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

Brain metabolites and arterial acid-base measurements were made one hr after bilateral carotid artery occlusion in 2 different models of hypertensive rats. Animals used included renovascular hypertensive rats (RHR) with an altered renin-angiotensin system and desoxycorticosterone hypertensive rats (DHR) with low plasma renin activity (PRA). The mean value for supratentorial lactate of 7.41 mM/kg in RHR was significantly higher than in DHR (3.90 MM/kg) or in control normotensive rats (3.10 - 2.56 mM/kg). Concomitantly, the lactate/pyruvate ratio tended to increase and ATP to decrease in RHR only. In these same rats (RHR) infratentorial lactate was also increased. The results suggest that bilateral carotid occlusion leads to anaerobic metabolism of the brain in RHR but not in DHR, suggesting that the renin-angiotensin system may play some role in the susceptibility to cerebral ischemia following carotid occlusion in the hypertensive rats.
Stroke
PMID:Brain metabolism following bilateral carotid occlusion in 2 different models of experimental hypertensive rats. 50 99

A self-administered questionnaire designed to identify people with transient cerebral ischemia (TIA) in large population groups was distributed to approximately 10,000 elderly persons living in public and private retirement facilities in the United States. The population resided in eight cities, and 74% completed the survey. Transient focal neurological symptoms compatible with a diagnosis of TIA within the previous year were reported by 6.4% of the respondents. Uncertain manifestations of TIA, i.e., dizziness, light-headedness, or loss of balance, were noted by an additional 15.4%; the remaining 78.2% had no manifestations of this disorder. A clinical history for TIA was taken by a neurologist in a sample of 1,712 respondents to determine the validity of the questionnaire responses. Thirty (7.1%) of 423 persons presumed by the questionnaire to have TIA met the standard clinical criteria for the diagnosis. An additional 8 cases of TIA were found by the neurologist among the 1,289 interviewed persons presumed by the questionnaire to have uncertain TIA or no evidence of the disorder. The twelve-month period prevalence of TIA was estimated to be 8.2 per 1,000 in the total respondent population and 5.8 per 1,000 among those without a history of prior completed stroke. Despite the high proportion of false-positive neurological symptoms of TIA elicited by the questionnaire, this survey instrument nevertheless screened out for further study the 6% of the population in whom 55% of the TIAs occurred.
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PMID:Use of a self-administered questionnaire for detection of transient cerebral ischemic attacks: I. Survey of elderly persons living in retirement facilities. 50 55

Over the past three years, high-dose barbiturate therapy has been used in the treatment of 60 patients with head injury (N = 45), encephalitis (N = 8), acute focal cerebral ischemia (stroke, N = 4), and global anoxia secondary to drowning (N = 3). High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Administration of barbiturates to patients with this problem will often reduce the requirement for osmotic agents, thereby facilitating medical management by avoiding hyperosmolality and fluid and electrolyte depletion. In a carefully controlled intensive care setting the risk of barbiturate therapy is low, though the costs and demands on personnel are great. Survival appeared to be improved in aptients with ,head injury and encephalitis. Although the ultimate outcome was not altered in patients with stroke or near-drowning, intracranial hypertension did not occur until barbiturate therapy was withdrawn. This experience provides an ethical basis to justify further randomized studies for determining whether or not barbiturates materially improve the neurological outcome following cerebral ischemic and traumatic insults.
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PMID:High-dose barbiturate therapy in humans: a clinical review of 60 patients. 53 17

A total of 289 carotid endarterectomies were performed in 204 patients. A decision to place a temporary shunt during carotid endarterectomy in this series was made entirely on the basis of intraoperative EEG monitoring. Retrospectively, the correlation between stump pressures and the results of intraoperative EEG monitoring in each case was determined. Evidence of ischemia developed in 6% of the total series on intraoperative EEG monitoring despite a stump pressure of greater than 50 mm Hg. The degree of disagreement between stump pressure and EEG varied according to clinical category in this series. In those endarterectomies performed for completed stroke, all cases requiring shunting had stump pressures less than 50 mm Hg. In those cases performed for symptoms of vertebral basilar insufficiency, however, 77% of the cases requiring an intraoperative shunt had stump pressures greater than 50 mm Hg. A review of the complication rate in the various study groups indicates that the use of intraoperative EEG is a safe indicator of cerebral ischemia during carotid endarterectomy regardless of stump pressure.
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PMID:Failure of carotid stump pressures. Its incidence as a predictor for a temporary shunt during carotid endarterectomy. 53 56

The microanastomosis of a scalp artery to a cortical vessel to augment cerebral blood flow is a significant advance in the treatment of patients with cerebral ischemia due to intracranial arterial obstruction. Results of nearly two thousand cases performed in the world since 1967 show clearly that the operation is excellent in the relief of transient ischemic attacks and in the prevention of iatrogenic stroke. Its place in the long term prevention of strokes is being evaluated. A personal series of 16 patients with 18 microvascular by-passes is reported. The indication, technique and pitfalls of this procedure is illustrated in this local series.
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PMID:Extracranial-intracranial microvascular by-pass in the treatment and prevention of cerebral ischemia. 53 15

