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

In a human acid pain model, which uses continuous intradermal pressure infusion of a phosphate-buffered solution (pH 5.2) to induce localized non-adapting pain, the flow was adjusted to result in constant pain ratings of about 20% or 50% on a visual analog scale (VAS). Six volunteers in each group participated in 4 different placebo-controlled double-blind cross-over studies to measure rapidly evolving cutaneous analgesia from topically applied new ointment formulations of acetylsalicylic acid (ASA) and salicylic acid (SA) as well as of commercial ibuprofen and benzocain creams. Similar, log-linear dose-response curves were found for both ASA and SA, significant in effect at 3 g/kg and higher drug contents and reaching saturation level at 15 or 30 g/kg, respectively, which, 20 min after application, caused a mean pain suppression of 95% using ASA and 80% using SA. Half-maximal effects were achieved using 3 g/kg ASA or 15 g/kg SA. The SA action was also clearly slower to develop. With an increased flow of the acidic buffer, producing lower effective tissue pH and more intense pain, the effect of ASA and SA decreased to 73% pain suppression. A competitive mechanism of both drug effects was suggested by the fact that, with 15 g/kg ASA and SA, pain reduction could be reversed by increasing the buffer flow by a factor of 1.75, on average. Commercial ibuprofen (50 g/kg) and benzocain creams (100 g/kg) were comparably as effective as ASA and SA, but the local anesthetic caused a loss of all cutaneous sensations while the touch threshold (von Frey) under the specific analgesics was the same as under the placebo ointment. Thus, topical applications of non-steroidal anti-inflammatory drugs (NSAIDS) dissolved in different ointment formulations have proven dose-dependently effective and specific in suppressing experimental acidotic pain by a local and competitive mechanism.
Pain 1996 Jan
PMID:Dose-dependent competitive block by topical acetylsalicylic and salicylic acid of low pH-induced cutaneous pain. 886 48

Patients with unilateral (n = 14) and bilateral (n = 4) herniorrhaphy participated in this study. With bilateral herniorrhaphy, at the end of the surgery, the wound was infiltrated with a solution of bupivacaine 0.5% and ketamine 0.3% on one side and a solution of bupivacaine 0.5% only, on the other. With unilateral herniorrhaphy, the patients were randomly assigned to one of two groups (n = 7). One group at the end of the surgery received the infiltration with a solution of bupivacaine 0.5% and ketamine 0.3%, the other group received the infiltration with a solution of bupivacaine 0.5% only. The duration of the local anesthetic (response to a von Frey filament) and postoperative analgesic (time to mild spontaneous pain) effects of the infiltrations, as well as wound pain threshold 24 h after surgery (pressure algometry), were determined. In patient with unilateral herniorrhaphy, the addition of ketamine for wound infiltration enhanced the duration of infiltration anesthesia (206 +/- 76 versus 343 +/- 108 min, P < 0.02) and analgesia (240 +/- 45 versus 420 +/- 151 min, P < 0.03). Similar enhancement of the local anesthetic effect was observed in patients with bilateral herniorrhaphy. The increase in pain threshold to pressure on the wound with the addition of ketamine was evident in bilateral herniorrhaphy patients and also with a combination of bilateral and unilateral results (1.39 +/- 0.40 versus 2.35 +/- 0.92 kg, P < 0.02). In the group of five volunteers, the subcutaneous infiltration with 0.3% ketamine produced a local anesthetic effect lasting only 10-20 min. The results indicate that ketamine acting via a peripheral mechanism can profoundly enhance anesthetic and analgesic actions of a local anesthetic administered for infiltration anesthesia.
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PMID:Ketamine enhances local anesthetic and analgesic effects of bupivacaine by peripheral mechanism: a study in postoperative patients. 1256 Mar 18

