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PubMed2005

Mild cognitive impairment is related to Alzheimer disease pathology and cerebral infarctions.

OBJECTIVES: To examine the extent to which persons with mild cognitive impairment have intermediate levels of Alzheimer disease (AD) pathology, cerebral infarcts, and Lewy body disease. METHODS: A total of 180 Catholic clergy participating in the Religious Orders Study underwent annual detailed evaluation and brain autopsy. Blocks of midfrontal, superior temporal, medial temporal lobe, inferior parietal, entorhinal cortex, hippocampus, and substantia nigra were paraffin embedded, and sectioned at 6 mum. Cortical neuritic plaques, diffuse plaques, and neurofibrillary tangles were visualized with Bielschowsky silver stain, and counted and summarized to yield a Braak stage, Consortium to Establish a Registry for Alzheimer's Disease (CERAD) diagnosis, National Institute on Aging (NIA)-Reagan diagnosis, and composite measure of AD pathology. The authors recorded the number and location of all gross chronic cerebral infarctions. Lewy bodies were identified with antibodies to alpha-synuclein. Multiple regression analyses were used to examine the relation of AD pathology and cerebral infarctions to clinical diagnosis proximate to death, controlling for age, sex, and education. RESULTS: A total of 37 had mild cognitive impairment, 60 did not have cognitive impairment, and 83 had dementia proximate to death. Nearly all persons had at least some AD pathology. Cerebral infarctions were present in 35.2%, and 15.6% had Lewy body disease. Persons with mild cognitive impairment were intermediate in terms of Braak stage and CERAD and NIA-Reagan neuropathologic criteria for AD compared to the other two groups. In multiple regression analyses, persons with mild cognitive impairment had intermediate levels of AD pathology from those without cognitive impairment and those with dementia (test for trend, F = 45.2, p < 0.001). Further, the relation between cognition and AD pathology in persons with mild cognitive impairment did not differ significantly from the relation between cognition and AD pathology in persons with dementia or those without cognitive impairment. Persons with mild cognitive impairment also had intermediate levels of cerebral infarctions (test for trend, p = 0.04). Only 3 (8.1%) persons with mild cognitive impairment had Lewy body disease. CONCLUSION: These data suggest that mild cognitive impairment may be the earliest clinical manifestation of common age-related neurologic diseases.

Age Factors↗
PubMed1990

Delayed intracranial hemorrhage following cerebral infarction in sickle cell anemia.

Clinical and necropsy findings in 11 patients with sickle cell anemia (SS) indicate that intracranial hemorrhage (IH) is a delayed sequela of the same vasculopathy that causes cerebral infarction during childhood. Evidence of prior cerebral infarction during childhood included hemiparesis, seizures, an episode of coma, or mental retardation. Computerized tomography (CT) scans showed cerebral infarcts with lucent areas and dilated ventricles or cerebral atrophy. CT or magnetic resonance imaging (MRI) scans after the intracranial hemorrhage demonstrated intraventricular or intracerebral hemorrhages. Angiography or autopsy in seven patients showed widespread vascular occlusion and narrowing of arterial vessels. Moyamoya with internal carotid artery occlusion was identified in two cases. At the time of the IH, three patients were being treated with prophylactic transfusion regimens. We hypothesize that the central nervous system vasculopathy progresses over time and that arterial narrowing in both large and small vessels secondary to endothelial hyperplasia is followed by neovascularization and hemorrhage. Recognition of this pattern of delayed intracranial hemorrhage following cerebral infarction should encourage more intensive evaluation aimed at developing rational interventional therapy prior to a terminal intracranial hemorrhage.

Adolescent↗
PubMed1997

Dietary lipids and incidence of cerebral infarction in a Japanese rural community.

OBJECTIVE: To assess the relationship between dietary lipids and incidence of cerebral infarction in a Japanese rural population. DESIGN: A cohort study from July 1977 through December 1992. SETTING: Akadani-Ijimino (A-I) district, Niigata Prefecture, Japan. SUBJECTS AND METHODS: All the residents, 1,182 men and 1,469 women, aged 40 years and over. Out of these members, 954 men and 1,329 women who were initially free of stroke completed a semiquantitative food frequency questionnaire in 1977, and were then subjected to a follow-up for 15.5 years. The occurrence of stroke was determined by the annual follow-up examination and registry. Dietary lipid was adjusted for total energy or fat intake by the residual method. Sex- and age-stratified and blood pressure- and atrial fibrillation-adjusted relative risk for cerebral infarction was estimated by the Cox proportional hazard model. RESULTS: There were 75 new cases of cerebral infarction during the observation period. The relative risk for cerebral infarction was less than one in the highest quartile level of total fat, saturated fatty acids (S), Keys score and westernized dietary pattern: 0.68-0.94. It ranged between 1.36 and 1.57 in the highest level of polyunsaturated (P), n-3 and n-6 fatty acids, and P/S ratio. CONCLUSION: This study suggests the possibility that the traditional Japanese diet, very low fat intake, was likely to increase the risk of stroke through the low level of serum cholesterol as an intermediary factor.

