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

Of the 202 patients undergoing home dialysis in the Trent region, 11 developed dialysis encephalopathy, 21 suffered spontaneous fractures, and 36 who had undergone dialysis for over four years had neither of these complications. Because the incidence of complications seemed to be unevenly distributed the water supplies were analysed. Water supplied to the homes of the patients with fractures or encephalopathy contained significantly less calcium and fluorine and significantly more aluminium and manganese than that piped to patients without these complications. The high aluminium concentrations in the bone of patients with encephalopathy was confirmed, but aluminium concentrations in the brains from three patients with encephalopathy were not increased. Patients who undergo dialysis in areas where water contains high aluminium concentrations should be supplied with deionisers.
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PMID:Composition of the domestic water supply and the incidence of fractures and encephalopathy in patients on home dialysis. 90 42

Several neurochemical parameters were studied in brain regions of rats chronically treated with a high concentration of manganese chloride (20 mg MnCl2.4H2O per ml. of drinking water) throughout development until adulthood. Large increases in Mn accumulation were found in all brain regions (hypothalamus, +530%; striatum, +479%; other regions, +152 to +250%) of Mn-treated adult rats. In these animals, Ca levels were decreased (-20 to -46%) in cerebellum, hypothalamus, and cerebral cortex but were increased (+186%) in midbrain. Mg levels were decreased (-12 to -32%) in pons and medulla, midbrain, and cerebellum. Fe levels were increased (+95%) in striatum but were decreased (-28%) in cerebral cortex. Cu levels were increased (+43 to +100%) in pons and medulla and striatum but Zn levels were decreased (-30%) in pons and medulla. Na levels were increased (+22%) in striatum but those of K and Cl remained unchanged. Type A monoamine oxidase activities were decreased (-13 to -16%) in midbrain, striatum, and cerebral cortex, but type B monoamine oxidase activities decreased (-13%) only in hypothalamus. Acetylcholinesterase activities were increased (+20 to +22%) in striatum and cerebellum. The results are consistent with our hypothesis that chronic manganese encephalopathy not only affects brain metabolism of Mn but also that of other metals.
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PMID:Neurochemical changes in rats chronically treated with a high concentration of manganese chloride. 140 72

We report an unusual case of an acute encephalopathy following injection of iohexol for myelographic study, which was reversible after a treatment with water restriction and glucocorticoids. The pathophysiologic mechanism appears to be related with hyponatremia. We conclude that drinking of large amounts of fluids must be not recommendable in order to avoid the developing of encephalopathy.
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PMID:Acute encephalopathy following lumbar myelography with iohexol. 141 56

To determine whether cytotoxic brain edema is associated with a decrease in diffusion, it was induced in rats, in the absence of ischemia, with an established model of acute hyponatremic encephalopathy. Cytotoxic brain edema secondary to acute hyponatremia was induced with intraperitoneal injections of 2.5% dextrose in water and subcutaneous injection of arginine-vasopressin. Coronal spin-echo magnetic resonance (MR) images were obtained with and without strong diffusion-sensitizing gradients before and after induction of acute hyponatremia. The apparent diffusion coefficient (ADC) was measured at two coronal section locations. In hyponatremic rats, the brain ADC was significantly reduced (P = .0153 and .0001) and was positively correlated with increased total brain water content (P = .0011). Plots of ADC versus total brain water showed a statistically significant inverse linear relationship between ADC and increasing brain water at the anterior coronal section location. The results indicate that the ADC may be a sensitive indicator of cytotoxic brain edema and thus may enable quantitative evaluation of such edema with diffusion-weighted MR imaging.
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PMID:Cytotoxic brain edema: assessment with diffusion-weighted MR imaging. 143 45