There is much evidence that tactile allodynia in rat models of mononeuropathy produced by sciatic nerve constriction is linked to disturbance of spinal GABAergic functions. Spinal cord stimulation (SCS) applied to such animals via chronically implanted electrodes may in some of the animals induce a significant increase of the withdrawal threshold in response to innocuous mechanical stimulation with von Frey filaments applied to the paw of the nerve ligated leg. The present study was performed in mononeuropathic animals with definite signs of tactile allodynia, which did not respond to SCS, GABA and the GABAB-agonist baclofen were administered intrathecally, in doses per se insufficient to influence the withdrawal thresholds, together with the previously ineffective SCS. This combination resulted in a marked and long-lasting increase of the thresholds. The GABAA-agonist muscimol given together with SCS also produced a similar, but less prominent threshold increase. The GABAB-antagonist 5-aminovaleric acid (5-AVA) produced a transient suppression of the threshold increase induced by SCS together with either GABA or baclofen. In contrast, the GABAA-antagonist bicuculline had no apparent inhibitory effect on the threshold augmentation produced by SCS combined with GABA or baclofen. It is concluded that SCS may operate by upgrading the spinal GABAergic systems and that its potential for producing pain relief is dependent upon the availability of responsive GABA-containing inhibitory interneurons. Moreover, it seems that the effects of SCS are more linked to the GABAB-than to the GABAA-receptor system.
Pain 1996 Aug
PMID:Effects of spinal cord stimulation on touch-evoked allodynia involve GABAergic mechanisms. An experimental study in the mononeuropathic rat. 888 Aug 52

Behavioral and electrophysiological methods were used to investigate the hyperalgesia and allodynia, and functional changes in lumbar spinal dorsal horn neurons, in a model of neuropathic pain (Selzer et al. 1990) involving ligation of one-third to one-half of one sciatic nerve in rats. One and 5 weeks following ligation, there was a significant reduction in hind limb withdrawal latency to noxious radiant heat on the operated side and, to a lesser degree, on the unoperated side. By 16 weeks, heat withdrawal latencies were reduced about equally (approximately 40%) on both sides. Withdrawal threshold to mechanical pressure was markedly reduced within 1 week on the operated side, and decreased in a time-dependent manner on the unoperated side. Heat withdrawal latency and von Frey withdrawal thresholds were not significantly affected in sham-operated rats. The same rats were tested in a paradigm measuring the isometric force of hind limb withdrawals elicited by graded noxious contact heat stimuli (38-52 degrees C, 5 sec). Withdrawal force increased monotonically with stimulus temperature starting at a threshold of approximately 40 degrees C. Stimulus-response functions were not significantly different between a sham-operated group and groups tested 5 (acute) and 16 weeks (chronic) after partial sciatic nerve ligation. Following behavioral testing, the animals were deeply anesthetized with pentobarbital sodium to allow electrophysiological recording of responses of single lumbar dorsal horn wide-dynamic range-type neurons to mechanical and noxious thermal stimulation of the hind paw. Recordings were made from 6 sham-operated rats (26 neurons ipsilateral and 31 contralateral to the operated leg), from 7 rats receiving partial sciatic nerve ligation 5 weeks previously (29 ipsilateral and 29 contralateral to ligation), and from 7 rats receiving partial sciatic ligation 16 weeks previously (18 ipsilateral, 29 contralateral to ligation). In several ligated rats we were unable to find heat-responsive neurons with cutaneous receptive fields on the hind paw ipsilateral to the ligation. For the neurons that were sensitive to heat, responses increased monotonically from a threshold of 40-42 degrees C. Neuronal stimulus-response functions for heat were not significantly different between ipsi- and contralateral (to operated) sides in the sham, 5-week or 16-week post-ligation groups, or between sham and 5- or 16-week post-ligation groups. Mechanical receptive field areas were not significantly different between ipsi- and contralateral sides in the sham and 5-week post-ligation groups, or between sham and 5-week post-ligation groups. However, receptive field areas were significantly larger in the 16-week post-ligation group (both ipsi- and contralateral to ligation) compared to sham and 5-week post-ligation groups. The results suggest that allodynia may be associated with a chronic enhancement of neuronal mechanosensitivity, but that the thermal hyperalgesia is not associated with enhanced neuronal responsiveness or force of withdrawal.
Pain 1996 Aug
PMID:Behavioral and electrophysiological assessment of hyperalgesia and changes in dorsal horn responses following partial sciatic nerve ligation in rats. 888 Aug 53

