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CENTRAL INHIBITORY SYSTEMS GABA g-Amino butyric acid (GABA) has been firmly established as the major inhibitory neurotransmitter in the central nervous system effective kamagra super 160 mg doctor who treats erectile dysfunction. The extensive distribution and influence of GABAergic terminals suggests the nervous system operates under considerable restraint discount kamagra super 160 mg with mastercard injections for erectile dysfunction forum, with GABA acting as a tonic controller of excitation. This is also true for the spinal cord where GABA is concentrated in interneurons of the superficial dorsal horn. About one-third of neurons in the superficial spinal cord, the main site of termination of Ad- and C-fibre afferents, contain GABA. In addition, there is evidence that GABA can co-exist with either glycine, galanin, enkephalin or neuropeptide Y in separate populations of neurons. GABAergic terminals contact more Ad-fibre terminals than C- fibre terminals, and in support of this anatomical data, the benzodiazepine (Bz), midazolam, has weak depressive effects on C-fibre-evoked responses, but marked effects on Ad-fibre-evoked responses. In addition, the GABAA antagonist bicuculline facilitates C-fibre-evoked activity less than the profound potentiation of Ad-fibre- evoked responses. Both presynaptic and postsynaptic GABAA receptor-mediated mechanisms are documented in the spinal cord. Several studies have demonstrated Bzs to be analgesic, whereas others have found no antinociceptive properties. In addition, there are contradictory reports of Bzs both potentiating and antagonising morphine analgesia. This diversity of results, however, is the product of many different experimental protocols, models of nociception and routes of administration. In addition, the sedative and myorelaxant effects of these compounds must be considered and these will always limit the usefulness of GABAergic agonists. In the spinal cord GABA can also activate the G-protein-linked GABAB receptor, also found pre- and postsynaptically. Baclofen modulation of nociceptive transmission is seen under inflammatory conditions in animals but in humans the drug appears to lack any analgesic effect. OPIATES Opiate receptors Almost all clinically used opioid drugs act on the mu opioid receptor, the receptor for morphine, and they can be highly effective analgesics in many patients unless the pain is due to nerve damage where some patients have inadequate control. The assessment of the analgesic effectiveness of opioids in both animals and in patients is complicated by the fact that the type of neuropathy and the extent, duration and intensity of the symptoms will vary. There is no real consensus from clinical studies on the efficacy of morphine in neuropathic pain states. Dose escalation with morphine was shown to produce good analgesia in one study and others have reported that, in general, morphine could be effective in a group of patients with neuropathy. Another study concluded that opioids were entirely ineffective and finally, opioid analgesia was less in PAIN AND ANALGESIA 467 468 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION neuropathic pain patients as compared to a group with nociceptive pain. Resolution of this problem has important implications yet a similar series of discrepant results can be found in the animal literature. Following the description and then isolation of opioid receptors, there were three known receptors for the opioids, the mu, delta and kappa opioid receptors, but a novel fourth receptor, the orphan receptor, has been characterised very recently. This newly discovered opioid receptor-like (ORL-1) receptor appears to be linked to an inhibitory receptor despite the endogenous agonist having been named nociceptin (orphanin FQ). The receptor system does not appear to be anything like the traditional opioids. The central effects of nociceptin include a low abuse potential compared to morphine, and so provide an opportunity for the development of alternative analgesics to morphine. However, sufficiently selective tools for the receptor are lacking; the peptide itself is the only agonist available at present, and the putative antagonist appears to be at best a partial agonist. The apparently paradoxical site-dependent antinociceptive/hyperalgesic effects of this peptide are yet to be resolved. The actions of all clinically used opiates can now be explained in terms of their acting as agonists at one of the four opiate receptors found in the brain, spinal cord and peripheral nervous system. The opioid receptors are for the endogenous opioids, peptide transmitters, b- endorphin, endomorphins, enkephalins, dynorphins and nociceptin. Thus all the problems of drugs based on peptides need to be overcome in order for the roles of these Table 21. Pethidine Antagonists Naloxone Naloxone Naloxone Not naloxone Beta FNA Naltrindole Not BNI Effector mechanism G-protein G-protein G-protein G-protein opens K‡ opens K‡ closes Ca2‡ opens K‡ channel channel channel channel Effects Hyperpolarisation of neurons, inhibition of neurotransmitter release Analgesia Similar to mu but Analgesia Analgesia Relief of anxiety less marked Aversion Hyperalgesia Euphoria Diuresis Nausea Constipation Cough suppression Dependence PAIN AND ANALGESIA 469 receptors to be elucidated. The use of morphine and naloxone, non-peptides with mu selectivity has been responsible for the wealth of knowledge about the mu receptor but much less is known about the delta and ORL-1 receptors. Kappa opioids have weak actions in many animal studies and also cause aversive effects Ð clinical studies with these drugs have been discontinued.

