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

In a series of pig brains submitted from field cases where water deprivation/sodium salt intoxication was suspected, histopathological examinations and chloride determinations were performed. A poor correlation was found between brain chloride concentration and neuropathology. The ranges of chloride concentrations found were similar for brains showing the encephalopathy of water deprivation/sodium salt intoxication, brains with other neuropathological diagnoses and brains without significant histopathological lesions. A close correlation was found between brain sodium and chloride in a further similar series, suggesting that determinations of sodium would not be more helpful diagnostically than determinations of chloride. A wide range of brain chloride values was also found in a group of healthy slaughtered pigs but the significance of this was not apparent. Brain chloride determinations have little value in the diagnosis of water deprivation/sodium salt intoxication in pigs, especially when performed in isolation without concurrent neuropathology and an adequate clinical history.
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PMID:Evaluation of brain chloride determinations in the diagnosis of water deprivation/sodium salt intoxication in pigs. 646 33

An outbreak of subacute poisoning occurred among nine members of a family; eight were ill with gastrointestinal symptoms, four developed encephalopathy, and two died. Abnormal liver function tests and leukopenia were common laboratory findings. Epidemiologic and environmental investigations traced the source of arsenic exposure to a farm well with water containing 108 ppm arsenic. The soil adjacent to the well was also contaminated with arsenic, possibly from waste pesticide. Presumably, arsenic gained access to the well through obvious leaks in the well's casing. To our knowledge, this is only the second reported outbreak of fatal arsenic poisoning from contaminated drinking water and one of few instances where illness followed exposure to a toxic substance which was disposed of, or possibly disposed of, in an indiscriminate manner.
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PMID:Outbreak of fatal arsenic poisoning caused by contaminated drinking water. 649 43

The serum aluminium concentration of 82 patients undergoing regular dialysis treatment in a large dialysis department was measured. Duration of known uraemia, total cumulative aluminium hydroxide consumption, present level of aluminium hydroxide consumption and chronic interstitial nephropathy as primary kidney pathology were all positively correlated to serum aluminium concentration. Serum aluminium concentration was positively correlated to the incidence of clinical osteodystrophy and negatively correlated to bone mineral content. There was, however, no correlation to parathyroid hormone concentration or parathyroidectomy. The highest serum aluminium concentration was accompanied by clinical dialysis encephalopathy. The centre uses reverse osmosis for water purification, and there has never been measurable aluminium contamination. On the basis of these findings it is concluded that: the source of aluminium in our patients is aluminium hydroxide consumption and not the dialysis water; aluminium plays no role in the development of osteitis fibrosa; the findings are consistent with the theory that hyperaluminaemia plays a role in the development of osteomalacia, and serum aluminium measurement may be useful in the diagnosis of dialysis encephalopathy.
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PMID:Serum aluminium in haemodialysis patients: relation to osteodystrophy, encephalopathy and aluminium hydroxide consumption. 650 90

Metrizamide (Amipaque), a water soluble nonionic contrast medium has less toxic effect in comparison with other contrast media, and it is now widely used for myelography, cisternography, ventriculography and cerebrospinal fluid dynamic imaging. However, as the number of cases in which this medium has been utilized has gradually increased, incidents of toxic manifestations have been reported. Among these, there are a considerable number of case reports referring to metrizamide encephalopathy, but only a few authors reported the appearance of triphasic waves on EEG when they occurred. The authors experienced one case of metrizamide encephalopathy accompanied by frequent appearance of triphasic waves on EEG. A 31-year old male was admitted to our hospital with the complaint of right homonymous hemianopsia. At that time he was fully conscious and mentally alert. On CT, 39 mm X 45 mm partially enhanced isodense mass was revealed on the enlarged sella turcica. Laboratory findings showed high titer of prolactin (10200 ng/ml). Premedication of 100 mg phenobarbital i.m. was followed by the tomography of the sella turcica, using 8 ml of 250 mgI/ml metrizamide injected into L 3-L 4 subarachnoid space. Several hours after the examination, he complained of slight nausea and was kept in bed with his head placed in an elevated position. The next morning, he was found to be in a drowsy state. He was disoriented and could not respond adequately to questions asked. His naming of daily necessities was also poor, although he knew how to use them.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of metrizamide encephalopathy with triphasic waves on EEG]. 654 77

The histories of five long term dialysis patients, all of whom showed the characteristic features of dialysis bone disease are considered. One population, on hospital dialysis, also suffered dialysis encephalopathy, whilst the home dialysis population did not. It is postulated that the excessive polyvalent ion content of the water supply to a new hospital building displaced aluminum from the bone stores and precipitated encephalopathy in three patients over three months. The relationship of bone lysis (corticosteroids, immobilisation and orthopaedic procedures) to encephalopathy is considered in the light of this experience.
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PMID:Dialysis encephalopathy associated with polyvalent ion contamination. 658 79

Of 26 patients who underwent distal splenorenal shunting 4 or more years ago (1969 to 1978), 10 died 3 to 87 months postoperatively (mean 38.5 months). Six deaths were due to liver failure, two to hemorrhagic peptic ulcer disease (the shunt remained patent in each patient), one to brain hemorrhage, and one to sepsis. Eight of the surviving patients resumed professional activity, one showed transient signs of encephalopathy, one had a single episode of recurrent variceal bleeding that could be managed conservatively, and no patient had ascites. Eight patients were investigated angiographically and endoscopically. Preoperative and postoperative measurements of the portal vein showed a decreased diameter in five patients and no opacification in the other three 29 to 97 months after surgery. At endoscopy four patients had small residual esophageal varices, one patient had none, and the other three had large varicosities with variceal pressures between 30 and 40 cm H2O in two and above 40 cm H2O in one. Although the incidence of postoperative encephalopathy and variceal bleeding was low after distal splenorenal shunting, the operation did not prevent a decrease in hepatopetal portal flow and did not always abolish the esophageal varices.
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PMID:Long-term follow-up after a distal splenorenal shunt procedure. A clinical and hemodynamic study. 660 May 87