Adult↗
PubMed1999

Serial MRI of cerebral infarcts before and after removal of an atrial myxoma.

We describe a cerebral infarct caused by atrial myxoma. A 30-year-old woman with an atrial myxoma presented with a right hemisensory deficit. MRI carried out before and after removal of the myxoma, showed multiple small bilateral white-matter infarcts which increased in number up to the surgery. A lesion in the left thalamus, which enlarged and showed contrast enhancement 4 months before surgery, resembled an old cerebral infarct by the time the myxoma was removed. The number of lesions stopped increasing after surgery. We suggest that atrial myxomas should be removed even in asymptomatic patients, to prevent cerebral infarcts due to embolism of tumour or thrombus.

Adult↗
PubMed1979

[Treatment with 10% glycerin in acute ischemic cerebral infarct. Doubleblind study].

56 patients with acute ischemic cerebral infarction were randomly allocated to intravenous treatment for 6 days with either 500 ml of a 10% glycerol solution or 500 ml of a 5% dextrose solution (placebo). The neurological status of the patients was evaluated by a blinded investigator before the beginning of the treatment, after 2 weeks and again after 6 months. According to the initial degree of neurological deficit, patients were stratified into a mild, intermediate and severe group (using a scoring system). After 2 weeks there was significantly less neurological deficit in the total glycerol-treated group than in the placebo group (2p less than 0.02). This favourable effect of glycerol was even greater in the patients with an initially intermediate degree of neurological deficity (2p less than 0.01). After 6 months there was no difference between the total glycerol-treated and the placebo group. A beneficial effect of glycerol treatment, however, was still demonstrable in the intermediate group (2p less than 0.05). Mortality was not influenced by glycerol treatment. No side effects of the glycerol treatment could be detected. Intravenous administration of 10% glycerol can thus be recommended in patients with acute cerebral infarction.

Adult↗
PubMed1980

Cerebral infarction: a disparity between Tc-99m-pertechnetate and Tc-99m-EHDP images.

A case of cerebral infarction that showed a disparity between Tc-99m-pertechnetate and Tc-99m-EHDP brain images is presented. Serial Tc-99m-ertechnetate and Tc-99m-EHDP brain images showed not only different lesion-to-nonlesion ratios but different distribution patterns. Tc-99m-labeled phosphate compounds may be useful in the estimation of prognosis in cerebral infarction as well as in differential diagnosis between cerebral infarction and cerebral tumors.

Cerebral Infarction↗
PubMed2002

[Clinical study on effect and therapeutical mechanism of composite Salvia injection on acute cerebral infarction].

OBJECTIVE: To investigate the curative effect and therapeutical mechanism of composite salvia injection (CSI) in treating ischemic cerebral infarction in the respect of oxygen free radical and apolipoprotein. METHODS: Sixty-eight cases of ischemic cerebral infarction within the first 72 hrs after onset were divided randomly into the CSI group (treated with CSI) and the control group (treated with Xueshuantong). Serum lipid peroxide (LPO) and superoxide dismutase (SOD) were measured by colorimetry and apolipoprotein A1 (ApoA1) and ApoB100 were measured with unidirectional immune diffusion method. RESULTS: Serum levels of LPO and ApoB100 were obviously lower, and levels of SOD and ApoA1 significantly higher in the CSI group than those in the control group (P < 0.05 or P < 0.01). The total effective rate of CSI in treating cerebral infarction was 88.24%, which was significantly higher than that of the control (P < 0.05). CONCLUSION: CSI shows definite effect in treating cerebral infarction, to reduce the oxygen free radical damage and regulate the apolipoprotein metabolism possibly was the important therapeutical mechanism.

Aged↗
PubMed1995

[Cerebral infarction after the cardiovascular operation].

From January, 1990 through July 1994, 615 adult patients were undergone cardiovascular operation under the cardiopulmonary bypass. Sixteen patients were suffered perioperative cerebral infarction. The etiology of the cerebral infarction was evaluated on the pre and postoperative brain CT findings by the neurologists. In the 283 coronary artery bypass operations, 4 patients suffered watershed infarction (WS) and 4 cerebral embolism. In the 252 valve operations, one WS and one embolism. In the 80 thoracic aortic operations, 5 WS and one embolism, respectively. The risk factors of WS were the elderly, emergency, the longer operative period, and the longer cardiopulmonary bypass period. The risk factor of the embolism were male, preoperative cerebral infarction, the calcified finding of the ascending aorta by the chest CT. It is important to take preventive strategies against the watershed infarction.

Adult↗
PubMed1999

Apolipoprotein(a) and cortical cerebral infarction.

