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)

29 cases of femoral mononeuropathy are reported. While the clinical features of the femoral neuropathy are easily identified, the etiology is often hard to establish. The cases reported tend to fall into three general categories: 1) cases without major diagnostic difficulties (e.g. diabetic neuropathy); 2) those in which the definite diagnosis results from combined evidence of laboratory and instrumental data (degenerative changes in the lumbar spine, compressions, entrapments, etc.); 3) those in which the negative result of the investigations prevents a positive diagnosis and hence a presumptive etiology (spondylosis, inflammatory process, ischemia of the nerve) may be formulated. Attention is drawn to the favorable course of the condition in the patients of this group.
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PMID:Problems of etiology in femoral neuropathies. 298 53

We report 2 cases of cadaveric renal transplantation in which the grafts were placed in the right iliac fossa. Postoperatively, both patients complained of ipsilateral thigh weakness. Electromyography and nerve conduction studies indicated femoral nerve neuropathy. Muscle weakness gradually resolved. Difficulty was encountered in placing both grafts, and each kidney and limb were subjected to prolonged ischemia. We suggest that the femoral neuropathy was ischemic in origin.
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PMID:Femoral neuropathy after renal transplantation. 299 77

We report a case of a mixed sensorimotor, predominantly axonal mononeuritis multiplex that developed after a severe meningococcal septicemia and disseminated intravascular coagulation (DIC) with associated distal limb necrosis. Ischemia resulting from the DIC-induced multiple vascular occlusions is suggested as the leading cause of this neuropathy.
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PMID:Peripheral neuropathy in meningococcal septicemia. 299 4

Some human and experimental neuropathies are characterized by endoneurial edema and increased intercapillary distance (ICD). This may potentially produce chronic endoneurial ischemia. To examine the relationship between nerve blood flow (NBF) and ICD we measured NBF in rats with experimental galactose neuropathy (EGN), a model where ICD is known to be increased. Simultaneous measurements of NBF in the center and subperineurial region were made in normal and edematous tibial nerves using hydrogen-sensitive microelectrodes and hydrogen polarography. NBF was significantly reduced in rats with EGN when compared with controls. A second finding was that in half the rats with EGN there was a greater reduction in NBF in the subperineurial region, a site of maximal ICD increase. In contrast, NBF was similar in central and peripheral regions in control rats. These findings support the hypothesis that an increase in ICD produces a reduction in NBF. Further support for the hypothesis is derived from a computer model of the effect of changes in ICD on endoneurial oxygen tension. We conclude that a chronic reduction in NBF may participate in the pathogenesis of edematous neuropathies.
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PMID:Relationship between nerve blood flow and intercapillary distance in peripheral nerve edema. 301 93

A total of 230 patients with facial neuropathies were under this study. Of these, in 29 members of 13 families the hereditary nature of the diseases transmission was clearly evident. The incidence of hereditary-familial form of the facial neuropathy was 12.6% with the rate of intrafamilial affliction being 23.3%. Two factors have been found to influence the morbidity: (1) genetic predisposition manifested by autosome-dominant type of temporal bone malformations; (2) exogenous factors leading to ischemia and compression of the facial nerve and thus promoting the phenotypic realization of genotypic predisposition.
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PMID:[Hereditary familial forms of neuropathy of the facial nerve]. 322 64

A case of visual loss due to orbital emphysema secondary to a blow-out fracture of the orbit is presented. Because vision returned to 20/20 following an optic nerve decompression procedure, we hypothesize that our patient developed a compressive optic neuropathy with ischemia due to the emphysema. Essential instructions concerning the injury that the emergency physician should give the patient suffering an orbital blow-out are also presented.
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PMID:Orbital emphysema: a potentially blinding complication following orbital fractures. 339 93

Anterior ischemic optic neuropathy (A.I.O.N.) may cause optic disc edema in type-I diabetes. A.I.O.N. affects diabetic patients of all ages. Such optic neuropathy is more likely to become bilateral in diabetics than in the non-diabetic subjects. A 41-year-old diabetic insulin-dependent woman presented A.I.O.N. in RE; 5 years later, the same affection occurred in LE. The clinical course was relatively benign in both eyes, with good functional restitution. The patient was treated by high doses of Sodium Salicylate and Sulfinpyrazone. The pathogenesis of optic disc edema in type-I diabetes is, according to Hayreh (1981), ischemia of different grade in the district of the posterior ciliary arteries: microangiopathy, rheological anomalies and atherosclerotic added lesions produce a variability of clinical pictures of increasing seriousness. Our case has an intermediate position in such a continuous spectrum. The VEP supported the diagnosia of A.I.O.N.
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PMID:Anterior ischemic optic neuropathy in type I diabetes. 345 16

Neuropathy, peripheral ischemia, and an altered host defense make the diabetic patient particularly prone to the development of infected foot ulcers. Successful treatment must be directed at these three primary pathologic situations. Since a limb-threatening infection carries a 25% risk of major amputation, early and prompt recognition and reporting of all foot problems are essential. Neuropathy requires total rest of the injured part. An altered host defense requires knowledge of the bacteria involved and proper use of antibiotics. It requires strict adherence to sound surgical principles that ensure debridement of all necrotic material and adequate dependent drainage of the wound while conserving as much viable skin and tissue for later revision or conservative amputations. Once sepsis is controlled, ischemic extremities can be revascularized. Because of the peculiar nature of the diabetic's vascular disease, revascularization procedures require the maximum skill and experience of the operating vascular surgeon. After revascularization, revisions or more conservative distal amputations can be achieved. Patient and physician education and understanding still remain essential not only to prevention but to successful management of all diabetic foot-related problems.
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PMID:The diabetic foot: amputations and drainage of infection. 355 24

Foot infections are common in the diabetic patient. They result from a interplay of neuropathy, ischemia, and metabolic alterations. The team approach in the management of diabetic foot infections can provide the most optimal and probably the most cost-effective care. The cornerstone of treatment is early recognition and prompt intervention. After diagnostic cultures are obtained, infections should be treated with appropriate antibiotics. Bony deformities should be corrected. The vascular status of the patient should be evaluated, and if necessary, treatment should be directed at improving blood flow to the affected foot.
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PMID:Team approach in the management of diabetic foot infections. 355 50

Pathological, morphometric, and teased fiber studies of sural nerve from 36 diabetic patients with (n = 32) and without (n = 4) neuropathy and from 47 healthy subjects provide evidence that in diabetic polyneuropathy: (1) fiber loss is primary; (2) demyelination and remyelination with or without onion bulb formation are secondary; (3) remaining fibers, on average, have the same ratio of small to large fibers as in healthy individuals, but with a greatly increased variability; and (4) the spatial distribution of fiber loss is both diffuse and multifocal. Criteria developed during the study of experimental models of ischemic neuropathy were employed to assess whether ischemic nerve damage had occurred in diabetic polyneuropathy. We conclude that there is increasing evidence that microvascular pathological abnormality and ischemia may be involved in the pathogenesis of human diabetic polyneuropathy. Cases with selective loss of small or large afferent fibers are probably extremes of a normal distribution and not different disorders.
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PMID:Fiber loss is primary and multifocal in sural nerves in diabetic polyneuropathy. 371 6


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