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Results for “Cerebral Infarction”

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At least 19 recordsLinked to original sources
PubMed1977

Reduction of coagulation factor XIII concentration in patients with myocardial infarction, cerebral infarction, and other thromboembolic disorders.

Coagulation factor XIII and plasma fibrinogen chromatographic assays have been performed serially in patients suffering from acute myocardial and cerebral infarction, and in others with disseminated intravascular coagulation. The findings were compared with 2 groups of "controls"; normal clinically-well subjects and hospitalized patients with cerebral infarction who exhibited minimal, stable, or improving neurological deficits. Substantial depression of factor XIII concentrations developed in the 3 patient groups, together with concomitant significant increases in the proportion and concentration of plasma high molecular weight fibrin(ogen) complexes (HMWFC). An inverse correlation (p less than 0.05) between coagulation factor XIII concentration and percentage of HMWFC was demonstrated in the early stages of the illness. These findings suggest that depression of coagulation factor XIII concentration in these states, is secondary to extravascular or intravascular coagulation and may reflect its degree.

Adult↗
PubMed1991

Cerebral blood flow and event-related potential in patients with multiple cerebral infarcts.

Cerebral blood flow and P300, a long-latency, positive component of the scalp-recorded, event-related potential (ERP), were measured in 26 patients with multiple cerebral infarcts (mean age, 65.0 years). Compared with age-matched normal subjects, patients with multiple cerebral infarcts had significantly lower cortical blood flow values and had prolongation of the P300 latency. There was a significant correlation between the P300 latency and the mean cortical blood flow values in patients with multiple cerebral infarcts. These results suggest that, in patients with multiple cerebral infarcts, the cognitive impairment associated with change of the ERP may be related to reduction of cortical blood flow.

Aged↗
PubMedDate not supplied

Platelet thrombi in experimental cerebral infarction.

Cerebral infarction was produced in paralyzed, ventilated rats by a 30 min period of right common carotid artery occlusion combined with systemic hypoxia (Pao2 21-25 mm Hg). After 30 min the arterial clamp was removed and the animals were reoxygenated and allowed to survive for 1 min (6 animals), 30 min (12 animals), or 1 1/2 to 2 h (6 animals). The animals were reanesthetized and sacrificed by perfusion-fixation with paraformaldehyde-glutaraldehyde. Light and electron microscopy revealed ischemic cell change in neurons in the ipsilateral cerebral cortex, striatum and hippocampus. These changes were mild to moderate in the early post-ischemic period and severe in the post-ischemic period. Cerebral infarction was present in one of the 30 min survivors and in all of the 1 1/2 to 2 h survivors. Electron microscopy showed platelet thrombi in the infarcted brain in 3 of the 7 animals with infarcts, and in an area of very severe ischemic cell change in a fourth animal. They were not present in areas of brain showing only mild to moderate ischemic cell change. These findings showed that platelet thrombi form in association with cerebral infarcts and suggested that they are induced by tissue necrosis rather than by neuronal ischemic cell change alone.

Animals↗
PubMed1979

Early and late mechanisms of increased vascular permeability following experimental cerebral infarction.

Cerebral infarction was produced in rats by a combination of transient unilateral common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase (HRP) and Evans blue were given 5 minutes prior to sacrifice to assess the integrity of the blood-brain barrier (BBB) at 1 minute, 30 minutes, and 2 hours following the ischemic insult. There was immediate permeability to HRP in the early (1 minute and 30 minutes) post-ischemic period, whereas, Evans blue was not seen until the late (1.5 to 2 hours) post-ischemic period. Ultrastructural examination showed two routes of barrier permeability to HRP. In the early post-ischemic period, HRP was transported by pinocytosis through endothelial cells in areas of brain containing ischemic neurons. In the late post-ischemic period, HRP diffusely leaked into the brain through the necrotic walls of vessels in areas of infarction. In contrast to previous reports, these results show that the BBB becomes permeable immediately following hypoxia-ischemia. In addition, this study shows that BBB permeability to HRP during cerebral ischemia occurs through two mechanisms: an active, energy-requiring permeability through enhanced pinocytosis within endothelial cells and a passive leakage of protein tracers through necrotic vessel walls.

Animals↗
PubMedDate not supplied

Gallium-67 citrate in cerebral infarction.

Cerebral scans were obtained on 30 "stroke" patients first with 99mTc pertechnetate and subsequently with 67Ga citrate. Of the 26 patients with abnormal 99mTc static scans, 17 (65%) showed the same abnormality in gallium citrate scans also. In 4 patients with positive technetium flow studies but negative static scans, no abnormality was seen in the scans obtained after gallium citrate injection. In none of the patients was the relative concentration of radioactivity in the lesion greater in the gallium image than in the technetium image. This study proves the nonspecificity of gallium citrate and thus its inability to differentiate cerebral tumor from cerebral infarction just on the basis of localization of gallium.

Aged↗
PubMed1977

Cerebral angiography in acute cerebral infarction.

