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

The clinical course and causes of death in 132 consecutive patients with fulminant hepatic failure and grade III or IV encephalopathy have been reviewed. 105 patients died and in 96 of these an autopsy examination was performed. In 36 patients there was cerebral oedema and the mean age of this group was significantly younger than the other fatal cases. In 28 patients death was attributed to major haemorrhage which originated in the gastrointestinal tract in 25. The prothrombin time ratio was not significantly greater in patients with major bleeding than in those without but they did have a significantly lower platelet count. Sepsis contributed to death in 12 patients. In 25 patients massive hepatic necrosis only was found at autopsy and death was considered to be due solely to hepatic failure. The degree of hepatocyte loss was assessed in 80 fatal cases by a histological morphometric technique on a needle specimen of liver taken immediately post-mortem. The proportion of the liver volume occupied by hepatocytes (hepatocyte volume fraction, HVF) was greatly reduced in all patients (normal 85+/-SD 5 percent) but the mean value was significantly higher in the patients dying with sepsis, cerebral oedema or haemorrhage than in the group in whom death was attributed solely to hepatic failure. There were ten patients in whom liver function was improving at the time of death which was due to cerebral (9) or haemorrhage (1). These observations suggest that many patients presently dying from fulminant hepatic failure may be expected to survive, once more effective therapy is available for the complications of the illness.
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PMID:Causes of death in fulminant hepatic failure and relationship to quantitative histological assessment of parenchymal damage. 17 38

Inorganic lead, added to the diet of suckling rat in high doses, produces an encephalopathy similar to that seen in the immature human. Pathologic changes of edema and hemorrhage are seen earliest and are most prominent in the cerebellum. In this study, we measured respiration in cerebral hemisphere and cerebellar mitochondria isolated from led-fed and age-matched normal rat pups. Lactating mothers were begun on ad libitum feedins containing 4% lead carbonate when their pups were 2 weeks old. Mitochondria were isolated by differential centrifugation. Oxygen consumption was measured polarographically, NAD-linked respiration was measured with oxidation of the substrate pair, glutamate and malate. Cytochrome oxidase (cytochrome c oxidase, EC. 1.9.3.1) activity was measured in the presence of tetramethyl-p-phenylenediamine dihydrochloride (TMPD) and ascorbate. Within 2 days of starting lead feedings, rat pups showed a significant loss in body weight (P less than 0.02) and, after 1 week, a significant loss in cerebral hemisphere wet weight (P less than 0.01) compared with controls. Overt encephalopathy appeared in pups from two of nine litters receiving lead feedings for 1 week and in half of the litters after 2 weeks of feedings. None of the lead-fed mothers developed encephalopathic signs. With oxidation of the NAD-linked substrate pair, there was a progressive decrease, relative to controls, in ADP/O ratios in both cerebellar and cerebral mitochondria from lead-fed animals. After 2 weeks these differences were significant in mitochondria from both regions (cerebellum, P less than 0.02; cerebrum, P less than 0.005). Respiratory control ratios were significantly lower in cerebellar mitochondria from lead-fed rats within 2 days of beginning feedings (P less than 0.02) and in mitochondria from both regions after 2 weeks of lead feedings (cerebellum, P less than 0.01; cerebrum, P less than 0.05). The decrease in control ratios in cerebellar mitochondria from animals receivint lead feedings for 1 week or less was due to a small decrease in state 3 respiration and a large, but inconsistent, increase in state 4 respiration. The decrease in control ratios in both cerebellar and cerebral hemisphere mitochondria after 2 weeks of lead feedings was due to a marked inhibition of state 3 respiration, relative to controls (cerebellum, P less than 0.01; cerebral hemisphers, P less than 0.05). In cerebellar mitochondria from lead-fed animals, cytochrome oxidase activity showed similar changes compared with controls: a highly significant (P less than 0.001) increase within 2 days of beginning feedings and a significant (P less than 0.01) decrease after 2 weeks of feedings.
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PMID:Early effects of inorganic lead on immature rat brain mitochondrial respiration. 17 53

Six forms of reversible adverse reactions to adenine arabinoside (vidarabine) were observed in a two-year period among 42 patients (19 of whom had lymphomas, leukemias, or other malignancies) who were treated for complicated infections with varicella-zoster or herpes simplex virus. Six patients received placebo. Ten patients received 10 mg of adenine arabinoside/kg per day; three received 15 mg/kg; 22 received 20 mg/kg; and one received 30 mg/kg. Patients were treated (by continuous intravenous injection) for an average of seven days. Toxic effects were nausea and vomiting, weight loss, weakness (often with impaired ambulation), megaloblastosis in erythroid series in bone marrow, tremors five to seven days after the start of therapy (including tremors in one patient with abnormal electroencephalograms that were consistent with toxic-metabolic encephalopathy), and thrombophlebitis at the intravenous site. Side effects clearly predominated in patients who received 20 mg/kg per day. Therefore, treatment with 10 mg/kg per day appears preferable until the relation of toxicity to dosage level can be clarified.
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PMID:Toxicity of adenine arabinoside in humans. 18 Jan 99

Five central nervous diseases are described and their relationships to previously recorded conditions are discussed. The conditions are congenital inclusion-body encephalopathy probably caused by a paramyxovirus infection, idiopathic neuraxial oedema of a newborn calf, focal symmetrical encephalomalacia of a young calf, yacca (Xanthorrhoea spp) poisoning of adult cattle leading to spinal demyelination, and focal demyelination and neuropathy in an adult cow.
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PMID:Encephalolopathies in cattle in Tasmania. 18 2

