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

Morphine sulfate (MS Contin), a proven analgesic in the treatment of cancer pain and chronic benign pain, seems to be a good analgesic for the treatment of burn pain. MS Contin is morphine sulfate incorporated in a wax cellulose matrix delivery system. This wax cellulose delivery system gives MS Contin its duration of action. Ten patients were enrolled in an open-labeled, nonrandomized study. The study was designed to examine the analgesic efficacy of MS Contin in the burn population. Each patient remained in the study for 6 days. The efficacy of the analgesic regimen was subjectively measured by the visual pain scale. The MS Contin group was retrospectively compared with a group of patients who were given continuous intravenous infusions of morphine. The two groups were matched according to age, burn size, surgical procedures, and hospital stay. The analgesic qualities of MS Contin were comparable to those of continuous intravenous morphine sulfate infusions. MS Contin is a possible candidate for the treatment of patients with burn pain because of its analgesic qualities, oral dosing, and duration of action.
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PMID:Use of morphine sulfate (MS Contin) in patients with burns: a pilot study. 145 94

Concern with the suboptimal management of pain in hospitalized patients has led to the development of a patient-controlled analgesia system. In this system, a preset amount of narcotic is delivered intravenously when the patient activates the demand button. We tested the safety and efficacy of this mode of treatment in eight patients with cancer suffering from severe pain. Respiratory rates, mental status, and pain relief were recorded at baseline and during the study period. Morphine sulfate doses ranged from 1 to 5 mg, and lockout intervals from 15 to 90 minutes. Patients had a higher analgesic demand, ie, self-administered more doses, during the first four hours than during the remaining time of treatment. Respiratory rates decreased during the first four hours of treatment, but no cases of significant respiratory depression were encountered during this period or thereafter in the study. Significant pain relief was produced in all patients without causing undue sedation. Patient acceptance of this mode of therapy was excellent, and the majority of patients preferred this type of analgesia to other forms of pain treatment. In conclusion, patient-controlled analgesic is effective and safe therapy for cancer pain.
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PMID:Patient-controlled analgesia for severe cancer pain. 242 59

Morphine sulfate in doses of 90 to 150 micrograms/3 microliters evoke a prominent behavioral syndrome characterized by 1) periodic bouts of spontaneous agitation during which the rat scratches and bites at the skin of the caudal dermatomes and 2) vigorous agitation, vocalization and coordinated efforts to bite and escape evoked by a light tactile stimulus applied to the flank, suggestive of a pain state (allodynia). The phenomenon is not reversed by naltrexone or is it subject to tolerance. The ordering of activity of an opioid alkaloid related agent in producing this touch-evoked agitation is: noroxymorphone-3-glucuronide, morphine-3-glucuronide, morphine-3-ethereal sulfate, dihydromorphine, noroxymorphone dihydrate, hydromorphone, dihydrocodeine tartrate, morphine sulfate, dihydroisomorphine, morphine-HCl, 6-acetylmorphine, N-normorphine-HCl and (+)-morphine. The following agents were essentially without effect at the highest doses examined: 3,6-diacetylmorphine, N-normeperidine-HCl, nalorphine-HCl, alfentanil, sufentanil, naloxone, naltrexone, methadone, dextrorphan tartrate, meperidine-HCl, oxycodone, levorphanol, oxymorphone, codeine phosphate, thebaine, nalbuphine and naltrexone-3-glucuronide. The observations that the sulfated and conjugated metabolites are 10 to 50 times more potent than their unmetabolized precursor suggest the possibility that, in high concentrations certain phenanthrene opioid alkaloids with a free 3-OH position, an ether bridge and no N-methyl extension will be subject to conjugation and this metabolite will alter the processing of otherwise innocuous tactile stimuli. The fact that the phenomenon appeared at least partially stereospecific may reflect upon the fact that other laboratories have shown that glucuronyl transferase may preferentially convert (-)-morphine to the 3-glucuronide and (+)-morphine to the 6-glucuronide which may be less active.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacology of the allodynia in rats evoked by high dose intrathecal morphine. 334 33

Morphine sulfate in controlled-release tablet form is a relatively new oral preparation being used for the relief of chronic severe pain, such as that related to cancer. A patient with adenocarcinoma of the prostate with bone metastases experienced dyspnea possibly related to the ingestion of these tablets. Discontinuing the drug quickly resulted in disappearance of the dyspnea. The respiratory effects of morphine and the particular risks posed to the elderly patient are discussed.
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PMID:Dyspnea possibly associated with controlled-release morphine sulfate tablets. 339 Nov 10

