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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our results with the ulnohumeral arthroplasty are presented. Seventeen patients were evaluated at an average followup greater than 36 months (range, 24-50 months). The average age of the patients was 52 years (range, 40-74 years). At final followup, 15 patients had complete pain relief at end ranges of motion whereas two patients had moderate pain after prolonged activity. Extension and flexion were improved by a mean of 12 degrees and 20 degrees, respectively, with a mean range of motion 14 degrees to 118 degrees. Postoperative radiographs showed a correctly placed drill hole with complete osteophyte resection. There were no neurologic or other complications and good stability of the elbow was observed in all patients. We think ulnohumeral arthroplasty is a good procedure for active patients with primary degenerative joint disease of the elbow.
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PMID:Ulnohumeral arthroplasty: results in primary degenerative arthritis of the elbow. 1505 96

The cellular events involved in acetyl-L-carnitine (ALCAR) analgesia were investigated in the mouse hot plate test. I.c.v. pretreatment with aODNs against the alpha subunit of G(q) and G(11) proteins prevented the analgesia induced by ALCAR (100 mg kg(-1) s.c. twice daily for 7 days). Administration of the phospholipase C (PLC) inhibitors U-73122 and neomycin, as well as the injection of an aODN complementary to the sequence of PLCbeta(1), antagonized the increase of the pain threshold induced by ALCAR. Pretreatment with U-73343, an analogue of U-73112 inactive on PLC, did not modify ALCAR analgesic effect. In mice undergoing treatment with LiCl, which impairs phosphatidylinositol synthesis, or pretreatment with TMB-8, a blocker of Ca(++) release from intracellular stores, the antinociception induced by ALCAR was dose-dependently antagonized. I.c.v. treatment with heparin, an IP(3) receptor antagonist, prevented the increase of pain threshold induced by the investigated compound, analgesia that was restored by co-administration of D-myo-inositol. On the other hand, i.c.v. pretreatment with the selective protein kinase C (PKC) inhibitors calphostin C and cheleritryne, resulted in a dose-dependent potentiation of ALCAR antinociception. The administration of PKC activators, such as PMA and PDBu, dose-dependently prevented the ALCAR-induced increase of pain threshold. Neither aODNs nor pharmacological treatments produced any behavioral impairment of mice as revealed by the rota-rod and hole board tests. These results indicate that central ALCAR analgesia in mice requires the activation of the PLC-IP(3) pathway. By contrast, the simultaneous activation of PKC may represent a pathway of negative modulation of ALCAR antinociception.
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PMID:Acetyl-L-carnitine requires phospholipase C-IP3 pathway activation to induce antinociception. 1522 7

The supraspinal cellular events involved in H(1)-mediated hyperalgesia were investigated in a condition of acute thermal pain by means of the mouse hot-plate test. I.c.v. administration of the phospholipase C (PLC) inhibitors U-73122 and neomycin antagonized the hyperalgesia induced by the selective H(1) agonist FMPH. By contrast, U-73343, an analogue of U-73122 used as negative control, was unable to modify the reduction of the pain threshold induced by FMPH. In mice undergoing treatment with LiCl, which impairs phosphatidylinositol synthesis, or treatment with heparin, an IP(3)-receptor antagonist, the hyperalgesia induced by the H(1)-receptor agonist remained unchanged. Similarly, pretreatment with D-myo inositol did not alter the H(1)-induced hypernociceptive response. Neither i.c.v. pretreatment with TMB-8, a blocker of Ca(2+) release from intracellular stores, nor pretreatment with thapsigargin, a depletor of Ca(2+) intracellular stores, prevented the decrease of pain threshold induced by FMPH. On the other hand, i.c.v. pretreatment with the selective protein kinase C (PKC) inhibitors calphostin C and chelerytrine resulted in a dose-dependent prevention of the H(1)-receptor agonist-induced hyperalgesia. The administration of PKC activators, such as PMA and PDBu, did not produce any effect on FMPH effect. The pharmacological treatments employed did not produce any behavioral impairment of mice as revealed by the rota-rod and hole-board tests. These results indicate a role for the PLC-PKC pathway in central H(1)-induced hyperalgesia in mice. Furthermore, activation of PLC-IP(3) did not appear to play a major role in the modulation of pain perception by H(1)-receptor agonists.
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PMID:H1-receptor stimulation induces hyperalgesia through activation of the phospholipase C-PKC pathway. 1522 8

