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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated levels of aluminum in brain tissue have been found in demented patients with Alzheimer's disease, with ALS-PD complex of Guam and with dialysis encephalopathy. A possible etiological relationship between enhanced aluminum exposure and impaired mental function was suggested both for ALS-PD of Guam (a region where high contents of aluminum in water are found) and for dialysis encephalopathy which appears in dialyzed patients exposed to high doses of aluminum in medications and in dialysate fluid. The role of aluminum in Alzheimer's disease is not known as is the question of life-long aluminum accumulation in healthy human beings. In this review we have limited ourselves to the issue of oral aluminum ingestion and the possible neurotoxic consequences of such exposure. The following topics are summarized: 1. Physiological mechanisms involved in ingestion and intestinal absorption of aluminum and the influences of pH and available organic complexing agents on these processes. 2. Effects of an aluminum-enriched diet on behavior and on brain metabolism. 3. Dietary sources of aluminum and elevated loads of this substance due to prolonged intake of aluminum-containing medications. The main conclusion of this summary is that aluminum is absorbed and may accumulate in different organs in both adults and infants. Two groups seem to be at particular risk for aluminum related toxicity: people with chronic renal failure treated with aluminum-containing medications and pre-term infants fed on aluminum containing formulate. It seems probable that at least upon short term exposure the healthy human body can defend itself adequately from aluminum's toxic effects. However, not enough information is available on possible effects of life-long exposure to aluminum in the environment, diet and medications, which over decades may lead to accumulation of this substance with expressions of toxicity. Therefore, the question of aluminum's relevance to dementive diseases cannot yet be adequately answered.
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PMID:Aluminum ingestion--is it related to dementia? 184 54

Aluminum contaminates several chemical compounds that are administered intravenously to patients. The most highly contaminated are calcium and phosphate salts, followed by albumin and heparin. Parenteral administration of aluminum bypasses the gastrointestinal tract, which serves as a protective barrier to aluminum entry into the blood. In the past, parenteral administration of aluminum as a contaminant of water used in hemodialysis and of casein hydrolysate, the former source of protein in parenteral nutrition solutions, was associated with a low-turnover osteomalacic bone disease and, in the case of uremic patients, encephalopathy. Groups currently at risk for aluminum accumulation in tissue resulting from parenteral administration include premature infants receiving long-term parenteral nutrition and patients receiving plasmapheresis therapy with albumin. Both groups may develop metabolic bone disease; the pathogenesis may involve aluminum. The Food and Drug Administration is currently considering regulation of aluminum in fluids used for parenteral nutrition. No changes are presently proposed with regard to albumin.
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PMID:The aluminum content of parenteral solutions: current status. 190 89

Brain edema and intracranial hypertension are a major cause of death in fulminant hepatic failure. We have shown that brain water measured in rats after hepatic devascularization (portacaval anastomosis followed in 24 to 48 hr by ligation of the hepatic artery) increases with the progression of encephalopathy. In this study, we examined whether intracranial hypertension develops in this model of fulminant hepatic failure. Using a fiberoptic pressure transducer, intracranial pressure rose from 3.3 +/- 1.1 mm Hg to 23.7 +/- 2.7 mm Hg (mean +/- S.E.M.) by the time the corneal reflex was lost; intracranial pressure was unchanged in control rats. Immediately after ligation of the hepatic artery, intracranial pressure was normal and remained stable until the last hours of the experiment, when it progressively rose, suggesting a loss of intracranial compliance. In addition, sudden and short episodes of marked increases in intracranial pressure (greater than 50 mm Hg) not related to seizure activity markedly decreased cerebral perfusion pressure. Internal carotid artery blood flow, an indirect measure of cerebral perfusion, decreased 29% +/- 12% by the end of the experiment. The time elapsed from ligation of the hepatic artery until loss of the corneal reflex (range 340 to 940 min) was related to the change in cerebral perfusion pressure, suggesting that an increase in systemic arterial pressure at the time of the initial rise in intracranial pressure may result in an increased length of survival. In this animal model, widely used to study the pathogenesis of hepatic encephalopathy, intracranial hypertension invariably appears in the terminal phase of the course. The development of intracranial pressure waves may be an indication that brain herniation is imminent.
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PMID:Intracranial pressure waves and intracranial hypertension in rats with ischemic fulminant hepatic failure. 191 75

The influenza B virus mouse model of Reye's syndrome was studied to learn more about the encephalopathy in Reye's syndrome. One to 3 days after intravenous influenza B/Lee virus, Balb/c mice became lethargic, seized and lapsed into a fatal coma. Wide-spread cerebral edema without inflammation developed 1-3 days after virus inoculation. Swollen astrocytic foot processes containing increased glial fibrillary acidic protein were located around capillaries. Viral particles were not seen by electron microscopy and complete viral replication did not occur. Immunohistochemical studies demonstrated influenza B viral antigen within many endothelial cells but not within other brain cells. Qualitative (Evans blue dye) and quantitative (percent brain water and technetium -99 pertechnetate) studies of the blood-brain barrier demonstrated abnormalities. This model reproduced many clinical, virologic and pathologic features of the Reye's syndrome encephalopathy. In addition, a non-permissive viral infection of brain endothelial cells occurred which may be important in the pathogenesis of the mouse encephalopathy and may participate in the encephalopathy of Reye's syndrome.
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PMID:The influenza B virus mouse model of Reye's syndrome: clinical, virologic and morphologic studies of the encephalopathy. 216 26

