Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cerebral Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1998

Relation of plasma homocyst(e)ine to cerebral infarction and cerebral atherosclerosis.

BACKGROUND AND PURPOSE: A number of investigations support the theory that the elevated plasma homocyst(e)ine is associated with occlusive vascular disease. The aim of this study is to examine whether moderate hyperhomocyst(e)inemia is an independent risk factor for cerebral infarction. In addition, we examined the association between plasma homocyst(e)ine and the severity of cerebral atherosclerosis. METHODS: We conducted a hospital-based case-control study with 140 male controls and 78 male patients with nonfatal cerebral infarction, aged between 39 and 82 years. Plasma homocyst(e)ine levels were analyzed in 218 subjects. Fifty-five patients were evaluated for cerebral vascular stenosis by MR angiography. RESULTS: The mean plasma level of homocyst(e)ine was higher in cases than in controls (11.8+/-5.6 versus 9.6+/-4.1 micromol/L; P=0.002). The proportion of subjects with moderate hyperhomocyst(e)inemia was significantly higher in cases than in controls (16.7% versus 5.0%; P=0.004). Based on the logistic regression model, the odds ratio of the highest 5% of homocyst(e)ine levels in control group was 4.17 (95% confidence interval, 3.71 to 4. 71)(P=0.0001). After additional adjustment for total cholesterol, hypertension, smoking, diabetes, and age, the odds ratio was 1.70 (95% confidence interval, 1.48 to 1.95) (P=0.0001). The plasma homocyst(e)ine levels of patients having vessels with 3 or 2 stenosed sites were significantly higher than those of patients having vessels with 1 stenosed site or normal vessels (14.6+/-1.4, 11.0+/-1.4 versus 7.8+/-1.5, 8.9+/-1.4 micromol/L respectively; P<0. 02). Multiple logistic regression analysis revealed that moderate hyperhomocyst(e)ienemia was significantly associated with the number of stenosed vessels (P=0.001). CONCLUSIONS: These findings suggest that moderate hyperhomocyst(e)inemia is an independent risk factor for cerebral infarction and may predict the severity of cerebral atherosclerosis in patients with cerebral infarction.

Adult↗
PubMed1995

[A case of systemic lupus erythematosus associated with cerebral infarction and cerebral hemorrhage].

This is a report of cerebral infarction and cerebral hemorrhage derived from systemic lupus erythematosus. A 49-year-old male was admitted to our hospital due to dysarthria and supranuclear facial palsy. He had been suffering from SLE and medicated incompletely since 9 years prior to admission. A CT scan showed a small infarction in the left parietal area. An angiography revealed a tapering stenosis of the left carotid siphon and an occlusion of the left vertebral artery at the cisternal portion. On the 13 days after the admission, he complained of a high fever and right hemiparesis. The CT scan disclosed newly multiple small infarctions in the left parietal area. The angiography showed the progressing of the tapering stenosis at the left carotid siphon, and demonstrated the narrowing of the left superior temporal artery and ophthalmic artery in addition to the disappearance of a left posterior communicating artery. High dose of steroid was given to him, but cerebral hemorrhage and huge left cerebral infarction were complicated. On the 26 days after the admission, his general condition was worsened and died. It was considered that the cerebral infarction and hemorrhage might be derived from the vasculitis of SLE.

Cerebral Angiography↗
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

Delayed imaging of Tc-99m-DTPA-HSA SPECT in subacute cerebral infarction.

Cerebral blood volume measurement by Tc-99m-DTPA-HSA SPECT was performed in a patient with subacute cerebral infarction to evaluate compensatory vasodilatation. Additional delayed imaging revealed focal increased radioactivity that was not found on the early images, indicating leakage of radioactive agents due to blood-brain barrier breakdown. Delayed SPECT may be helpful to detect areas unsuitable for estimating regional blood volume.

Acute Disease↗
PubMed1998

Ultrasonographically assessed carotid intima-media thickness and risk for asymptomatic cerebral infarction.