The antinociceptive effect of the D(2) antagonist prochlorperazine was examined in the mouse hot-plate and abdominal constriction tests. Prochlorperazine (1-2 mg kg(-1) s.c./i.p.) produced an increase of the pain threshold in the mouse hot-plate test. The antinociception produced by prochlorperazine was prevented by the D(2) selective agonist quinpirole, the unselective muscarinic antagonist atropine, the M(1) selective antagonist pirenzepine, and by the choline uptake inhibitor hemicholinium-3 hydrobromide (HC-3). Moreover, prochlorperazine antinociception was abolished by pretreatment with an aODN against the M(1) receptor subtype, administered at the dose of 2 nmol per single i.c.v. injection. By contrast the analgesic effect of prochlorperazine was not prevented by the opioid antagonist naloxone and the GABA(B) antagonist CGP-35348. Prochlorperazine also elicited a dose-dependent increase in ACh release from rat cerebral cortex. In the antinociceptive dose-range, prochlorperazine did not impair mouse performance evaluated by the rota-rod and hole-board tests. On the basis of the above data, it can be postulated that prochlorperazine exerted an antinociceptive effect mediated by a central cholinergic mechanism.
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PMID:Prochlorperazine induces central antinociception mediated by the muscarinic system. 1522 80

The role of intracellular calcium in acute thermal nociception was investigated in the mouse hot-plate test. Intracerebroventricular (i.c.v.) administration of TMB-8, a blocker of Ca++ release from intracellular stores, produced hypernociception. By contrast, i.c.v. pretreatment with thapsigargin, a depletor of Ca++ intracellular stores, produced an increase of the mouse pain threshold. Furthermore, non-analgesic doses of thapsigargin prevented the hypernociception produced by TMB-8. In mice undergoing treatment with heparin, an InsP3-receptor antagonist, or ryanodine, a ryanodine receptor (RyR) antagonist, a dose-dependent reduction of the pain threshold was observed. Pretreatment with D-myo inositol, compound which produces InsP3, and 4-chloro-m-cresol, a RyR agonist, induced an antinociceptive effect. The heparin hypernociception was prevented by D-myo inositol, but not by L-myo inositol, used as negative control. In the same experimental conditions, the antinociception induced by D-myo inositol was prevented by a non-hyperalgesic dose of heparin. Similarly, the reduction of pain threshold produced by ryanodine was reversed by non-analgesic doses of 4-chloro-m-cresol, whereas the antinocicpetion induced by 4-chloro-m-cresol was prevented by non-hyperalgesic doses of ryanodine. The pharmacological treatments employed did not produce any behavioral impairment of mice as revealed by the rota-rod and hole-board tests. These results indicate that a variation of intracellular calcium contents at a supraspinal level is involved in the modulation of acute thermal nociception. In particular, the stimulation of both InsP3- and Ry-receptors appears to play an important role in the induction of antinociception in mice, whereas a blockade of these receptors is involved in an hypernociceptive response to acute thermal pain.
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PMID:Role of intracellular calcium in acute thermal pain perception. 1552 27

According to recent clinical data, motor cortex stimulation (MCS) is an alternative treatment for central pain syndromes. We present our minimally invasive technique of image guidance for the placement of the motor cortex-stimulating electrode and assess the clinical usefulness of both neuronavigation and vacuum headrest. Five patients suffering from central pain underwent MCS with the guidance of a frameless stereotactic system (BrainLab AG, Munich, Germany). The neuronavigation was used for identification of the precentral gyrus and accurate planning of the single burr hole. The exact location was reconfirmed by an intraoperative stimulation test. Postoperative clinical and neuroradiological evaluations were performed in each patient. The navigation system worked properly in all 5 neurosurgical cases. Determination of the placement of stimulating electrode was possible in every case. All patients obtained postoperative pain relief. No surgical complication occurred, and the postoperative course was uneventful in all patients. This preliminary experience may confirm image guidance as a useful tool for the surgery of MCS. Additionally, minimal and safe exposure can be achieved using a single burr hole and vacuum headrest.
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PMID:Image-guided motor cortex stimulation in patients with central pain. 1557 39

The wrist joint is frequently affected by arthritis, which leads to pain, loss of function and ultimately deformity. Various designs of wrist arthroplasty have been introduced to attempt to relieve pain and provide a functional range of motion. The first generation of wrist implant was a one-piece silicone elastomer. Later generations have designs that have two parts that articulate against each other. However, wrist implants have not achieved the same clinical success to date, compared with hip and knee implants, and there is a high revision rate associated with them. This paper describes a new design concept for wrist arthroplasty, based around the idea of combining the principles of an articulating implant with that of a flexible elastomer implant. The design consists of assembling a radial, carpal/metacarpal, plate and flexible parts together. The radial and carpal/metacarpal parts are to be made from ultra high molecular weight polyethylene. The bearing surfaces of the radial and carpal/metacarpal parts articulate against the flat surfaces of the plate, made from cobalt chrome molybdenum alloy. The radius on the bearing surface of the radial part enables flexion/extension, while the radius on the carpal/metacarpal surface enables radial/ulnar deviation. The articulation of the carpal/metacarpal part against the plate also allows for rotation as well as flexion/extension. The flexible part, made from Elast-Eon, which is a silicone polyurethane elastomer, is inserted through the hole of the plate and into the holes of the radial and carpal/metacarpal parts.
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PMID:A new design concept for wrist arthroplasty. 1577 56