Hyponatraemia occurs in nearly half of patients in hospital with cirrhosis and ascites, and is due to the excessive retention of free water which results from the kidney's inability to excrete it normally. The morbidity and mortality associated with hyponatraemia is largely attributable to central nervous system disturbances. The degree to which brain water content increases depends on the duration of hyponatraemia and on compensatory mechanisms. Altered steroid and peptide hormones in cirrhotic patients may contribute to the development of hyponatraemic encephalopathy, symptoms of which overlap with hepatic encephalopathy and uraemia. The occurrence of central pontine myelinolysis is unrelated to the rate of correction of hyponatraemia. The appearance of hyponatraemia in cirrhotic patients, long regarded as a poor prognostic sign, may be a function of unrecognized underlying impaired renal function. Therapy for hyponatraemia remains suboptimal.
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PMID:Hyponatraemia in patients with cirrhosis. 221 72

We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.
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PMID:MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy. 223 93

When the aluminium content of the water supply to our Haemodialysis Unit rose from less than 0.5 mumol/l to 6 mumol/l over a two month period, we carried out bone biopsies and desferrioxamine infusion tests on twelve (12) patients who had been on haemodialysis for less than one year (mean 8 months) and had normal serum aluminium levels. The patients had no bone symptoms. Eight patients had positive aluminium bone stains. The aluminium osteomalacia group (n = 8) had a mean PTH of 1.4 ng/ml s.e. 0.3 whereas the non-ALO group had a mean PTH of 2.9 ng/ml s.e. 0.7. The difference in mean PTH is significant (p less than 0.05). There was no evidence of encephalopathy, fractures or microcytic anaemia in the ALO positive group. The aluminium contamination of the water supply occurred because of a change in the reservoir purification system from sand-filtration to alum.
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PMID:Acute epidemic aluminium osteomalacia secondary to water supply contamination. 236 22

Closed-circuit dialysis using the Redy sorbent cartridge to regenerate the dialysate has been incriminated in previous reports as a cause of severe fracturing osteomalacia and fatal encephalopathy in several patients treated with this procedure for 15-36 months. In a retrospective study, we compared 15 unselected patients who had received Redy dialysis for 66 +/- 14 months with 15 control patients dialysed with single passage of dialysate. Redy and control patients were matched for age, sex, and duration of dialysis. They belonged to two dialysis centres, situated in the same geographical area and having a common water supply. Mean serum and bone aluminium concentrations were slightly greater in the Redy group but the differences were not significant. Pathological fractures had occurred in two Redy patients and in one control, but could not be attributed to aluminium-induced bone disease. Although the histochemical staining for aluminium in bone was positive in six patients, diagnosis of aluminium-induced bone disease was made in one case only. The results of bone histomorphometry did not differ significantly between the two groups. Our findings may be explained by the strict application of the measures required to avoid aluminium contamination of the Redy dialysate, i.e. sufficient rinsing before dialysis, use of almost aluminium-free water, and of acetate-buffered dialysate.
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PMID:Risk of aluminium intoxication in long-term acetate Redy dialysis. 250 78

Brain water content was measured by gas-chromatography in rats following intraperitoneal injection of drugs and fatty acids related to the etiology of Reye syndrome. A statistically significant increase in brain water content was observed following injection of 5% glucose solution, valproic acid, acetyl salicylic acid, calcium hopantenate, margosa oil, 4-pentenoic acid, linolenate and arachidonate. Seizures occurred in all animals given valproic acid, margosa oil and 4-pentenoic acid, and in 25% of those given 5% glucose solution + anti-diuretic hormone. The results of these studies may help in the selection of appropriate agents for experimental induction of acute encephalopathy and brain edema in animal models of Reye syndrome.
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PMID:Effects of drugs and fatty acids related to Reye syndrome on brain water content in rats. 251 90

In view of the increasing pollution of our environment and forest decline, growing interest has been focused on aluminum toxicity. Aluminum is one of the most abundant metals and commonly present in tap water, beverages, food, cosmetics, and pharmaceutical preparations. Thus everybody is exposed to aluminum to a greater or lesser extent. It is now beyond any doubt that aluminum intoxication may cause encephalopathy, fracturing vitamin D resistant osteomalacia, and microcytic anemia in patients with chronic renal insufficiency as well as in experimental animals. The risk of aluminum intoxication has also to be considered in several other groups. These include elderly individuals with physiologically impaired excretory renal function who are treated with aluminum-containing antacids, patients with chronic liver disease, infants who are fed highly aluminum-contaminated formula at a time when their excretory renal function has not jet fully developed, patients on total parenteral nutrition, and, possibly, patients with Alzheimer's disease.
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PMID:[Aluminum toxicity]. 251 13


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