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

In 59 patients with respiratory insufficiency due to chronic obstructive pulmonary disease (COPD) the relationship between the state of consciousness, the blood gases and blood ammonia were studied. Interindividually, a significant correlation was found between the encephalopathy and SaO2, PaCO2 or ammonia, and also between the blood gases and ammonia. On the other hand, an intraindividual study, performed on patients with minor cerebral dysfunction, showed that only PaCO2 was significantly correlated with the stage of consciousness. Ammonia did not appear to have a neurotoxic influence. The ammonia level seemed to be influenced primarily by other factors than the blood gases, although there was a borderline influence of SaO2 on aterial ammonia and a significant influence of PaCO2-HCO3 and pH on venous ammonia.
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PMID:Respiratory failure: correlation between encephalopathy, blood gases and blood ammonia. 0 6

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

Acute lead encephalopathy was induced in adult guinea pigs with daily oral doses of lead carbonate. Cerebral capillaries were examined by electron microscopy, and the blood-brain barrier (B-BB) evaluated with Evans blue and horseradish peroxidase. Brain lead levels were also determined during the developing encephalopathy. There was no cerebral capillary alteration or demonstrable B-BB dysfunction. Brain lead concentrations increased over the 5-day period. The encephalopathy in the absence of any vascular alteration suggests that lead can produce a primary toxic effect at the neuronal level.
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PMID:Acute lead encephalopathy in the guinea pig. 121 Nov 9

Acute lead encephalopathy was induced in adult guinea pigs by administering daily oral doses of lead carbonate. During the development of the encephalopathy, the structural and functional integrity of the blood-brain barrier was evaluated with electron microscopy and tracer probes. Blood, cerebral gray matter, liver, and kidney were analyzed for lead, calcium, and magnesium content. The animals regularly developed an encephalopathy after four doses of lead. There were no discernible pathomorphologic alterations in the cerebral capillaries or perivascular glial sheaths. Furthermore, no evidence of blood-brain barrier dysfunction was demonstrated with Evans blue-albumin complex or horseradish peroxidase. Blood-brain barrier permeability to radiolead was not increased in the intoxicated animals. During the development of the encephalopathy there was a progressive rise in the lead concentration in all tissues. Concurrently, there was a significant rise in brain calcium. These results suggest that the encephalopathic effects of lead may be mediated directly at the neuronal level.
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PMID:Blood-brain barrier dysfunction in acute lead encephalopathy: a reappraisal. 122 64

Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 16 patients with hepatic encephalopathy before and/or after treatment. CSF lactate was significantly increased to 1.92 +/- 0.11 mmol/l in hepatic encephalopathy before the treatment in comparison to 1.40 +/- 0.05 mmol/l in control subjects. In 9 of 11 patients with moderate or stage 2 encephalopathy, CSF lactate levels were below 2 mmol/l. In contrast, in 4 of 5 patients with stage 3-4 encephalopathy, CSF lactate levels were higher than 2 mmol/l. CSF lactate was decreased with the recovery of neurological symptoms by the treatment. These findings indicate that CSF lactate levels reflect the severity of metabolic impairment of the brain. Hypocapnia was frequently observed in these encephalopathic patients, and arterial PCO2 correlated inversely with CSF lactate and linearly with CSF HCO3-, suggesting that CSF lactic acidosis contributes to hyperventilation in hepatic encephalopathy. It is concluded from present results that metabolic disorder of neuronal cells might be one of the important factors for the development of hepatic encephalopathy.
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PMID:Cerebrospinal fluid lactate in patients with hepatic encephalopathy. 311 61

