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)

Many reports have indicated that electro-acupuncture analgesia (EAA) was mediated by endorphins. Among them is B-endorphin which can be released from the anterior lobe of the pituitary. To examine the role of B-endorphin in EAA and observe CNS metabolic (functional) and behavioral effects of dexamethasone the present study employed the (14C) 2-deoxyglycose (2DG) method. Seventeen adult male Sprague-Dawley rats in five groups received the following different types of somesthetic stimulation to examine the local cerebral glucose utilization (LCGU) and tail-flick response latency: control group (N = 3), pain group (N = 4), EA group (N = 3), pain + EA group (N = 3; from another ongoing study) and dexamethasone group (N = 4). Dexamethasone reduced tail-flick response latency in response to electroacupuncture, and produced metabolic (functional) changes in a number of CNS structures implicated in electroacupuncture produced analgesia effects (some changes were statistically significant, many others were not). Specific brain structures exhibiting statistically significant changes (p less than 0.05) in LCGU when compared to the pain + EA group are: the parafascicular and habennlar nuclei of the thalamus and the posterior cingulate gyrus. In comparison of dexamethasone group with the other four experimental groups of rats, the following trend in LCGU changes was observed: pain + EA group greater than pain group = EA group = dexamethasone group greater than control group. In addition, dexamethasone had a sedative effect. The results suggest that dexamethasone is reducing EAA and having suppressive effects on CNS metabolism and behavior.
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PMID:Effects of dexamethasone on electroacupuncture analgesia and central nervous system metabolism. 289 1

Angioneurotic oedema is a rare disease caused by Cl esterase inhibitor deficiency. Hereditary angioneurotic oedema includes type I (quantitative and functional) deficiency and type 11 (functional) deficiency. Its prophylactic treatment during pregnancy, based on danazol therapy if the fetus is male, may avoid acute attacks of generalized or laryngeal oedema. It must be instituted before delivery and carried into the postpartum period. If the fetus is female, epsilon aminocaproic acid may be used. The acquired form of angioneurotic oedema can be due to antibodies to C1 esterase inhibitor. A prophylactic therapy is not well established, but high doses of corticosteroids are recommended. Operative delivery is best avoided when possible. Regional analgesia is indicated for labour or caesarean section to prevent pain and stress and to avoid the difficulties associated with laryngeal oedema and tracheal intubation. In the treatment of an acute attack, Cl esterase inhibitor concentrates (1500 units) may be given i.v. We present two cases, one of hereditary and one of acquired angioneurotic oedema, both presenting during pregnancy and both delivered vaginally under epidural analgesia with successful outcome.
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PMID:Parturition and angioneurotic oedema. 1532 Nov 58

Pain in chronic pancreatitis (CP) shows similarities with other visceral pain syndromes (i.e., inflammatory bowel disease and esophagitis), which should thus be managed in a similar fashion. Typical causes of CP pain include increased intrapancreatic pressure, pancreatic inflammation and pancreatic/extrapancreatic complications. Unfortunately, CP pain continues to be a major clinical challenge. It is recognized that ongoing pain may induce altered central pain processing, e.g., central sensitization or pro-nociceptive pain modulation. When this is present conventional pain treatment targeting the nociceptive focus, e.g., opioid analgesia or surgical/endoscopic intervention, often fails even if technically successful. If central nervous system pain processing is altered, specific treatment targeting these changes should be instituted (e.g., gabapentinoids, ketamine or tricyclic antidepressants). Suitable tools are now available to make altered central processing visible, including quantitative sensory testing, electroencephalograpy and (functional) magnetic resonance imaging. These techniques are potentially clinically useful diagnostic tools to analyze central pain processing and thus define optimum management approaches for pain in CP and other visceral pain syndromes. The present review proposes a systematic mechanism-orientated approach to pain management in CP based on a holistic view of the mechanisms involved. Future research should address the circumstances under which central nervous system pain processing changes in CP, and how this is influenced by ongoing nociceptive input and therapies. Thus we hope to predict which patients are at risk for developing chronic pain or not responding to therapy, leading to improved treatment of chronic pain in CP and other visceral pain disorders.
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PMID:Systematic mechanism-orientated approach to chronic pancreatitis pain. 2557 79