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

Resistance to ischemic conduction block (RICB) was studied in rats with streptozotocin (STZ) induced hyperglycemia, hyperglycemia by glucose injection, and glycerin-induced hyperosmolarity. Ischemia was produced by tight ligation at the base of the tail. The time required for nerve action potentials (NAP) to disappear was defined as the disappearance time of NAP (DT-NAP). Both STZ and glucose rats showed a marked prolongation of DT-NAP at 2 hours after injection of STZ (up to 120 minutes) or glucose (up to 95 minutes), as compared with the control rats (less than 45 minutes). Hyperosmolar rats showed no prolongation of DT-NAP. The amplitude of NAP remained at the initial level for at least 2 hours after ligation of the sciatic nerve, whereas NAP disappeared within 45 minutes after ligation of the abdominal aorta. These findings indicate that the RICB can be produced by means of hyperglycemia without the presence of diabetic neuropathy and is the most sensitive indicator of hyperglycemia.
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PMID:Resistance to ischemic conduction block of the peripheral nerve in hyperglycemic rats: an electrophysiological study. 338 66

The recent recognition of the prevalence of asymptomatic ST-segment depression in patients with coronary artery disease demonstrates the poor sensitivity of using angina as a sign of myocardial ischemia. Possibly the greatest application of ambulatory ST-segment monitoring for the detection of asymptomatic ischemia is in diabetic patients. Coronary artery disease represents the ultimate cause of death in more than half of such patients and usually manifests itself prematurely at an advanced stage. The long-held clinical belief that infarction may be silent, or less painful, in patients with diabetes is supported by several retrospective studies (32 to 42 percent of diabetic patients lack angina at infarction, compared with only 6 to 15 percent of nondiabetic patients). Explanations for this observation have been remarkably deficient in the literature. One group has shown that in diabetic patients with painless infarction, the autonomic nerve fibers of the heart display typical lesions of autonomic neuropathy that may affect afferent sensory impulse transmission compared with those in several matched control groups. Except for a recent report from Italy, there are no data on the prevalence of asymptomatic ischemia in diabetic patients. There are obvious reasons to address this issue more comprehensively: first, given the high incidence of painless myocardial infarction, the frequency of asymptomatic ischemia may be very high; second, because the ability to evaluate patients with standard treadmill testing is limited in patients with peripheral vascular disease and diabetic neuropathy, ambulatory monitoring may be used on a more widespread basis; and third, given the higher than average incidences of sudden death and left ventricular dysfunction in diabetic patients compared with nondiabetic patients, ambulatory monitoring may represent a method of assessing the role of episodic ischemia in explaining these other cardiac events.
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PMID:Asymptomatic myocardial ischemia in diabetic patients. 370 56

In Japan, diabetic patients are known to be able to sit on the floor for a prolonged time because of mildness or absence of ischemic paresthesia. In order to investigate this resistance to ischemia quantitatively, the mixed nerve function of the median nerve was studied during 30 min of ischemia using surface electrodes in 60 diabetic patients and 15 normal subjects. In studies of 33 unequivocal diabetics, potential amplitudes decreased during ischemia more slowly than in the controls, and at 15 min of ischemia, potential amplitudes were greater in all 33 diabetics than in the 15 normal subjects. The relationship between the resistance to ischemia and various aspects of diabetes was studied further in the 60 diabetics including the 33 aforementioned patients. Resistance to ischemia was found in almost all diabetics and no significant correlation was shown with values for fasting blood glucose and HbA1c, other diabetic complications or duration of diabetes. However, values for potential amplitudes declined to the normal range in seven of 18 patients after strict glucose control. These results suggest that resistance to ischemia is the earliest manifestation of peripheral nerve dysfunction and is different from classical diabetic neuropathy. Furthermore, the method employed in this study is simple, noninvasive and clinically very useful.
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PMID:Effect of ischemia on peripheral nerve function in diabetes mellitus. 378 Mar 80

This is a review article on diabetic neuropathy. The different patterns of diabetic neuropathies, including focal and multifocal, distal symmetrical and autonomic neuropathy are exposed. Length dependent degeneration of fibers is suggested by the pattern of sensory loss and by morphological findings. The various hypotheses on the mechanisms of the neuropathy, including the possible role played by ischemia and by the accumulation of sorbitol in Schwann's cells, are reviewed. The therapeutic implications of the clinical, pathological and biochemical abnormalities are discussed.
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PMID:[Metabolic neuropathies. I. Diabetic neuropathies]. 391 41

