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)

To determine if dialysis modality may be an independent factor in the level of cognitive function in chronic dialysis patients, cognitive function was studied in 17 pairs of continuous ambulatory peritoneal dialysis (CAPD) and center hemodialysis (CHD) subjects matched for sex, age, diabetic status, and interval since dialysis onset. Data on current metabolic, medical, psychological, and vocational function status were obtained. Neuropsychological (NP) measures included the Number Cancellation Protocol (NCP), Trailmaking test forms A and B (TMT A, TMT B), Symbol Digit Modalities (SDM), and the Rey Auditory Verbal Learning Test (RAVLT). The CAPD subject group had consistently more efficient cognitive function than the CHD subject group. Regardless of modality, the groups of subjects under age 51 and those who were vocationally active had significantly better NP performance. No cognitive function differences were found in groups categorized by sex or duration of dialysis. Creatinine levels were more highly correlated with NP scores than were BUN levels, with higher creatinine levels associated with better cognitive function. Serum calcium, CO2, total protein, albumin, and SGOT levels also were correlated with NP scores. CAPD may be more effective than HD in reversing uremic encephalopathy by mechanisms mostly unrelated to serum creatinine and BUN levels. Longitudinal studies will be needed to determine if dialysis modality is an independent factor in the degree of reversal of uremic encephalopathy.
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PMID:Relationship of dialysis modality and other factors to cognitive function in chronic dialysis patients. 317 71

To evaluate the influence of necrotic liver tissue on the cerebral metabolism and cerebral function in acute liver failure, comparison was made between hepatectomy and total liver devascularization in pigs. In both groups the cerebral blood flow and glucose uptake were significantly decreased. The cerebral oxygen uptake was not reduced. The EEG frequency gradually fell from 12-14 Hz to 1-2 Hz, with intermittent and finally persistent flattening of cortical activity. The visual evoked potentials were unchanged throughout the observation period. The vascular autoregulation and the CO2-reactivity of cerebral circulation disappeared, indicating complete vasoparalysis. As no difference was found between the two groups, it is concluded that the encephalopathy was not due to intoxication from necrotic liver tissue in the abdominal cavity, but to deprivation of liver function.
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PMID:Cerebral flow and metabolism in experimental liver failure. A comparison between hepatectomy and total hepatic devascularization in pigs. 376 31

Low plasma levels of branched-chain amino acids, leucine, isoleucine, and valine are postulated to play an etiologic role in hepatic encephalopathy. Supplementation is advocated to reverse encephalopathy and improve nutritional status and survival. We measured in vivo leucine metabolism in normal individuals (n = 5) and in two groups of patients with cirrhosis (n = 8) with a primed continuous infusion of L-[15N, 1-13C] leucine to quantitate the following parameters of leucine metabolism: nitrogen and carbon fluxes, oxidation, contribution to protein synthesis, breakdown of endogenous protein to leucine, deamination and reamination to/from ketoisocaproate. Studies were performed in the fasting and fed states with a conventional enteral diet (Propac) and a branched chain-enriched diet (one third Propac plus two thirds Hepatic-Aid). In vivo leucine metabolism was similar in the fasting and fed states in normal individuals in patients with cirrhosis and with both diets when studied at a protein intake of 0.6 gm/kg ideal body weight/day. When fed these diets, oxidation increased (p less than 0.05) and breakdown decreased (p less than 0.05). The Hepatic-Aid diet increased (p less than 0.05) nitrogen and carbon fluxes significantly more than did the standard diet. Four additional patients with cirrhosis on a diet with more protein were studied (0.75 gm/kg ideal body weight/day). Carbon and nitrogen fluxes, oxidation, synthesis, and deamination were increased (p less than 0.05) when patients with cirrhosis were fed the Propac diet compared with those who fasted. The Hepatic-Aid diet further increased (p less than 0.05) all parameters except synthesis and did not decrease protein breakdown. These data show that patients with cirrhosis metabolize leucine in vivo in a manner identical to that of normal subjects and that leucine-enriched formulas increase oxidation to CO2 without improving protein synthesis.
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PMID:In vivo measurement of leucine metabolism with stable isotopes in normal subjects and in those with cirrhosis fed conventional and branched-chain amino acid-enriched diets. 403 63

