Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Older people often describe their headaches as starting with vague neck discomfort and eventually moving to the temples and forehead. These are muscle-tension headaches, by far the most common type in the elderly. Although cervical osteoarthritis often is at fault, depression can be a significant factor, patricularly when headaches are chronic. There is no sure cure for tension headache, and often, several of the many remedies-ethyl chloride spray, moist heat, massage, antidepressant drugs, analgesics, local anesthetics, etc.-must be tried before an effective one is found. But just as important to successful therapy are concern, compassion, and a willingness to listen on the part of the physician. True migraine headaches are rare in the elderly. More prevalent is the type of vascular headache associated with giant cell arteritis, which is severe and resistant to any form of analgesic except the strongest narcotics. Vascular headaches also may result from congestive heart failure (which produces venous congestion in the cranial cavity), transient ischemia, increased intracranial pressure, and a variety of metabolic disturbances.
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PMID:The types of headache that affect the elderly. 95 13

Osteochondritis dissecans (OCD) is a common entity in both the juvenile and adult populations, with an incidence of 3 to 6/10,000 in adults. Much of the early literature grouped juvenile and adult osteochondritis dissecans, osteochondral fracture, and accessory ossification into the same category. Conclusions were then drawn on the combined group. Nonetheless, this is a diverse group. This review discusses only OCD. There have been multiple etiological theories of OCD, ranging from trauma to ischemia to accessory centers of ossification and to genetics. It is evident that the true etiology is probably multifactorial. Bone scan, computed tomographic scan, and magnetic resonance imaging advances have enhanced the physician's ability to make the diagnosis of osteochondritis dissecans as well as to stage operative intervention. There is a vast difference between juvenile and adult OCD, as seen in the natural history, prognosis, and treatment options. In general, the juvenile patients have better results overall. The indications for operative intervention for these juvenile patients are a nonhealing attached fragment, fully or partially detached lesions of the articular surface, and loose bodies. Nonoperative treatment in the adult patient has been shown to accelerate degenerative arthritis, which involves all 3 compartments of the knee. Therefore, symptomatic lesions and loose bodies comprise the surgical indications for adult OCD. An understanding of this disease process will help the physician optimize the patient's results.
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PMID:Osteochondritis dissecans of the knee: a historical review of etiology and treatment. 220 81

In a 67 year-old man, an aseptic necrosis of the right hip joint developed side by side with an early oteoarthrosis characterized by an extensive narrowing of the upper interlinear space. The histological study revealed a diffuse ischemia which had evolved differently in the various regions of the femoral head. A well-limited necrosis appeared in a part of the weight-bearing zone, and osteoarthrosis developed in another one. In contrast with classical osteoarthrosis secondary to malformation, the osteoarthrotic lesions of the weight-bearing zone were caused by the ischemic angio-fibrosis of the bone marrow. At the beginning there was a resorption by the subjacent fibro-vascular tissue of the end-plate and of the deep layer of the cartilage. The osteosclerosis of this zone, in particular the eburnated plate, was formed mostly of fibre bone which rapidly became necrotic. Outside the weight-bearing zone, the subchondral angio-fibrosis and the non-inflammatory vascular pannus modified the articular surface.
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PMID:Contiguous development of idiopathic osteonecrosis and osteoarthrosis in ischemia of a femoral head (radiological and morphological study). 376 83

Disorders and complaints in the neck and shoulder regions are common among industrial workers and are often attributed to occupational musculoskeletal stress. The possible pathophysiological mechanism of occupational stress on the neck and shoulders is reviewed. A mechanical origin for cervical disc degeneration and osteoarthrosis is reported for a few occupational groups. However, a mechanical origin for osteoarthrosis is debatable. A work posture involving elevated arms may accelerate degeneration of shoulder tendons through impairment of circulation due to static tension and humeral compression against the coracoacromial arch. Furthermore, work tasks with repetitive arm movements may evoke shoulder tendinitis or tendo-vaginitis, probably due to friction. Three possible routes to neck-shoulder muscular pain are discussed; mechanical failure, local ischemia and energy metabolism disturbance.
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PMID:Occupational musculoskeletal stress and disorders of the neck and shoulder: a review of possible pathophysiology. 636 2