Cerebral infarction (CI) is still a leading cause of death in Japan. Thus, the management of risk factors for CI as primary prevention is one of the most important tasks in multiphasic health testing and services. To determine whether carotid intima-media thickness (IMT) is a risk for CI, ultrasonographically assessed carotid IMT was compared between normal subjects (N) and subjects with asymptomatic CI (ACI) in 243 subjects who underwent human brain dry dock. ACI was found in 68 people (28.0%). Age, body mass index, and mean blood pressure were higher in ACI than in N. Also, atherogenic index was higher in ACI than in N. Carotid IMT was significantly thicker in ACI than in N. Furthermore, incidence of atherogenic plaque in ACI was significantly higher than that in N. In conclusion, not only aging, obesity, blood pressure, and plasma lipids, but also carotid IMT may be a risk for ACI.

Adult↗
PubMed1984

[Indication for, the method of, and result of the prophylactic use of barbiturate therapy (B-therapy) against cerebral infarct from cerebral arterial vasospasm due to ruptured aneurysm].

A review of 45 cerebral vasospasm cases for cerebral infarct under computer tomography (CT) scanner and based on activities of daily living (ADL) resulted in the finding that, of 19 cases with vasospasm of "diffuse, severe" grade, 14 cases were rated "poor (disabled)" to "dead": CT-diagnosed cerebral infarct was found in 4 out of 6 cases. From this, it was believed that indication for B-therapy was clinically significant vasospasm (diffuse, severe), which falls under the clinical grade of III or IV by Hunt and Kosnik without considering such incidental condition as severe vasospasm. After B-therapy, 45% showed ADL of at least "fair". CT-diagnosed cerebral infarct was found in 4 out of 10 cases. None died from complications as a result of B-therapy. The examination of ineffectual cases pointed to the importance of the first choice application of B-therapy, the continuation of the therapy as long as vasospasm continues, and the sustenance of cerebral perfusion pressure by the use of vasopressor (Dopamine) to offset the hypotensive effect of barbiturate. With these points of care exercised, the B-therapy is believed to achieve good results.

Adult↗
PubMedDate not supplied

A case of hyperLp(a)aemia, associated with systemic lupus erythematosus, suffering from myocardial infarction and cerebral infarction.

We describe a case of systemic lupus erythematosus (SLE) with nephrotic syndrome who suffered from myocardial infarction and cerebral infarction associated with hyperLp(a)aemia. The proband was an 18-year-old Japanese male who was found to have hypercholesterolemia and hyperLp(a)aemia, with a serum total cholesterol level of 361 mg/dl and a serum Lp(a) level of 197 mg/dl. His father and mother showed higher Lp(a)levels (26 and 56 mg/dl, respectively) than those in normals (18 +/- 0.6 mg/dl, mean +/- SE). Lp(a)glycoprotein phenotypes were examined. The proband had the phenotype S2/4, which is associated with high Lp(a) concentration. His parents had the phenotype S3/4 and S2/4. No cardiovascular diseases were noted in other members of his family. After treatment with CS-514, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lp(a) levels decreased from 197 to 121 mg/dl, but still remained abnormally high. LDL apheresis using a Liposorber system was attempted in this patient. Total and LDL cholesterol levels decreased by 57 and 62%, respectively. Lp(a) levels decreased by 68%. These results suggest that LDL apheresis may be an alternative therapy in drug resistant hyperLp(a)aemia.

Adolescent↗
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↗
PubMed1993

On the degree of platelet, coagulation and fibrinolysis activation after cerebral infarction and cerebral haemorrhage and the clinical outcome.

Thrombocytic, haemostatic and fibrinolytic quantities were investigated in 47 patients with cerebral infarction and 34 patients with cerebral haemorrhage. Sixteen of the infarction patients and ten patients of the haemorrhage group were on acetylsalicylic acid medication. Of the remaining 55 patients without acetylsalicylic medication 21/31 = 67.7% of the patients in the infarction group and 9/24 = 37.5% of the patients in the bleeding group had unphysiologically enhanced ADP-induced platelet aggregation. With regard to the coagulation and fibrinolysis markers no significant differences were found between the two groups. In both groups, coagulation activity markers (fibrin monomer and thrombin-antithrombin III), as well as D-dimers were significantly higher than in controls in a high proportion of cases. In 5/47 of the infarction patients and in 3/34 of the haemorrhage patients the fibrin monomer levels were elevated to such an extent, that it can be considered as low grade disseminated intravascular coagulation. In the cerebral haemorrhage group, 80.3% of the patients who subsequently died showed a significantly enhanced fibrin monomer concentration, compared with 28.6% of those who survived. The corresponding frequencies for D-dimer were 100% compared with 66.7%. In the cerebral infarction group, the only analytical quantity showing a significant difference between patients with a fatal outcome and those with a non-fatal outcome was ADP (2 mumol/l) induced platelet aggregation (83.3% in the fatal group, 40.0% in the non-fatal group).

