Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inadequacy of pain treatment has been demonstrated in many patient groups suffering from acute pain. The injectable nonsteroidal anti-inflammatory drugs (NSAIDs), including indomethacin, diclofenac, ketoprofen and ketorolac, provide relief from the pain associated with several different conditions. When administered alone or in combination with low doses of opioids, NSAIDs provide good pain relief after musculoskeletal trauma or operation. The main advantage of these agents is that they may form the first-line therapy for pain relief and thus decrease the need of opioids. This avoids respiratory depression which can be associated with opioids. In contrast to opioids, NSAIDs do not cause respiratory depression or have marked adverse effects on the central nervous system. However, they may be associated with adverse effects of the gastrointestinal tract, liver and kidneys, and may increase pre- and postoperative bleeding and cause allergic reactions. These effects are related to the ability of NSAIDs to inhibit prostaglandin synthesis. Use of NSAIDs has to be considered carefully in patients with asthma, allergy to aspirin and NSAIDs, atopy, peptic ulcer or bleeding disorders (such as abnormalities in blood coagulation or coagulation deficits). These considerations are especially important in elderly patients. Having taken these contraindications into account, many clinical studies have demonstrated that NSAIDs are at least as safe as opioids when administered in the short term. However, few studies have specifically monitored adverse effects or included patients over 65 to 70 years of age. In addition, patients with risk factors have often been excluded from the trials. Therefore, the risk-benefit ratio of NSAIDs requires further assessment.
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PMID:A risk-benefit appraisal of injectable NSAIDs in the management of postoperative pain. 828 Apr 5

Transient global amnesia (TGA) is a transient, benign neurological syndrome, characterized by global loss of memory, preserved consciousness and self-awareness, associated with some behavioral changes (in particular, repetitive questioning). It generally resolves within 24 h. Mild brain stem symptoms can often be demonstrated during the attack, but major neurological abnormalities never occur. The only sequel is a permanent amnesic gap for the duration of the episode. The episode is often preceded by typical precipitating events, such as physical activity, emotional stress, acute pain, comprising haemodynamic changes of the body. The diagnosis is easy provided one is acquainted with the syndrome. The prevalence of vascular risk factors is low and the risk for stroke is not increased. Although much evidence indicates the possibility of a causative ischaemia in the inferomedial parts of the temporal lobes, an atherothrombo-embolic TIA is not the cause of TGA, and TGA is unrelated to cerebrovascular disease in general. In the author's view, the cause of TGA is a transient ischemic attack (TIA) but a haemodynamic one of the vertebrobasilar system, producing a transient dysfunction of inferomedial parts of the temporal lobes, regions that are particularly sensitive to impaired blood supply. For a full pathogenetic explanation of TGA, clarification of the underlying mechanisms is a prerequisite. This touches on the genesis of migraine and Leao's spreading depression phenomenon. The term 'amnesic TIA' would reflect the pathogenesis more appropriately.
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PMID:Transient global amnesia. 829 84

