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 343 records · Page 19Linked to original sources
PubMedDate not supplied

[The role of blood lipids in the different aetiologies of cerebral infarction].

INTRODUCTION: In order to determine the role lipids play in cerebral infarction (CI), the different aetiological subgroups of this disease should first be separated. AIMS AND METHOD: We conducted case control studies to identify whether there is a relation between blood lipid levels and the occurrence of cerebral infarction caused by atheromatosis (CIA). Our study involved a total of 98 patients with cerebral infarction of an atherothrombotic or lacunar aetiopathogenesis that were included in the CIA category. Two control groups were set up: one consisted of 23 patients with non atheromatous cerebral infarction (NACI), which included other aetiologies (cardioembolic, unusual and unspecified), and the other was made up of 101 healthy subjects who had not had a stroke. RESULTS: The group of patients with CIA presented higher average cholesterol rates than the group of subjects with NACI (p= 0.005). Nevertheless, compared to the control group they had higher average levels of cholesterol (p= 0.003), triglycerides (p= 0.011), VLDL (p= 0.028) and LDL (p= 0.000), as well as a higher average atherogenic index (p= 0.028). Furthermore, the average levels of LDL (p= 0.030) and the atherogenic index (p= 0.008) were seen to be statistically higher in the group of subjects with NACI than in the control group. Lastly, it must be pointed out that no differences in the average HDL levels were found between the three groups studied (p= 0.500). The presence of high blood pressure and a history of ischemic heart disease in patients with CI did not modify the variations that were observed in the lipids. CONCLUSIONS: Patients with CIA have a more atherogenic lipid profile than healthy individuals, while subjects with NACI are situated midway between the two groups

Arteriosclerosis↗
PubMed2002

Silent cerebral infarction and cognitive function in middle-aged neurologically healthy subjects.

We sought to clarify whether apparently silent cerebral infarcts and periventricular hyperintensities are associated with depressed cognitive function in middle-aged subjects. Subjects were 84 middle-aged neurologically normal adults who wished to undergo a screening examination of the brain. We performed magnetic resonance imaging (MRI) of the brain and neuropsychologic tests in all subjects. Silent cerebral infarcts and periventricular hyperintensities, respectively, were detected in 21 and 14 of 84 subjects. Mini-mental state (MMS) and Raven's colored progressive matrices (RCPM) scores were significantly lower in subjects with than without silent cerebral infarcts. By two-factor analysis of variance, MMS score was affected by silent cerebral infarcts or periventricular hyperintensities, with interactions between the two lesion types (P < 0.05). Silent cerebral infarcts may be an independent factor in the pathogenesis of intellectual dysfunction, but truly independent analysis is difficult because many subjects with silent cerebral infarcts also have periventricular hyperintensities.

Adult↗
PubMed2005

Cerebral infarction in IgG multiple myeloma with hyperviscosity.

Cerebral infarction is an uncommon complication in multiple myeloma with hyperviscosity. Serum hyperviscosity may cause a variety of clinical manifestations including bleeding from mucosal membranes, congestive heart failure, retinopathy, and various neurologic deficits. These manifestations have been attributed to the presence of large quantities of asymmetrical molecules of high molecular weight in the serum. We recently experienced a case of multiple myeloma with acute cerebral infarction, which caused by hyperviscosity, as an initial manifestation in IgG multiple myeloma, and reviewed the relevant literature of myeloma presenting with the stroke. A 68-yr-old woman abruptly developed hypesthesia and monoplegia in the left leg. The stroke confirmed by the brain MRI and MR angiography, which revealed acute infarction at the right anterior cerebral artery territory. On admission, routine blood tests showed a slight decrease in hemoglobin and a marked increase in erythrocyte sedimentation rate. Peripheral blood smear, serum protein electrophoresis, serum visocity, and bone marrow aspiration showed that she had IgG multiple myeloma with hyperviscosity. She was treated by chemotherapy with cyclophosphamide and discharged with the improved clinical condition.

