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

Patients with chronic liver disease, yet without severe encephalopathy, were found to show evidence of increased brain utilization of glucose. The changes were abolished after an intravenous infusion of 15 g ornithine alpha oxoglutarate, given over a period of 15 minutes. The possible implications of these observations are discussed.
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PMID:Effect of ornithine alpha oxoglutarate on brain metabolism in patients with chronic liver disease. 23

Bile acid levels were measured in the sera, cerebrospinal fluid (CSF), and brain tissue of 10 patients immediately after death from fulminant hepatic (FHF). Serum bile acids in FHF were predominantly conjugated, and total bile acid levels were higher in all 10 patients than in normal controls (85.9 +/- SE 8.4 compared with 5.7 +/- 0.4 nmol/ml, P less than 0.001). Small but significant amounts could be detected in CSF (range 1.2-5.3 nmol total bile acid/ml) and brain biopsies (1.0-18.8 nmol/g wet weight) of FHF patients, whereas none could be detected in CSF and brain biopsies of patients dying without evidence of liver disease. There was no relationship between serum, CSF, or brain levels and duration of coma, or presence of cerebral oedema found in five FHF patients at necropsy. However, serum bile acid levels were similar in FHF to those found in chronic liver disease without encephalopathy and lower than those found to inhibit brain respiration in vitro. A primary role for these compounds in the pathogenesis of coma in FHF therefore seems unlikely.
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PMID:Serum, cerebrospinal fluid, and brain levels of bile acids in patients with fulminant hepatic failure. 60 89

The dog with an end-to-side portacaval shunt (PCS) has been extensively used as a model to investigate hepatic encephalopathy (HE) as it demonstrates a plasma amino acid pattern similar to patients with chronic liver disease. In adult mongrel dogs, the effect of PCS on plasma and CSF amino acids, octopamine (OCT), phenylethanolamine (PEA) and CSF 5-hydroxyindolacetic acid (5-HIAA), were studied. Moreover, the effect of correction of plasma amino acids by infusional techniques was investigated.Tyrosine, tryptophan and phenylalanine levels increased dramatically during the development of HE in plasma and CSF, while valine, leucine and isoleucine decreased in plasma only, but CSF levels remained stable. Plasma and CSF octopamine and phenylethanolamine and CSF 5-HIAA increased markedly as clinical features in the dogs' behavior, characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence and finally coma. Once in coma, the dogs were infused with an amino acid mixture (F080) calculated to normalize the plasma amino acid pattern. After one to eight hours, the dogs began to awake. Simultaneously, blood, and CSF aromatic amino acids returned to their control values, as did OCT, PEA and CSF 5-HIAA. If F080 infusion was stopped, biochemical alterations would appear within one week, again accompanied by clinical hepatic encephalopathy.The results indicate that the altered levels of aromatic and branched chain amino acids, octopamine and PEA in plasma and CSF correlate well with the development of HE and that correction of the plasma amino acid abnormalities improves encephalopathy simultaneously with correction of neurotransmitter derangements in CSF.
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PMID:Alterations in plasma and CSF amino acids, amines and metabolites in hepatic coma. 63 94

In rats after portacaval anastomosis (an animal model of chronic liver disease), transport of tryptophan and other members of the large neutral amino acid group from blood to brain was markedly enhanced. Increased transport activity was apparently restricted to the neutral amino acid transport system, since brain uptake of glucose, inulin, and tyramine was unaffected while blood-brain arginine transport was significantly reduced. These results strikingly confirm the hypothesis that carrier-mediated blood-brain transport is the limiting factor determining the availability of the neutral amino acids to the brain. The encephalopathy associated with cirrhosis may be the result of abnormal neurotransmitter metabolism and neurotransmission secondary to increased neutral amino acid transport activity and an increased brain content of members of the neutral amino acid group.
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PMID:Blood-brain neutral amino acid transport activity is increased after portacaval anastomosis. 66 19

A patient with recurrent episodes of consciousness disturbance following partial gastrectomy is presented. Angiographic examination revealed a great portasystemic shunt, which probably developed following the postoperative splenic vein thrombosis. This is suspected a rare cause of the condition. In chronic liver disease, recurrent encephalopathy which is caused by portasystemic shunt is well known as one of the most frequent complications. It is very uncommon in adults, however, when the liver is not concerned in the shunt formation. In the present paper the authors report an unusual case of recurrent consciousness confusion which is due to the great portasystemic shunt probably caused by postgastrectomy splenic vein thrombosis.
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PMID:An unusual case of portasystemic encephalopathy caused by splenic vein occlusion following gastrectomy. 68 65

