Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In five patients who had been on chronic maintenance haemodialysis for more than eight months a syndrome involving altered consciousness, asterixis, and abnormal electroencephalogram developed after they had been given flurazepam and diazepam. All five patients were adequately treated by haemodialysis. Hepatic, pulmonary, and cardiac decompensation were not present. The encephalopathy and other abnormalities cleared when the drugs were withdrawn. Symptoms were also produced by accidental rechallenge.
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PMID:Drug-induced encephalopathy in patients on maintenance haemodialysis. 6 91

Hepatic encephalopathy (H.E.) is associated with and perhaps caused by changes in plasma-aminoacid patterns--decreased branched-chain aminoacids (B.C.A.A.) and increased aromatic aminoacids (A.A.A.). The decreased B.C.A.A. may be in part secondary to hyperinsulinaemia, but the B.C.A.A. are catabolised by both fat and muscle. The increase in A.A.A. may reflect a "catabolic stimulus" reflected in hyperglucagonaemia, particularly in severe hepatic failure and H.E., and a decreased insulin/glucagon ratio. Endogenous protein, lean body-mass, or liver then releases large amounts of A.A. and the A.A.A. cannot be catabolised by the failing liver, and thus accumulate in the circulation. With decreased plasma-B.C.A.A., the molar ratio of B.C.A.A. and A.A.A. decreases allowing the toxic A.A.A. to penetrate the blood-brain barrier in increased amounts and encephalopathy develops. Appropriate therapy for H.E. must include reversal of the "catabolic state" by providing sufficient B.C.A.A. and calories to decrease the flux of A.A.A. from muscle and liver, and the restoration of the normal molar ratio of B.C.A.A. and A.A.A.
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PMID:Insulin, glucagon, aminoacid imbalance, and hepatic encephalopathy. 6 15

Two unusual cases of subacute necrotizing encephalopathy are described. In one, a marked hirsutism led to a suspicion of adrenal tumor or other endocrinopathy. In the other case, there was an agenesis of the corpus callosum, the second instance in which a malformation of the corpus callosum was associated with this condition. Electron micrographs from a case of Leigh's disease showed examples of marked axonal swelling and occasional splitting of the lamellae of the myelin sheath, probably responsible for the spongy state seen under light microscopy. That such marked changes were not seen in the "internal control" tended to exclude postmortem changes. The ultrastructure and histologic structure of striated muscle appeared normal in the one case examined.
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PMID:Subacute necrotizing encephalopathy (Leigh's disease): two unusual cases. 6 6

The EEGs of 7 children with Reye's syndrome (fatty liver and encephalopathy) were continuously recorded on magnetic tape for times ranging from 12 to 80 h. During these times the major therapy consisted of exchange blood transfusions. The tapes were automatically processed on a LINC-8 computer using a peak-detection algorithm. The main parameters investigated were the delta and theta indices, the mean EEG frequency, the mean peak-to-peak amplitude, and the frequency versus amplitude characteristics of the delta waves. In 5 patients who responded to therapy, a marked decrease in the delta activity and an increase in mean frequency were noted subsequent to exchange transfusions. In all 5 cases the delta waves exhibited a similar pattern of decreasing amplitude and increasing frequency following therapy. However, in 2 patients with a fatal outcome, no favorable EEG response was observed during treatment, and a simultaneous decline in both delta frequency and delta amplitude was noted as the clinical condition worsened. The results of this study indicate that continuous EEG monitoring in Reye's syndrome may be an important clinical adjunct in evaluating the effectiveness of exchange transfusion therapy and in signaling the need for further treatment.
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PMID:Computerized evaluation of electroencephalographic changes accompanying exchange transfusion in Reye's syndrome. 6 30

Computerized EEG was performed in 20 patients with renal failure before and after haemodialysis (HD), applying spectral analysis and Hjorth's EEG descriptors in EEG quantification, correlation and factor analysis as statistical procedures to analyse the connections of EEG, blood variables and psychological performance. The main results were: (1) Moderate uraemic encephalopathy -- according to Kiley's (1971) standards -- was present in most of our patients, before and after HD. (2) Before HD, EEG slowing was most strongly connected with the creatinine level and EEG acceleration with hyperkalaemia, which in most cases accompanied a high urea level. (3) Significant EEG changes after HD were: decrease of percentage delta activity, increase of Hjorth's 'mobility', decrease of Hjorth's 'complexity'. (4) The theta/alpha ratio (Matousek 1968) was significantly correlated with the patient's general clinical state after HD. (5) Visual discrimination, memory and maximal tapping speed improved significantly after HD. Only Hjorth's EEG parameters were correlated with test performance in that patients with low voltage and fast EEGs did worse in visual discrimination.
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PMID:EEG and haemodialysis. A structural survey of EEG spectral analysis, Hjorth's EEG descriptors, blood variables and psychological data. 7 46

