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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The back pain syndrome which accompanies involutional osteoporosis presents a marked heterogeneity. Acute pain may be due to vertebral fractures, whereas chronic pain may eventually accompany established osteoporosis in which clinical and instrumental evidence are present. Back pain is the consequence of the mechanical (internal or external pressure) or chemical stimulation of pain receptors present in bone tissue, along the vessels, in cartilage, joints, disk, ligaments, and also in soft tissue and muscle (with secondary antalgic contracture). The compression of spinal nerves may contribute to the pain as well. An evident alteration of mood is usually present and represents an important element in the syndrome. This phenomenon interferes with the evolution of pain, in particular as regards its intensity. Besides scales for the evaluation of pain and inability, it is possible to check objective data by means of particular algometers (not easy to employ) or by electromyographic measurements of antalgic secondary contracture of spinal muscle. Gait examination (basography) of patients with painful hip prosthesis may provide objective evaluation regarding specific antalgic activity on bone of drugs. Usually the effective drugs for osteoporosis possess antalgic properties as well, with different mechanisms of action. Three drugs with evident activity are taken into consideration: calcitonin, ipriflavon, aminobutane-bisphosphonate (alendronate). Though each of them possesses some particular activity, the main mechanism of action is dependent on their effect on the local microenvironment, particularly at the level of bone tissue (calcium, cytokine and prostaglandin local concentration), on the modulation of osteoclast activity. In particular alendronate (intermittently administered intravenously) exerts the most evident antalgic activity. Subjective chronic back pain relief is accompanied by (secondary) reduction of antalgic contracture at vertebral muscle level. The activity of the substance against the painful hip prosthesis (documented by basographic gait recording) leads us to conclude that the substance really exerts a direct antalgic action at the level of bone tissue.
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PMID:[Treatment experience with chronic spinal pain in involutional osteoporosis]. 129 92

Two cases of acute attack of pseudogout associated with primary hyperparathyroidism are reported. Case 1 suffered from acute pain and swelling of the right ankle and dorsal of the right foot. Case 2 suffered from unknown fever and pain of the bilateral jaw, shoulder, elbow, wrist and knee joints. Postoperative radiological studies revealed the association of chondrocalcinosis in both cases. Synovial fluid in case 2 was aspirated and analyzed for calcium pyrophosphate dihydrate crystal by microscopic examination.
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PMID:Two cases of acute pseudogout attack following parathyroidectomy. 179 38

Acute pain in the lower extremity, which has previously been attributed to synovitis or fasciitis, develops in about 15 percent of osteoporotic patients treated with sodium fluoride. This report describes 11 osteoporotic women in whom this syndrome developed while they were being treated with sodium fluoride (mean dose 78 mg per day; range, 60 to 90). [99mTc]Hydroxymethylene diphosphonate scintiscanning showed an increased number of foci of abnormal uptake in the lower extremities (p less than 0.05), when compared with results of scintiscanning in 12 nonsymptomatic osteoporotic women treated with sodium fluoride and 12 osteoporotic women treated with oral calcium carbonate only. The increased uptake was not restricted to the areas of pain. Roentgenography revealed stress microfractures in five of the 11 symptomatic patients. It is concluded that the acute lower extremity pain syndrome during fluoride therapy usually results from intense regional bone remodeling, which may be complicated by stress microfractures.
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PMID:Mechanism of acute lower extremity pain syndrome in fluoride-treated osteoporotic patients. 396 37

