuate stimuli distally but not proximally to the injection site (P<0.05). It is concluded that there is no HA to cold stimuli within the area of mechanical 2 degrees HA. However, cooling acts as a conditioning stimulus and expands the area of capsaicin-induced punctuate HA.
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Glial cell line-derived neurotrophic factor (GDNF) has been hypothesized to play an important role in the modulation of nociceptive signals especially during neuropathic pain. The present study examined the expression of GDNF and GFRalpha-1 (the high-affinity receptor of GDNF) in dorsal root ganglions (DRG) in a rat model of neuropathic pain induced by chronic constriction injury (CCI) to the sciatic nerve. ⋯ The present study demonstrated that endogenous GDNF and GFRalpha-1 might play an anti-hyperalgesic role in neuropathic pain of rats. In addition, we found a down-regulation of somatostatin (SOM) in DRG and spinal dorsal horn after expression of GFRalpha-1 was knocked down, which suggested the possible relationship between the anti-hyperalgesic effect of GDNF and GFRalpha-1 on neuropathic pain and endogenous SOM.