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

The hydrogen clearance method was used to measure local and total cerebral blood flow (CBF) in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage (SAH). CBF remained stable after SAH unless SAH was associated with a fall in cerebral perfusion pressure. In addition, cerebrovascular resistance did not increase after SAH. These results suggest that vasoactive agents in fresh whole blood, and the arterial spasm they produce when added to cerebrospinal fluid (CSF), play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.
Stroke
PMID:The effect of a simulated subarachnoid hemorrhage on cerebral blood flow in the monkey. 0 Aug 20

Central nervous system (CNS) involvement is rare in scleroderma unless there are concomitant abnormalities in renal or lung function or malignant hypertension. A 43-year-old woman with typical scleroderma developed subacute encephalopathy despite absence of the above abnormalities. Cerebral angiography demonstrated a focal arteritis. The patient improved while being given corticosteroids. We believe this case indicates that cerebral arteritis can occur in scleroderma.
Stroke
PMID:Cerebral arteritis in scleroderma. 50 2

Large doses of phenytoin were administered on 159 occasions to 139 adult patients. Most patients had had more than three seizures or were in status epilepticus. Based on response to treatment, patients could be divided into two groups. Those with excellent response (recurrent seizures, 10%; mortality, 1%) included known epileptics with exacerbation of seizures (n = 75), atypical alcohol withdrawal (6), or miscellaneous conditions (17). Those with poor results (recurrent seizures, 57% mortality, 38%) included patients with anoxic or metabolic encephalopathy (14), stroke or other vascular disease (14), brain tumor (5), or trauma (5).
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PMID:Intravenous phenytoin in acute treatment of seizures. 57

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

A 51-yearold man with moderate intermittent hypertension had a rapidly progressive, profound dementia in the absence of significant localizing neurological signs. Postmortem examination disclosed the vascular alterations and diffuse white matter degeneration which characterize subcortical arteriosclerotic encephalopathy (SAE) or Binswanger's disease. The case underscores the need to consider vascular disease as an etiology of dementia -- even in the absence of focal neurological deficit.
Stroke
PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's disease). A vascular etiology of dementia. 100 40

Cultures of a mouse cell line (PAM) were treated with 71 multiple sclerosis (MS) and 45 non-MS samples. Of the cultures treated with MS material, 80 percent (58) showed a reduction in cell yield (compared to untreated controls) of at least 20 percent by the third passage after inoculation. The MS samples were from 40 MS cases, and a total of 36 cases yielded at least one positive sample. The agent responsible for the decrease was not limited to nervous tissue, but was also found in serum, cerebrospinal fluid, spleen, kidney, and lymph node of MS patients. Positive samples were present at every stage of the disease. None of the non-MS samples yielded cell counts significantly different from untreated controls. The non-MS category included 12 samples from healthy individuals, 13 assorted non-central nervous system disease samples, and the following central nervous system disease samples: six subacute sclerosing panencephalitis, three Huntington's chorea, two Parkinsonism, six amyotrophic lateral sclerosis, one stroke, one encephalopathy, and one epilepsy. Brain homogenates from mice inoculated with MS tissues elicited the decrease, whereas brain homogenates from mice inoculated with non-MS samples did not.
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PMID:Multiple sclerosis-induced reduction in the yield of a mouse cell line. 112 Jun 12

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.
Stroke
PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

The possibilities of the use of electroencephalography for evaluating intellectual-mnemonic disorders in elderly patients with cerebral atherosclerosis have been studied. The study included 95 subjects aged 60 to 74 years with varying intensity of circulatory atherosclerotic encephalopathy (without brain stroke). The psychological tests were performed according to Wechsler's methods. To evaluate the EEG, visual and automatic spectral analyses were employed. The data obtained were analyzed by means of discriminant, correlation and regression methods. A certain relationship was found between the results of the psychological tests and the EEG readings. The method of automatic EEG analysis is proposed, which allows revealing intellectual disorders in patients suffering from cerebral atherosclerosis. Its comparability with the data obtained by means of visual EEG analysis is discussed.
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PMID:[Correlations of cognition disorders and the EEG data in elderly patients with circulatory encephalopathy]. 131 45

Cavinton was used for 10 years in 967 patients with different cerebrovascular diseases. The highest effect was seen in patients with early forms and primarily chronic forms: vegetovascular (neurocirculatory) dystonia, initial manifestations of brain blood supply insufficiency, circulatory encephalopathy in the first and second stages. Improvement of the subjective status and a decrease of the intensity of vestibulocerebellar disorders were recorded by the end of the treatment in 75-85% of such patients. In ischemic brain stroke, regress of general cerebral and focal symptoms was more rapid and significant in the adequate reaction type of cerebral hemodynamics to cavinton administration (a rise of pulse blood content of the brain and a reduction of the vascular tone according to the REG data) and was less noticeable in the hypertonic and, in particular, in the hypotonic type. Cavinton should not be used in severe general cerebral hypertensive crises, as well as in elderly or senile patients with acute cardio-cerebral or cerebro-cardiac syndrome, postinfarction cardiosclerosis, marked disorders of heart rhythm.
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PMID:[10-year experience with using Cavinton in cerebrovascular disorders]. 131 51

In order to determine the patient blood flow hydrodynamic properties in terms of the Toms-effect, the time blood flow was measured in special apparatus twice: (1) before and (2) after addition of poly(ethylene oxide) WSR-301 (Union Carbide, USA) in concentration of 2 x 10(6) g/ml of blood sample (50 ml with 500 units of heparin) taken from 26 patients with acute ischaemic stroke, 8 patients with vascular encephalopathy after stroke, 5 patients with vascular encephalopathy following atherosclerosis with or without arterial hypertension. The blood samples taken from 8 healthy persons formed the control group. Haematocrit (HCT) and asymptotic blood viscosity were studied also. It was established that hydrodynamic blood flow resistance (HBFR) did not depend on HCT and viscosity, but was significantly higher in all patient groups than in normal persons (p less than 0.05). Addition of polymer solution decreased HBFR of patient blood more intensively that in the control group. We believe that it indicates an insufficiency of an unidentified factor in native human blood.
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PMID:Blood flow hydrodynamic resistance in patients with ischaemic stroke or vascular encephalopathy and possibilities of its correction in vitro. 135 73


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