Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.
 ...
PMID:Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease). 56 79

Ischemia-provoking factors such as vasospasm, decreased cerebral perfusion pressure, and intravascular thrombosis may be present after subarchnoid hemorrhage (SAH). When these factors were not present during controlled SAH, a primary depression of cerebral glycolysis associated with normal stores of energy-rich phosphates was found. Although cerebral blood flow usually changes in response to changes in cerebral metabolic needs, this influence on the circulation was not evident in the early hours after SAH. After 3 to 4 hours an erratic decrease in blood flow occurred, probably related to vasospasm, and there were measurable decreases in energy-rich phosphates similar to those occurring after more severe and prolonged ischemias. These findings are indicative of abnormally erratic vascular responses to metabolic cues and may play a role in producing the encephalopathy of SAH.
 ...
PMID:Brain energetics and circulatory control after subarachnoid hemorrhage. 82 8

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
 ...
PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

To determine whether cytotoxic brain edema is associated with a decrease in diffusion, it was induced in rats, in the absence of ischemia, with an established model of acute hyponatremic encephalopathy. Cytotoxic brain edema secondary to acute hyponatremia was induced with intraperitoneal injections of 2.5% dextrose in water and subcutaneous injection of arginine-vasopressin. Coronal spin-echo magnetic resonance (MR) images were obtained with and without strong diffusion-sensitizing gradients before and after induction of acute hyponatremia. The apparent diffusion coefficient (ADC) was measured at two coronal section locations. In hyponatremic rats, the brain ADC was significantly reduced (P = .0153 and .0001) and was positively correlated with increased total brain water content (P = .0011). Plots of ADC versus total brain water showed a statistically significant inverse linear relationship between ADC and increasing brain water at the anterior coronal section location. The results indicate that the ADC may be a sensitive indicator of cytotoxic brain edema and thus may enable quantitative evaluation of such edema with diffusion-weighted MR imaging.
 ...
PMID:Cytotoxic brain edema: assessment with diffusion-weighted MR imaging. 143 45

The neurometric method as introduced by John was used to study three groups of patients with cerebral ischemia, three groups of patients with renal disease and an additional normal control group. The traditional neurometric approach was slightly modified: relative band power values were not expressed as a percentage of the total power per derivation but as a percentage of the "global power"; frequency matrices were used in addition to power matrices. From the study of the three groups of patients with one-sided supratentorial ischemia it appeared that sensitivity and specificity are completely satisfactory when using neurometrics in patients with severe ischemia in the middle cerebral artery territory studied within 48 hours of the onset of the stroke. However, in ischemia patients with less pronounced clinical signs and especially in patients without persistent neurological deficit the sensitivity is much lower. In studying dialysed and non-dialysed renal patients signs of an (often subclinical) encephalopathy could be detected in approximately 37% of all patients. Follow-up studies of the ischemia patients and the renal patients over a period of several years revealed a parallelism between clinical scores and qEEG scores in the ischemia patients; almost all qEEG improvement occurred in the first three months after the stroke. The qEEG profile of the groups of dialysed patients tended to be more or less stable over a period of several years.
 ...
PMID:Neurometrics in cerebral ischemia and uremic encephalopathy. 151 Aug 71

Magnetic resonance (MR) images obtained in 15 patients with delayed encephalopathy after acute carbon monoxide (CO) intoxication were reviewed. Images had been obtained 4-9 weeks after exposure to CO, during the relapse of neuropsychiatric symptoms after initial recovery. Bilateral symmetric confluent high signal intensity in the periventricular white matter and centrum semiovale was seen on long-repetition-time images (n = 15). The high intensity extended into the corpus callosum (n = 11), subcortical U fibers (n = 12), and external (n = 9) and internal (n = 7) capsules. Bilateral diffuse low-intensity signal in the thalamus and putamen on T2-weighted images, suggesting iron deposition, was demonstrated in 10 patients. Bilateral ischemia or necrosis of the globus pallidus was seen in nine patients. In three of four patients with follow-up MR imaging studies, a decrease in extent and signal intensity of white matter lesions accompanied lessening of clinical symptoms. These results suggest that the main pathologic feature of delayed encephalopathy associated with CO intoxication is a reversible demyelinating process of the cerebral white matter.
 ...
PMID:Delayed encephalopathy after acute carbon monoxide intoxication: MR imaging features and distribution of cerebral white matter lesions. 160 67