We examined the effect of ischemia on nerve conduction in experimental diabetic neuropathy (EDN) and related electrophysiological changes to nerve adenosine triphosphate (ATP), creatine phosphate (CP), and lactate under anoxic conditions. Rats rendered diabetic with streptozotocin had a resistance to ischemic conduction block (RICB). Caudal nerve action potential (NAP) was well maintained for 10 min in controls and for 15 min in EDN, after which time NAP declined in both groups but more rapidly in normal rats. Time to 50% reduction in nerve ATP and CP was 10 and 3 min, respectively, in controls and delayed to 20 and 8 min in EDN. Rate of utilization of high-energy phosphate (approximately P) was linear for 5 min in controls to be followed by a progressive decline. In EDN rate of utilization of approximately P was linear to 15 min to be followed by a more gradual decline than in normal nerves. These findings suggest that the maintenance of nerve transmission in anoxic-ischemic states depends on anaerobic metabolism and that RICB in EDN is due in part to the ability of diabetic nerves to maintain a higher level of anaerobic glycolysis and for a longer time than normal nerves.
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PMID:Ischemic conduction failure and energy metabolism in experimental diabetic neuropathy. 398 44

Morphological change of endoneurial and perineurial vessels accompanied severe loss of myelinated axons in peripheral nerves of each of 17 patients with diabetic neuropathy. Vascular mural thickening averaged 18.9 +/- 9.9 micron2 in diabetic capillaries (n = 11) vs. 6.9 +/- 4.1 micron2 in controls (n = 7). Electron microscopy revealed vigorous endothelial proliferation as well as thickening and reduplication of basal lamina in each instance. Particular attention was paid to vessels which penetrate the perineurium en route to the endoneurial interstitium, since they provide a major portion of the endoneurial blood supply. Luminal narrowing and mural thickening of these vessels was compounded by basal laminar thickening of the perineurium. Fenestrated endoneurial capillary endothelium was noted in one case. Both demyelination and axonal degeneration were observed with intra-axonal glycogen accumulation in some axons. Morphometric analysis revealed extensive myelinated nerve fiber loss in diabetic nerves. These morphological findings emphasize the impact of diabetic microangiopathy on specialized endothelium and suggest that local anatomic factors in the perineurial sheath render the nerve vulnerable to chronic ischemia.
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PMID:Microangiopathy in human diabetic neuropathy. 409 Sep 41

Estimates of the number, density, and size distribution of myelinated fibers at selected levels of roots, spinal tracts, and sampled levels of peripheral nerves may be used in the detection and characterization of alterations of motor, sensory, and autonomic neurons and their axons with development, aging and disease. Use of imaging techniques, now available, increases the reliability, versatility, and speed of such analysis. In this study, the authors evaluated the spatial pattern of fibers in sampled frames and contour areas of transverse sections of nerve fascicles, utilizing, the coefficient of variation and index of dispersion (ID), the latter extensively employed by plant ecologists. The ID was used for recognization of increased, normal, or decreased variability of density within fascicles, between fascicles, and between nerves in health and in various experimental neuropathies. In addition, various morphometric measurements were made in transverse sections at defined levels along the hind limb nerves of rats in acute and chronic ischemia, after rhizotomy and in galactose neuropathy. These stereomorphometric studies, emphasizing the number, size, shape, and spatial pattern of fibers, revealed differences among experimental neuropathies and may be found to be helpful in the characterization and prediction of pathologic mechanisms in neuropathies of unknown cause. Specifically, these approaches could be used for study of whether fiber loss in human diabetic neuropathy is multifocal and determination of the levels of such losses.
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PMID:Spatial pattern of nerve fiber abnormality indicative of pathologic mechanism. 633 25

Cronassial, a combination of four different cerebral gangliosides, was evaluated in a six month double blind controlled study involving 25 patients with symptomatic diabetic neuropathy (12 receiving Cronassial, 13 receiving placebo). Clinically there was mild but definite improvement in the Cronassial patients. Small increases in sensory conduction velocities in Cronassial patients were also seen; their significance require further clarification. Measurements of neuronal responses du ischemia suggest that Cronassial may enhance anaerobic metabolism.
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PMID:Ganglioside (Cronassial) therapy in diabetic neuropathy. 637 52

Motor nerve conduction velocities (MNCVs) of ventral peripheral tail nerves of unanaesthetized streptozotocin diabetic rats were examined in comparison to age matched normal rats under normal and ischemic conditions. A miniature blood pressure cuff was applied to the base of the tail and was adjusted to provide complete vascular occlusion for 30 min. MNCVs were recorded during ischemia and in the post-ischemic period. MNCVs were markedly reduced during ischemia in normal rats but were unchanged in diabetic rats. Conversely, the sensation of heat induced pain was retained to an equal extent in normal and diabetic rats during ischemia states. The abnormal resistance to ischemia of MNCV of peripheral nerves is an early and sensitive index of nerve dysfunction and precedes slowing of MNCV in diabetic rats. The results suggest that initial peripheral nerve abnormalities in diabetic rats may be related to biochemical changes rather than axonopathy and may have heuristic significant for clinical diabetic neuropathy.
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PMID:Motor and sensory conduction in peripheral nerves of unanaesthetized streptozotocin diabetic and normal rats during ischemia. 710 55


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