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

1. Prevent predictable pain, such as occurs postoperatively. Anticipatory pain management is particularly important in the elderly, who frequently attempt to "tough it out" without much analgesia. 2. Assume the patient is in pain if the situation is potentially painful, even without verbal complaints. Confused elders may be unable or unwilling to verbalize pain. For example, a confused 90-year-old woman with an acute hip fracture should be treated for pain, even if she does not complain of it. Elders, especially if demented, may not have the usual external "pain behaviors." 3. Do not routinely use antiemetics, especially phenothiazines. The incidence of postoperative nausea and vomiting is probably less in the elderly, and antiemetics are strongly anticholinergic and poorly tolerated in the frail elderly. 5. Do not use IM narcotics at all, except as "rescue analgesia" or when acute pain has subsided. Their high peak, low trough profile leads to a respiratory depression, excess pain cycle which is poorly tolerated in the elderly IV, or even oral, morphine is better tolerated. 6. Use multiple modalities for analgesia; for example, intercostal nerve block and epidural opioids, or IV-PCA and IV NSAIDs. This will enhance analgesia and reduce narcotic toxicity. This is especially important in frail elders, who often tolerate systemic narcotics poorly. 7. Use site-specific analgesia. Certain operative sites, such as the upper extremity, are especially amenable to local nerve blocks. Others, such as thoracotomy, are especially painful and need potent analgesia. For upper-extremity surgery, consider interscalene nerve block and NSAIDs. For thoracotomy, use extrapleural, intercostal nerve block and epidural narcotics. Local bupivacaine and NSAIDs work well after inguinal herniorrhaphy. For knee surgery, consider intra-articular morphine and NSAIDs. 8. Whenever possible, add a scheduled parenteral, rectal, or oral NSAID, in order to spare narcotics, enhance analgesia, and decrease inflammatory mediators. Unless the patient has a contraindication or there is a strong concern about hemostasis or peptic ulceration, NSAIDs should generally be administered. The major concern in frail elders is acute renal failure; therefore, ensure good hydration and avoid use of NSAIDs if renal function is diminished. NSAIDs should be used on a scheduled (not prn) basis.
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PMID:Postoperative pain management in the frail elderly. 885 47

Chronic musculoskeletal pain, a common problem seen in the primary care setting, is often frustrating for both the patient and the clinician. Despite its prevalence, chronic pain is often poorly understood and inconsistently managed by health care providers. Unlike acute pain, chronic pain serves no biologic function and persists long after the tissue has healed from injury. Patients with chronic pain may become isolated from friends and family, lose their jobs, and develop depression. Nonpharmacologic techniques such as acupuncture, massage, and relaxation may be helpful to the patient with chronic pain. In addition to nonsteroidal antiinflammatory drugs, antidepressants and opioid analgesics are useful for treating chronic musculoskeletal pain. This article explains that pathophysiology of chronic pain, lists aspects of chronic pain that distinguish it from acute pain, and develops a general primary care plan for patients with chronic musculoskeletal pain.
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PMID:Primary care management of chronic musculoskeletal pain. 923 45

Morphine is a potent opioid analgesic widely used for the treatment of acute pain and for long-term treatment of severe pain. Morphine is a member of the morphinan-framed alkaloids, which are present in the poppy plant. The drug is soluble in water, but its solubility in lipids is poor. In man, morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) are the major metabolites of morphine. The metabolism of morphine occurs not only in the liver, but may also take place in the brain and the kidneys. The glucuronides are mainly eliminated via bile and urine. Glucuronides as a rule are considered as highly polar metabolites unable to cross the blood-brain barrier. Although morphine glucuronidation has been demonstrated in human brain tissue, the capacity is very low compared to that of the liver, indicating that the M3G and M6G concentrations observed in the cerebrospinal fluid (CSF) after systemic administration reflect hepatic metabolism of morphine and that the morphine glucuronides, despite their high polarity, can penetrate into the brain. Like morphine, M6G has been shown to be relatively more selective for mu-receptors than for delta- and kappa-receptors while M3G does not appear to compete for opioid receptor binding. The analgesic properties of M6G were recognised in the early 1970s and more recent work suggests that M6G might significantly contribute to the opioid analgesia after administration of morphine. The analgesic potency of M6G after intracerebroventricular (ICV) or intrathecal (IT) administration in rats is from 45-800 timer greater than that of morphine, depending on the animal species and the experimental antinociceptive test used. Furthermore, the development of a sensitive high-performance liquid chromatography (HPLC) assay for the quantitative determination of morphine, M6G and M3G has revealed that M6G and M3G were present in abundance after chronic oral morphine administration and that the area under the plasma concentration-time curve exceeded that of morphine. M3G has been found to antagonise morphine and M6G induced analgesia and ventilatory depression in the rat, which has led to the hypothesis that M3G may influence the development of morphine tolerance. M3G exhibits no analgesic effect after ICV or IT administration. Some studies do, however, indicate that M3G may cause non-opioid mediated hyperalgesia/allodynia and convulsions after IT administration in rats. These observations led to the hypothesis that M3G might be responsible for side-effects, hyperalgesia/allodynia and myoclonus seen after high-dose morphine treatment.
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PMID:Morphine metabolites. 906 Oct 94