Using noninvasive measurement of cranial blood flow, we previously demonstrated that full-term asphyxiated neonates have decreased cerebral perfusion that can persist up to 5 days of age. In an attempt to test their postischemic cerebrovascular CO2 reactivity, we measured cranial blood flow in ten asphyxiated term (39 +/- 0.8 weeks and 3078 K 400 gm) infants with and without inhaled carbon dioxide (3 percent). The end tidal CO2 (PaCO2) increased significantly, from 28.8 +/- 1.0 mm Hg to 32.3 +/- 2.0 mm Hg after CO2 inhalation (p less than 0.01), whereas the cranial blood flow showed no significant change (38.5 +/- 5.0 ml/min/100 gm brain weight to 37.6 +/- 6.0 ml/min/100 gm brain weight). We conclude that term infants with hypoxic-ischemic encephalopathy have low cranial blood flow at 3 days of age. Their cerebrovascular response to inhaled CO2 is variable and suggests some impairment.
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PMID:Hypoxic-ischemic encephalopathy: cerebrovascular carbon dioxide reactivity in neonates. 644 May 73

Estimated cerebral blood flow (eCBF) was measured sequentially in seven term infants with evidence of hypoxic-ischemic encephalopathy (HIE) and compared with that of normal-term infants. The eCBF was determined by a noninvasive method involving brief bilateral jugular venous occlusion with simultaneous measurement of occipitofrontal circumference. There was a significant decrease in eCBF on day 2 (30 +/- 4 ml/min/100 g brain weight) and on day 4 (36 +/- 5 ml/min/100 g brain weight) compared with control values (56 +/- 4 ml/min/100 g brain weight; 54 +/- 4 ml/min/100 g brain weight) (P less than 0.01). The alveolar CO2 was significantly lower on days 2 and 4 in the HIE group (P less than 0.001), and these values increased to control values by day 6. There was no significant correlation between estimated cerebral blood flow and alveolar CO2 in infants with HIE. We conclude that term infants with evidence of hypoxic-ischemic encephalopathy demonstrate lowered eCBF in the first 4 days of life.
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PMID:Estimated cerebral blood flow in term infants with hypoxic-ischemic encephalopathy. 679 82

Since in a previous study hypoxia and subsequent hypotension were considered to be essential for the pathogenesis of carbon monoxide encephalopathy (CO-encephalopathy), experiments were conducted to see whether a combination of nitrogen hypoxia and subsequent systemic hypotension of similar degree and duration as in the previous experimental CO poisoning could induce the same lesion in the CNS of cats. The partial pressure of blood oxygen was reduced to less then 26 mm Hg by increasing the concentration of nitrogen in N2/O2 gas to be inhaled in 1.5h and then the aortic blood pressure (BP) was reduced to 60-80 mm Hg by blood depletion and ganglion-blockage for 1h. In 11 of the 15 cats, lesions were produced in the CNS which were similar by light and electron microscopy to those in CO-encephalopathy. In control groups which were treated by hypoxemia only, hypotension only or a combination CO2-gas inhalation and hypotension without hypoxemia, such lesions were not found in the cerebral white matter. Considering the pathogenesis of lesions in the cerebral white matter in both nitrogen hypoxia and CO-poisoning, two factors i.e., hypoxemia and subsequent systemic hypotension, are common and essential. Further, the enormous vasodilatation in the cerebral white matter induced by hypoxemia and subsequent drop in BP seem to cause a more severe circulatory disturbance in the cerebral white matter than in the cortex.
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PMID:Comparative study on pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats. 709 Jul 35

In 17 patients, breathing room air and pure oxygen, with histologically proven cirrhosis of the liver and portocaval encephalopathy grade I, static and dynamic lung volumes, closing capacity and arterial blood gases were determined. Furthermore, CO2, response curves were provided and mouth occlusion pressure measurements were carried out. The residual volume was found to be increased (130 +/- 8% of predicted) which resulted in decreased vital capacity (79 +/- 2% of predicted) with total lung capacity being normal (94 +/- 2% of predicted). Closing capacity was increased to 134 +/- 5% of the predicted value. Gas exchange for oxygen was impaired (AaDO2 = 262 +/- 30% of predicted). Arterial PO2, however, was within normal range PaO2 = 84 +/- 3.6 mm Hg) due to hyperventilation (PaCO2 = 28.1 +/- 0.8 mm Hg). Hypoxic ventilatory stimulation could be excluded because inspiration of pure oxygen caused no change of PaCO2 (PaCO2 = 27.3 + 0.7 mm Hg and PaO2 = 465 + 16.9 mm Hg with FIO2 = 1.0). The slope of the CO2 response curves was normal, the mouth occlusion pressures, however, were higher than the predicted value: up to PaCO2 of 55 mm Hg. The slope of these curves being smaller than predicted. The results show that in patients with portocaval encephalopathy the lung function is disturbed due to premature airway closure with consequently decreased regional ventilation: perfusion ratios and that regulation of ventilation is impaired by a loss of sensitivity for CO2 with high basal output of the respiratory centers not related to CO2.
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PMID:[Lung function, gas exchange and regulation of ventilation in patients with portocaval encephalopathy (author's transl)]. 742 66

