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

Forty-seven children treated for lead poisoning (PbB 50 to 365 microgram/dl) were compared to siblings next in age (PbB less than 40 microgram/dl) by a battery of psychologic tests. Symptoms were present in 18 but none had frank encephalopathy. Physical and neurologic examinations revealed no residual damage. Mean psychologic test scores showed no significant difference between patients and controls except in the arithmetic subtest, in which patients' scores were not related to lead concentration. Intelligence tests failed to distinguish children successfully treated from their sibling controls.
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PMID:IQ following treatment of lead poisoning: a patient-sibling comparison. 9 4

Chromium is required for maintenance of normal glucose tolerance. After complete bowel resection and five months of total parenteral nutrition, severe glucose intolerance, weight loss, and a metabolic encephalopathy-like confusional state developed in a patient. Serum chromium levels were at the lowest normal level. Supplementation of 150 microgram of chromium per day reversed the glucose intolerance, reduced insulin requirements, and resulted in weight gain and the disappearance of encephalopathy. The low levels of chromium and response to chromium supplementation suggest that chromium deficiency can arise in long-term total parenteral nutrition.
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PMID:Chromium deficiency during total parenteral nutrition. 10 57

Four cases on a combination of lithium and thioridazine developed severe neurotoxic symptoms, e.g., delirium, seizures, encephalopathy and grossly abnormal EEG's. All patients had been on lithium without thioridazine prior to and after the neurotoxic episode with no complications or EEG changes. The possible risk of combining lithium and neuroleptics (thioridazine) is discussed and repeated EEGs are recommended as a preventive measure.
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PMID:Neurotoxicity with combined use of lithium and thioridazine. 10 47

Two women, aged 41 and 51 years, developed jaundice, encephalopathy, and hypoprothrombinemia during rapid weight loss four and 12 months after jejunoileal bypass for refractory obesity. Both were treated for liver failure and received a prolonged course of nutrition parenterally and orally. Serial liver biopsy specimens demonstrated extensive alcoholic-like hepatitis and cirrhosis that improved with nutritional repletion and reanastomosis. Postoperative biopsy specimens later demonstrated minimal portal fibrosis in one patient and inactive mild cirrhosis in the other. Although previous reports indicate that patients usually die when they develop liver failure of this severity after jejunoileal bypass, prolonged intensive nutritional repletion was associated with sufficient clinical and histologic improvement in these two patients so that intestinal reanastomosis could be performed safely.
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PMID:Liver failure with steatonecrosis after jejunoileal bypass: recovery with parenteral nutriton and reanastomosis. 10 83

Clinical and Neuropathological data on sixteen cases of progressive myoclonic encephalopathy are reported. This neurological syndrome appears after an average duration of thirty two months of haemodialysis and leads to death in four and a half months, and is characterized by myoclonus, speech disorder, epileptic seizures, and mental-status changes. At first, clinical signs and symptoms are related to haemodialysis, later they become permanent. An early diagnosis is based on EEG which is the only useful laboratory test, demonstrating bisynchronous slow-wave bursts. The caracteristic histopathologic findings are neuronal depopulation, lipofuscin accumulation, and appearance of Neurofibrillary degeneration, especially in Motor cortex, red nucleus and dentato-olivary systems. It seems to be justified to attribute P.M.D.E. to aluminium chronic poisonning; the source of the aluminium intoxication is not aluminium containing phosphate-binding gels but intravenously administreted tape-water. The intracellular binding of aluminium is shown from a histochemical study employing fluorescent stain Morin.
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PMID:[Progressive myoclonic encephalopathy in dialysis patients. Clinical, electroencephalographic and neuropathological study. Pathogenetic discussion]. 10 55

A new and sensitive method for determination of octanoate in serum by gas-liquid chromatography is described. It was validated by mass spectrometry. Octanoate concentrations were determined in the serum of 61 fasting cirrhotic patients of which 47 also had hepatic encephalopathy. Concentrations in arterial and venous blood were higher in cirrhotic patients with encephalopathy than in those without and higher in the latter than in controls. Arterial concentrations were higher than venous concentrations and octanoate and ammonia varied independently. A predominant endogenous origin is likely. Data obtained from studies using palmitic acid labeled at different loci suggest that recovered serum octanoate was formed mostly by incomplete oxidation of long chain fatty acids. Sodium octanoate infusion to rhesus monkeys studied polygraphically induces a temporary coma.
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PMID:[Hyperoctanoatemia and the hepatic encephalopathy of cirrhosis. 150 dosages in 61 patients (author's transl)]. 11 76

