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

Formalin-fixed brain slices from four cases of subcortical arteriosclerotic encephalopathy in which a firm diagnosis could be made both clinically and pathologically have been studied by magnetic resonance imaging (MRI). The slices were subsequently embedded in paraffin-wax or celloidin and sections were cut in the same plane as the MRI slices. There was a good correlation between the extent and severity of the abnormal MRI signal and the pathological changes. Areas of diffuse MRI abnormality corresponded with areas of axonal and myelin loss with gliosis, and small "lacune"-like lesions corresponded with lacunar infarcts histologically. Sparing of the subcortical U-fibres was seen histologically and on MRI. The abnormal signal probably originates from increased tissue water attributable to gliosis and an expanded extracellular space.
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PMID:Pathological findings correlated with magnetic resonance imaging in subcortical arteriosclerotic encephalopathy (Binswanger's disease). 261 28

Six new cases of psychogenic water intoxication are discussed in the light of 150 observations published in the literature since 1935. 87% of all patients were schizophrenic, and 13% had other psychoses and a variety of functional and organic psychopathies. Psychogenic polydipsia is a prerequisite of psychogenic water intoxication. Water intake either overrides an intact osmoregulation (46% of all cases) or, allied to an inadequate urinary dilutional capacity (54%), leads to a transitory, sometimes repeated, and (in 8% of all cases) lethal water intoxication and hypoosmolality. - The consequence of hypoosmolality is metabolic encephalopathy, with agitation, convulsions and coma as its most common symptoms. Profuse diuresis, enuresis and urinary retention, gastric dilatation, watery vomiting and watery diarrhea are diagnostically helpful symptoms of polydipsia typically denied by the patients. Hypoosmolality/hyponatremia are the hallmarks of water intoxication. However, fewer than 50% of all patients present with the expected maximal urinary dilution. Inadequate ADH activity and increased sensitivity of the renal tubule to antidiuretic hormone are the pathogenetic factors in this inappropriate urinary dilution, while psychosis, psychotropic drugs, diuretics, nicotine and alcohol withdrawal are possible causes and cofactors of polydipsia and inadequate urinary dilution. New aspects of treatment are discussed.
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PMID:[Psychogenic water intoxication]. 264 58

Aluminum intoxication is common in patients with chronic renal failure because of absorption of aluminum during dialysis from aluminum-containing dyalysate water and ingestion of phosphate binders containing aluminum. Aluminum accumulation in the body is followed by bone disease, encephalopathy and anemia. Bone diseases can be recorded in 44% of the patients treated with long-term dialysis. Two early histologic types of retarded bone turnover can be seen, i.e. osteomalacia and aplastic bone disease. In dialyzed patients, osteomalacia is usually followed by low PTH level in human serum. On the contrary, studies on uremic rats have shown that previous parathyroidectomy can prevent aluminum intoxication, because hyperparathyroidism in an early phase of chronic renal failure increases aluminum absorption from the gut and its accumulation in the body. As the pathogenesis of aluminum-induced alterations is unclear, the prevention of bone disease should be provided through lowering the aluminum intake in dialyzed patients. Bone biopsy is unavoidable for the early detection and diagnosis of the disease. Promising results in the treatment of aluminum intoxication have been obtained using deferoxamine, a chelating agent.
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PMID:[Aluminum poisoning]. 267 63

Inorganic bismuth salts are poorly soluble in water: solubility is influenced by the acidity of the medium and the presence of certain compounds with (hydr)oxy or sulfhydryl groups. The analysis of bismuth in biological material is not standardised and is subject to large variation; it is difficult to compare data from different studies, and older data should be approached with caution. The normal concentration of bismuth in blood is between 1 and 15 micrograms/L, but absorption from oral preparations produces a significant rise. Distribution of bismuth in the organs is largely independent of the compound administered or the route of administration: the concentration in kidney is always highest and the substance is also retained there for a long time. It is bound to a bismuth-metal binding protein in the kidney, the synthesis of which can be induced by the metal itself. Elimination from the body takes place by the urinary and faecal routes, but the exact proportion contributed by each route is still unknown. Elimination from blood displays multicompartment pharmacokinetics, the shortest half-life described in humans being 3.5 minutes, and the longest 17 to 22 years. A number of toxic effects have been attributed to bismuth compounds in humans: nephropathy, encephalopathy, osteoarthropathy, gingivitis, stomatitis and colitis. Whether hepatitis is a side effect, however, is open to dispute. Each of these adverse effects is associated with certain bismuth compounds. Bismuth encephalopathy occurred in France as an epidemic of toxicity and was associated with the intake of inorganic salts including bismuth subnitrate, subcarbonate and subgallate. In the prodromal phase patients developed problems in walking, standing or writing, deterioration of memory, changes in behaviour, insomnia and muscle cramps, together with several psychiatric symptoms. The manifest phase started abruptly and was characterised by changes in awareness, myoclonia, astasia and/or abasia and dysarthria. Patients recovered spontaneously after discontinuation of bismuth. Intestinal lavage, forced diuresis and haemodialysis have been tried without positive effects on the clinical condition of the patient or on blood bismuth concentration, and the use of dimercaprol as an antidote has produced reports of both positive and negative findings. To confirm the diagnosis of bismuth encephalopathy, it is essential to find elevated bismuth concentrations in blood, plasma, serum or CSF. A safety level of 50 micrograms/L and an alarm level of 100 micrograms/L have been suggested in the past, but no proof is available to support the choice of these levels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pharmacokinetics and toxicity of bismuth compounds. 268 29