The results of a retrospective study of patients undergoing carotid endarterectomy for hemispheric and/or nonhemispheric symptoms of transient ischemic attacks are presented. During an approximately 3-year period of follow-up observation, recurrent cerebral ischemia following carotid endarterectomy was two to three times more frequent among patients with nonhemispheric transient ischemia than among those with hemispheric transient ischemia. Patients with symptoms of both hemispheric and nonhemispheric transient ischemia had the highest frequency of transient ischemic attacks and stroke during the follow-up period and also had the greatest surgical morbidity and mortality. The results of this study suggest that carotid endarterectomy has little or no therapeutic value in treating patients with vertebral-basilar ischemia.
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PMID:The value of carotid endarterectomy in treating transient cerebral ischemia of the posterior circulation. 55 76

Study of the blood platelet functional activity and intensity of hemolysis in 41 patients with transient disorders of cerebral circulation and comparison of the results with the corresponding indices in healthy individuals, in 40 patients with hypertensive disease free of crisis, and in 25 patients with cerebral atherosclerosis led to the conclusion that the character of cerebral stroke is already determined in the pre-stroke period. It depends on the functional state of the blood platelets in many respects. In patients with hypertensive disease in a period clear of crisis, for instance, there is a tendency towards hypoaggregation possible associated with the presence of latent hemolysis. Platelet hypofunction progresses in the period of hypertensive encephalopathy and still more during its transformation into hemorrhagic stroke. On the contrary, in patients with atherosclerosis but no symptoms of cerebral ischemia the adhesion-aggregation activity of the platelets does not differ essentially from that in healthy individuals. With the development of signs of ischemia of the brain, the platelet activity grows considerably, particularly when transient cerebral circulatory disorders transform into ischemic stroke.
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PMID:[Importance of the thrombocytes and hemolytic syndrome in the pathogenesis of transient cerebral circulatory disorders in hypertension patients]. 63 13

Cerebral ischemia was produced in gerbils by ligation of the right common carotid artery and the resulting clinical manifestations and pathological alterations, along with electroencephalographic findings, were followed from 30 minutes to 24 hours. Protein synthesis was evaluated with brain slices in vitro and subsequent cellular and subcellular fractionations. One group of animals developed clinical signs of cerebral ischemia and stroke very rapidly and often died within 12 hours. In these animals cerebral infarction was diffuse in the right side of brain within a few hours post-operatively and there was persistent suppression in the electroencephalographic recordings. Amino acid incorporation into protein of subcellular fractions was decreased to 50% of the opposite side at 30 minutes and further declined to less than 10% in 8 to 10 hours. Another group of animals survived to 24 hours in spite of severe neurological manifestations, and protein synthesis was about 15% of the control side at 24 hours. The suppression of protein synthesis was observed both in the neuronal and neurologlial fractions indicating similar vulnerability of these cellular elements toward cerebral ischemia as shown with cerebral anoxia in the past. It was emphasized that the correlation of clinical manifestations and biochemical data is very important to extract meaningful information from biochemical investigations in this model.
Stroke
PMID:Experimental stroke in gerbils: correlation of clinical, pathological and electroencephalographic findings and protein synthesis. 64 9

Difficulties in achieving focal temporary cerebral ischemia in experimental animals have delayed study of the prevention and treatment of cerebral infarction. We have succeeded in producing focal cerebral infarction by temporary occlusion of brain arteries. Infarction confined to the anterior portion of the thalamus was obtained by simultaneous occlusion of the 4 cerebral arteries: internal carotid, anterior cerebral, middle cerebral and posterior communicating arteries for 60-120 minutes. This experimental model in dogs is unique, since thalamic infarction can be produced with high frequency, and the dogs can be kept alive and managed for sufficient periods after temporary artery clipping. With this model it is possible to investigate cerebral infarction not only from the pathophysiological viewpoint, but also from the viewpoint of prevention and treatment of cerebral infarction in man.
Stroke
PMID:Experimental cerebral infarction. Part 1: Production of thalamic infarction in dogs. 64 16

The efficacy of pentobarbital in the delayed treatment of acute cerebral ischemia was investigated in cats. Cerebral ischemia was produced by left middle cerebral artery (LMCA) ligation. Ten cats received 50 mg/kg of pentobarbital prior to ligation; a second group of 10 cats received the same dose of pentobarbital 2 hrs after ligation, and the control group of 7 cats received no pentobarbital. Brains were removed after spontaneous or induced death and the volume infarction was determined histologically. It was found that the volume of brain infarction in the group receiving pentobarbital 2 hrs after ligation was significantly less than that of the control group, which received no pentobarbital; but the volume of infarction in the former group was significantly greater than that found in the experimental group, which received pentobarbital prior to ligation. However, the mortality after LMCA ligation was higher in the 2 experimental groups, which received pentobarbital therapy, than in the control group, which did not receive pentobarbital. An hypothesis was advanced, which speculated that secondary adrenal insufficiency and altered cardiovascular function accounted for the increased mortality after pentobarbital treatment of patients with ischemic stroke.
Stroke
PMID:Delayed pentobarbital therapy of acute focal cerebral ischemia. 64 22


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