Inorganic lead produces cerebral dysfunction and clinically definable encephalopathies in man. To date there have been few studies on the biochemical changes in brain following exposure to inorganic lead. Studies correlating toxicity with behavioral and brain neurochemical changes following lead exposure have been hindered because adult laboratory animals are resistant to the central nervous system effects of lead poisoning. Such studies have been impeded by lack of suitable experimental models until Pentschew and Garro showed that brain lesions develop in neonatal rats when a pregnant rat newly delivered of her litter is placed on a 4% lead carbonate containing diet. Lead passes into the developing sucklings via maternal milk. Lead-poisoned new-borns have pronounced retardation of growth and during the fourth week of ilfe develop the severe signs of lead encephalopathy, namely, extensive histological lesions of the cerebellum, brain edema, and paraplegia. There is an approximate 85-fold increase in the lead concentration of both the cerebellum and cerebral cortex relative to controls, but edema and gross vascular changes are confined to the cerebellum. Ingested lead had little effect on RNA, DNA, and protein concentrations of developing rat cerebellum and cerebral cortex. However, there was a reduction of between 10 and 20% in the DNA content of the cerebellum around 3 weeks of age in the lead-exposed sucklings. This suggests a failure of cell multiplication in this part of the brain.A critical evaluation of this experimental approach indicated that under similar dietary conditions experimental lactating rats eat 30% less food than controls resulting in: (a) sustained loss in body weight of nursing mothers and that (b) offsprings who develop paraplegia and cerebellar damage do so after gaining access to lead containing diet. We have studied mothers' food consumption and body weight changes and blood, milk, and brain lead content; and newborns' body and brain weight changes, blood and brain lead content, and brain serotonin (5HT), norepinephrine (NE), dopamine (DA), and gamma-aminobutyric acid (GABA). We have found that a lactating mother rat eating 5% lead acetate (2.73% Pb) produced milk containing 25 ppm lead. When the mothers' diet is changed at day 16 from 5% PbAc to one containing 25 ppm Pb, and neonates allowed free access to the solid diet, the sucklings still have retarded body growth but do not develop paraplegia or grossly apparent vascular damage of the cerebellum. However, during the fourth week these animals exhibit a less severe form of "encephalopathy" consisting of hyperactivity, tremors, and stereotype behavior. Pair-fed controls coetaneous to experimental groups do not display such activities. There was no change in brain 5HT, GABA, or NE, but a 15-20% decrease in brain DA. Change in DA relative to other monoamines suggests a relationship between CNS dysfunction due to lead and DA metabolism in the brain.The experimental design as discribed provides a model of CNS dysfunction due to lead exposure without debilitating histopathologies. It is possible that our findings on increased motor activity and changes in brain dopamine may correspond to early responses to lead exposure before recognized overt signs of toxicity.
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PMID:Animal models of human disease: severe and mild lead encephalopathy in the neonatal rat. 483 Nov 41

Organic brain syndrome is reported to occur occasionally in patients who are treated with lithium carbonate alone, or in combination with neuroleptics. Such neurotoxicity is often associated with moderate to low serum lithium levels and is usually reversible upon the cessation of lithium treatment. The authors report on a 57 year old manic-depressive and alcoholic patient who, after four years of lithium treatment, developed symptoms of CNS hypersensitivity which reappeared several times when he was challenged with lithium during a two month period. The possible role of an underlying, subclinical encephalopathy, caused by episodic drinking, is considered.
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PMID:Acquired transient CNS hypersensitivity to lithium therapy. 611 Apr 72

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.
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PMID:Antacid therapy--changes in mineral metabolism. 629 43

Toxic irreversible encephalopathic syndromes developed in 2 patients treated with lithium carbonate and haloperidol. Symptoms consisted of lethargy, fever, tremulousness, confusion, and extrapyramidal and cerebellar dysfunction, accompanied by leucocytosis and elevated serum enzyme, blood urea nitrogen, creatinine and fasting blood glucose levels. One patient suffered widespread irreversible brain damage; the other was left with persistent dyskinesias. Although causal factors have not been identified, this report and others in the literature suggest that diffuse irreversible encephalopathy may occasionally develop in individuals with abnormal brain sensitivity to the lithium carbonate/haloperidol combination. Evidence for this is based on the fact that in our patients and others mentioned in the literature the dosage and blood levels of lithium were not high.
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PMID:Toxic irreversible encephalopathy induced by lithium carbonate and haloperidol. A report of 2 cases. 641 23

The present report describes a rare of a 77-year-old woman who developed encephalopathy and metabolic acidosis associated with hyperammonemia, at the introduction of hemodialysis by chronic renal failure. With the intravenous infusion of HCO3-, levels of acidosis and hyperammonemia decreased rapidly. Concomitantly the disturbance of consciousness was improved. Results of plasma amino acid patterns of pre and post infusion of HCO3- showed improvement of the metabolism of the urea cycle, increased urea synthesis and decreased plasma ammonium levels. The role of the hepatic urea cycle has been considered to be exclusively the elimination of potentially toxic ammonia. In the conventional view, the acid base balance of the body obtains stabilized homeostasis by the function of the principal organs, lungs and kidneys. But, it has been recently shown that urea cycle is an important factor in the maintenance of pH homeostasis, due to regulated metabolism of HCO3-. Both HCO3- and NH4+ are converted to urea indicating the urea cycle's involvement in acid base homeostasis. 2HCO3- + 2NH4+-->urea+CO2+3H2O In this case, with the infusion of HCO3, the metabolism of the urea-cycle was improved and plasma ammonium levels were decreased. This indicates that HCO3- is an important factor for the metabolism of ammonia.
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PMID:[A case of hyperammonemia in chronic renal failure successfully treated with the infusion of NaHCO3]. 841 69


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