Magnetic resonance (MR) has begun to play an important role in neonatal neurology. Several MRI techniques have been applied to the diagnosis of hypoxic ischemic encephalopathy. Cerebral perfusion examined by intravoxel incoherent motion, a non-invasive tool, seems to be opening new inroads for detecting variations (neurophysiological modifications) in cerebral flows during hypoxic ischemic encephalopathy. MR spectroscopy allows identification of specific biochemical alteration of spectra patterns at various moments of hypoxic ischemic distress, including: (1) primary expression of metabolic disorders induced by the lack of blood and O2, revealed by a peak of the water-suppressed H1 spectrum, the earliest and most persistent-marker; (2) a secondary marker for the establishment of permanent lesions of anoxic-ischemic origin revealed that variations of the phosphocreatine/inorganic phosphorous index in the P31 spectrum are of diagnostic and prognostic significance in this phase. In relation to different neuropathological, structural lesions, MRI becomes particularly important in diagnosing the acute phase of cerebral edema and the different types of infarct. MRI is especially fruitful in monitoring the evolution of the lesion, providing an evaluation of myelinization, and defining the neuropathological outlook. Spectroscopic studies on human neonates have helped establish the therapeutic effects of mannitol in cerebral metabolism. MR studies on neonate animals seem to open new therapeutic prospect for CA antagonists.
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PMID:State of the art of magnetic resonance (MR) in neonatal hypoxic-ischemic encephalopathy. 269 12

Near drowning remains one of the most frequently encountered environmental injuries in the United States. Physicians can do much to educate their patients on prevention. Both at the scene and in the emergency department, physicians should direct initial attention to aggressive respiratory management, because hypoxia is the primary cause of mortality and morbidity in the near-drowning victim. An apparently lifeless victim of cold-water immersion may go on to full recovery with such management. In patients who survive the initial insult, the degree of hypoxic encephalopathy is the major determinant of outcome.
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PMID:Immersion injury. Drowning and near drowning. 272 38

Hepatic dysfunction after portacaval shunting (PCS) has been attributed to loss of portal perfusion to the liver. Proponents of selective systemic shunting state that reduced encephalopathy and hepatic dysfunction with this procedure result from the maintenance of portal perfusion to the liver through the hypertensive mesenteric venous circulation. We questioned the importance of maintaining the diminished portal flow to the cirrhotic liver because hepatofugal flow is known to develop in many of these patients. We sought to further define mechanisms that may contribute to the maintenance of critical flow to the liver in compensated hepatic cirrhosis. We demonstrated a primary relationship between mesenteric venous hypertension (MVH) and increased hepatic arterial blood flow after diversion of portal blood flow. Fifteen dogs had vena caval stenosis above an end-to-side PCS to establish MVH and deprive the liver of portal blood flow. Another 15 dogs had end-to-side PCS alone. A half hour after shunting, hepatic arterial blood flow had increased significantly in all dogs. Hemodynamic parameters remained stable throughout. Six weeks later, mesenteric pressure increased 98% +/- 3% with intracaval stenosis (from 9.6 +/- 0.1 to 19.0 +/- 0.3 cm H2O). Mesenteric pressure was unchanged with PCS alone (9.0 +/- 0.1 cm H2O). Increased hepatic arterial flow was significantly elevated in all dogs above pre-shunt values by 6 weeks postshunt. With MVH, however, further augmentation in hepatic arterial flow was noted in the chronic state (1.5 +/- 0.1 vs 0.9 +/- 0.1 ml/min/gm, p less than 0.05). There was significant correlation between MVH and increased hepatic arterial flow in the chronic state (r = 0.79, p = 0.05). Hepatic arterial flow 6 weeks after PCS with MVH was associated with lower blood ammonia and improved hepatocellular function compared with animals with PCS alone. These results support the hypothesis that MVH is important in maintaining blood supply--beyond providing driving force for sustained portal flow to the liver. This is an important consideration in the medical and surgical management of portal hypertension, a condition in which profound reduction in portal pressure may negatively affect compensatory hepatic arterial blood flow.
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PMID:Mesenteric venous hypertension: importance after portal systemic shunting? 274 Sep 86