The role of ryanodine receptors (RyRs) in the induction of muscarinic antinociception was investigated in a condition of acute thermal pain by means of the mouse hot-plate test. I.c.v. administration of non-hyperalgesic doses of ryanodine (0.001-0.06 nmol per mouse i.c.v.), an antagonist of ryanodine receptors (RyRs), dose-dependently prevented the antinociception induced by both physostigmine (100-150 microgkg(-1) s.c.) and oxotremorine (40-70 microgkg(-1) s.c.). A shift to the right of the dose-response curve of both cholinomimetic compounds was observed. Pretreatment with non-analgesic doses of 4-chloro-m-cresol (4-Cmc; 0.003-0.3 nmol per mouse i.c.v.), an agonist of RyRs, reversed in a dose-dependent manner the antagonistic effect produced by ryanodine of muscarinic antinociception. The pharmacological treatments employed neither modified the animals' gross behavior nor produced any behavioral impairment of mice as revealed by the rota-rod and hole-board tests. These results indicate that a variation of intracellular calcium contents at the central nervous system level is involved in muscarinic antinociception. In particular, the stimulation of RyRs appears to play an important role in the increase of the pain threshold produced by physostigmine and oxotremorine in mice.
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PMID:Ryanodine receptors are involved in muscarinic antinociception in mice. 1605 78

The present study examined the influence of innocuous skin cooling on the perception and neurophysiological correlates of brief noxious CO2 laser stimuli. In nine normal subjects, brief CO2 laser pulses of four different intensities (duration 50 ms; diameter 5 mm; intensity range 5.8-10.6 mJ/mm2) were delivered at random every 5-10 s on the dorsum of the hand. Innocuous skin cooling was performed by a thermode (20 degrees C; 3x3 cm) with a central hole for the laser test stimuli. Quality and intensity (VAS) of perceptions, reaction times and laser evoked potentials (LEPs) were examined. Signal detection theory analysis was performed to evaluate discrimination performance and decision criterion. During innocuous skin cooling, detection threshold increased from 4.8+/-1.81 to 8.2+/-1.05 mJ/mm2 and pain threshold from 8.7+/-1.53 to 13.5+/-1.57 mJ/mm2. proportion of detected stimuli decreased from 87% to 48% and pain reports from 42% to 10%. The well localized 'pricking' sensation mediated by Adelta-nociceptors almost vanished. The intensity of sensations (VAS scores) was considerably reduced. Sensory discriminative performance was significantly depressed but decision criterion remained unchanged. Reaction times were delayed. The late-LEPs, correlates of Adelta-nociceptor activations, were also significantly depressed while the ultra-late LEPs, correlates of C-nociceptors, were not affected. Taken together, these results strongly suggest that innocuous skin cooling interfered with the sensory processing of laser heat stimuli and more prominently with those related to Adelta-nociceptive input.
Eur J Pain 2005 Oct
PMID:Innocuous skin cooling modulates perception and neurophysiological correlates of brief CO2 laser stimuli in humans. 1613 81

F 13640 is a newly discovered high-efficacy 5-HT(1A) receptor agonist that produces exceptional analgesia in animal models of tonic and chronic, nociceptive and neuropathic pains by novel molecular and neuroadaptive mechanisms. Here we examined the effects of F 13640 and remifentanil (0.63 mg/kg with either compound) when injected i.p. either before or 15 min after rats underwent orthopedic surgery. Surgery consisted of the drilling of a hole in the calcaneus bone and of an incision of the skin, fascia and plantar muscle of one foot. During surgery, the concentration of volatile isoflurane was progressively incremented depending on the animal's response to surgical maneuvers. Other experiments examined the dose-dependent effects of F 13640 (0.04 to 0.63 mg/kg) on surgical pain as well as on the Minimum Alveolar Concentration of isoflurane. Both F 13640 and remifentanil markedly reduced the intra-operative isoflurane requirement. F 13640 also reduced measures of postoperative pain (i.e., paw elevation and flexion). With these postoperative measures, remifentanil produced short-lived analgesia followed by hyperalgesia. F 13640 significantly reduced both surgical pain and the isoflurane Minimum Alveolar Concentration from 0.16 mg/kg onward. F 13640 produced powerful intra- and postoperative analgesia in rats undergoing orthopedic surgery. Unlike the opioid, remifentanil, F 13640 caused no hyperalgesia with ongoing postoperative pain, and should remain effective with protracted postoperative use.
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PMID:The novel analgesic, F 13640, produces intra- and postoperative analgesia in a rat model of surgical pain. 1622 46


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