beta-Oxidation of [1-14C]palmitic acid was examined in homogenates of astrocytes cultured from neonatal mouse brain. Under optimal reaction conditions (< or = 50 micrograms protein, 10 min at 37 degrees C), oxidation increased as a function of palmitate concentration (15 microM to 2 mM) and reached a maximum rate of 1.98 +/- 0.29 nmol/min/mg protein (mean +/- SEM) at 0.2 mM substrate. Eadie-Hofstee analysis of data from four experiments yielded apparent values for Vmax of 1.87 nmol/min/mg protein, and for Km, 35-40 microM. There were no dramatic changes in the oxidation rate in cells between 10 and 36 days in culture. During the 10-min assays, less than 0.05% of the radioactivity was converted to 14CO2 by the astrocytes; water-soluble products accounted for 1-2% of the total substrate added. Studies with KCN indicated that 60-70% of the total activity occurred in the mitochondria. We have been studying the structural and functional changes associated with the cerebral encephalopathy of Reye's syndrome (RS). Three-week-old astrocytes exposed to serum from RS children for the final 7 days of culture exhibited minor mitochondrial pleomorphism and had increased numbers of other intracellular organelles. Examination of the effects of agents implicated in RS indicated that oxidation of [1-14C]palmitate was not altered by Na+ salicylate (1-3 mM), but was inhibited by the industrial surfactant, Toximul MP-8 (> or = 10 micrograms/ml), 4-pentenoic acid (> or = 0.1 microM), or with 4 days' exposure to ammonia (10 nM). The latter treatment also resulted in an increase in protein synthesis, cell volume, and malondialdehyde formation. These results suggest that some of the "toxins" implicated in RS inhibit fatty-acid oxidation in the astrocytes and produce other lipid-related abnormalities that could be related to encephalopathy.
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PMID:Beta-oxidation of [1-14C]palmitic acid by mouse astrocytes in primary culture: effects of agents implicated in the encephalopathy of Reye's syndrome. 146 46

A retrospective study of transjugular intrahepatic shunts performed between June 1990 and June 1991 is reported. Twelve patients were actively bleeding at the time of the procedure; 12 other patients had had one to five bleeding episodes within the previous 2 weeks, and one patient had massive ascites from Budd-Chiari syndrome. Most patients had severe liver disease: 21 Child's class C, three Child's class B, and one Child's class A. Transjugular intrahepatic shunting was technically successful in all cases. Portal vein pressures were reduced on average from 36 +/- 7 cm H2O to 22 +/- 6 cm H2O. Variceal bleeding ceased after transjugular intrahepatic shunting in all patients who were actively bleeding. Five patients died (30-day mortality, 20%), and eight patients subsequently underwent elective liver transplantation. The transjugular intrahepatic shunts in the 12 other patients have remained patent an average of 5.5 months. Shunt occlusion occurred in three patients at 21, 24, and 102 days, respectively. All three occlusions were successfully reopened with percutaneous techniques, yielding a primary shunt patency of 88% and secondary shunt patency of 100%. Complications included new onset encephalopathy in one patient, which cleared with medical therapy and transient renal failure in one patient. These preliminary data suggest that transjugular intrahepatic shunting is a safe and effective therapy for the short-term treatment of patients with variceal hemorrhage, particularly in patients with severe liver disease awaiting transplantation. The long-term benefit of transjugular intrahepatic shunting awaits further follow-up.
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PMID:Transjugular intrahepatic portosystemic shunts: preliminary results in 25 patients. 149 51