Aged↗
PubMed2004

The effect of desflurane on ameliorating cerebral infarction in rats subjected to focal cerebral ischemia-reperfusion injury.

To obtain more information on the cerebral ischemia and reperfusion injury under desflurane anesthesia, we compared the infarct volume and lactate dehydrogenase (LDH) activity in rats subjected to focal cerebral ischemia during different concentration of desflurane anesthesia. Male Long-Evans rats weighing 270-350 g were anesthetized with desflurane in air at 1.0, 1.25 or 1.5 MAC whereas rats in the control group received intraperitoneal chloral hydrate (400 mg/kg) anesthesia. Cerebral infarction was induced by microsurgical procedures with ligation of the right middle cerebral artery (MCA) and clipping of the bilateral common carotid arteries (CCA) for 60 minutes. The rats were sacrificed 24 hours later, serial brain slices of 2mm thickness were taken and stained for the measurement of the infarct area. Cellular damage was evaluated by measuring the LDH level in the plasma. Desflurane (1.0, 1.25 or 1.5 MAC by inhalation) and chloral hydrate (400 mg/kg; ip.) did not produce any changes in pH, blood gases, heart rate or mean arterial blood pressure. In the rats subjected to focal cerebral ischemia, the volume of infarction was significantly less in the desflurane groups in all three different concentrations than in the chloral hydrate group. The changes of LDH activity in plasma also correlated with the result of the infarct volume. Our study suggests that desflurane may offer a neuroprotective effect such as decreased infarct volume after focal cerebral ischemia.

Animals↗
PubMed1987

[Cerebral amyloid angiopathy complicated by multiple cerebral infarcts and intracerebral hemorrhages: case report].

Recently, cerebral amyloid angiopathy is stressed as an unusual and infrequent cause of cerebral infarct or intracerebral hemorrhage. This report described a case of cerebral amyloid angiopathy complicated by multiple cerebral infarcts and multiple intracerebral hemorrhages. This 70-year-old man was admitted to our hospital on November 10, 1984 for evaluation of the gradual onset of dysarthria. Examination showed only slight dysarthria. There was no history of hypertension or dementia. A computed tomography (CT) showed enlarged ventricles with cortical atrophy and multiple low-density lesions, deep in the left frontal, left parietal, right parietal lobes, and in the both basal ganglias. The patient discharged from the hospital with only slight dysarthria. On November 20, 1984, he was admitted to our hospital again, because he was found unresponsive on the floor. He was somnolent but arousable. Examination showed disorientation, impairment of recent memory and impairment of calculation, A CT scan demonstrated three small intracerebral hemorrhages in the left frontal, right parietal lobes and left basal ganglia. On the fifth hospital day he deteriorated acutely, becoming semicomatose and hemiparetic on the right side. A repeated CT scan showed two new intracerebral hemorrhages in the left frontal lobe. Cerebral angiograms showed only minimal changes due to the occupying lesions in the above mentioned area. The hematomas was evacuated via left fronto-parietal craniotomy. The specimens removed with hematoma (stained with hematoxylin-eosin, Congo red and thioflavin T) showed extensive amyloid angiopathy. Postoperatively he made a good recovery, although he had residual mental dysfunctions. He expired by pneumonia on March 30, 1985.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2002

[Trend analyses in the incidence of acute intracerebral hemorrhage events and acute cerebral infarction events in urban areas in Beijing].

OBJECTIVE: To study the trends of incidence on acute intracerebral hemorrhage events and acute cerebral infarction events in the population aged 25 - 74 in urban areas of Beijing from 1984 to 1999. METHODS: In monitoring the trends and determinants in the cardiovascular disease (MONICA) project and subsequent study, acute intracerebral hemorrhage events and acute cerebral infarction events were registered in a standardized way in men and women aged 25 to 74 years from 1984 - 1999. RESULTS: Both intracerebral hemorrhage attack rates decreased but cerebral infarction attack rates increased significantly; The proportion of intracerebral hemorrhage events in stroke events decreased from 42.0% to 16.0% while the proportion of cerebral infarction events in stroke events increased from 55.8% to 81.6%, the changes in incidences of acute intracerebral hemorrhage events and acute cerebral infarction events in various age groups were different. CONCLUSION: Cerebral infarction was the most important risk causing stroke, so prevention of cerebral infarction should be strengthened in the area.