The dog with an end-to-side portacaval shunt has a plasma amino acid pattern similar to that in man with chronic liver disease and encephalopathy. When dogs with end-to-side portacaval shunts manifested symptoms of hepatic encephalopathy, superior caval catheters were placed and one of three solutions was infused. Whereas almost all animals given a commercially available synthetic amino acid mixture died, a special mixture formulated to normalize plasma amino acids was associated with 100 percent survival and few neurological symptoms. The results suggest that manipulation and normalization of plasma amino acids in animals with hepatic failure may be efficacious in providing adequate nutrition while minimizing hepatic encephalopathy. Moreover, these experiments may shed some light on the mechanism of human hepatic encephalopathy.
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PMID:The role of plasma amino acids in hepatic encephalopathy. 80 82

We present data on 10 patients (5 men and 5 women, aged 21-56 yrs) with end-stage liver disease or tumour who underwent orthotopic liver transplantation at Groote Schuur Hospital between October 1988 and June 1991. Standard surgical techniques were used for procuring the donor liver, the recipient hepatectomy and the implantation of the liver. The venovenous bypass method was used in all but 2 patients. Postoperative immunosuppression was usually achieved with cyclosporin, azathioprine and low-dose steroids. Six patients were treated with prophylactic OKT3. Rejection episodes were treated with bolus doses of intravenous steroids. The indications for liver transplantation included chronic active hepatitis progressing to cirrhosis (5), biliary cirrhosis in association with inflammatory bowel disease (1), sclerosing cholangitis (2), alpha 1-antitrypsin deficiency (1), and tumour (1). All patients with chronic liver disease had experienced at least one complication, examples of which included encephalopathy, bacterial peritonitis, ascites, variceal bleeding and septicaemia. Serious postoperative complications included acute rejection of the transplanted liver, renal and liver failure that responded to intensive care support and medical management. One patient died on the 11th postoperative day with complications of bleeding oesophageal ulcer, shock and fungaemia. The remaining patients are alive and well 1-31 months after transplantation.
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PMID:Orthotopic liver transplantation at Groote Schuur Hospital. 150 34

Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (rCMRO2), and oxygen extraction fraction (rOEF) were measured using positron emission tomography (PET) in four patients with cirrhosis (two males and two females, aged 57 to 69 years) in comparison with those in five age-matched controls with previous transient global amnesia. PET studies were carried out when the patients were fully alert and oriented after the episodes of encephalopathy. In the patients, rCBF tended to be lower, while rCMRO2 was significantly lowered in almost all hemisphere cortices, more markedly in the frontal cortex. Our results suggest that the brain oxygen metabolism is diffusely impaired in patients with advanced cirrhosis, and the frontal cortex seems to be more susceptible to the systemic metabolic derangements induced by chronic liver disease.
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PMID:Marked reduction of cerebral oxygen metabolism in patients with advanced cirrhosis: a positron emission tomography study. 154 88

One hundred and forty-six patients with chronic liver disease have been studied. Some of them (15) showed a clinical picture characterized by cryptogenetic liver cirrhosis associated with hypotriglyceridemia and hypobetalipoproteinemia. These patients had compensated cirrhosis and no history of alcohol abuse; they did not suffer major illness in the past and had no signs of portosystemic encephalopathy. The pathogenetic mechanism of this association and the possible role of genetic factors are discussed. The HLA system has been studied and the A2 antigen found with high frequency, raising the possibility that patients with this syndrome may represent a particular subgroup among these with liver cirrhosis.
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PMID:[Cryptogenetic liver cirrhosis with hypobetalipoproteinemia. Typing of the HLA histocompatibility system]. 157 90

Visual event-related P300 potentials, conventional visual evoked potentials, and psychometric tests were applied to patients with noncirrhotic chronic liver disease and to clinically nonencephalopathic and encephalopathic cirrhotics to compare their diagnostic efficacy in detecting early portosystemic encephalopathy (PSE). Sixty-four investigations were performed in 58 patients. The latencies of the P300 parameters were significantly longer in both the encephalopathic and nonencephalopathic cirrhotics than in the noncirrhotics, indicating distinctly abnormal cortical processing of visual stimuli in cirrhotic patients. The visual P300 potentials showed the highest sensitivity and specificity for grade I PSE. Abnormal P300 test results were also found in 78% of the clinically nonencephalopathic cirrhotics, while psychometric tests showed abnormalities in only 41%. The P300 latencies were similar in alcoholic and nonalcoholic cirrhotics. Significant inverse correlations were found between the P300 latencies and measures of quantitative liver function such as galactose-elimination capacity and aminopyrine breath test. It is concluded that visual event-related P300 potentials are a sensitive index of subclinical and grade I PSE. Furthermore, the degree of cognitive dysfunction detected by this method in patients with liver cirrhosis appears to be related to the reduction in hepatic metabolic capacity.
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PMID:Visual event-related P300 potentials in early portosystemic encephalopathy. 161 38


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