The pharmacology, pharmacokinetics, efficacy, adverse effects, and dosage and administration of tramadol are reviewed. Tramadol is a synthetic analogue of codeine that binds to mu opiate receptors and inhibits norepinephrine and serotonin reuptake. It is rapidly and extensively absorbed after oral doses and is metabolized in the liver. Analgesia begins within one hour and starts to peak in two hours. In patients with moderate postoperative pain, i.v. or i.m. tramadol is roughly equal in efficacy to meperidine or morphine; for severe acute pain, tramadol is less effective than morphine. Oral tramadol can also be effective after certain types of surgery. Tramadol and meperidine are equally effective in postoperative patient-controlled analgesia. In epidural administration for pain after abdominal surgery, tramadol is more effective than bupivacaine but less effective than morphine. In patients with ureteral calculi, both dipyrone and butylscopolamine are more effective than tramadol. For labor pain, i.m. tramadol works as well as meperidine and is less likely to cause neonatal respiratory depression. Oral tramadol is as effective as codeine for acute dental pain. In several types of severe or refractory cancer pain, tramadol is effective, but less so than morphine; for other types of chronic pain, such as low-back pain, oral tramadol works as well as acetaminophen-codeine. Common adverse effects of tramadol include dizziness, nausea, dry mouth, and sedation. The abuse potential seems low. The recommended oral dosage is 50-100 mg every four to six hours. Tramadol is an effective, if expensive, alternative to other analgesics in some clinical situations.
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PMID:Tramadol: a new centrally acting analgesic. 907 93

Pain is the main reason prompting patients to consult their physicians. In acute conditions, pain has a very particular significance as a warning sign, enabling the physician to attempt a diagnosis. Nevertheless, its detrimental effect upon the individual (even in the case of acute pain) and its cost to society are now widely acknowledged. There can be no doubt about the physical component of pain, but the psychological and social aspects should not be ignored, particularly in the case of chronic pain. There is no single therapeutic approach to pain and, more often than not, successful treatment comprises a combination of several. Pharmacological treatments are undeniably the most common approach. In clinical practice, recent advances have been based upon an improved understanding of 'old' substances such as morphine and, at the same time, research continues in the hope of finding the 'ideal' analgesic-effective in most situations but without adverse effects: this appears to be a somewhat utopian arm at present, considering the number of different causes of pain. An improved understanding of the physiological mechanisms of pain has led, within the field of clinical practice, to several methods of differentiating pain. These depend on whether or not pain responds to morphine, or on the type of pain: pain due to an excess of nociception, pain resulting from deafferentation (caused by damage to nerve pathways) in the central or peripheral nervous system and psychogenic (idiopathic) pain. Likewise, there are several different ways of classifying analgesic treatments: according to the intensity of pain, as with use of the WHO ladder (which is based on the notion of steps) for the treatment of cancer pain; according to the presumed physiopathological mechanism and, in particular, the response to morphine, and according to the presumed central or peripheral mechanism of the drugs. In reality, peripherally acting drugs can also have a central mechanism of action, just as drugs known to have a central mechanism of action can also have peripheral activity. As a result, several therapeutic classes have been identified. Firstly NSAIDs, which act by inhibiting the enzymes that synthesise prostaglandins, cyclooxygenases (COX-1, COX-2), but which also act upon lipo-oxygenases: Their efficacy is interesting, although somewhat limited by both their ceiling effect and the frequent adverse gastrointestinal reactions they produce. Specific inhibitors of COX-2 could well reduce the risk of adverse effects. Opioids constitute the first-line treatment for pain, particularly severe pain. There are several classifications for these drugs. Firstly, weak opioids (such as codeine) and strong opioids (such as morphine) are differentiated. Secondly, a distinction is made between pure agonists (such as morphine), partial agonists (such as buprenorphine), agonist-antagonists (such as nalbuphine) and antagonists (such as naloxone). Finally, agents are distinguished on the basis of their chemical structure (synthetic, semi-synthetic or natural derivatives). These molecules act upon different receptors (mu, delta, kappa, sigma) and, although peripheral mechanisms have been described, their activity occurs mainly at spinal and supraspinal levels. They provide a potent analgesic effect but are also responsible for various adverse effects-nausea, vomiting, sedation, constipation and respiratory depression-which seriously limit their use. As long as the indication is appropriate, these drugs should not be withheld because of fear of dependence or abuse. It has been observed that other adjuvant therapeutic approaches, generally used to treat conditions other than pain, provide pain relief in certain situations. These include corticosteroids, which are-widely used in rheumatology and oncology, and antidepressants, which are frequently used to treat chronic pain, especially that with a neuropathic component. Anti-epileptics are also used, particularly for excrutiating
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PMID:[Review of current pharmacologic treatment of pain]. 919 Mar 20