Acute Disease↗
PubMed2005

Caffeic acid phenethyl ester ameliorates cerebral infarction in rats subjected to focal cerebral ischemia.

The effects of caffeic acid phenethyl ester (CAPE), an antioxidant derived from propolis, on the infarct volume elicited by focal cerebral ischemia were studied on Long-Evans rats. Cerebral infarction was induced by microsurgical procedures with ligation of the right middle cerebral artery (MCA) and clipping of bilateral common carotid arteries (CCA) for 60 min. The rats were sacrificed 24 h later and serial brain slices of 2 mm thickness were taken and stained for the measurement of infarct area. CAPE was administered intravenously 15 min before MCA occlusion. Pretreatment of CAPE (0.1, 1 and 10 microg/kg) significantly reduced the total infarct volume from 169.6 +/- 14.5 mm3 (control) to 61.0 +/- 24.1 mm3 (0.1 microg/kg CAPE), 47.4 +/- 9.1 mm3 (1 microg/kg CAPE), and 42.4 +/- 8.7 mm3 (10 microg/kg CAPE), respectively. Plasma nitric oxide (NO) content was significantly increased in rats subjected to focal cerebral ischemia. It is concluded that CAPE possesses neuroprotective properties in focal cerebral ischemia injury in rats possibly through its antioxidant effect and/or via the upregulation of NO production.

Animals↗
PubMed2006

Reduction in the motor unit number estimate (MUNE) after cerebral infarction.

BACKGROUND: The mechanism of the decrease in motor unit number estimates (MUNEs) after cerebral infarction has not been studied systematically. We examined the relationship between the degree to which MUNEs decreased and the other clinical features of patients with the infarction. METHODS: Using a multiple point stimulation technique, we obtained the MUNE of the hypothenar muscle group in 13 age-matched control subjects and 30 patients with cerebral infarction. In all patients, we obtained the Japan Stroke Scale (JSS) and head MR images. In eight patients with acute cerebral infarction, admitted within 24 h after onset, we also obtained head MR angiograms and single-photon emission CT. FINDINGS: There was a decrease in the MUNE of the hypothenar muscle group on the affected side of 24 patients with cerebral infarction and hand weakness. The decrease in the MUNE started from 4 to 30 h after the infarction, when T1-weighted MR images of the brain involved were normal. The degree to which the MUNE decreased correlated with the part of the JSS showing the upper extremity weakness. INTERPRETATIONS: A decrease in the MUNE of the hypothenar muscle group within 30 h after cerebral infarction may be due to trans-synaptic inhibition of the spinal alpha motor neurons innervating this muscle.

Action Potentials↗
PubMed2003

[A cross-sectional study on angiotensin-converting enzyme and angiotensin II type I receptor gene polymorphism and cerebral infarction].

OBJECTIVE: To explore the relation of angiotensin-converting enzyme (ACE) gene polymorphism, angiotensin II type I receptor (ATIR) gene polymorphism and other factors on cerebral infarction. METHODS: One thousand three hundred fifty-one subjects from Tangshan coalmine were enrolled with study method of cluster sampling. Face to face interviews were conducted to fill in questionnaires by trained interviewers. ACE gene, ATIR gene and inflammation factors including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-8, IL-10, C reactive protein (CRP), fibrinogen (Fg), fibrin monome polymerized velocity (FMPV), absorbance maximum (A(max)), FMPV/A(max), were measured. RESULTS: No different prevalence rates of ACE genotype were found on cerebral infarction. The distributions of AA genotype of ATIR gene in the cerebral infarction was higher than that of the controls. The prevalence of AA genotype was higher than other groups, but the prevalence of combined genotype did not show much difference. Under the existence of factors that related to cerebral infarction, AA genotype frequencies were higher than those of non-smoking and with hypertension. IL-6, ATIR gene polymorphism, sex, FMPV/A(max) were strongly related to cerebral infarction. The level of IL-6 was higher than the normal ones. CONCLUSIONS: The prevalence of cerebral infarction obviously increased in the hypertensive groups having AA genotype of ATIR gene. In the cerebral infarction groups, the level of IL-6 was higher than that in the normal population, indicating that these can be resulted from local inflammation and immunity reactivity. Environmental and genetic factors in the pathogenesis of cerebral infarction might have coordinating functions.

