Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

82 patients with chronic pain resulting from mononeuropathy were treated with psychotropic drugs in an open therapeutic study. In this study we found that treatment with a combination of clomipramine (Anafranil) and small doses of neuroleptics was significantly superior to therapy with neuroleptics alone. In a subsequent double-blind study, it was attempted for the first time to determine the efficacy of clomipramine compared to that of acetylsalicylic acid in 48 patients with painful mono- and polyneuropathies. The test was carried out in a cross-over trial with two sequence groups. We evaluated assessments of pain by both patients and doctors, and were able to prove statistically that clomipramine possesses a significantly greater efficacy compared to that of acetylsalicylic acid. By taking into account recent anatomical, biochemical and pharmacological studies, it can be concluded that clomipramine probably has-in addition to the action on peripheral receptors-a direct effect upon pain modulation systems. It seems possible that clomipramine activates serotonin-containing neurons of the endorphin-mediated analgesia system that control pain transmission in the CNS.
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PMID:An open and double-blind cross-over study on the efficacy of clomipramine (Anafranil) in patients with painful mono- and polyneuropathies. 612 61

The contribution of a peripheral action of morphine in the augmented antinociceptive effect of this substance was re-evaluated in a well established rat model of peripheral unilateral mononeuropathy (chronic constriction of the common sciatic nerve), using a relatively low dose of systemic morphine (1 mg/kg i.v.) and local low doses of specific antagonists of kappa- (nor-binaltorphimine) or delta-(naltrindole) opioid receptors. Vocalization thresholds to paw pressure were used as a nociceptive test. Escalating doses of nor-binaltorphimine (10-30 micrograms injected locally into the nerve injured paw) significantly and dose dependently reduced the effect of morphine on this paw but not on the contralateral paw, an effect which plateaued at 30 micrograms. By contrast, the local injection of naltrindole (30-40 micrograms into the nerve injured paw) had no effect on morphine analgesia. The doses of opioid receptor antagonists used, injected i.v., in the contralateral paw, or alone in the nerve injured paw had no significant effect. These results suggest that the peripheral effect of systemic morphine in this model of neuropathic pain could be mediated not only by mu- but also by kappa-opioid receptors.
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PMID:Further evidence for a peripheral component in the enhanced antinociceptive effect of systemic morphine in mononeuropathic rats: involvement of kappa-, but not delta-opioid receptors. 896 Aug 76

We previously reported that ketamine analgesia in acute pain was produced by the activation of the monoaminergic descending inhibitory system. Recent studies have confirmed that the NMDA receptor antagonists attenuate the hyperalgesia in neuropathic pain. In this study, we investigated the suppressive effects of a clinically available NMDA antagonist, ketamine, and the mechanisms of its effects on neuropathic pain in rats with peripheral mononeuropathy. A unilateral chronic constriction injury (CCI) model was introduced by loose ligation of the sciatic nerve of the rats. The CCI rats showed hyperalgesia to thermal and mechanical pressure stimuli on the injured side of their hind paws. Intraperitoneal (IP) ketamine (25 or 50 mg.kg-1) and intrathecal (IT) ketamine (25-500 micrograms) reversed, dose-dependently, both thermal and mechanical hyperalgesia. Pretreatment with IT yohimbine (alpha-2 adrenergic antagonist) or IT methysergide (serotonergic antagonist) did not show the suppressive effects of IP ketamine (50 mg.kg-1) on hyperalgesia. Concentrations of norepinephrine (NE) and serotonin (5HT) in the spinal dorsal horn were measured using high performance liquid chromatography. The CCI rats showed increased NE and 5HT concentrations on both ligated and unligated sides of spinal dorsal horn, compared with shamoperated rats. IP ketamine (50 mg.kg-1) in the CCI rats did not boost the spinal NE or 5HT levels. These results indicate that the anti-hyperalgesic effect of ketamine is derived from a direct action on the spinal cord, but not from the activation of monoaminergic descending inhibitory systems.
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PMID:[Suppressive effects of ketamine on neuropathic pain]. 951 24