Five patients with dialysis encephalopathy were transferred to deionized water; all died after a variable period, 4 of progressive dementia. Six other patients with encephalopathy were started either on deionized or reverse osmosis water as well as desferrioxamine on dialysis. Serial EEG's were performed in this group. In 2 patients the EEG's showed rapid and sustained improvement after the institution of desferrioxamine, whereas there had been no EEG change after 15 and 32 months of reverse osmosis water. In 2 patients there was similar clinical and EEG improvement, related to water change and the institution of desferrioxamine. Two patients died of progressive dementia in spite of both water change and desferrioxamine. Thus, while not a panacea, desferrioxamine has a definitive therapeutic effect on the clinical and EEG manifestations of dialysis encephalopathy, when used in conjunction with deionized or reverse osmosis water.
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PMID:The effect of low aluminum water and desferrioxamine on the outcome of dialysis encephalopathy. 664 Oct 27

The effects of chronic manganese chloride administration (1 mg MnCl2.4H2O/ml of drinking water) and ageing on the regional distribution of monoamine oxidase (MAO, EC 1.4.3.4) were studied in 2-month- and 24-28-month-old rats. In both the control and Mn-treated rats, the serotonin oxidation (type A) rates decreased in hypothalamus, pons and medulla, striatum, midbrain and cerebral cortex, but not in cerebellum, in ageing. On the other hand the benzylamine oxidation (type B) rates in hypothalamus, striatum and cerebral cortex increased in ageing. In all regions except the cerebellum, there was a uniform decrease in the A/B ratio. This decrease was verified by differential inhibition studies using clorgyline and L-deprenyl, specific type A and type B inhibitors respectively. The dopamine-oxidising rates decreased in all regions, except the cerebral cortex and the cerebellum, in ageing control rats. This age-related decrease was not seen in the striatum and midbrain of manganese-treated rats. In these rats the other effect was an age-related increase in the rate of oxidation of all the amines in the cerebellum, not observed in control rats. These selective effects of manganese are only seen when comparing age-related changes in both groups of animals, since comparison of manganese-treated rats with age-matched controls showed a significant difference only in the rate of serotonin oxidation in the cerebellum of 2-month-old rats. The relationship of these observations to the effects of ageing and manganese encephalopathy on specific amine systems is discussed.
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PMID:The regional distribution of monoamine oxidase activities towards different substrates: effects in rat brain of chronic administration of manganese chloride and of ageing. 678 76

Available enteral hyperalimentation solutions used to treat undernourished cirrhotic, ascitic patients with protein intolerance are excessive in water, sodium, and in some cases protein. This study investigated the use of enteral formulae tailored to the water, sodium, and protein tolerance of 10 undernourished subjects with ascites due to alcoholic liver disease (n = 8) and postnecrotic cirrhosis (n = 2). During a 10- to 60-day (mean +/- 80 = 37 +/- 19) hyperalimentation period, three subjects were treated with a low Na (1g Na/2000 kcal), high caloric density formula (2 kcal/ml); previous encephalopathy in seven remaining subjects required infusion of a low Na, low protein (40 g/day) modular high caloric density formula. The high caloric density formula protein content in 6/7 subjects was increased to 80 to 143 g without adverse effect. Nine subjects tolerated the program well and showed improvement in the following indices: serum albumin, creatinine/height, and midarm muscle and fat areas. In selected cases, enteral hyperalimentation solutions with appropriate composition can be safely and effectively administered to cachectic cirrhotic subjects with ascites.
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PMID:Enteral hyperalimentation in undernourished patients with cirrhosis and ascites. 680 58

Lead encephalopathy was produced in immature Sprague-Dawley rats with an intraperitoneal (IP) injection of 60 micrograms/g body weight of lead acetate administered daily from the fifth day after birth. Macroscopic and light microscopic study of the nervous system, estimations of the blood-brain barrier permeability to proteins and brain water content were performed every two days thereafter. Lead levels in total blood, plasma, and several brain areas were measured at the same intervals by flameless atomic absorption spectrometry. Electron microscopic study of the cerebellum was done 2, 6, and 12 days after beginning lead administration. After two days of lead administration and before any pathological change occurred the increase in lead level was greater in the cerebellum than in other brain areas. After four to six days, hemorrhagic lead encephalopathy developed and was most prominent in regions with higher lead levels. From day 11 to 14, there were two possible courses: a) improvement of the clinical status and morphological findings in 25% of the animals, or b) progression of abnormal clinical signs and death. Cerebral edema, both intra- and extracellular, may have contributed to the fatal evolution. The mechanism of this edema appeared complex and may have involved resorption failure. Good correlations were observed among progression of the clinical signs, high water content in the brain, morphological evidence of cerebral edema, and a high cerebellar lead level. In contrast, high blood lead levels could be associated with clinical improvement, normal brain water content, and regression of the pathological findings. These data suggest that differences in evolution are more likely related to differences in the development of resistance of the cerebral capillary to lead, or in the efflux of lead, rather than to the blood lead concentrations.
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PMID:Regressive or lethal lead encephalopathy in the suckling rat. Correlation of lead levels and morphological findings. 682 89


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