The pathogenesis of brain edema in acute liver failure is poorly understood. We have previously shown that rats with ischemic acute liver failure (portacaval anastomosis followed by hepatic artery ligation) exhibit brain edema and intracranial hypertension, with swelling of cortical astrocytes as the most prominent neuropathological abnormality. Because ammonia has been shown to induce swelling of astrocytes in vivo and in vitro, we examined the relationship between brain ammonia, amino acids generated from ammonia metabolism and brain water content in this model. Four groups of animals were studied: rats subjected to two sham operations, rats subjected to portacaval anastomosis and a sham operation, rats subjected to a sham operation and hepatic artery ligation and rats subjected to portacaval anastomosis and hepatic artery ligation. The last group of animals was studied at three progressive stages of encephalopathy. Cortical gray matter water increased from 80.26% +/- 0.22% (sham + sham) to 82.46% +/- 0.06% (last stage of devascularization). In cerebral cortex, brain ammonia increased to a maximum of 5.4 mmol/L. Glutamine, generated in glial cells from ammonia and glutamate, increased sixfold to 24 mmol/L and remained at this level throughout all stages of encephalopathy. Alanine, which may be generated from the transamination of glutamine, increased in parallel to the increase in water (r = 0.80, n = 15). In this model of fulminant liver failure and associated brain edema, brain ammonia increases to levels associated with in vitro swelling of brain slices and glial cells. The accumulation of osmogenic aminoacids such as glutamine and alanine may contribute to the selective astrocyte swelling seen in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ammonia and related amino acids in the pathogenesis of brain edema in acute ischemic liver failure in rats. 154 26

Magnetic resonance spectroscopy (MRS) is a flexible tool with real clinical utility. Examples from our experience in over 250 cases of clinical proton MRS are presented. Shorter echo time and reproducible water suppression increases the number of metabolites which can be detected and identified. Case reports illustrate the significance of altered ratios of N-acetylaspartate, choline, total creatine, myo-inositol, glutamate, glutamine, lactate, glucose, ketones, and, as an incidental finding, ethanol. Significant new information has resulted by applying proton MRS in chronic hepatic encephalopathy, diabetes mellitus and severe hypoxic encephalopathy ('near-drowning'). Potentially useful measurements have been made in normal brain maturation, ethanol related diseases, dementia (normal-pressure hydrocephalus), urea cycle defect and neuronal disease presenting as seizures. Metabolite imaging, particularly with proton, is clinically valuable, documenting the heterogeneity of biochemical disorders in seemingly focal lesions. A new method of specific 31-phosphorus--phosphocreatine imaging provides information in partially denervated skeletal muscle and is expected to have applications in brain.
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PMID:Clinical tools for the 90s: magnetic resonance spectroscopy and metabolite imaging. 156 13

Hyponatremia is the most commonly observed electrolyte abnormality in hospitalized children. The most serious consequences of hyponatremia and its treatment involve the central nervous system (CNS). Important factors determining the development of clinical symptomatology include: the rate of fall in serum sodium, and the severity and duration of hyponatremia. Acute hyponatremia is associated with increased brain water resulting in varying grades of encephalopathy whereas the osmoregulatory mechanism allows normalization of CNS water content in chronic hyponatremia. It is recommended that the therapy for hyponatremia be initiated on the basis of the presence or absence of symptoms. An increase of 4-6 mmol/l in serum sodium over 10-15 min is recommended in symptomatic patients. Rapid correction of chronic hyponatremia may result in osmotic dehydration syndrome and therefore should be avoided.
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PMID:Hyponatremia: pathophysiology and treatment, a pediatric perspective. 161 42

Levels of cholecystokinin (CCK) immunoreactivity and distribution of CCK immunoreactive cells were studied in the cerebral cortex of LEC (Long Evans Cinnamon) rats with hepatic encephalopathy. CCK immunoreactivity in water extract of cerebral cortex of LEC rats with hepatic encephalopathy (n = 7) was 41.5 +/- 2.6 (mean +/- S.E.M. pmol/g wet wt.) and that of LEC rats without encephalopathy (n = 8) was 67.1 +/- 6.9, the difference being significant (P less than 0.01). CCK immunoreactive cells assessed by immunohistochemistry were also markedly decreased in the cortex of LEC rats with hepatic encephalopathy of stage IV. Thus, CCK reduction was observed in the cerebral cortex of LEC rats with hepatic encephalopathy which are provided as a model for analysis of the pathogenesis of acute hepatic encephalopathy.
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PMID:Reduced cholecystokinin in the brain of LEC rats with hepatic encephalopathy. 175 73


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