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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of neuropathy, structural changes, and ischemia in the development of foot ulcerations in diabetic patients is well established. As a result, it is now possible to determine which patients are at risk for ulceration and to place them in education programs or clinics with multidisciplinary care. In such situations, a high rate of ulcer healing and a decrease in amputation can be achieved. However, the roles of specific therapeutic interventions, particularly local wound healing agents and antibiotics, are not yet understood. Well-characterized patients need to be studied in comparative antibiotic trials for infection and in double-blind, placebo-controlled trials of wound-healing agents. Until such trials are completed, dogmatic advocacy or condemnation of a given therapy should be avoided.
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PMID:Diabetic foot ulcers: etiology, treatment, and prevention. 155 93

In recent years, our operative approach to ulceration and gangrene in the diabetic foot has changed markedly. We now investigate all such patients for ischemia, even in the presence of neuropathy and localized infection. This strategy is based on a rejection of the concept of a microvascular occlusive lesion, an improved understanding of the pattern of atherosclerotic occlusion, an emphasis on arteriographic delineation of the foot arteries, and increasing success with extreme distal arterial reconstruction, especially vein bypass grafts to the dorsalis pedis artery. From 1984 through 1990, 2883 procedures were performed at our institution on patients with diabetes mellitus. There was a statistically significant decrease in every category of amputation, which correlated precisely with the increasing rate of dorsalis pedis artery bypass. Our indications for surgery, in-hospital mortality, and the bypass-associated amputation rate did not change.
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PMID:Trends in the care of the diabetic foot. Expanded role of arterial reconstruction. 157 32

The findings in nine patients are presented who suffered from acute bilateral visual loss occurring within less than one week, and all showed optic disc edema. CT scans revealed no abnormalities and the CSF-pressure measured in 6 patients was normal. Four of the patients (22 to 53 years old) recovered completely under orally given prednisolone (about 100 mg/day). The recent history of three patients suggested that the optic neuropathy was associated with an infection. This parainfectious process may be identical to the bilateral optic neuritis described in children. Four older patients (55 to 63 years) did not respond to steroid therapy. Their vision did not significantly improve. They showed attenuated retinal arteries; therefore it can be assumed that ischemia plays a role in the pathogenesis of this second type of optic neuropathy. In none of the cases a toxic optic neuropathy could be confirmed. One patient who experienced a visual loss down to finger counting after throat-surgery without marked blood loss recovered partially after steroid treatment.
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PMID:[Bilateral optic neuropathy with papilledema]. 158 43

Neuropathy, mechanical stress, and macrovascular disease are involved in the pathogenesis of diabetic foot ulceration. Implicit in the development of gangrene and ulceration is the recognition that these factors interact with the microcirculation, resulting in the failure of skin capillary flow to meet nutritive requirements. There is little evidence to associate structural microangiopathy with foot microcirculatory failure. Significant functional abnormalities of the microcirculation have been defined. In accord with the haemodynamic hypothesis early hyperaemia and capillary hypertension promote more sinister late functional abnormalities with increasing duration of diabetes. These late functional abnormalities include loss of autoregulation and reduced hyperaemic responses which interact with loss of neurogenic flow regulation, disturbed endothelial function, and abnormal rheology to produce the familiar clinical picture of the diabetic foot. Ischaemia secondary to multi-segment arterial disease induces additional abnormalities of microcirculatory function which are superimposed on the pre-existing diabetic microvascular structural and functional microangiopathy.
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PMID:Aetiology of diabetic foot ulceration: a role for the microcirculation? 160 Jul 1

The toxic oil syndrome is a multisystemic disease caused by the ingestion of adulterated rapeseed oil. The basic lesion is a peculiar vasculitis that affects mainly the intima, showing the features of an endovasculitis. Vessels of every type and size are involved, affecting practically every organ. The vascular lesions begins with endothelial damage that varies from cellular swelling to cellular necrosis. It then progresses by mixed cellular inflammatory infiltration of the intima and, in some cases, of the media and adventitia. In some cases the infiltrate is rich in eosinophils and a few show foamy histiocytes. Proliferation of myointimal cells and in advanced stages fibroblastic proliferation causes narrowing or obliteration of the vascular lumen. Thromboembolic complications perpetuate the vascular lesion and compound the ischemia and parenchymal atrophy of several organs. The peripheral nerve lesions begin with an inflammatory neuropathy with lymphocytic perineuritis and progress to perineural fibrosis with secondary axonal degeneration. Skeletal muscle lesions exhibit an interstitial inflammatory myopathy at first, followed by a neurogenic muscular atrophy. A direct effect of unidentified toxic substances, possibly free radicals, may cause the endothelial lesion. Other factors, such as immunopathologic mechanisms of delayed hypersensitivity, may contribute to the progression of the vascular lesions.
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PMID:Extracardiac vascular and neural lesions in the toxic oil syndrome. 165 52