Withdrawal responses to heat and mechanical stimuli applied to the plantar surface of the rat hindpaw were measured before and after an intraplantar injection of capsaicin. In separate groups of rats, capsaicin doses of 1, 10 and 30 micrograms, and the vehicle were given into the center of the plantar surface in a volume of 10 microliters. Withdrawal latency evoked by radiant heat and the frequency of withdrawal evoked by mechanical stimuli (von Frey monofilaments) were obtained from both hindpaws before and after injection. Hyperalgesia to heat was defined as a decrease in withdrawal latency and mechanical hyperalgesia was indicated by an increase in withdrawal response frequency. Intraplantar injection of capsaicin evoked nocifensive behavior characterized by lifting and guarding the injected paw which typically lasted up to 3 min following injection. Capsaicin produced a decrease in withdrawal latency to heat and increased the frequency of withdrawal to mechanical stimuli in a dose-dependent manner. These effects were observed on the injected paw only. The duration of hyperalgesia produced by capsaicin was also dose-dependent. Withdrawal latencies to heat were decreased up to 45 min following capsaicin while withdrawal responses to mechanical stimuli remained elevated up to 4 h. The area of mechanical hyperalgesia included most of the plantar surface and extended approximately 9 mm proximal and distal to the injection. Injection of the vehicle did not significantly alter withdrawal responses to heat or mechanical stimuli. These studies demonstrate that intraplantar injection of capsaicin in rats produces hyperalgesia to heat and mechanical stimuli. This model should be useful for correlative behavioral, physiological and pharmacological studies of underlying mechanisms of capsaicin-evoked hyperalgesia.
Pain 1996 Sep
PMID:Enhanced withdrawal responses to heat and mechanical stimuli following intraplantar injection of capsaicin in rats. 889 46

The authors investigated 28 patients with "idiopathic" trigeminal neuralgia who had undergone no previous invasive procedures; together these patients had a total of 50 affected trigeminal divisions. Quantitative sensory perception thresholds were measured before operation. Preoperative measurements in the affected divisions indicated raised thresholds for touch (von Frey filaments) and temperature, but not for pinprick or heat pain, in agreement with the findings of Nurmikko. Only the tactile threshold was also significantly affected in the unaffected divisions on the affected side. The authors discuss their findings in relation to the pathophysiology of trigeminal neuralgia, concluding that the origin of the condition is almost certainly central to the gasserian ganglion.
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PMID:Trigeminal neuralgia: a quantitative sensory perception threshold study in patients who had not undergone previous invasive procedures. 901 Apr 17

Nineteen patients with "idiopathic" trigeminal neuralgia, who had not undergone any previous interventional procedures, possessed a vessel or vessels compressing the preganglionic nerve root that was demonstrated by magnetic resonance tomographic angiography. Pain was relieved immediately in all of these patients after they underwent microvascular decompression without observed nerve damage. Although preoperative measurement of sensory perception thresholds showed elevations in the thresholds for touch (von Frey filaments) and warmth and coolness sensations, these thresholds normalized during the postoperative period. An apparent deficit in the pinprick (sharpness) sensation appeared postoperatively, but the deficit gradually regressed and completely disappeared by 1 year after surgery; this phenomenon may have been a statistical anomaly. The patients' pain disappeared immediately postoperatively and remained absent throughout the follow-up period. The authors conclude that damage to the nerve or nerve root is not essential for the relief of trigeminal neuralgia.
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PMID:Sensory effects of microvascular decompression in trigeminal neuralgia. 901 Apr 18