The relative analgesic efficacy of zomepirac sodium 100 mg and fenoprofen calcium 200 mg was evaluated in patients with pain due to surgical removal of dental impactions. This is the first study to make a direct comparison of their effectiveness. This study is especially important since zomepirac sodium was recently removed from the market as an analgesic for acute pain. Zomepirac sodium was extremely popular among clinicians and was considered the most effective of the peripherally acting analgesics. Patients were requested to take a single dose of study medication when they had moderate to severe pain. The study medications were identical in appearance and randomly allocated under double-blind conditions. The medication was evaluated over the next 4 hours according to subjective analgesic measurement scales. The primary measures of efficacy included total pain relief ( TOTPAR ), sum pain intensity difference ( SPID ), overall evaluation, and time to remedication . Of the 136 patients entered, 117 were included in the efficacy analysis. Both active agents demonstrated marked superiority to placebo (p less than 0.001) for all efficacy measures but were inseparable from each other. The mean analgesic efficacy values for both zomepirac sodium and fenoprofen calcium were almost identical. The nineteen subjects who reported side effects were evenly distributed among the three groups. No serious side effects occurred. The results of this study indicate that fenoprofen calcium 200 mg and zomepirac sodium 100 mg are equally efficacious, with similar onset, peak, and total analgesic effects.
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PMID:Comparative efficacy of fenoprofen calcium and zomepirac sodium in postsurgical dental pain. 658 96

Over the past few years periarthritis calcarea - also known as hydroxyapatite rheumatism - has attracted increasing interest. The periarticular calcification hitherto regarded as a secondary finding is today a well-defined disease entity occurring either in localized or generalized form, i.e. around one or more joints respectively. Although the origin of this calcification is now known, various hypothetical causes have been discussed in the literature. In the light of studies on familial clustering and the HL-A constellation, it is now evident that genetic factors have a definite role to play in the etiology of the disease. Even though no metabolic defect has been identified as yet, it is impossible to state with certainty that no metabolic cause is involved. As in gout, periarthritis calcarea is liable to cause attacks of acute pain that last for several days and then disappear. In consequence, the clinical picture is misleadingly similar to that of arthritis. The subsequent disappearance of the periarticular calcium deposits previously shown to be present can be considered a cardinal symptom of the disease. To detect this calcification it is necessary to use the electron microscope, since the crystals are too small to be seen with the light microscope. Periarthritis calcarea undoubtedly ranks as a crystallopathy. Since its origin is unknown, causal therapy such as exists for gout cannot be adopted. Treatment is restricted to purely symptomatic measures.
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PMID:[Periarthritis calcarea]. 705 Dec 77

Ergometrine (ergonovine) tests were performed in patients with unstable angina on the 1st day of hospitalization, on 2nd--3rd days during which patients received only nitroglycerin sublingually for acute pain relief (33 observations), and after "stabilization" of their condition by calcium antagonists or/and beta-blockers (34 observations). Reactions to ergometrine were classified as spastic when pain was accompanied by ST segment elevations of T wave changes and as nonspecific when intravenous ergometrine resulted in ST segment depression and/or anginal attack. Spastic reactions to ergometrine observed in the acute period as a rule disappeared with "stabilization" of patients condition. Spontaneous rapid disappearance of spastic reactions was noted in 4 of 15 patients. Spastic reactions also disappeared in 13 of 17 patients while they were on active antianginal therapy. Disappearance of spastic reactions was observed more frequently in patients treated with calcium antagonists than with beta-blockers. Nonspecific reactions never disappeared spontaneously. Persisting despite therapy any positive reaction to ergometrine was prognostically unfavorable.
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PMID:[Unstable angina pectoris: results of repeated ergometrine tests]. 709 72

Experimental and clinical evidence testifies to an antinociceptive action of salmon calcitonin (sCT), administered in different ways, on the central nervous system. These studies were performed almost exclusively in acute pain models. The purpose of the present study was to investigate the effects of sCT, injected directly into the lateral cerebral ventriculi, on the firing of single nociceptive thalamic neurons, detected by electrophysiological techniques in an experimental model of prolonged or chronic pain, such as rats rendered arthritic by injection of Freund's adjuvant into the left hindfoot. The noxious test stimuli used were either extension or flexion of the ankle or mild lateral pressure on the heel. With increasing doses of sCT (5, 10, 20, 40 micrograms, 5 microliters/i.c.v.) it was possible to observe correspondingly increasing inhibitory and long-lasting effects on the evoked firing, with a significant dose-effect relationship. In agreement with electrophysiological findings, preliminary data, obtained with a patch clamp technique, on depression of calcium fluxes through neuronal membrane, induced by sCT, oriented the attention to a direct action of sCT on CNS.
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PMID:Antinociceptive activity of salmon calcitonin: electrophysiological correlates in a rat chronic pain model. 846 41

