Articles: hyperalgesia.
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In a rat model of morphine tolerance, we examined the hypotheses that thermal hyperalgesia to radiant heat develops in association with the development of morphine tolerance and that both the development and expression of thermal hyperalgesia in morphine-tolerant rats are mediated by central NMDA and non-NMDA receptors and subsequent protein kinase C (PKC) activation. Tolerance to the analgesic effect of morphine was developed in rats utilizing an intrathecal repeated treatment regimen. The development of morphine tolerance and thermal hyperalgesia was examined by employing the tail-flick test and paw-withdrawal test, respectively. ⋯ MK 801 (5, 10 nmol, not 2.5 nmol) and CNQX (80, 160 nmol, not 40 nmol), but not GM1 (160 nmol), also reliably reversed thermal hyperalgesia in rats rendered tolerant to morphine when tested 30 min after each drug treatment on day 10 (48 hr after the last morphine treatment). The data indicate that thermal hyperalgesia develops in association with the development of morphine tolerance and that the coactivation of central NMDA and non-NMDA receptors is crucial for both the development and expression of thermal hyperalgesia in morphine-tolerant rats. Furthermore, intracellular PKC activation plays a critical role in the development of thermal hyperalgesia in morphine-tolerant rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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Different types of hyperalgesia were studied after experimental induction of inflammation in small skin areas of healthy volunteers either by topical application of capsaicin solution (1% in 70% ethanol) or by briefly freezing a skin area of similar size to -28 degrees C. Sensory tests were performed 30 min after capsaicin application and 22 h after freeze lesions. Heat pain thresholds were lowered after both treatments, probably due to nociceptor sensitization. ⋯ It was found in the 1 degree zone after freezing and absent in the capsaicin model. Differential nerve blocks revealed that it is probably mediated by sensitized C-fibres. In conclusion, different types of inflammatory changes may result in characteristic different patterns of hyperalgesia.
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Anesthesia and analgesia · Feb 1994
Randomized Controlled Trial Comparative Study Clinical TrialPreemptive effect of fentanyl and ketamine on postoperative pain and wound hyperalgesia.
The aim of this study was to test the hypothesis that the induction and maintenance of anesthesia with the use of fentanyl or ketamine reduces postoperative pain and wound hyperalgesia beyond the period when these effects can be explained by the direct analgesic action of these drugs. Twenty-seven patients scheduled for elective hysterectomy were investigated in a double-blind, randomized study. Patients were divided into three groups. ⋯ The intensity of spontaneous incisional pain and movement-associated pain was measured with a visual analog self-rating method. The surgical wound hyperalgesia was assessed by measuring pain threshold to pressure on the wound by using an algometer, and also by measuring the intensity of pain to suprathreshold pressure on the wound with the visual analog self-rating method. Forty-eight hours after surgery, the pain threshold was 0.90 +/- 0.06 kg in controls, 1.69 +/- 0.19 kg (P < 0.001) in the fentanyl group, and 1.49 +/- 0.15 kg (P < 0.01) in the ketamine group.(ABSTRACT TRUNCATED AT 250 WORDS)
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Repetitive C-fiber stimulation induces a state of facilitated processing of sensory information in the dorsal horn, while chronic nerve compression gives rise to a hyperalgesic state, characterized by spontaneous neuronal activity generated by voltage-sensitive sodium channels, as well as spinal facilitation. This study investigates the effects of systemic local anesthetic on thermal hyperalgesia evoked by chronic nerve compression and on the pain behavior responses to subcutaneous formalin. ⋯ Intravenous lidocaine acts by distinct mechanisms to diminish the hyperesthetic state induced by peripheral nerve injury and to reduce the degree of spinal sensitization induced by C-afferent fiber activation.
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Case Reports Randomized Controlled Trial Clinical Trial
Response of chronic neuropathic pain syndromes to ketamine: a preliminary study.
Hyperactivity of N-methyl-D-aspartate (NMDA) receptors may be one of the factors in the genesis of neuropathic pain. Ketamine is an NMDA-blocking agent widely used in human medicine. Ketamine (at 250 mcg/kg i.v. slow push) was administered to 6 patients for control of chronic neuropathic pain syndromes in double-blind placebo-controlled fashion. ⋯ Continuous subcutaneous infusion of ketamine administered to 1 patient with PNS-related neuropathic pain caused no additional improvement in pain control but caused intolerable cognitive and memory side effects. In contrast, side effects during single-dose injections were mild and well tolerated. Ketamine affected the evoked pain and associated after-sensation in chronic neuropathic pain syndromes more than the ongoing constant pain.