Morphine sulfate is the narcotic analgesic most commonly used for pain treatment in terminally ill patients. This case report demonstrates a new method of morphine administration. A 56-year-old terminally ill cancer patient with severe pain from metastatic adenocarcinoma of the lung required continuous nasogastric feeding and around-the-clock narcotic analgesics. The patient was safely and effectively converted from a continuous intravenous morphine infusion to continuous nasogastric morphine-enteral feedings. This method of administration may benefit patients receiving continuous enteral tube feedings who either require high-dose morphine therapy or are unable to use the oral administration route.
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PMID:Continuous nasogastric morphine infusion. 342 37

Pain relief following stimulation of the periaqueductal gray matter (PAG) or periventricular gray matter (PVG) in man has been ascribed to stimulation-induced release of endogenous opioid substances. Forty-five patients were studied and followed for at least 1 year after placement of chronic stimulating electrodes in the PAG or PVG to determine if pain relief due to stimulation could be ascribed to an endogenous opioid mechanism. Three criteria were assessed: the development of tolerance to stimulation; the possibility of cross-tolerance to morphine; and reversibility of stimulation-induced pain relief by the opiate antagonist naloxone. Sixteen patients (35.6%) developed tolerance to stimulation, that is, they obtained progressively less effective pain relief. Twelve (44.4%) of 27 patients undergoing stimulation of the thalamic sensory relay nuclei for treatment of chronic pain (a presumably non-opioid mechanism) also developed tolerance. Morphine sulfate was administered in a blind, placebo-controlled protocol to 10 patients who had become tolerant to PAG-PVG stimulation and none showed evidence of cross-tolerance. Fifteen of 19 patients, already tolerant to morphine at the time of PAG-PVG electrode implantation, experienced excellent pain relief by stimulation, also indicating a lack of cross-tolerance. Twenty-two patients who experienced excellent pain relief from chronic PAG-PVG stimulation received intravenous naloxone in a double-blind, placebo-controlled protocol. Pain intensity as assessed by the visual analog scale was increased to the same degree by both placebo and naloxone. Eight patients showed no increase in pain intensity with either placebo or naloxone. Although tolerance to PAG-PVG stimulation developed in these patients, the frequency of tolerance was similar to that seen in patients undergoing thalamic sensory nuclear stimulation. Since the latter technique presumably relieves pain by a non-opioid mechanism, the development of tolerance to PAG-PVG stimulation does not, in itself, confirm an opioid mechanism. Cross-tolerance between PAG-PVG stimulation and morphine was not seen and cross-tolerance to PAG-PVG stimulation in patients already tolerant to morphine was rare. The pain-relieving effect of PAG-PVG stimulation was reversed to an approximately equal degree by naloxone and placebo. The authors do not believe that, in most patients, pain relief elicited by PAG-PVG stimulation depends on an endogenous opioid mechanism. It appears that other, non-opioid mechanisms are primarily responsible for such pain relief.
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PMID:Pain relief by electrical stimulation of the periaqueductal and periventricular gray matter. Evidence for a non-opioid mechanism. 349 33

D-Phenylalanine, along with morphine, acetylsalicylic acid and zomepirac sodium were evaluated for their antinociceptive actions in monkeys (M. fascicularis) trained to autoregulate nociceptive stimulation using a discrete-trials, aversive-threshold paradigm. Morphine sulfate produced dose-related increases in aversive threshold which were reversible after administration of naloxone (12.5 or 25 micrograms/kg i.m.). D-Phenylalanine (500 mg/kg p.o.) produced a small increase in aversive threshold which was not statistically significant and not naloxone reversible. Acetylsalicylic acid (200 mg/kg p.o.) but not zomepirac sodium (200 mg/kg p.o.) in combination with D-phenylalanine (500 mg/kg) produced a small statistically significant increase in aversive threshold. Our results argue against the hypothesis that D-phenylalanine is responsible for increasing aversive thresholds via opiate receptor mechanisms involving increased activity of enkephalins at synaptic loci. Previous studies by others in rats and mice showed that D-phenylalanine and acetylsalicylic acid produced increases in nociceptive thresholds which were naloxone reversible. Our failure to find opiate receptor mediated analgesia in a primate model with demonstrated opiate receptor selectivity and sensitivity is discussed in terms of previous basic and clinical research indicating an analgesic role for D-phenylalanine. Possible species difference in drug action is discussed in terms of inhibition by D-phenylalanine of carboxy-peptidase-like enkephalin processing enzymes as well as inhibition of carboxypeptidase-like enkephalin degrading enzymes.
Pain 1986 Feb
PMID:D-phenylalanine: a putative enkephalinase inhibitor studied in a primate acute pain model. 351 91