Cerebral angiography in the acute phase of clinically diagnosed stroke syndromes was evaluated in a prospective study of 104 consecutive patients over an eight month period at the Massachusetts General Hospital to determine the diagnostic yield. Of 68 patients subsequently documented to have retinal or cerebral hemispheric infarction, 63 (92.6%) had angiographic demonstration of occlusive lesions which appeared to correlate with the clinical deficit. These results are discordant with prior angiographic reports, 2,17,18,20 suggesting that delayed carotid artery angiography fails to show occlusive lesions (embolic) which may be shown acutely.

Acute Disease↗
PubMed1977

[Radioisotope scanning in the diagnosis of cerebral infarction].

Cerebral scanning was performed in 52 cases of brain infarctions (in 43 cases in the system of middle brain arteries and in 9 cases in the vertebro-basillar basin). For this purpose in 46 of the studied cases human albumin serum, labeled readioactive I131 was used and in 6 cases-Tc 99m. Positive scannograms were received only in 16 patients with infarctions in the system of the middle brain arteries. The clinical picture in both groups of patients with positive and negative scannograms did not differ significantly from each other. This may indicate the fact that the process of accumulating radioactive isotopes in brain infarctions depends upon manifold reasons: the state of collateral circulations, the traits of angioarchitectonics in the affected area, the level of metabolism in the focus of lesions, disturbed permeability of the menatoencephalic barrier, etc. In doubtful cases for the differential diagnosis between brain infactions and tumors the most valid criteria in scanning is the dynamics of the focus of accuumulation of radioactive isotopes.

Adult↗
PubMedDate not supplied

Relative role of factors associated with cerebral infarction and cerebral hemorrhage. A matched pair case-control study.

Comprehensive ascertainment of all possible new cases of stroke appearing between January 1, 1970 and June 30, 1971, and admitted to three major hospitals in Winnipeg, Manitoba, has been achieved by reviewing the Manitoba Health Services Commission claim reports. The medical records of these cases were reviewed, pertinent data were abstracted, and rigid criteria for diagnosis were followed. Also, data were obtained from death certificates, autopsy reports and long-term hospital records. A total of 606 ascertained cases (410 infarction, 137 hemorrhage, and 59 undetermined type) were matched for age, sex, residence and year of admission with 606 controls from admissions for other than cardiovascular and cerebrovascular disorders. The data were analyzed for elucidating the possible risk factors for infarction (INF) and hemorrhage (HGE). The findings suggested that hypertension was the main risk factor in hemorrhage, whereas in infarction, along with hypertension, other factors such as diabetes, heart enlargement in chest x-ray, ECG abnormalities, and smoking were suggested as risk factors. There was an association also between infarction, on one hand, and the history of receiving anticoagulants, diuretics, and medications for the heart, and the occurrence of myocardial infarction, on the other hand. These features indicate that infarction and ischemic heart disease have similar risk factors. Hemoglobin and hematocrit were higher in infarction cases than in their controls only when measured at stroke admission. No difference was revealed when they were measured prior to stroke. Their association with infraction therefore may be secondary to other factors and of no significance for its risk.

Aged↗
PubMed2026

Integrated analysis of gut microbiota, serum metabolomics, and proteomics reveals novel associations with clinical symptoms in patients with cerebral infarction.

BACKGROUND: Cerebral infarction (CI) is a major cause of adult disability and mortality worldwide. Mounting evidence supports the critical role of the gut-brain axis in cerebrovascular disease progression. This study aimed to characterize the alterations in gut microbiota, serum metabolome, and serum proteome in patients with CI, and to identify multi-omics signatures associated with clinical symptoms. METHODS: A total of 20 CI patients and 20 healthy controls (HC) were enrolled. Fecal microbiota was profiled using 16&#xa0;S rRNA gene high-throughput sequencing. Serum metabolomics and proteomics were analyzed using ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) and data-independent acquisition (DIA) proteomics, respectively. Spearman correlation and multi-omics integration were applied to explore the associations among microbiota, metabolites, proteins, and clinical indicators. RESULTS: CI patients displayed significant gut microbiota dysbiosis, with a markedly lower gut microbiota health index (GMHI) and higher microbiota disorder index (MDI) compared with HC (P&#x2009;<&#x2009;0.001). The genera g_norank_o_RF39 and Oxalobacter were significantly enriched in CI patients, whereas Clostridium_sensu_stricto_1 and Agathobacter were enriched in HC. Metabolomic analysis identified 445 differential metabolites, mainly involved in glycerophospholipid metabolism, phenylalanine metabolism, and caffeine metabolism. Proteomic analysis revealed 140 differentially expressed proteins linked to inflammatory responses, calcium signaling, and NF-&#x3ba;B signaling. Multi-omics integration showed that signature gut microbiota was strongly correlated (P&#x2009;<&#x2009;0.005) with key serum metabolites and proteins implicated in CI pathogenesis. CONCLUSIONS: This integrated multi-omics study revealed distinct gut microbiota, serum metabolomic, and proteomic alterations in CI patients. The microbiota-metabolite-protein regulatory axes provide novel insights into the gut-brain axis in CI and may serve as potential diagnostic biomarkers or therapeutic targets.

Humans↗