At present in vivo NMR spectroscopic studies of brain glutamate and glutamine concentrations relative to encephalopathy have mainly been performed in hepatic encephalopathy (HE). In vivo proton NMR studies were performed in rats with hyperammonemia and acute HE due to acute liver ischemia as well as in rats with hyperammonemia due to either repeated urease i.p. injection or i.p. administration of methionine sulfoximine, a well known inhibitor of glutamine synthetase. In man, in vivo proton NMR is described in patients with chronic liver disease: cirrhosis of different etiology and associated with different degrees of HE. In the experimental models proton NMR spectroscopy of the cerebral cortex revealed an increase in glutamine concentration, a decrease in glutamate concentration and a decrease in phosphocholine compounds. In humans no clear distinction between cerebral cortex glutamate and glutamine concentration could be made by in vivo 1H NMR spectroscopy. However, the combined glutamate/glutamine peak increased in a way compatible with an increased cerebral cortex glutamine concentration during chronic HE. In the cirrhotic patients too a decrease in cerebral cortex phosphocholine compounds was observed, the explanation of which is unclear. Both the experimental work and the clinical observations support the hypothesis that impairment of the glutamate/glutamine cycle between astrocytes and neurons plays a role in the pathogenesis of hepatic encephalopathy.
 ...
PMID:What the clinician can learn from MR glutamine/glutamate assays. 167 85

Cerebral ischemia in the neonate is an important cause of hypoxic-ischemic encephalopathy. Thus, it is important to have an economical and readily available animal model in which to study the local control of the cerebral circulation in the perinatal period. This study demonstrates that the newborn rabbit, a rather immature species at birth, is a suitable neonatal model in which to measure local cerebral blood flow with quantitative iodo[14C]antipyrine autoradiography. One or 2 d after birth, local cerebral blood flow in the newborn rabbit is low, but flow varies distinctly between regions [e.g. 8.9 +/- 1.5 mL.kg-1.s-1 (53 mL.100 g-1.min-1) in the nucleus tractus solitarius and 3.4 +/- 0.7 mL.kg-1.s-1 (20 mL.100 g-1.min-1) in the frontal cortex]. During early postnatal development (i.e between 1 and 8 d), local cerebral blood flow does not change greatly. However, by 17 d, 22 of 26 brain regions exhibit significant marked increases (200-350%) in local cerebral blood flow when compared with blood flow in the newborn. Between 17 and 40 d postnatally, cerebral blood flow continues to increase in 16 of 26 regions (e.g. thalamic areas). In four of the cerebral cortical areas, elevations in flow continue during the period between 40 d of age and adulthood. In contrast to the generalized increases in flow occurring postnatally, a few brain regions (i.e. within the pons and medulla) exhibit only minor changes in cerebral blood flow. The differential pattern and lower basal levels of cerebral blood flow in the neonate compared with the adult may be important determinants in regional susceptibility of the brain to ischemia.
 ...
PMID:Local cerebral blood flow in the newborn rabbit: an autoradiographic study of changes during development. 189 57

Content of 5-, 8-, 11-, 12- and 15-monohydroxyeicosatetraenoic acids was markedly increased in blood of patients with cerebral atherosclerosis accompanied by discirculatory encephalopathy and brain infarction. These values were lower in the patients with infarction as compared with healthy people. After tourniquet ischemia of limbs concentration of the eicosatetraenoic acids was altered in blood of patients: in one group the concentration of all the lipoxygenase metabolites of arachidonic acid was increased, in the other group of patients it was decreased. Development of atherosclerosis appears to be related to activation of lipoxygenases and production of monohydroxyeicosatetraenoic acids.
 ...
PMID:[Level of monohydroxyeicosatetraenoic acid in the blood of patients with cerebral blood circulation disorders]. 194 87

The effects of hyperammonemia on brain function have been studied in three different experimental models in the rat: acute liver ischemia, urease-treated animals and methionine sulfoximine-treated animals. To quantify the development of encephalopathy, clinical grading and electroencephalographic spectral analysis were used as indicators. In all three experimental models brain ammonia concentrations increased remarkably associated with comparable increases in severity of encephalopathy. Furthermore, in vivo 1H-nuclear magnetic resonance spectroscopy of a localized cerebral cortex region showed a decrease in glutamate concentration in each of the aforementioned experimental models. This decreased cerebral cortex glutamate concentration was confirmed by biochemical analysis of cerebral cortex tissue post mortem. Furthermore, an increase in cerebral cortex glutamine and lactate concentration was observed in urease-treated rats and acute liver ischemia rats. As expected, no increase in cerebral cortex glutamine was observed in methionine sulfoximine-treated rats. These data support the hypothesis that ammonia is of key importance in the pathogenesis of acute hepatic encephalopathy. Decreased availability of cerebral cortex glutamate for neurotransmission might be a contributing factor to the pathogenesis of hyperammonemic encephalopathy. A surprising new finding revealed by 1H-nuclear magnetic resonance spectroscopy was a decrease of cerebral cortex phosphocholine compounds in all three experimental models. The significance of this finding, however, remains speculative.
 ...
PMID:Changes in brain metabolism during hyperammonemia and acute liver failure: results of a comparative 1H-NMR spectroscopy and biochemical investigation. 197 48


1 2 3 4 5 6 7 8 9 10 Next >>