Severe water and electrolyte disturbances were observed in a patient after a bout of very heavy beer drinking (30 liters in 6 days). On admission she was found to have hypokalemia (2.2 mEq/I), metabolic alkalosis (pHa: 7.55-total CO2: 40 mEq/I), and more particularly hyponatremia (109 mEq/I), responsible for the typical neurological signs of water intoxication (hyponatremic encephalopathy). There was a positive cumulative return of sodium (570 mEq) and chloride (900 mEq) levels, and normal conditions were restored without significant modifications in water balance or weight. No other etiology, apart from the beer, was discovered. Heavy drinking of beer alone can therefore provoke chloride and sodium depletion, probably because beer, which is poor in NaCl, must produce urinary loss of these electrolytes. The high osmolarity of beer may explain this latter phenomenon. This particular cause of hyponatremia should be recognized, if only to avoid confusing the clinical signs of alcoholic intoxication with those due to water intoxication.
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PMID:[Hyponatremia after very heavy beer drinking (author's transl)]. 744 30

Patients with mitochondrial disease may present to the Intensive Care Unit (ICU) with a variety of neurological and general medical disorders. Eleven patients were admitted to a neurological ICU between 1970 and 1992 because of respiratory insufficiency, status epilepticus and/or metabolic encephalopathy associated with mitochondrial disease. Respiratory impairment occurred in eight patients and was associated with nocturnal hypoventilation due to respiratory muscle weakness, aspiration due to bulbar weakness and abnormalities of central control leading to a reduced CO2 drive, irregular respiratory patterns and sleep apnoea. Seven patients received continuous respiratory support during the acute illness; three were subsequently weaned to domiciliary ventilation, and four died. Five patients had stroke-like episodes, which in two were recurrent. Four patients developed tonic-clonic grand mal epilepsy associated with myoclonic fits (2 patients), absences (2), focal fits (1) and status epilepticus (2). Encephalopathy was associated with recurrent lactic acidosis (2 patients), cardiac failure (2), hyponatraemia (2), renal abnormalities (3) and complete heart block (1). Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.
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PMID:Management of mitochondrial disease on an intensive care unit. 776 70

Intracellular pH and ammonium ion concentration are potent modulators of cerebral amino acid metabolism. Furthermore, intracellular acidosis and hyperammonemia accompany conditions such as ischemic encephalopathy and seizures and may contribute to the pathological sequelae observed. In vivo NMR spectroscopy permits multiple, non-destructive measurements of important cerebral metabolic intermediates in the same animal. We describe here the use of 1H, and 31P NMR spectroscopy to investigate the effects of acute changes in intracellular pH and ammonium ions on cerebral glutamate, glutamine, and lactate levels in vivo. We then show how 1H NMR can be used to indirectly follow the flow of 13C label from [1-13C] glucose into the cerebral glutamate pool, allowing us to measure cerebral TCA activity in normal and chronically hyperammonemic rats. Male Sprague-Dawley rats (160-210 gm), fasted 24-hours, were tracheotomized, paralyzed and ventilated on 30% O2/70% N2O. NMR spectroscopy was performed at a field strength of 8.4 Tesla using a Bruker AM-360 wide bore spectrometer. An elliptical surface-coil (8 x 12 mm) was double-tuned to either the 1H and 31P or 1H and 13C frequencies. After retraction of extracranial tissues, the coil was positioned over the skull 2 mm posterior to the bregma. Tail arteries and veins were cannulated allowing periodic measurements of PO2, pCO2, pH and glucose in arterial blood and intravenous infusions. Respiratory acidosis was induced in rats by the addition of CO2 to the ventilation gas mixture. Arterial pCO2 increased within 5 min from a pre-hypercarbic value of 36.4 +/- 6.1 mm Hg to 200-220 mm Hg and was maintained at this level for over 1 hour. Hypercarbia led to rapid cerebral acidification. Intracellular pH decreased from 7.18 +/- 0.08 (pre-hypercarbic period) to 6.68 +/- 0.06 (n = 4) at 10 min and remained stable throughout the NMR observation period. Glutamate decreased to 53 +/- 4% of control after 60 min of hypercarbia, while glutamine increased to 126 +/- 7% of control. Acute hyperammonemia was produced by a programmed intravenous infusion of 250 mM ammonium acetate, which rapidly raised and maintained the concentration of ammonium ions in the blood at approximately 500 microM. Shortly after the start of the infusion (10-20 min), the levels of glutamine and lactate rose continuously throughout the experiment, reaching levels of 170 +/- 25% and 260 +/- 60% of control, respectively (n = 12) after 50 min. Glutamate decreased during the same time interval to 80 +/- 4% of control (n = 12).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral metabolic studies in vivo by combined 1H/31P and 1H/13C NMR spectroscopic methods. 842 59


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