Direct and indirect evidence suggests that Na+/K(+)-ATPase activity is reduced or insufficient to maintain ionic balances during and immediately after episodes of ischemia, hypoglycemia, epilepsy, and after administration of excitotoxins (glutamate agonists). Recent results show that inhibition of this enzyme results in neuronal death, and thus a hypothesis is proposed that a reduction and/or inhibition of this enzyme contributes to producing the central neuropathy found in the above disorders, and identifies potential mechanisms involved. While the extent of inhibition of Na+/K(+)-ATPase during ischemia, hypoglycemia and epilepsy may be insufficient to cause neuronal death by itself, unless the inhibition is severe and prolonged, there are a number of interactions which can lead to a potentiation of the neurotoxic actions of glutamate, a prime candidate for causing part of the damage following trauma. Presynaptically, inhibition of the Na+/K(+)-ATPase destroys the sodium gradient which drives the uptake of acidic amino acids and a number of other neurotransmitters. This results in both a block of reuptake and a stimulation of the release not only of glutamate but also of other neurotransmitters which modulate the neurotoxicity of glutamate. An exocytotic release of glutamate can also occur as inhibition of the enzyme causes depolarization of the membrane, but exocytosis is only possible when ATP levels are sufficiently high. Postsynaptically, the depolarization could alleviate the magnesium block of NMDA receptors, a major mechanism for glutamate-induced neurotoxicity, while massive depolarization results in seizure activity. With less severe inhibition, the retention of sodium results in osmotic swelling and possible cellular lysis. A build-up of intracellular calcium also occurs via voltage-gated calcium channels following depolarization and as a consequence of a failure of the sodium-calcium exchange system, maintained by the sodium gradient.
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PMID:Inhibition of sodium-potassium-ATPase: a potentially ubiquitous mechanism contributing to central nervous system neuropathology. 166 97

The present paper has been written in order to determine the morphological alterations in the sural nerve from patients with chronic arteriosclerotic occlusive disease. Eight patients with Peripheral Vascular Disease (PVD) and six age-matched control subjects were studied. Morphometric data revealed two groups of patients, one of them with mild disease (n = 5), and the other one with severe damage (n = 3), consisting in loss of myelinated fibres and increase in the number of small fibres (p less than 0.05). Teased nerve fibres and electron microscopic studies also showed two types of patients, with respect to the myelin or the axonal alterations. The unmyelinated fibre population was affected equally in both groups. In conclusion, this study supports the idea that ischemia is able to cause structural alterations in the peripheral nerve, and that it can play a role in the development of neuropathy.
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PMID:Morphological abnormalities in the sural nerve from patients with peripheral vascular disease. 166 55

The effect of lower-limb ischemia on the severity of neuropathy was examined in 48 diabetic patients with peripheral vascular disease. The severity of the vascular disease, as determined by medical history, physical findings, and laboratory data, was scored for each leg. Neuropathy was rated clinically and based on the results of nerve conduction studies of the common peroneal, posterior tibial, and sural nerves. A significant correlation was found between the vascular scores and neurologic variables of the two legs, most strikingly so in electrophysiologic data, with coefficients of .6 to .7. Nondiabetic control patients showed no evidence of neuropathy, regardless of the severity of ischemia, whereas diabetic controls without limb ischemia showed symmetrical neuropathy. These findings support the hypoxic theory in the pathogenesis of diabetic neuropathy.
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PMID:Vascular insufficiency quantitatively aggravates diabetic neuropathy. 184 25

In order to learn more about the vulnerability of nerve fibres to ischemia, a quantitative study of nerve fibre abnormalities was performed on biopsy specimens of the superficial branch of the peroneal nerve from 26 patients with vasculitic neuropathy: 20 had necrotizing arteritis, 5 a lymphocytic, and 1 a leucocytoclastic vasculitis on nerve and/or muscle biopsy. The density of myelinated fibres ranged from 25 to 7880 per mm2 (n = 8470 +/- 706 (SD]. There was a marked inequality in the density of nerve fibres between the fascicles of individual nerves with a mean coefficient of variation of 41 +/- 37 (SD) % versus 7.4 +/- 3.0% in controls. Loss of myelinated fibres, which was greater for fibres larger than 7 microns in diameter, was more severe than that for unmyelinated axons. Regeneration, which was assessed by the number of clustered axons, decreased when the density of myelinated fibres decreased, suggesting that severe nerve ischaemia precludes axonal regeneration. Wallerian degeneration affected on average 58% (range 5-100%) and segmental demyelination, mainly of the secondary type, on average 1.94% (range 1-10%) of teased fibres. It was concluded that (1) myelinated fibres are more vulnerable to ischaemia than unmyelinated axons; (2) large myelinated fibres are affected before the smaller ones; (3) segmental demyelination is uncommon in this context; (4) severe nerve ischaemia precludes axonal regeneration.
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PMID:Vulnerability of nerve fibres to ischaemia. A quantitative light and electron microscope study. 188 86

Primary amyloidosis and myeloma associated amyloidosis causes neuropathy in 10% of the cases, and hemodialysis associated amyloidosis causes carpal tunnel syndrome. However, most severe amyloid neuropathy is observed in familial amyloidotic polyneuropathy (FAP). FAP type I is an autosomal dominant systemic amyloidosis characterized by sensory dominant systemic amyloidosis characterized by dissociated sensory disturbance and autonomic dysfunction. Amyloid deposition is noted universally in endoneurium of peripheral nerve, especially prominent in sural, sciatic nerve, dorsal root ganglia and sympathetic ganglia. Moderate deposition was also noted in dorsal spinal root. Amyloid was absent in CNS. The number of small myelinated fibers is decreased. Unmyelinated axons are severely depleted and amyloid fibrils are observed around the wall of small vessels. Amyloid fibril protein consists of variant transthyretin (TTR:prealbumin) with one amino acid substitution of methionine-for-valine at position 30. Other types of FAP show another one point mutation in TTR molecule. Transgenic mouse model of FAP was produced by microinjecting cloned human variant TTR gene into mice. Amyloid were demonstrated in thyroid, kidney and intestine and so on, but not in peripheral nerve in these mice. Pathogenesis of neuropathy of FAP is not known, but mechanical compression to the nerve, ischemia and metabolic abnormality may play some role combined to cause of nerve fiber damage. The effect of deposition on physiochemical functions of the neuron and mechanism to accumulate in nervous system of the TTR remain to be elucidated.
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PMID:[Amyloid neuropathy]. 196 18


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