Morphine sulfate Contin (MSC) is an investigational matrix delivery system for oral morphine sulfate that allows for prolonged blood levels of morphine. Twenty-six patients with inadequately controlled cancer-related pain were examined in an open but controlled study using MSC. Initially, all patients were converted from the prestudy analgesic regimen to an equianalgesic amount of immediate-release morphine sulfate (IRMS) on a q4h dose schedule that was in turn titrated to the level of adequate pain relief. Patients then were switched to MSC q8h and eventually to q12h, starting at doses representing the same total daily amount of morphine that was in the final IRMS dose. Of the 18 patients who completed the study, all achieved satisfactory levels of analgesia on MSC, seven at q8h and 11 at q12h dosing intervals. All patients reported better analgesia while taking MSC compared with their previous regimen. Side effects associated with MSC included sedation and constipation but not nausea or respiratory difficulty. Significant drug tolerance did not develop during a mean follow-up period of four weeks (range, 1-18 weeks). MSC is an effective oral opioid analgesic that allows an increased dose interval without increased side effects or decreased potency. It can improve the quality of life of cancer patients by allowing them to be maintained without frequent dosing or parenteral medication.
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PMID:Management of cancer pain with oral controlled-release morphine sulfate. 368 May 67

Antinociception following central opioid microinjection in rats was assessed weekly via a tail-flick procedure during chronic tricyclic antidepressant (TCA) treatment. (1) Daily TCA: Subcutaneous injections of desipramine (DMI), 30 mg/kg, chlorimipramine (CMI), 10 mg/kg, or saline, 1 ml/kg, were given daily for 22 days. Morphine sulfate (M), 5 micrograms, was microinjected into the ventrolateral periaqueductal gray (VLPAG) at 7 day intervals. On day 1, DMI or CMI enhanced M analgesia whereas saline did not. Augmentation of M disappeared by days 8 and 15 for CMI and DMI, respectively, and was replaced by attenuation which was still observed on day 22 for both TCAs. L-Tryptophan (LT), 100 mg/kg, i.p., on days 15 and 22 temporarily restored TCA enhancement of M. Fourteen days after cessation of all daily TCA treatments, enhancement of M by CMI was similar to that observed on day 1, whereas recovery of DMI-induced facilitation was incomplete. (2) Weekly TCA: Weekly treatment with DMI, CMI, or saline in the same doses as above had similar effects. M analgesia was enhanced by the TCAs but not saline on day 1; this facilitation was absent by day 15. Attenuation of M by DMI or CMI was evident on day 22; 2 weeks after cessation of all weekly TCA treatments, complete recovery of TCA-induced augmentation was observed. Loss of M facilitation during chronic daily or weekly TCA administration may be related to reduction of central opioid and/or 5-HT2 receptors.
Pain 1984 Dec
PMID:Contrasting effects of acute vs. chronic tricyclic antidepressant treatment on central morphine analgesia. 609 58

Morphine sulfate (0.75 micrograms) was microinjected into (rat) rostral and caudal trigeminal areas singly and simultaneously, using cannula-electrode combinations. Also, 0.5 micrograms or 1.0 micrograms of morphine was injected into nucleus reticularis paragigantocellularis (PGC). Both single trigeminal nuclear microinjections significantly elevated the latency to a defensive face-rub reaction to noxious facial heat, bilaterally. There was no summation effect with the conjoint injection of 1.5 micrograms total to rostral and caudal nuclear areas. The 0.5 micrograms injection in PGC had a significantly larger effect than did the 0.75 microgram trigeminal injections. The caudal but not the rostral trigeminal injections did elevate the threshold for aversive reaction to caudal trigeminal nuclear stimulation of the injected tissue. This finding contrasts with the previously reported fact that as much as 1.0 microgram of morphine in PGC has no effect on this aversive reaction threshold to brain stimulation.
Pain 1983 Feb
PMID:Analgesia for orofacial nociception produced by morphine microinjection into the spinal trigeminal complex. 684 24


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