Few clinical or experimental studies have carried out systematic investigations of cutaneous and deep sensibility in areas with referred muscle pain. Therefore, no clear signs of increased or decreased psychophysical responses to various somatosensory stimuli are found in referred pain areas. In the present study, a total of 7.1 ml 5% hypertonic saline was infused over 900 s into the m. tibialis anterior of 11 subjects. This produced local muscle pain and pain referred to the ventral aspect of the ankle. A continuous recording of the ongoing pain intensities of the local and referred pain was carried out on two electronic visual analogue scales (VAS). Before, during and 30 min after the period with referred pain, radiant heat (argon laser) stimuli, single and repeated electrical stimuli, and pressure stimuli were applied to the referred pain area. Stimulus-response (SR) functions were obtained by means of pain intensity ratings of the different stimuli at 75%, 112.5% and 150% of the individual pain threshold (PT) intensity. The pain intensities of contact heat (thermode) stimuli at 40 degrees C, 47 degrees C and 50 degrees C and pin-prick stimuli with von Frey hair were also assessed in the referred pain area. The saline-induced local muscle pain intensity was higher than the intensity of the referred pain (P < 0.05). The referred pain intensity was significantly higher in the 20-460 s interval than in the 460-900 s interval (P < 0.05). This difference was not seen for the local muscle pain. During the period with referred pain, significantly decreased responses to radiant heat and pressure stimuli were found at 112.5% and 150% of PT intensity (P < 0.05). Further, significantly increased responses to single and repeated electrical stimuli at 75% and 112.5% of PT intensity (P < 0.05) were also found. After the period with referred pain, a considerably decreased response to single and repeated, electrical stimuli (P < 0.05) was present together with significantly increased responses to contact heat stimuli at 40 degrees C and radiant heat stimuli at 75% of PT intensity (P < 0.05). The present results suggest that ongoing muscle pain can cause modality-specific (and bi-directional) sensory changes in the referred pain area. This could explain why previous studies have reported both decreased and increased responses in referred pain areas.
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PMID:Stimulus-response functions in areas with experimentally induced referred muscle pain--a psychophysical study. 903 Apr 20

The effects of the intrathecal alpha 2-agonists tizanidine and clonidine and the somatostatin analog octreotide on an experimental rat model of tactile allodynia were investigated to determine the therapeutic potential for treating chronic neuropathic pain. Allodynia was induced by ligating the rat sciatic nerve. The mechanical threshold for paw withdrawal was assessed by applying von Frey hairs to quantify analgesic actions. Mean 50% paw withdrawal thresholds were converted to the percentage of maximum possible effect (%MPE) where %MPE = (postdrug threshold-predrug threshold) divided by (15 g-predrug threshold) x 100. Dose-response curves were plotted for suppression of paw withdrawal 30 minutes after intrathecal injection of various doses of tizanidine, clonidine, and octreotide. Thresholds on the non-lesioned side were greater than 15 g. The lesioned side had baseline thresholds of less than 4.5 g. Dose-response curves were established for the antiallodynia effects of each drug. Tizanidine and clonidine at a 25-micrograms dose increased the threshold to greater than 97% of the MPE, but caused transient hindpaw weakness or sedation. No side effect was observed at a 10-micrograms dose, at which the threshold was 88-96% of MPE. Intrathecal octreotide modestly increased the threshold to only 49-67% of MPE, showing a lesser analgesic effect, although no side effect was observed at a 4-micrograms dose. The antiallodynic effects of intrathecal tizanidine and clonidine were more potent than that of octreotide.
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PMID:Effects of intrathecal nonnarcotic analgesics on chronic tactile allodynia in rats: alpha 2-agonists versus somatostatin analog. 904 98

We examined the hypothesis that peripheral morphine can modulate pain and hyperalgesia/allodynia in the human capsaicin model. Subcutaneous injections of 1 mL morphine (1 mg/mL) in one arm and of 1 mL 0.9% saline in the other arm were made prior to bilateral intradermal injections of 50 microL (6 mg/mL) capsaicin. All injections were made on the volar aspect of the arm. Before and after the capsaicin injections, spontaneous pain and pain evoked by repetitive von Frey filament stimulation was rated on a numerical rating scale; furthermore, pressure pain thresholds were determined. The area in which von Frey filament stimulation evoked pain and the area of visible flare were mapped after the capsaicin injection. Capsaicin injection resulted in spontaneous pain on the saline-injected side not significantly different from that on the morphine-injected side. However, capsaicin injections gave rise to significantly less pain evoked by mechanical stimuli, as well as to a significantly smaller area of mechanical hypersensitivity, on the morphine-injected side compared with the saline-injected side. These results suggest that morphine can modulate sensitization mechanisms involved in the development of capsaicin-induced mechanical hypersensitivity.
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PMID:Peripherally administrated morphine attenuates capsaicin-induced mechanical hypersensitivity in humans. 905 8


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