35 patients with syndrome of reflex sympathetic dystrophy (RSD) were examined clinically by means of psychological tests, method of evoked skin sympathetic potentials (ESSP) and nociceptive flexor reflex R III. RSD syndrome had central origin (after strokes) in 17 patients (group I) while in 18 patients it arose after some peripheral damages (group II). RSD syndrome was characterised in both groups by triad of symptoms: acute pain, autonomic disorders and osteoporosis. Decreased life quality, high anxiety and depression were quite characteristic for the patients with RSD. Both significant prolongation of latent period and decrease of amplitudes of ESSP were observed on the damaged limb in both groups of patients. These damages were evidently connected with disorders of central-peripheral autonomic interactions in paretic limbs in group I, in group II they were conditioned by damages in peripheral sympathetic sudomotor fibers. Significant increase of both thresholds of pain perception and flexor reflex was found in patients with RSD while the value of the coefficient of their correlation was decreased. Such disorder might be caused by initial insufficiency of antinociceptive functions and that permitted to suggest the hypothesis about the role of this factor in pathogenesis of RSD syndrome and in development of chronic pain its leading symptom. The conclusion was drawn that development of RSD syndrome was not associated with location, severity and character of the damage, but it was conditioned mainly by the state of functions of cerebral antinociceptive systems as well as by emotional and personal peculiarities of the patients.
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PMID:[Reflex sympathetic dystrophy]. 921 82

CAREFUL ASSESSMENT: In pediatric clinics, it has become habitual to prescribe analgesics in all painful situations. Particular attention must be paid to pain experienced by the child and obtaining objective evidence allowing valid assessment prior to treatment. ACUTE PAIN: Usually clearly expressed by crying screams, agitation, retraction and protection of the painful area, signs of acute pain are nonspecific and not proportional to its intensity. PROLONGED PAIN: Sadness and depression confound the expression of prolonged pain. Diagnosis may be difficult; an association between a potentially painful situation, pain relieving positions, and retraction behavior is specific. ESTABLISH CONFIDENCE: For both the child and his family, an atmosphere of confidence and a clear explanation of the lesions and their treatments are essential to break the viscious cycle of pain and anxiety. EXAMINING A CHILD WITH PAIN: Patience is the essence of examining children, facial mimics, reactions, movements and positions all provide essential information. ASSESSING PAIN INTENSITY: Using the visual analogue scale, VAS, children over 5 years of age can show where the pain is on a drawing of the body. For those under 5, questioning the family and looking for specific signs is an essential source of information. The DEGR scale can be used to score prolonged pain in children from 2 to 6 or 8 years of age.
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PMID:[Analgesics in pediatrics. Before prescribing: recognize and evaluate pain, reassure]. 923 66


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