Eighteen adult chacma baboons were fed Cannabis sativa, the plant material being incorporated into their food. They were divided into three equal groups. Group 1 animals were fed on 2% cannabis in food for 4 months, after which 2 animals remained on 2%, 2 were given 4% and 2 6% cannabis in food for the next 4 months. They became mildy apathetic. Five gained weight. Serum glucose, potassium and CO2 values decreased. Neuropathological examination of their brains did not show any significant abnormality. Group 2 animals were fed 10% cannabis for several weeks. They ate less and lost weight, and later became very apathetic. Right temporal biopsies were done in all and in 3 the tissue was analysed for glutamine, glutamate, tryptophan, ammonia and cyclic AMP. No significant change was found. Serum glucose and CO2 levels rose and potassium levels fell. Blood cholesterol values decreased in 3 of the 9 males. Group 3 animals were fed 6% cannabis for 2--4 months. Radio-immunoassay of sera and urine showed the presence of cannabinoids. They became apathetic, and 5 lost weight. Serum glucose and potassium levels (measured in the males) decreased. No neuropathological lesions were found in the brains, apart from an incidental leptomeningitis in 1 animal which died suddenly. The question of cannabis encephalopathy is discussed.
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PMID:Effects of the oral administration of Cannabis sativa (dagga) on chacma baboons (Papio ursinus). 11 92

A case of anoxic encephalopathy is reported, with study on a whole-auditory-pathways basis, and the method of processing tissues is outlined. Pathologic changes are found throughout the central part of the auditory pathway. The importance of including the superior ventral cochlear nucleus (SVCN) with cochlear structures in correlating findings with audiometric data is supported. The previously advanced tonotopic frequency pattern, with zonal vulnerability, of the spheroid cells of SVCN is supported.
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PMID:The auditory pathology of anoxia. 11 18

The aluminum present as a contaminant in ATP preparations can cause strong inhibition of yeast hexokinase P-II activity at pH 7.0 or below but has little or no inhibitory effect at a pH of 7.5 or greater. The inhibition is reversed by citrate, 3-phosphoglycerate, malate, phosphate, and catecholamines, all of which have previously been described as activators of hexokinase at low pH. We suggest that these agents activate the enzyme only by virtue of their ability to coordinate with aluminum present in the assay system. The presence of aluminum is also responsible for the "negative cooperativity" observed at low pH with respect to Mg . ATP concentration--i.e., the inhibition by aluminum is uncompetitive at low Mg . ATP concentrations but becomes competitive at high Mg . ATP concentrations. The inhibition is thought to be due to formation of a complex of Al . ATP with the enzyme, with a dissociation constant (Ki) of 0.1 microM. Yeast hexokinase P-I is somewhat less sensitive to A1 than is hexokinase P-II, and yeast glucokinase is not detectably affected. The hexokinase in rat brain (type I) shows a pH-dependent inhibition by Al similar to that observed with the yeast hexokinases, whereas the rat muscle (type II) enzyme is less sensitive, suggesting a possible relationship to aluminum encephalopathy in man.
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PMID:Proton-dependent inhibition of yeast and brain hexokinases by aluminum in ATP preparations. 11 25

Enteral hyperalimentation in four patients with severe alcoholic hepatitis and anorexia increased spontaneous food intake, increased their nitrogen balance and the patients improved clinically. Seven patients with alcoholic hepatitis, who were clinically ill and able to eat only 410-1,100 calories per day, were given a 900 mosM/l. parenteral "hyperalimentation" solution by a peripheral vein (P-900). The intravenous nutrition provided daily 51.6-77.4 gm. amino acids in addition to oral intake. All patients improved. None developed detectable encephalopathy after 16-42 days of P-900 therapy. Five additional patients had ascites and alcoholic hepatitis. The daily infusion of 2,000 ml. P-900 was not associated with hyponatremia, renal failure or encephalopathy in four of these five patients who improved and continued their diuresis. P-900 therapy was discontinued in one because of progressive hyponatremia. The observations indicate that over and above the maximum tolerable oral nutrition, intravenous nutrition can be effectively utilized by clinically ill, jaundiced patients with alcoholic hepatitis without precipitating encephalopathy or interference with standard therapy of ascites.
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PMID:Hyperalimentation in alcoholic hepatitis. 11 34


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