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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with atherosclerotic encephalopathy (AE) the major indices of blood rheology, hemostasis and its cells' functional state were under investigation. Different patterns of blood rheology changes were detected with increased counts of pathological red blood cells and hypercoagulability. These disorders correlated with the rate of major neurological signs and syndromes, and with the disease stage as well. A multilevel positive effect of hemosorption was shown in different pathogenic links of AE related to disorders in lipid metabolism, blood rheology, shape and functional activity of erythrocytes, shifts in the homeostatic systems. This suggested the use of hemosorption as a tool in prevention of ischemic stroke.
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PMID:[Rheologic properties of the blood and the system of hemostasis in patients with circulatory encephalopathy treated by hemosorption]. 278 48

Blood serotonin levels have been measured by spectrofluorometry in 145 patients with various manifestations of acute disorders of the cerebral circulation (ADCC): with ischemic stroke, cerebral hypertensive crises, transient impairments of the cerebral circulation, and with circulatory encephalopathy (DE) in the presence of arterial hypertension combined with atherosclerosis. In ADCC patients the blood serotonin has been measured 7 times, in DE ones 3 times. This level has been found changed in the patients with ischemic stroke and with cerebral hypertensive crises for a long time after the cerebral circulation impairment. Serotonin levels correlated with the condition severity and course in ADCC and DE. The vestibulocerebellar syndrome in DE has been treated more effectively, particularly with trental. The blood serotonin level may be regarded as a prognostic criterion of the disease outcome and of the treatment efficacy.
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PMID:[Dynamics of blood serotonin contents in acute disorders of cerebral circulation and circulatory encephalopathy]. 279 19

The extent of molecular defects in the mitochondrial energy-transducing system was examined in autopsied tissues of a 14-year-old male with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) in order to elucidate the underlying molecular and genetic abnormalities. The patient also had other multiorganic disorders: hypertrophic cardiomyopathy, nephrotic syndrome, and pseudohypoparathyroidism. Enzymic activities of complex I and IV were severely decreased, and those of complex III and V were mildly decreased in the mitochondria isolated from various tissues, but the severity of the deficiencies varied from tissue to tissue. In contrast, complex II and citrate synthase activities were normal or were decreased to a lesser extent than the enzymic activities of other complexes in all the tissues examined. These results suggest that the energy-transducing complexes, namely complexes, I, III, IV, and V, that contain mitochondrially synthesized subunits, were selectively affected. Immunoblot analysis demonstrated that the decreased enzymic activities were based on decreased contents of subunits in these complexes. The multiorganic manifestation of the disorder may result from wide and uneven distribution of abnormal mitochondria that have pleiotropic molecular defects in the energy-transducing complexes among the organs of the patient.
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PMID:Pleiotropic molecular defects in energy-transducing complexes in mitochondrial encephalomyopathy (MELAS). 280 15

A 29-year-old single woman had recurrent stroke-like episodes. She developed loss of consciousness, myoclonic seizures, and lactic acidosis. She died at the age of 30. A muscle biopsy study revealed mitochondrial myopathy, and the postmortem biochemical analysis demonstrated decreased cytochrome c oxidase activity in the skeletal muscles by 20% of normal control. The brain had multiple ischemic lesions in the cerebral cortex without major vascular occlusions. We present this case as an autopsy case of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with a partial deficiency of cytochrome c oxidase. The analytical electron microscopic study of the calcified small vessels in the globus pallidus revealed increased calcium, phosphorus and iron. No accumulation of chromium, nickel or zinc was noted in this case, which was different from the previously reported cases of basal ganglia calcification.
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PMID:An autopsy case of mitochondrial encephalomyopathy: biochemical and electron microscopic studies of the brain. 284 99

Identical twins developed myoclonic epilepsy in their teens. One twin remained mildly affected but the other went on to develop sensorineural deafness and ataxia with lactic acidosis and ragged red fibres leading to a diagnosis of mitochondrial encephalopathy. Multiple stroke-like episodes with hemiparesis followed, indicating progression from a MERRF to a MELAS phenotype. Biochemical studies revealed a severe deficiency of mitochondrial NADH-ubiquinone reductase and a moderate deficiency of cytochrome aa3. Western immunoblotting experiments using polyclonal antibodies raised against human placental cytochrome oxidase identified a similar profile of bands to those seen in controls, supporting the view that cytochrome aa3 deficiency in this case may be a secondary consequence of a failure of assembly related to a severe proximal respiratory chain defect.
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PMID:Progression from MERRF to MELAS phenotype in a patient with combined respiratory complex I and IV deficiencies. 285 17