Aged↗
PubMed1995

[A case of cerebral infarction in a young adult following an abuse of cocaine and other drugs].

We reported a case of cerebral infarction in a young adult following an abuse of cocaine and other drugs. A 27-year-old male was admitted to our hospital because of the abrupt onset of right hemiplegia and dysarthria. Brain CT and MRI examinations showed cerebral infarction in the region of the left caudate head and the left corona radiata. Cerebral angiography revealed total occlusion at the origin of the left middle cerebral artery, with neither vascular malformation nor atherosclerotic change. There were no obvious causes that might lead to cerebral infarction in young adults, including potential cardiac sources of embolism, abnormalities of blood coagulation, or collagen vascular diseases. From his history we learned he had started abusing cocaine and other drugs at the age of 16 years, and that he had been addicted to these drugs up to at least 2 months earlier than the onset of cerebral infarction, so we suggested his drug abuse might have affected the occurrence of cerebral infarction. We would like to emphasize that using 'drugs' should be taken into consideration as a possible cause of cerebral infarction in young adults.

Adult↗
PubMed2005

[Analysis of 994(G--> T) mutation in the plasma platelet-activating factor acetylhydrolase gene in the patients with cerebral infarction].

OBJECTIVE: To investigate the relationship between plasma platelet-activating factor acetylhydrolase (PAF-AH) gene 994(G--> T) mutation in exon 9 and the patients with cerebral infarction in Chinese Hans. METHODS: The authors conducted a case-control study including 108 patients in three groups (atherosclerotic cerebral infarction group, lacunar infarction group and cerebral embolism group) and 215 normal subjects as controls. Genomic DNA was analyzed for the mutant allele by a specific polymerase chain reaction. RESULTS: The frequency of the mutant genotype in the 102 patients with cerebral infarction was 35.19%(32.41% heterozygotes and 2.78% homozygotes), and was 38.10%(34.92% heterozygotes and 3.18% homozygotes) in the atherosclerotic cerebral infarction group, being all significantly higher than the control group's 20.46% (18.60% heterozygotes and 1.86% homozygotes)(P< 0.01); however, the frequencies of the mutant genotype in the lacunar infarction group and cerebral embolism group were 32.35% (29.41% heterozygotes and 2.94% homozygotes) and 27.27% (27.27% heterozygotes and 0 homozygotes) respectively, being not statistically different from those of the controls (P> 0.05). CONCLUSION: These findings show that the 994(G--> T) mutation of plasma PAF-AH gene may be an independent risk for atherosclerotic cerebral infarction, but not for lacunar infarction.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1992

[A prospective trial of hemodilution therapy in acute cerebral infarction].

Ninety two 50-year-old-or-more patients with acute (less than 72 hours) cerebral infarction involved middle cerebral artery region and hematocrit of 40% or more were prospectively randomised to either hemodilution group (by rapid venesection, venous infusion of autologous plasma and 500 ml dextran 40) or standard therapy group. Effects of hemodilution on acute cerebral infarction were evaluated by clinically neurological deficit scores, hemorheological parameters and size of infarction. The results of our clinical trial are: 1. Clinical efficacy of hemodiluted patients is significantly superior to that of standard treatment patients. Effective rates are 63.04% and 41.30% respectively (P less than 0.05). 2. At 48th hour after hemodilution there are profound decreases in hematocrit, blood viscosity at high shear rate and blood viscosity at low shear rate. These changes last more than four weeks. Whereas in standard group, hemorheological parameters do not evidently change. 3. Sizes of cerebral infarction do not distinctly change in both groups between at entry and at the fourth weekend after treatment.

