Articles: hyperalgesia.
-
Reg Anesth Pain Med · Sep 2000
Randomized Controlled Trial Clinical TrialEffect of oral ketamine on secondary hyperalgesia, thermal and mechanical pain thresholds, and sedation in humans.
Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist, and has been proven effective in alleviating secondary hyperalgesia in human subjects when injected intravenously. After oral ingestion, ketamine is metabolized into norketamine, which in vitro possesses NMDA receptor antagonistic effect. The aim of this study was to investigate the effects of oral administration of ketamine on secondary hyperalgesia evoked by standardized tissue injury. ⋯ Oral ketamine 0.5 or 1.0 mg/kg has no effect on secondary hyperalgesia or thermal or mechanical pain thresholds in human volunteers.
-
Randomized Controlled Trial Clinical Trial
Preinjury treatment with morphine or ketamine inhibits the development of experimentally induced secondary hyperalgesia in man.
We examine the effect of morphine or ketamine (N-methyl-D-aspartate receptor antagonist; NMDA) treatment on secondary hyperalgesia. Drug treatment started preinjury and continued into the early postinjury period. Hyperalgesia was induced by a local 1 degrees burn injury covering 12.5 cm(2) on the medial side of the calf. ⋯ In a previous study, we found that postinjury treatment alone with morphine did not affect secondary hyperalgesia, whereas ketamine did so significantly. The differential response to morphine administered pre- or postinjury may be relevant to the recently shown NMDA receptor mediated interaction of central hyperexcitability and morphine antinociception. The effect of ketamine supports the hypothesis of the role of NMDA receptor mediation in central hyperexcitability.
-
Randomized Controlled Trial Clinical Trial
Effect of preoperative oral dextromethorphan on immediate and late postoperative pain and hyperalgesia after total abdominal hysterectomy.
Dextromethorphan is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist known to inhibit wind-up and NMDA-mediated nociceptive responses of dorsal horn neurons. Experimental and clinical studies indicate that NMDA-receptor antagonists may potentiate the effect of analgesics such as morphine, local anesthetics and NSAIDs. Results from previous clinical studies of dextromethorphan in postoperative pain are conflicting, possibly related to administration of insufficient doses of the drug. ⋯ There were no significant differences in side-effects (nausea, vomiting, sedation). In conclusion, oral dextromethorphan 150 mg reduced PCA morphine consumption immediately (0-4 h) after hysterectomy, without prolonged effects on pain or wound hyperalgesia. A positive correlation between the magnitude of wound hyperalgesia at 24 h after operation, and total 24 h postoperative PCA morphine consumption was demonstrated.
-
Randomized Controlled Trial Clinical Trial
Spatial mapping of the zone of secondary hyperalgesia reveals a gradual decline of pain with distance but sharp borders.
The purpose of this study was to examine how pain to punctate mechanical stimuli varies with position within the zone of secondary hyperalgesia. Secondary hyperalgesia was produced by an intradermal injection of capsaicin (50 microg) into the volar forearm of human volunteers (n=9). Before and at 20, 60 and 100 min after the capsaicin injection, a computer-controlled electromechanical stimulator was used to deliver controlled-force stimuli to the skin via a 12-mm wide, 100-microm thick blade probe. ⋯ This finding unlikely reflects a ceiling effect because pain ratings within the zone of secondary hyperalgesia increased linearly with force. The relatively uniform pain ratings to the blade stimuli within the zone of secondary hyperalgesia and the sharp border that delimits the zone of hyperalgesia indicate that this sensory disturbance approaches being an 'all-or-nothing' phenomenon. Thus, a two-state model for central plasticity is needed to explain secondary hyperalgesia.
-
Randomized Controlled Trial Comparative Study Clinical Trial
Pain and allodynia/hyperalgesia induced by intramuscular injection of serotonin in patients with fibromyalgia and healthy individuals.
The aim of this study was to investigate the effect of injection of serotonin (5-HT) into the masseter muscle on pain and allodynia/hyperalgesia. Twelve female patients with fibromyalgia (FM) and 12 age-matched female healthy individuals (HI) participated in the study. The current pain intensity (CPI) and the pressure pain threshold (PPT) of the superficial masseter muscles were assessed bilaterally. 5-HT in one of three randomized concentrations (10(-3), 10(-5), 10(-7) M) or isotonic saline was then injected into either of the two masseter muscles in a double-blind manner. ⋯ In the HI-group pain developed significantly after injection irrespective of whether 5-HT or saline was injected, but significantly more so after 5-HT at 10(-3) M than saline injection. CPI decreased quickly and then remained on a very low level for most of the experiment. 5-HT at both 10(-5) M and 10(-3) M caused a significantly greater decrease of PPT than saline. In conclusion, our results show that 5-HT injected into the masseter muscle of healthy female subjects elicits pain and allodynia/hyperalgesia, while no such responses occur in patients with fibromyalgia.