There are no large studies on long-term treatment of nursing home patients with pressure sores. A 4-year experience of treating 95 nursing home patients on air-fluidized beds was reviewed. Treated patients were elderly (median age 73 years) and neurologically impaired (79% with dementia, cerebral vascular accident, or anoxic encephalopathy). The index pressure sores (deepest truncal sore for each patient) were large (median surface area 35.3 cm2) and commonly located on the sacrum (41%) and trochanters (38%). Only 13 of 95 (14%) index sores healed completely, and only two small sores healed in less than 30 days. No others treated less than 30 days had greater than or equal to 50% reduction in sore surface area. Patients were grouped according to whether or not treatment was less than 30 days, and for those treated greater than or equal to 30 days, according to whether or not greater than or equal to 50% reduction in sore surface area occurred. None of the easily measured patient characteristics examined were associated with longer or more successful treatment. These results indicate that although air-fluidized beds can be used to treat pressure sores successfully, even in severely debilitated nursing home patients, no simple criteria can be used to predict which patients will benefit from this treatment. Because long periods of time are necessary for treatment [median trial length 79 days and 17 of 95 (18%) trials greater than 180 days], substantial patient-care expenditures result.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Air-fluidized bed treatment of nursing home patients with pressure sores. 291 93

"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

Gaseous metabolism and carboanhydrase activity of erythrocytes of the capillary and venous blood were studied in 115 persons, including 19 apparently normal subjects, 66 patients with ischemic stroke, and 30 with discirculatory encephalopathy. Patients with cerebral stroke presented gross disorders in the function of carboanhydrase and gaseous metabolism from the first day of the disease which was expressed in an increased oxygenation of the venous blood and hypocapnia, whose severity was correlated with the gravity of the disease course. The authors have established an important pathogenetic role in gaseous metabolism impairment of erythrocyte carboanhydrase, whose activity in the capillary bed in hypocapnia was drastically inhibited, compromising, therefore, the entry of carbon dioxide into erythrocytes, which deteriorated oxyhemoglobin dissociation. The authors consider the possibility of normalizing gaseous metabolism in stroke patients via eliminating CO2 deficit in tissues.
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PMID:[Erythrocyte carboanhydrase and gas metabolism in patients with ischemic stroke]. 312 92

The spinal cords of 2 autopsied patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) were examined. Histologically, the spinal cords showed a spongy state due to the presence of distended myelinated fibers with enlarged periaxonal spaces. Ultrastructurally, the affected fibers showed extensive microvacuolation of the inner myelin sheath with occasional vesicular changes. The presence of macrophages near the degenerated myelin was a frequent finding. The stripping of myelin lamellae by macrophage was observed, with frequent appearance of denuded axons. Furthermore, prominent morphological changes were observed in oligodendrocytes. These findings indicate that demyelination, probably secondary to the degeneration of oligodendrocytes, occurs in the spinal cord of MELAS.
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PMID:Alterations of oligodendrocytes and demyelination in the spinal cord of patients with mitochondrial encephalomyopathy. 317 95

Two patients with visual agnosia underwent visual recognition and neuropsychological tests to characterize their perceptual functioning. Both had an initial "apperceptive profile" and evolved from cortical blindness. One had carbon monoxide intoxication and incidental agenesis of the splenium of the corpus callosum; the other had the clinical features of MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke-like syndrome). The agnosia profile showed impaired object recognition but adequate visual matching and copying of unrecognized items. The patients were successful on form discrimination, mental rotation, and visuospatial skills, but did poorly on figure-ground discrimination, visual integration, facial discrimination, and constructional tasks. Their performances were characterized by slow, serial analysis of visual features and a decreased useful field of view. The pattern of results suggests a form of visual agnosia caused by disturbances of parallel distributed processing.
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PMID:Visuoperceptual function in visual agnosia. 318 10


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