The classic features of idiopathic femoral head necrosis - increased roentgenologic density, the subchondral crescent-fracture and distortion of the femoral head - are now known to be late manifestations of the disease. The early changes have been studied prospectively in 34 patients receiving corticosteroids in high dosage and 11 patients with femoral head necrosis attributed to alcohol abuse. In five patients with unilateral femoral head necrosis, intraosseous pressure studies and core biopsy were carried out on the apparently unaffected side. The earliest pathologic changes were a relative increase in cancellous bone fat at the expense of myeloid tissue, swelling and necrosis of the fat cells, and variable areas of cell death in the trabeculae. All of these were fairly widespread throughout the proximal femur. Intraosseous pressures were raised, suggesting the presence of venous stasis. Fat cell size was measured in undistorted femoral heads with osteonecrosis and in a comparable series with osteoarthritis. There was a significant (P less than 0.001) increase in fat cell size and a virtual absence of sinusoids in histologic sections from those with osteonecrosis. It is posited that idiopathic osteonecrosis results from the following sequence: fatty accumulation and replacement of myeloid tissue, followed by compression of vascular sinusoids, venous stasis, ischemia, fat necrosis and then bone necrosis. The earliest stages in this chain of events are clinically asymptomatic and produce no radiologic abnormality. The results of treatment by core decompression in 22 hips are discussed. This is an effective prophylactic measure in all early cases and it has a place even in the management of more advanced cases, especially if the patient is considered too young for hip arthroplasty.
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PMID:Idiopathic necrosis of the femoral head: pathogenesis and treatment. 732 18

Bearing in mind earlier studies which established a link between arteriosclerosis and mineral loss, or fragility of the bones, and also our recent study showing that patients with arterial disorders of the lower limbs also suffered from osteoporosis, we carried out a histological study of the number and appearance of the intraosseous vessels and trabecular bone volume in the femoral heads of patients undergoing surgery for either fracture of the femoral neck or osteoarthritis of the hip. The number of thick-walled vessels, arterioles or arterial capillaries was significantly diminished in the femoral heads of patients with fractures of the femoral neck (p = 0.007). In addition, in the latter patients, arteriosclerotic vascular lesions (rupture of the internal elastic lamina, medial thickening and fibrosis) were more frequent than in patients with osteoarthritis of hip. The possibility that, through chronic ischemia, arteriosclerosis may lead to disturbance of bone remodelling and loss of the mechanical properties of bone has not been contradicted by these findings.
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PMID:Study of the intraosseous vessels of the femoral head in patients with fractures of the femoral neck or osteoarthritis of the hip. 749 58

E.Z. former world champion and holder of several gold and silver medals from Olympic Games as long-distance runner, underwent at the age of 71 comprehensive investigations. In 1993 following methods were used to establish E.Z. body build and health: Family, personal and sports history, anthropometry, somatotype, body composition posture values, sports medicine examination, ECG at rest, X-rays of the lung and heart, echocardiography at rest, systolic time intervals at rest, spirography at rest, hematology, biochemistry, X-rays of bones, exercise ECG changes and spiroergometry. Today, a typical feature of E.Z.'s bodybuild is a great amount of body fats, flabby musculature, faulty posture, restricted mobility of the spinal column and surprisingly good foot arches. The clinical findings are appropriate for his age, on his ECG at rest are signs of subendocardial ischemia above the left ventricle, atrial fibrillation and ventricular extrasystoles (Lown 1 a-b). Exercise ECG resulted in a deepening of the ischaemic changes already at a working load of 50 W. Hematology revealed normochromic macrocyt anaemia, biochemistry a borderline mineralogram, hyperuricaemia, higher S-GMT and HDL-C, T-C at the limit of normal values. X-rays of the bones were remarkable in two findings of that age. The pelvis, lumbar spine and knee joints were free of the usual pathological findings (osteoarthrosis), but presented with an exceptionally advanced osteoporosis.
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PMID:Medical and anthropological study of a world and Olympic champion, long-distance runner, 35 years after the end his racing career. 864 15