The most common crystal-related arthropathies-gout, calcium pyrophosphate dihydrate disease or "pseudogout," and calcific periarthritis/tendinitis-may be appropriately diagnosed and managed by the primary care physician. Definitive diagnosis via synovial tap is recommended, as the clinical picture may not identify some cases. The acute pain and swelling of attacks, regardless of etiology, generally respond to treatment with nonsteroidal anti-inflammatory drugs and local or occasionally systemic corticosteroids. Once a causative crystal has been identified and a diagnosis established, a plan for long-term management and prevention of recurrences may be devised. Thus, uric-acid-lowering therapy may be indicated in a patient who has experienced recurrent attacks of gout, whereas control of serum phosphate levels might be effective in some individuals with hyperphosphatemia and hydroxyapatite-associated periarthritis or arthritis. Crystal deposits in joints can be destructive as well as painful. Treatment, therefore, has two objectives: To relieve the pain of the acute attack, thus restoring normal function, and to prevent the accumulation of crystals that can lead to degenerative disease. Identification and subsequent treatment of preventable or correctable underlying disorders may be one of the most gratifying aspects of managing crystal-induced arthropathies.
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PMID:Crystal-induced arthritis: an overview. 860 27

There are several problems related to the diagnosis and treatment of the acute painful tooth associated with a deep carious lesion, including the fact that there is little or no correlation between the clinical signs and symptoms and also that the diagnostic tools are not reliable. It is important to understand the problems experienced by dental practitioners and how they routinely make diagnosis and formulate treatment plans. The way general dental practitioners diagnosed, categorised and treated teeth with acute pain was ascertained by a questionnaire completed by practitioners attending postgraduate courses. The results indicate that dental radiographs and the dental history were most frequently used and that few practitioners had, and fewer used electric pulp testers. The concept of using simple clinical categories which correspond to treatment categories does not seem to be in widespread use, though the generally accepted role of calcium hydroxide as an indirect and direct capping material is widespread. The use of corticosteroid materials is not as widespread in younger practitioners as in their older colleagues and the use of emergency pulpotomy is infrequent.
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PMID:The diagnosis, classification and treatment of acute pulpal pain by UK general dental practitioners: results of a survey. 894 6

Ginseng root, a traditional oriental medicine, contains more than a dozen biologically active saponins called ginsenosides, including one present in only trace amounts called ginsenoside-Rf (Rf). Previously, we showed that Rf inhibits Ca2+ channels in mammalian sensory neurons through a mechanism requiring G-proteins, whereas a variety of other ginsenosides were relatively ineffective. Since inhibition of Ca2+ channels in sensory neurons contributes to antinociception by opioids, we tested for analgesic actions of Rf. We find dose-dependent antinociception by systemic administration of Rf in mice using two separate assays of tonic pain: in the acetic acid abdominal constriction test, the ED50 was 56+/-9 mg/kg, a concentration similar to those reported for aspirin and acetaminophen in the same assay; in the tonic phase of the biphasic formalin test, the ED50 was 129+/-32 mg/kg. Rf failed to affect nociception measured in three assays of acute pain: the acute phase of the formalin test, and the thermal (49 degrees C) tail-flick and increasing-temperature (3 degrees C/min) hot-plate tests. The simplest explanation is that Rf inhibits tonic pain without affecting acute pain, but other possibilities exist. Seeking a cellular explanation for the effect, we tested whether Rf suppresses Ca2+ channels on identified nociceptors. Inhibition was seen on large, but not small, nociceptors. This is inconsistent with a selective effect on tonic pain, so it seems unlikely that Ca2+ channel inhibition on primary sensory neurons can fully explain the behavioral antinociception we have demonstrated for Rf.
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PMID:Ginsenoside Rf, a trace component of ginseng root, produces antinociception in mice. 959 2


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