Nerve injury may lead to chronic neuropathic pain syndromes. We determined whether the extent of central nervous system microglial activation that accompanies nerve injury is age dependent and correlated with behavioral manifestations of pain. We used the Bennett and Xie sciatic nerve chronic constriction injury model (Bennett, G.J., Xie, Y.-K., A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man, Pain, 33 (1998) 87-107) to induce neuropathic pain in three age cohorts of Fischer 344 FBNF1 hybrid rats (4-6, 14-16, and 24-26 months). Rats were assessed for thermal sensitivity (hyperalgesia) of their hind paws pre-injury (day 0) and up to 35 days post injury. On various days post injury, the L4-L5 levels of their spinal cords were reacted for localization of an antibody to OX-42, a marker for microlgia. OX-42 immunoreactivity (ir) was quantified by use of a Bioquant density analysis system. OX-42 ir was heavy in areas of sciatic nerve primary afferent terminations and in the motor columns of its neurons. Aging increases OX-42 ir in the absence of injury. After injury, OX-42 ir increased further, but the increases over control levels decreased with age. Ligation-induced analgesia and hyperalgesia were both correlated with the increases in OX-42 ir, regardless of age.
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PMID:Microglial proliferation in the spinal cord of aged rats with a sciatic nerve injury. 1085 27

In addition to its involvement in the transmission of neuropathic pain, the dorsal column system has been shown to have analgesic effects when electrically stimulated. The segmental or supraspinal origin of the analgesia, however, has not been clearly delineated. The aim of this study is to demonstrate the contribution of supraspinal mechanisms to the inhibition of allodynia and hyperalgesia in two different rat models of mononeuropathy. Mononeuropathy was induced, under deep anesthesia, in several groups of rats (n=7 each) following either the chronic constriction injury or the spared nerve injury model. Mechanical and cold allodynia were assessed by the Von Frey monofilaments and by the acetone drop test, respectively. Thermal hyperalgesia was assessed by the paw withdrawal and hot plate tests. Bipolar electrodes for dorsal column stimulation were implanted chronically in all rats on the dorsal aspect of the medulla at the level of the obex. Selective dorsal column bilateral lesions were performed at the upper cervical level in some groups of rats. Dorsal column nuclear stimulation, rostral to selective dorsal spinal lesions, produced strong inhibitory effects on the allodynia and hyperalgesia observed in both models of mononeuropathy. These effects were comparable to those observed following similar stimulations in rats with an intact spinal cord. Our results demonstrate strong inhibitory effects of dorsal column stimulation on neuropathic pain. This inhibition can be attributed to the activation of brainstem pain-modulating centers via rostral projections of the dorsal column nuclei.
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PMID:Attenuation of neuropathic pain by segmental and supraspinal activation of the dorsal column system in awake rats. 1207 97

Systemic opioid dosing until adequate analgesia in neuropathic pain may involve intolerable and untreatable side effects. Peripheral opioid receptor mechanisms may participate in the antinociceptive effect of systemic morphine. We evaluated the effect of peripherally injected morphine alone, and the ability of the functional antagonist at the glycine site of the N-methyl-D-aspartate (NMDA) receptor complex (+)-HA966 to modulate the antinociceptive effect of peripheral morphine in a rat model of neuropathic pain. Mononeuropathy was induced by placing four ligatures around the common sciatic nerve. Experiments were performed 2 weeks after the nerve ligature, when the pain-related behavior reached a stable maximum. Rats received injections of either subcutaneous (+)-HA966 (2.5mg/kg) or saline administered 20 min before morphine (50-150 microg injected into the nerve-injured hindpaw). The antinociceptive effect was tested against mechanical (vocalization threshold to hindpaw pressure) or thermal (struggle latency to hindpaw immersion into a 46 degrees C hot water bath) stimuli. In both tests, morphine alone (100-150 microg) produced antinociception. Pretreatment with (+)-HA966 did not potentiate the analgesic effectiveness of the two highest doses of morphine, but it did produce analgesia when combined with a low dose of morphine (50 microg), which did not produce analgesia by itself. These effects were reversed by intraplantar naloxone methiodide (50 microg injected into the nerve-injured hindpaw) indicating a peripherally opioid-mediated mechanism of action. The present studies suggested that combined administration of glycine/NMDA receptor antagonists, and peripherally acting morphine may be an interesting approach in the treatment of neuropathic pain.
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PMID:The glycine/NMDA receptor antagonist (+)-HA966 enhances the peripheral effect of morphine in neuropathic rats. 1240 30