Degenerative hip arthritis is caused by the joint failing to bear the normal walk load, because of changes in the anatomical components and of some factors leading to static or dynamic unbalance of the joint surfaces. Degenerative arthritis usually evolves slowly, but its evolution is rapid under certain circumstances and in elderly patients. In such cases destruction is severe and irregular erosions are observed in the femoral heads, which become small and move to the superior lateral edge of the acetabulum. Osteophytes and reactive osteosclerosis are uncommon. Severe pain, functional inability and lower limb shortening are quite constant findings. The patient is often immobilized in bed and risks his/her life. Since the pathogenesis of destructive arthritis is still debated and its clinical features are severe, the knowledge of the natural history and of the underlying factors appears to be very important. The only therapy is arthroprosthesis and prevention becomes, therefore, necessary. On the basis of radiographic findings, we selected three groups of elderly patients hospitalized from 1992 to 1995; of them, 178 had destructive arthritis. The control group consisted of 102 patients with degenerative arthritis and 188 with normal hip joints. The radiographic patterns were related to some clinical and laboratory findings, which are the suspected pathogenetic factors. Two main factors emerged, with high statistical development risk (p < 0.01): hypoxia from femoral head ischemia, due to atherosclerotic vasculopathy and associated anemia, and the articular biodynamic changes which, through minor repeated trauma, cause the lesions, with the appearance of stress fractures.
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PMID:[Destructive arthrosis of the hip. Natural history, pathogenesis, and radiographic features]. 897

Dysbaric osteonecrosis was induced successfully in adult sheep after 12 to 13, 24-hour exposures to compressed air (2.6-2.9 atmospheres absolute) during a 2-month period. All exposed sheep had decompression sickness and extensive bone and marrow necrosis in their long bones. Radiographic analysis of these progressive lesions showed mottled to distinct medullary opacities and endosteal thickening characteristic of dysbaric osteonecrosis. Six months after the last hyperbaric exposure, neovascularization of once ischemic fatty marrow was centripetal from the diaphyseal cortex. Proliferating endosteal new bone, fatty marrow calcification, and appositional new bone formation were widespread. Juxtaarticular osteonecrosis involved marrow fibrosis and loss of osteocytes in subchondral cortical bone. Tidemark reduplication in juxtaarticular bone and cartilage thinning suggested possible early osteoarthritis induction by recurrent episodes of transient ischemia after multiple hyperbaric exposures. Dysbaric osteonecrosis appears to involve a bone compartment syndrome of elevated intramedullary pressure initiated by decompression induced N2 bubble formation in the fatty marrow of the long bones. An animal model that can be used to investigate the pathogenesis, diagnosis, and treatment of dysbaric osteonecrosis is discussed.
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PMID:Dysbaric osteonecrosis in divers and caisson workers. An animal model. 937 84

Oxaceprol, an established drug for treatment of degenerative joint disease, has recently been shown in vitro to reduce leukocyte adhesion to cultured endothelial cells and leukocyte extravasation in vivo in an arthritis animal model. The aim of this study was to examine the effects of Oxaceprol on the microcirculation of striated skin muscle. In the dorsal skinfold chamber of the awake Syrian golden hamster I/R injury was induced by applying a 4-hour complete pressure ischemia. Prior to the ischemia, after 30 minutes, 2 hours and 24 hours of reperfusion the following parameters were assessed in a blinded study: macromolecular leakage, leukocyte rolling fraction, adherent leukocytes, and functional capillary density (FCD). Rhodamine 6G to stain leukocytes in-vivo and FITC Dextran (MW 150,000) was used as a plasma marker. 15 minutes prior to reperfusion the animals received either an i.v. bolus infusion of Oxaceprol (50mg/kg) or an equivalent volume of saline, which was followed by a 45-minute continuous infusion at the same dose. At the conclusion of the experiment samples were collected from the chamber tissue for histological quantification of leukocyte extravasation using an esterase stain. Oxaceprol treatment resulted in a significant decrease of postischemic leukocyte adherence after 0.5 h and 2h of reperfusion. The histological sections revealed a significant reduction in the number of extravasated leukocytes. There was a reduction of macromolecular leakage and treatment also resulted in a preservation of tissue perfusion, as was indicated by a significant increase in FCD in the treatment group compared to the ischemia group. In summary, Oxaceprol was able to protect the tissue from ischemia/reperfusion injury.
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PMID:Effects of oxaceprol on the microcirculation in ischemia/reperfusion injury. 953 26


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