Adenosine Diphosphate↗
PubMed1986

Beagle puppy model of perinatal cerebral infarction. Regional cerebral prostaglandin changes during acute hypoxemia.

Perinatal cerebral infarction, or stroke, is a not uncommon finding in newborns who survive after intensive care. Asphyxia, with its component parts hypoxemia and hypotension, represents the most common cause of perinatal cerebral infarction and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated regional alterations in cerebral blood flow (CBF) in response to hypoxemic insult. This work examines the effects of hypoxemia on regional cerebral prostaglandin levels in the developing brain, since some observers believe that local CBF is controlled in part by prostaglandins. In this study, newborn beagle pups were anesthetized, subjected to tracheotomy and artificially ventilated to maintain normoxemia and normocarbia. Mean arterial blood pressure (MABP) was continuously monitored by means of an indwelling catheter and transducer, and craniectomies were performed. When the pups were physiologically stabilized, they were randomly assigned to receive acute hypoxemic insult (pO2 14.0 +/- 1.55 mm Hg, mean +/- standard deviation) accomplished by altering the oxygen concentration in the inspired air) or to receive no insult (mean pO2 84.3 +/- 13.0 mm Hg). Fifteen minutes following stable hypoxemic or normoxic conditions, all pups underwent in vivo freezing of the intracranial contents under anesthesia followed by rapid sacrifice. No significant differences were noted between the MABP, pH, or pCO2 values for the control and hypoxemic pups during the experimental period. Regional cerebral prostaglandin data demonstrated a significant increase in prostaglandin (PG)E2 in the gray matter of hypoxemic pups when compared to the normoxic controls (p less than 0.02). No significant differences were noted for 6-keto-PGE1 alpha, the stable metabolite of prostacyclin, or thromboxane (TX)B2, the stable metabolite of TXA2, in the gray matter. In addition, although 6-keto-PGE1 alpha was significantly lower in the periventricular white matter of the hypoxemic pups (p less than 0.05), there were no changes in the white matter in either PGE2 or TXA2. This regional differential synthesis of PGE2 in response to hypoxemic insult may explain the relative failure of CBF to the periventricular white matter and thus the neuropathological alterations attributed to it.

Acute Disease↗
PubMed1999

[Association of silent cerebral infarction with cerebral hemispheric--sub-tentorial infarction in patients with supra-nuclear dysarthria or dysphagia].

Little information is available concerning the latent effects of silent cerebral infarction (SCI) on dysarthria (DA), dysphagia (DP), or both. A detailed analysis of MR images of multiple cerebral infarction was carried out to determine whether SCI is associated with the development of DA or DP. In this study MR images of the supra- and sub-tentorial regions were obtained from 14 patients presenting with persistent DA and DP (DA + DP group) and 9 patients presenting with DA alone (DA group) after the first episode of cerebral infarction. The DA + DP inducing lesion was identified from the change in signal intensity and the side with symptoms in 6 patients. Involvement of 3 lesions of the bilateral cortical branches, striatum, and pons on the line connecting the contra-lateral SCI with the lesion were noted in 4 patients (67%, vs. 40% for the DA group). Latent association of SCI with the development of supra-nuclear DA and DP was noted in 1 patient each from the DA + DP and DA groups. The results of this study support the concept that SCI patients include those in which SCI is involved in the development of supra-nuclear DA or DP, and suggest that SCI should be treated.

Aged↗
PubMed2004

[Therapeutic application of cell transplantation and increased neurogenesis in cerebral infarction].