Cytologic changes in neurons of the neocortex of mice consequent to suboptimal fixation have been investigated systematically in Golgi-rapid preparations. With few exceptions, there is no alteration in cellular morphology if the brain is refrigerated after death, and fixed by immersion within 3 hours. With latencies of fixation of 6 hours or more, autolytic changes supervene which modify the general histologic appearance and the morphology of individual cells. In general, the degree of tissue and cellular change is proportional to the latency between death and tissue fixation. Similar alterations in cellular morphology and general tissue appearance are found in Golgi-rapid impregnations of human brains obtained at autopsy. However, the degree of tissue autolysis in the human specimens bears a less predictable relationship to the latency of fixation after death. The duration of preterminal metabolic encephalopathy appears to be equally decisive as a determinant of tissue preservation.
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PMID:The Golgi rapid method in clinical neuropathology: the morphologic consequences of suboptimal fixation. 7 72

Three single CSF proteins with different molecular size (albumin, immunoglobulin G, and alpha2-macroglobulin) were determined by the method of electroimmunoassay in 61 children with febrile convulsions (FC) in order to evaluate the permeability of the blood-CSF barrier (B-CSF-B). Forty-two children with acute extracerebral infection served as controls. In contrast to a group of 22 children who suffered from acute meningoencephalitis or encephalitis, the CSF values of 48 children with FC were within normal limits. Thus even a very mild form of inflammatory encephalopathy-undetectable with conventional CSF investigation-was excluded in the majority of the children with FC. In 11 patients, however, CSF concentrations of albumin and alpha2-macroglobulin were abnormally raised, indicating a B-CSF-B distrubance. Elevated albumin values were found most frequently. In several children with FC lasting more than 20-30 min, B-CSF-B damage was probably caused by prolonged seizure activity since there is a linear correlation between albumin concentration and duration of convulsions. Several other factors known to raise the children's risk of developing epilepsy in later life were associated with the protein pattern of B-CSF-B disturbance in some of the children. In these cases, the cause of abnormal permeability of B-CSF-B is unknown and the condition might have existed prior to the occurrence of seizures.
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PMID:Febrile convulsions and blood-cerebrospinal fluid barrier. 7 3

In patients maintained on regular haemodialysis in Newcastle upon Tyne the development of osteomalacia is substantially reduced when water used to prepare dialysate is deionised. After 1--4 years of dialysis, osteomalacia was evident in 15% of patients on deionised water in 70% of patients on softened water from the same source. The close association of dialysis encephalopathy and osteomalacia suggests a common aetiology. Both diseases occur in centres with a high tap-water aluminium content. Serum-aluminium concentrations were raised in patients undergoing regular haemodialysis in the Northern Region of England. Those using softened water had higher concentrations than those using deionised water. Patients on softened water who had encephalopathy or dementia had serum-aluminium concentrations similar to those of patients using the same water-supplies without symptoms of these diseases, but they had been treated for longer. The evidence that aluminium absorption from dialysate causes osteomalacia and encephalopathy is strong enough to justify the expense of treating water by deionisation, reverse osmosis, or both in centres where tap-water aluminium is high.
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PMID:Osteomalacic dialysis osteodystrophy: Evidence for a water-borne aetiological agent, probably aluminium. 7 95

Brain-aluminium concentrations were found to be significantly higher in 7 patients dying with dialysis encephalopathy (mean 15.9 microgram aluminium/g dry weight) than in 11 dialysed controls (4.4 microgram/g) and in 2 uraemic patients who were not dialysed (2.7 microgram/g). The grey matter from the patients with dialysis encephalopathy contained about three times as much aluminium as white matter. The results suggest that dialysis with untreated and/or softened tap-water (aluminium concentration 0.1-1.2 mg/1) makes the major contribution to brain-aluminium levels; dialysis with deionised water (aluminium concentration normally less than 0.02 mg/1) and intake of phosphate-binding AL(OH)3 gel are less important. Brain aluminium levels remain elevated for up to four years after restoration of good renal function by transplantation. The association of dialysis encephalopathy with high levels of aluminium in the brain and in the dialysis water emphasises the potential neurotoxicity of aluminium in man.
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PMID:Brain-aluminium concentration in dialysis encephalopathy. 7 45

Five patients experienced severe encephalopathy within hours of receiving their initial dose of cranial irradiation for the treatment of central-nervous-system leukaemia. Neurological findings included cranial-nerve palsies, seizures, ataxia, depressed consciousness, increased intracranial pressure, and signs of herniation. Symptoms developed within 3-30 hours of the first radiation treatment of 50-200 rad. Each patient had also received one or more injections of intrathecal chemotherapy before encephalopathy developed. The aetiology of this syndrome is uncertain but may involve transient cerebral oedema and/or an altered blood-brain barrier produced by the combination of intrathecal chemotherapy and cranial irradiation.
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PMID:Acute encephalopathy after initiation of cranial irradiation for meningeal leukaemia. 7 11


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