Brain edema is a fatal complication of fulminant hepatic failure and its pathogenesis remains unclear. To determine its presence in a model of ischemic hepatic failure, rats were subjected to a portacaval anastomosis followed by hepatic artery ligation. Brain water was measured using the sensitive gravimetric method. Preliminary studies revealed marked hypothermia in devascularized animals kept at room temperature (26.9 degrees +/- 2.8 degrees C). An additional group of devascularized rats was kept in an incubator. As expected for hypothermia, such animals had a lower arterial pressure and heart rate; the duration of encephalopathy was markedly prolonged. Water content of the cortical gray matter was only increased in normothermic devascularized rats: 80.14% +/- 0.31%, normal; 80.06% +/- 0.22%, portacaval shunt only; 80.42% +/- 0.26%, devascularized at room temperature; 81.29% +/- 0.38%, devascularized at controlled temperature (p less than 0.001). Such differences could not be detected using the dry-weight technique in whole cerebral hemispheres. Astrocyte changes in the cortical gray matter were noted in both edematous and nonedematous devascularized groups, coupled with the presence of vesicles containing horseradish peroxidase in the endothelial capillary cell. This suggests that in this model, brain edema may be due to both a cytotoxic mechanism and changes in the permeability of the blood-brain barrier. Future studies with this widely used model will require strict control of temperature to allow interpretation of experimental results. A therapeutic role for hypothermia in the management of brain edema deserves further attention.
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PMID:Effect of body temperature on brain edema and encephalopathy in the rat after hepatic devascularization. 291 49

In order to compare the effectiveness of aluminum removal in uremic patients during extracorporeal treatment, 17 patients with endstage renal failure were given a desferrioxamine infusion of 40 mg/kg body weight after an ordinary dialysis treatment. Forty-eight hours later 7 patients were treated with hemodialysis, 6 with hemofiltration and 4 with a combination of hemodialysis and hemoperfusion. The clearance of aluminum was measured at different intervals. It was found that the aluminum clearance was 75 +/- 18 ml/min in hemofiltration compared to 30 +/- 10 ml/min in hemodialysis (p less than 0.001). A combination of hemodialysis and hemoperfusion with a charcoal column containing 100 g activated charcoal in series gave a total aluminum clearance of 56 +/- 11 ml/min. The total amount of aluminum in the ultrafiltrate after hemofiltration was found to be approximately 3 times as high (1,728 +/- 156 micrograms) as the total amount of aluminum in the hemodialysis water that had passed a single pass system during a 4-hour dialysis (576 +/- 104 micrograms). Our results indicate that hemofiltration or a combination of hemodialysis and hemoperfusion should be used to remove aluminum in patients with signs of severe aluminum accumulation such as encephalopathy or painful bone disease, because these methods are 2-3 times as effective as ordinary hemodialysis. In patients where aluminum has been accumulated but no severe symptoms occur hemodialysis gives a significant clearance of the aluminum desferrioxamine complex.
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PMID:Aluminum removal with hemodialysis, hemofiltration and charcoal hemoperfusion in uremic patients after desferrioxamine infusion. A comparison of efficiency. 231 28

"Energy metabolism" is deranged in a wide variety of disorders of the nervous system. This term refers rather loosely to the pathways responsible for the utilization of the major substrates of brain. Primary disorders of energy metabolism are those in which the primary insult affects the cellular machinery required for energy metabolism. A typical example would be a defect in a gene coding for a mitochondrial protein. Biochemically, defects which appear to be hereditary and which lead to disease of the central nervous system have been described in each of the pathways of energy metabolism: glycogenolysis (the break-down of glycogen to glucose); glycolysis (the break down of glucose to pyruvate and lactate); the pyruvate dehydrogenase complex (which oxidizes pyruvate to enter the Krebs tricarboxylic acid cycle); the tricarboxylic acid cycle itself (which completes the oxidation of carbohydrates and other substrates to carbon dioxide); electron transport (which carries out their oxidation to water); the pentose phosphate pathway (an alternate pathway for glucose oxidation); and several "minor" mitochondrial pathways. Clinically, the spectrum of syndromes associated with primary disorders of energy metabolism is wide. Common manifestations include psychomotor retardation, with associated lactic acidosis and/or hypoglycemia. The laboratory abnormalities may be intermittent. Syndromes which have been culled out include congenital lactic acidosis, Leigh disease, intermittent ataxia, Kearns-Sayre-Shy syndrome (KSS), myoclonus epilepsy with ragged red fibers (MERRF), and mitochondrial myopathy-encephalopathy-lactic acidosis-stroke (MELAS). As with other families of inborn errors, both clinical and biochemical heterogeneity occur. Patients with apparently similar clinical syndromes can turn out to have different inborn errors, and patients with abnormalities of the same gene product can have clinically distinguishable syndromes. Secondary disorders are those in which the derangements of energy metabolism are presumably secondary to some other insult but may still be important for the cellular pathophysiology. These include the metabolic encephalopathies and probably a number of well-known neurodegenerative disorders. In the hereditary ataxias, abnormalities of mitochondrial markers are common but do not correlate consistently with the disorders as conventionally classified; a new classification into axonal ataxias, multiple system degenerations, and ataxic encephalopathies may be easier to relate to the pathophysiology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Energy metabolism in disorders of the nervous system. 297 43


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