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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↗
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↗
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↗
PubMedDate not supplied

Importance of the hematocrit as a risk factor in cerebral infarction.

The relationship between the indicence of cerebral infarction and the hematocrit was studied using 432 consecutive autopsied patients with the average age of 77.1 years. The incidence of cerebral infraction was higher in patients with hematocrit values of more than 46%, (the average in younger adult subjects). The increase in the frequency of cerebral infarction with high hematocrit values was more conspicuous in patients with severe cerebral atherosclerosis than in those with slight cerebral atherosclerosis. High blood pressure per se did not influence the relationship between the hematocrit value and the incidence of cerebral infarction. With hematocrit values of more than 41%, cerebral infarction occurred more frequently in patients over 78 years of age than in the younger patients, but the difference was not significant statistically. High hematocrit values are associated with a higher risk of cerebral infarction in deep subcortical structures of the brain than for cartical infarctions. The pathogenetic and preventive implications of these results are discussed in the light of blood rheology.

Age Factors↗
PubMed1976

[Cerebrospinal fluid flow dynamics in cerebral infarction--Numerical study with RI Anger camera (author's transl)].

Although the cerebral blood flow dynamics in cerebral infarction has already been studied by many investigators, the CSF flow dynamics in cerebral infarction has not been well discussed. The purpose of this paper is to investigate CSF flow dynamics in chronic cerebral infarction by RI cisternography and our new quantitative method. In 12 patients with cerebral infarction, the flow of CSF was estimated following intrathecal injection of 169Yb-DTPA or 111In-DTPA. In this study, in addition to the conventional cisternograms, quantitative evaluation of CSF flow was performed in 6 patients by our method. Our previous work included the quantitative CSF flow dynamics in 26 various cerebral disorders using RI Anger camera. This method consisted of following procedure: 30 minutes after RI injection, RI activity was studied continuously for 30 minutes, afterwards playing back the record to calculate the changes of RI activity in the optimal regions of interest. These operations were performed with Anger camera, accessory digital ratemeter and tape-recorder. The changes of RI activity which appeared to be linear is called flow rate in our study for convenience. In this report, the region of interest was selected at Sylvian cistern. 6 patients had abnormal cisternograms consisting of reflux of tracer into the ventricle and delayed migration of tracer to the basal cisterns and diminished flow of tracer in the affected hemisphers. In 5 patients whose cisternograms could not demonstrate the laterality of RI perfsion over the cerebral hemishere, a marked difference of flow rate between right and left Sylvian cisterns was found. These findings probably indicated the correlation between cerebral blood flow dynamics and CSF flow dynamics in cerebral infarction. Moreover, it was confirmed that our method could be of clinical use to evaluate CSF flow dynamics quantitatively. The possible mechanisms of CSF flow disturbance in the affected hemisphere following cerebral infarction was discussed.

Adult↗
PubMed1979

[Histopathological study on experimental cerebral infarction in rat (author's transl)].

An experimental model of cerebral infarction in rat brain was successfully established by means of the unilateral internal carotid injection of carbon microspheres. A histopathological investigation of the infarcted brain was performed. The results were as follow: 1. No cerebral infarction was made by the unilateral internal carotid ligation alone. 2. Focal cerebral edema was most marked at the white matter of the embolized hemisphere. 3. The edema was also conspicuous in the deep cerebral gray matter, especially in hippocampus. Degeneration and pyknosis of the neurons were observed at the same area. 4. Transudative hemorrhage in the focal cerebral edema was usually observed in the thalamus. 5. Edematous change in the cortical gray matter was not so marked as compared with the hippocampus and thalamus. 6. Carbon microsphere was not found in the capillaries of ipsilateral choroid plexus. The present experimental model of cerebral infarction will be useful in elucidating the pathological mechanisms of the cerebral infarction.

Animals↗
PubMedDate not supplied

Experimental cerebral infarction. Part 1: Production of thalamic infarction in dogs.

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.

Animals↗
PubMed1979

Anticoagulant treatment to prevent cerebral infarction.

The indications for anticoagulant treatment to prevent cerebral infarction or progression of cerebral infarction are now clear. The indications are: (1) Prevention of recurrent embolization from a cardiac source (long-term anticoaguland treatment). (2) Transient ischemic attacks (particularly vertebrobasilar system) if a surgically accessible causative lesion, polycythemia, and thrombocytosis are not present (anticoagulants for a few months.) (3) Progressing stroke in either systme assuming that the neurological defect is partial and CT scan shows no evidence of bleeding (anticoagulants for a few months.) (4) Rarely, completed stroke (long-term).

Anticoagulants↗
PubMed1979

[Classification and course of cerebral infarcts on computer tomography (author's transl)].

The typical computer tomographic signs of ischaemic cerebral infarct are discussed on the basis of 631 cases. Infarcts have three typical stages. Stage I, one week, fresh infarct with signs of oedema (space-occupying lesion with an unsharp margin, slightly reduced density, lack of contrast uptake). Stage II, second to fourth week, reduction in the oedema. Frequently very marked contrast enhancement of the cortex and basal nuclei. Stage III, later than four weeks. Development of malacic cysts, with further reduction in density and size. Development of homolateral atrophy. The computer tomographic diagnosis of cerebral infarcts during Stage I is often very difficult. Distinction from infiltrating tumour is often possible only after further observation. The diagnosis of cerebral infarcts in stages II and III is possible in most cases. Haemorrhagic cerebral infarcts do not follow a temporal pattern as accurately as anaemic infarcts. They show circular increase in contrast of slowly diminishing size. The increased contrast persists considerably longer and is clearly distinguished from that in an anaemic cerebral infarct.

Adolescent↗