A 27 year old agricultural worker presented about one month after treating cereal seeds with an alcoxyalkyl mercurial derivative, an encephalopathy with a confusional state, a cerebellar stato-kinetic syndrome, an intention tremor and grand mal epileptic fits. Treatment with dimercaprol produced a clinical improvement on the fourth day with a fall in blood mercury from 3.5 mug to 2.2 mug whilst urinary excretion of mercury remained low. A fortnight later the patient was completely cured. Although less common than collective poisoning by ingestion, organo-mercurial encephalopathies due to occupational exposure are a real danger although it is not known whether the relative rareness of published cases is due only to lack of observance of security rules or to individual sensitivity which might be due to increased absorption of mercury through the lungs or skin. This case shows that although alkyl mercurial derivatives are reputed to be the most dangerous, alcoxyalkyl derivatives may also cause encephalopathies. Also, as long as non-toxic substances remain unavailable for use in agriculture, one should emphasise the necessity of careful observance of the security rules during manipulation of these products.
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PMID:[Encephalopathy due to organomercuric compounds]. 18 29

All general anesthetics include a risk to life. The etiology and circumstances of complications with cardiac arrest are studied. Accent is placed on the frequency of fatal accidents for benign operations and on the poor prognosis of accidents with hypoxia. The prevention of accidents and their sequelae, such as encephalopathy, requires one to foresee and treat efficaciously as soon as possible cardiac arrest. To reach these objectives, efforts should be made on preparation of the patients, on the equipment and its maintenance, on the grouping of units where fatal accidents most frequently occur, on the creation of departments of anesthesia with re-awakening wards, on the training of medical and surgical teams with better supervision of young anesthetists.
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PMID:[Prevention of anesthesia accidents]. 19 Jun 97

During 1974, eight of 37 (22%) Bordetella organisms isolated from patients in Cincinnate were Bordetella parapertussis. This is in contrast to other experience in the United States where parapertussis has comprised less than5% of the Bordetella species isolated and suggest that B parapertussis infection may be more common in this country than generally recognized. The failure to appreciate the presence of this infection may result from the lack of cultures taken from children with mild disease and the failure todistinguish B parapertussis from B pertussis. Ccultures were obtained from family members of three of the children with B parapertussis, and B pertussis was isolated from members of two families, including the mother and sister of a child who died of pneumonia and encephalopathy. These cases suggest that patients with severe disease associated with B parapertussis should be carefully evaluated for the possibility of dual infection caused by b pertussis.
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PMID:Bordetella parapertussis. Recent experience and a review of the literature. 19 93

Several viral, fungal, and protozoal diseases of the eye are significantly associated with immunologic deficiencies. Of the viral agents, cytomegaly and herpes simplex and zoster cause a discrete necrotizing retinopathy that has the characteristics of vascular occlusion. Measles may result in a delayed retinopathy that is predominantly macular and associated with subacute progressive encephalopathy. Of the fungal agents, Candida and Aspergillus are apt to involve the eye, beginning as choroidal lesions with extension forward to involve the pigment epithelium and retina secondarily. Mucor and Cryptococcus are less common. Toxoplasmosis is the one ocular protozoal disease whose incidence is increased by immunosuppression, and, like the viral diseases, is characterized by a discrete necrotizing retinopathy and probably results from activation of dormant organisms in the retina. Autoimmunity undoubtedly plays an important role in eye disease but its ocular pathogenesis is obscure.
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PMID:Immunosuppression and eye disease. First Vail lecture. 19 82

A case of hyperinsulinism occuring in a newborn, with a birthweight of 4,050 g, is reported. The hypoglycaemia was refractory to the usual therapy (increase of glucose administration per os, and I.V., corticosteroids, glucagon, diazoxide). At surgery, undertaken at 9 days of age, an adenomatous nodule was removed along with the left part of the pancreas. Death occurred at 18 days, after the child had developed a transitory acidoketosic diabetes and an encephalopathy. Measurement of insulin by radio-immunoassay revealed a strong increase in the ratio insulin/glycaemia, characteristic of nesidioblastoma, as well as a high concentration of insulin in the tumor as compared to normal tissue. On the ultrastructural level, the observed features differed from those seen in children and adults and showed an abnormal overload of dense deposits in the cytoplasm of some histiocytes.
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PMID:[Islet cell adenoma with neonatal onset. Clinical, hormonological and ultrastructural study of a case]. 19 46

Experiment studies were performed on rats that were administered mercury chloride sublimate with a special gastric cannule in a single 6 mg dose for four consecutive days. As a result of the investigations some changes in the phosphates and esterases activity were revealed. The diminution of AcP, AIP, ATP-ase and AChE activity as well as in the increase in TPP-ase activity in the neurocytes, and also the appearance on NsE activity in many oligodendrocytes was observed. The fall in ATP-ase activity was, above all, observable in cerebral and cerebellar capillaries, which is, in the authors opinion, a manifestation of enzymatic damage to the blood-brain barrier due to a toxic action of mercuric chloride. In the discussion attention was drawn to differences in the degree of enzymatic activity between a mercuric chloride intoxication and that with mercurous chloride, as well as attempt was made to explain the pathogenetic mechanism of this phenomenon. Furthermore, notice was brought to the fact that in the course of sublimate encephalopathy no changes are observed in BuTJ activity.
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PMID:Phosphatases and esterases activity in the brain following an acute sublimate intoxication. 19 75


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