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Berquist TH generic 160 mg kamagra super visa erectile dysfunction at age 18, Ehman RL buy kamagra super 160mg with visa erectile dysfunction drugs with the least side effects, King BF, Hodgman CG, Ilstrup DM (1990) Value of MR imaging in differentiating benign from malignant soft tissue masses: study of 95 lesions. Hajdu SI (1981) Soft tissue sarcomas: classification and nat- Diagnosis of soft-tissue masses with MR imaging: can benign ural history. CA Cancer J Clin 31:271-280 masses be differentiated from malignant ones? Weiss SW, Goldblum JR (2001) Enzinger and Weiss’s Soft benign soft tissue tumors. Rydholm A (1983) Management of patients with soft-tissue tu- (1982) Results of the national soft-tissue sarcoma registry. J Bone signal intensity in skeletal muscle adjacent to malignant tu- Joint Surg Am 54-A:1262-1266 mors: pathologic correlation and clinical relevance. Rydholm A, Berg NO (1983) Size, site and clinical incidence 162:251-255 of lipoma. Acta Orthop Scand 54:929-934 Muscle edema in musculoskeletal tumors: MR imaging char- 8. Disler DG, Alexander AA, Mankin HJ, O’Connell JX, acteristics and clinical significance. J Magn Reson Imaging Rosenberg AE, Rosenthal DI (1993) Multicentric fibromatosis 1:441-449 with metaphyseal dysplasia. Rock MG, Pritchard DJ, Reiman HM, Soule EH, Brewster RC sis of MRI parameters predicting malignancy in 141 soft tis- (1984) Extra-abdominal desmoid tumors. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Am 66-A:1369-1374 Verfahr : 156:587-591 IDKD 2005 Tumors and Tumor-Like Lesions of Bone M. Vanel2 1 Radiology, Cleveland Clinic Foundation, Cleveland, OH, USA 2 Institut Gustav Roussy, Villejuif, France Introduction Primary bone tumors as a group are bimodal, the first peak occurring during the second decade of life and the Primary malignant bone tumors are rare. In the year most common non-hematological primary malignancy of 2000, the National Cancer Institute’s Surveillance, bone, occurs predominantly in individuals younger than Epidemiology and End Results (SEER) program estimat- age 20, and in 80% of these patients the tumor is found ed 1,220,000 new cancer cases in the USA. The predilection for the patients, 20-85% may develop bone metastases [3, 4]. Chondrosarcomas show a gradual new cases of primary bone cancer in 1999, with a rate of increase in incidence rates up to the age of 50. Half of eight per million of the female population and 10 per mil- chondrosarcomas occur in the long bones; other major lion for the male population. Ewing’s sarcoma is similar ity, or perhaps because of it, radiologists need to be fa- to osteosarcoma in its age incidence and affinity for the miliar with these lesions, which can mimic or be mimic- long bones but, unlike osteosarcoma, it occurs almost ex- ked by benign and non-neo-plastic reactive lesions, so that clusively in the white population (Table 1). Other selec- imaging beyond the radiograph and biopsy is performed tive primary tumors will be discussed under separate on a logical and knowledgeable basis. The relative frequencies of bone sarcomas ac- 18-fluoro-2-deoxyglucose (18-FDG) accumulation has cording to histological type, sex, and race are shown in been demonstrated in a variety of malignant tissues, in- Table 1. No classification system, however, is so all- cluding sarcomas, and this information can be used to encompassing as to include traumatic reactive and infec- augment the information obtained from conventional tive lesions, all of which have to be considered by the ra- imaging techniques such as computed tomography (CT) diologist when faced with a seemingly neoplastic lesion. Relative frequencies of bone sarcomas by histological type, sex and race (from) Total White Black Histological type No. Unlike other imaging techniques, In general terms, the important features for staging prima- imaging with 18-FDG PET relies on metabolic rather ry bone tumors are local disease extent, the presence or ab- than anatomic parameters. As such, it has been shown in sence of metastatic disease, and histologic grade of the tu- multiple tumor types that intense FDG uptake is predic- mor. There are several staging classifications for bone tu- tive of high metabolic activity and therefore higher tumor mors, each with its own criteria for categorization. In a study of 89 patients with sarcoma, both bone According to the AJCC staging, the rules for classification and soft-tissue types, tumors were assessed with 18-FDG of primary bone tumors include clinical staging (which en- PET and the results compared to both histopathological compasses imaging), pathological staging, and histological grading and markers of cellular proliferation and gene grading. The standardized uptake value on PET to primary definitive therapy, including physical examina- was found to be associated with tumor grade, tumor cel- tion, imaging and biopsy. The radiograph is the mainstay in lularity, mitotic activity, proliferation markers and p53 determining whether a lesion of bone requires further stag- overexpression.

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