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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In most published studies women are more sensitive to experimental pain than men. Enhanced central pain processing in women has been suggested, but psychosocial factors might also have affected the findings. Data from five completed healthy volunteer studies were analyzed to investigate gender differences in development of secondary hyperalgesia. Cutaneous hyperalgesia was induced with the heat/capsaicin sensitization model. Outcome measures were areas of secondary hyperalgesia to brush and von Frey hair stimulation after heat and capsaicin sensitization, rating of pain during heat/capsaicin sensitization, and heat pain detection thresholds. There was a trend toward smaller areas of secondary hyperalgesia in women. After adjusting for estimated gender differences in forearm surface area, areas to brush but not von Frey hair stimulation after capsaicin sensitization were larger in women. Peak pain, but not total pain, during prolonged noxious thermal stimulation was higher in women. There was no gender difference in pain ratings during capsaicin sensitization or in heat pain detection thresholds. The results provided only limited support to the hypothesis that gender differences in clinical pain syndromes can be explained by enhanced central sensitization in women. ⋯ Our findings suggest that gender differences in nociceptive transmission and neuronal sensitization are small and provide only limited support to the hypothesis that gender differences in acute and chronic pain syndromes can be explained by enhanced central sensitization in women.
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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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Opioid-induced delayed hyperalgesia and allodynia have been reported in human and animal models. The authors evaluated the influence of different opioids used during clinical anesthesia on nociceptive sensitivity and incisional pain in mice. The role of the inducible nitric oxide synthase on surgical pain and opioid-induced pronociception also was investigated. ⋯ The authors' study demonstrates that the intraoperative administration of fentanyl or remifentanil enhances the extent and duration of postoperative pain. The results suggest a role of the nitric oxide systems in the cause of acute postoperative pain and opioid-induced pronociception.
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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.