The effects of a synthetic peptide analog of thymulin (PAT) were tested on nociceptive behavior in two animal models for peripheral mononeuropathy and in another two models for capsaicin-induced hyperalgesia. Treatment with PAT (0.25-25 microg/rat, i.p.) produced significant reduction of the mechanical allodynia and heat hyperalgesia in rats subjected to either chronic constriction injury (CCI) or spared nerve injury (SNI) models for mononeuropathy. Cold allodynia was moderately reduced in the CCI model. The inhibition of neuropathic manifestations peaked at 1-2 h post-treatment and disappeared in 3-4 h. Daily treatment with PAT, however, produced progressive attenuation of all neuropathic manifestations in the SNI model. On the other hand, pretreatment with similar doses of PAT produced dose-dependent reduction of the hyperalgesia induced by intraplantar injection of capsaicin (10 microg in 50 microl). The highest dose of PAT (50 microg) produced significant reduction of abdominal aversive behavior induced by i.p injection of capsaicin (20 microg in 100 microl). Compared with the effects of treatment with morphine or meloxicam (injected at single doses known to produce analgesia), PAT exerted equal or stronger inhibitory effects on neuropathic manifestations. The reported results suggest a possible direct action of PAT on afferent nerve fibers but its mechanisms remain to be determined.
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PMID:A thymulin analogue peptide with powerful inhibitory effects on pain of neurogenic origin. 1276 77

Although epidural anaesthesia and analgesia are widely used in obstetrics, there are no large contemporary prospective series detailing associated complications. Prospective data was collected on all obstetric epidural blocks performed for labour and delivery in a single institution between July 1989 and August 1994. A data entry sheet was compiled and entered onto a computer database. Confidence intervals for proportions were calculated using standard methods. Information from 10 995 epidural blocks was analysed. Epidural analgesia in labour was the primary indication in 7648, and anaesthesia for caesarean section in 3311. Minor complications included failed or abandoned insertion (incidence 0.5%), reinsertion of the epidural catheter (5%), and inadequate anaesthesia (1.7%) or analgesia (0.9%). Three percent were associated with venous puncture and 0.6% with accidental dural puncture. Maternal mortality was zero. Unexpectedly high blocks occurred on eight occasions (0.07%), two requiring intubation and ventilation. Three women (0.06%) experienced mild respiratory depression after postoperative epidural opioid. There was no major local anaesthetic toxicity or neurological deficit. The incidence of potentially life-threatening morbidity was thus 0.02% although in both cases outcome was good. The only persisting complication was neurological, an apparent epidural catheter-induced traumatic mononeuropathy.
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PMID:Complications of obstetric epidural analgesia and anaesthesia: a prospective analysis of 10,995 cases. 1532 Dec

The present study provides an important implication for the management of chronic neuropathic pain, focusing on prostaglandin (PG) and nitric oxide (NO) in the spinal cord. To determine if spinally administered cyclooxygenase (COX) inhibitor or nitric oxide synthase (NOS) inhibitor had preemptive analgesia on thermal hypersensitivity induced by chronic constrictive nerve injury, Sprague-Dawley rats were chronically implanted with an intrathecal (i.t.) catheter. The left sciatic nerve was loosely ligated with 2-mm polyethylene tubing to produce painful mononeuropathy. Animals received tenoxicam (7.5, 15 or 30 micromol/10 microl, i.t.), NS-398 (15 or 30 micromol), or L-NAME (30, 150 or 300 micromol) immediately before the nerve injury, followed by daily injection extending into the four postoperative days. The hindpaw was immersed into a hot (42 degrees C, 44 degrees C and 46 degrees C) or cold (10 degrees C) water bath. The paw immersion test revealed significant thermal hyperalgesia and allodynia 5 day after nerve injury in vehicle control animals. Tenoxicam (7.5, 15 or 30 micromol) or L-NAME (30, 150 or 300 micromol) dose-dependently attenuated hyperalgesia and allodynia. Equimolar dose of NS-398 (15 or 30 micromol) also diminished these nociceptive behaviors. Higher dose of either drug primarily produced longer duration of inhibition. The inhibitory effect of tenoxicam (30 micromol) on hyperalgesia was more effective than that of an equimolar dose of NS-398 or L-NAME. These results demonstrated that intrathecally administered COX inhibitor or NOS inhibitor provides preemptive analgesia on thermal hypersensitivity following chronic constrictive nerve injury in rats.
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PMID:Preemptive effects of intrathecal cyclooxygenase inhibitor or nitric oxide synthase inhibitor on thermal hypersensitivity following peripheral nerve injury. 1536 58

A 31-year-old woman had bone harvested from the left anterior iliac crest as a graft for an augmentation genioplasty. For postoperative analgesia, she was given a bupivacaine infusion into the iliac wound. She developed a temporary left femoral mononeuropathy from which she recovered completely.
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PMID:Transient femoral neuropathy after harvest of bone from the iliac crest. 1554 91


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