Cerebral ischemia often results in neuronal loss, leading to the neurological deficits in stroke patients. To obtain the functional recovery after stroke, cell transplantation and enhancement of endogenous neurogenesis may have potential application. Recent evidence has demonstrated that neural stem cells exist in the adult mammalian brain. After cerebral ischemia, newly born neurons were found not only in hippocampal dentate and olfactory bulb but also in hippocampal CA1 and striatum, where neurons were lost after ischemia. Administration of neurotrophic factors or genes encoding them into the lateral venticule could enhance endogenous neurogenesis in experimental ischemia model. Furthermore, we have recently developed non-invasive gene transfer into macrophages infiltrating an infarct to stimulate proliferation of neural stem cells in cerebral infarction. Several strategies including gene therapy and pharmacological approach will be tried in stroke patients in near future. However, it remains unclear whether the number of new-born neurons from endogenous neural stem cells is sufficient for replacement of damaged neurons. Cell transplantation will have the advantage of preparing the large amount of transplanted cells. Human neural stem cells, embryonic stem cells and bone marrow-derived cells will be donor cells in stroke patients. Surprisingly, neuron-like cells derived from human teratoma cell line were already applied in stroke patients. However, ethical aspect will have to be discussed carefully before cells from other individuals are used as donor cells in stroke patients.

Cerebral Infarction↗
PubMed2003

Cerebral infarction and cerebral salt wasting syndrome in a patient with tuberculous meningoencephalitis.

A 38-year old female with underlying systemic lupus erythematosus was admitted with tuberculous meningoencephalitis. After an initial good response to anti-tuberculous treatment, she developed cerebral infarction and profound hyponatremia. This was due to cerebral salt wasting syndrome, which has only previously been described in 2 cases. The difficulties in diagnosis and management of this case are discussed.

Adult↗
PubMed1985

Myocardial infarction and cerebral infarction in a Danish suburban community.

A comparison was made of 485 cases of cerebral infarction (CI), registered prospectively in Frederiksberg, Copenhagen, with 495 cases of myocardial infarction (AMI), recorded retrospectively in the same population. The overall annual incidence of AMI was 6.5 per 1,000 population for males, 3.8 for females; the rates for CI were 2.4 and 2.5, respectively. The age-incidence curves, particularly those for AMI, were significantly steeper in the females than in the males. Correspondingly, the male predominance in the AMI-group subsided with age. Age-specific incidence-rates rose exponentially with advancing age; for each sex and diagnosis the relationship can thus be expressed as a simple mathematical formula, which may facilitate comparisons of incidence patterns in different communities. Theories explaining the similarities and differences of the age-incidence curves for AMI and CI are discussed.

Adult↗
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↗
PubMedDate not supplied

Can raising cerebral blood flow improve outcome after acute cerebral infarction?

Cerebral blood flow correlates poorly with outcome after stroke, and most therapies aimed at increasing cerebral perfusion have not succeeded in predictably reducing neurological deficit. Newer approaches such as hemodilution and thrombolysis may prove to be more effective but might be most advantageous if combined with efforts to correct postischemic disturbances in cellular metabolism.

Blood Viscosity↗
PubMed2004

Possible vascular-bed-specific role of interleukin-6 in young women with a history of myocardial infarction, lacunar cerebral infarction and deep vein thrombosis.

The level of interleukin-6 (IL-6), a cytokine with prothrombotic properties, and its associations with metabolic, coagulation and fibrinolytic parameters were investigated in 68 young women (23-49 years, mean 40 years old) six months to six years after myocardial infarction (MI, N=22), lacunar cerebral infarction (LACI, N=16) and deep vein thrombosis (VT, N=30); all women were in the reproductive period, aged <45 years at the time of acute thrombotic event. Forty-seven age-matched women comprised a control group. Basic and multivariate analysis disclosed different patterns of IL-6 increase in all three groups of patients. In the MI group IL-6 was significantly elevated independently of factors known to increase IL-6 levels; the increase was most pronounced in patients with high lipoprotein(a). This result suggests a prothrombotic association of lipoprotein(a) with IL-6. In the whole LACI group IL-6 was not significantly increased. However, patients with elevated levels of IL-6 had abdominal obesity and elevated fibrinogen, suggesting the possibility that this combination might represent a specific risk profile. In VT group elevated IL-6 level was found in the group of previous users of oral contraceptives (OC). This might be relevant, since it is known that OC could importantly increase (previously elevated) IL-6 level in selected women. Our results suggest the hypothesis that the role of IL-6 might be vascular-bed-specific and further propose that increased IL-6 level might represent a novel, non-classical risk factor for development of MI, LACI and VT in specific subgroups of young women, which have to be clarified in further studies.

Adult↗