Acute Disease↗
PubMed1996

[Regional cerebral blood flow and periventricular hyperintensity in silent cerebral infarction--comparison with multi-infarct dementia].

In order to investigate relationship between regional cerebral blood flow (rCBF) and the white matter lesions on MRI in silent cerebral infarction, we quantitatively measured rCBF by 123I-IMP autoradiography method (IMP ARG method) and single photon emission tomography (SPECT) in 36 patients with silent cerebral infarction (SCI group), 22 patients with multi-infarct dementia (MID group), and 16 control subjects without periventricular hyperintensity (PVH) and lacunar infarction on MRI (CL group). Regions of interest (ROIs) on rCBF images were set in the frontal (F), temporal (T), parietal (P), occipital (O) cortex, and the cerebral white matter (W). The severity of PVH on MRI T2-weighted image was divided into four grades (grade 0-3). Our results: 1) Though the frequency of hypertension was significantly higher in SCI group and MID group compared with CL group, no significant difference was seen in the mean age among these three groups. 2) rCBF in the white matter and cerebral cortices except the occipital cortex in SCI group was significantly low compared with CL group (gamma CBFSCI/gamma CBFCL: W 0.87, F 0.87, P 0.88, O 0.92). 3) rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex, in MID group was significantly low compared with SCI group (gamma CBFMID/gamma CBFCL: W 0.69, F 0.71, T 0.74, P 0.75, O 0.81). 4) The mean grade of PVH in MID group was significantly higher that that in SCI group (SCI 1.1 vs MID 2.5). 5) The severity of PVH was significantly correlated with each rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex. Our findings suggest that the quantitative measurement of rCBF by IMP ARG method is useful for the follow-up study in the patients with silent cerebral infarction as well as the evaluation of the severity of PVH on MRI.

Aged↗
PubMedDate not supplied

Silent cerebral infarction in patients with type 2 diabetic nephropathy. Effects of antiplatelet drug dilazep dihydrochloride.

BACKGROUND: To determine whether diabetic nephropathy is a risk factor for silent cerebral infarction and whether antiplatelet drug dilazep dihydrochloride decreases the occurrence of silent cerebral infarction in type 2 diabetes patients with microalbuminuria. METHODS: Two hundred four type 2 diabetes patients (124 men, 80 women; age, median 56 years, range 42-74 years) and 60 healthy age-matched subjects (no diabetes, normal renal function) were recruited for brain magnetic resonance imaging. The diabetes patients included 40 without nephropathy (group A), 42 with microalbuminuria (20-200 microg/min) (group B), 44 with macroalbuminuria (>200 microg/min) and normal renal function (blood creatinine <132.7 micromol/L) (group C), 33 with chronic renal failure but not undergoing haemodialysis (blood creatinine >132.7 micromol/L; mean creatinine 335.9 micromol/L) (group D) and 45 undergoing haemodialysis (duration; median 4 years, range 3-6 years) (group E). RESULTS: Silent cerebral infarction was found in 20, 29, 34, 45, 53 and 8% of group A, B, C, D, E and control patients respectively. The incidence of silent cerebral infarction was increased with diabetic nephropathy. Thirty group B patients with no silent cerebral infarction were divided into two groups: (B1) 15 treated with dilazep dihydrochloride and (B2) 15 not treated with dilazep dihydrochloride. Treatment continued for 24 months. The incidence of silent cerebral infarction was significantly lower in the dilazep-treated patients (6.7%) than in the untreated patients (33.3%) (p < 0.01). CONCLUSIONS: These data suggest that diabetic renal dysfunction increases the risk of silent cerebral infarction and that dilazep dihydrochloride prevents its onset in early type 2 diabetic nephropathy patients.

Adult↗