OBJECTIVE: The present study aimed to elucidating the correlation of apolipoprotein(a) [apo(a)] with cerebral infarction at the levels of molecule and protein. METHODS: The serum Lp(a) level, by means of ELISA, the polymorphism of apo(a) protein, by SDS-PAGE/Western blotting combined with silver staining assays, and the sequence polymorphisms in 5' control region, the first exon and intron of apo(a) gene, by PCR-SSCP/AFLP assays, were detected in 85 healthy controls and 12 cases of cortical cerebral infarction. RESULTS: The serum Lp(a) level was markedly higher in the patients (152.59+/-3.41 mg/L) than that in the controls (56.21+/-3.67 mg/L) (t=4, 15, P<0. 001), even between the subjects with the same apo(a) phenotype. The frequency of low molecular weight phenotype was significantly higher in the patients than that in the controls (0.5238 vs. 0.2941). There were 2 sites of sequence variance in the 5' control region of apo(a) gene in our studied population, which were of significant difference between patients and controls, and were related to the variation of serum Lp(a) level. CONCLUSION: Our study found that the low molecular weight phenotype of apo(a) was closely associated with cerebral infarction, suggested that the variation of serum Lp(a) level be determined by not only the size of apo(a) gene but also its sequence, which indicated that both the size and sequence of apo(a) are associated with the susceptibility to cerebral infarction.

Aged↗
PubMed1980

Computerized tomographic enhancement patterns in cerebral infarction.

Intravenous contrast computerized tomography (CT) was performed in 200 patients with cerebral infarction. Of 100 patients who had CT performed after bolus injection of 50 mL of 60% iodinated contrast material, enhancement was seen in five (5%). This compared with enhancement seen in 65% of patients with cerebral infarction studied after drip infusion of 300 mL of 30% iodinated contrast material. The enhancement occurred between the end of the first week and and the end of the fourth week after development of neurological abnormalities. Follow-up CT showed disappearance or marked reduction in the intensity of enhancement within 21 days of the initial CT study. Peripheral ring or diffuse enhancement were nospecific, but certain patterns were highly specific for infarction and included dense enhancement within deep nuclear gray matter (putamen, caudate, thalamus) and tubular-shaped or gyral enhancement with intervening low-density portions and minimal or no mass effect. Cerebral infarction was confirmed in all cases by clinical course, angiography, or subsequent CT.

Cerebral Angiography↗
PubMed1988

Magnetic resonance imaging of cerebral infarction: time course of Gd-DTPA enhancement and CT comparison.

Thirty-five patients (7 females and 28 males) with cerebral infarction and suspicion of cerebral infarction of 4 h to 27 months duration were studied 45 times with magnetic resonance (MR) imaging using Gd-DTPA. Spin echo (SE) images were obtained before and after the administration of Gd-DTPA (0.1 or 0.15 mmol/kg) and compared with the enhanced CT. MR imaging using Gd-DTPA was more sensitive than enhanced CT and very useful for detecting a new focus of cerebral infarction, especially in the cases with multiple infarcted areas and for showing the extent of cortical and subcortical infarction. In most cases the MR enhancement was obvious in the subacute stage, especially after cerebral embolism, and the signal intensity of the lesion tended to show a gradual increase. The diagnosis of embolism was accepted on the basis of acute onset without prior TIA, coupled with angiography showing the embolus itself and/or a capillary blush and a wide area of infarction.

Adult↗
PubMed1991

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

We investigated shrinkage of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery in 33 patients who were admitted less than or equal to 2 days after the stroke and who were followed by computed tomography for greater than 1 year with no recurrences. The thalamic area was measured on the computed tomograms, and the ratio of the ipsilateral area to the contralateral area was calculated. All values were compared with values from the initial computed tomogram taken less than or equal to 2 days after the stroke. The values of the ratio on follow-up computed tomograms decreased gradually in 15 patients. In these cases, the area of the ipsilateral thalamus was significantly reduced after 1 year (p less than 0.01) and marked atrophy was observed. These results demonstrate the significance of remote changes over a long period of time after focal cerebral infarction.

Atrophy↗
PubMed1995

Determinants of black-white differences in the risk of cerebral infarction. The National Health and Nutrition Examination Survey Epidemiologic Follow-up Study.

OBJECTIVE: To determine whether blacks in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study remained at increased risk for cerebral infarction after adjusting for stroke risk factors and sociodemographic factors. METHODS: A cohort study involving 8203 whites and 1362 blacks who participated in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. During the 13-year follow-up, 538 and 122 cerebral infarctions occurred in whites and blacks, respectively. RESULTS: The black-white risk for cerebral infarction varied by age (P = .007 for race-age interaction). Compared with whites of the same age, blacks aged 35 to 44 years were at significantly increased risk for cerebral infarction (relative risk, 2.62; 95% confidence interval, 1.23 to 5.57), while older blacks, those older than 64 years, were not at increased risk (relative risk, 1.14; 95% confidence interval, 0.90 to 1.46). The relative risk for cerebral infarction decreased to 2.07 (95% confidence interval, 0.97 to 4.42) in younger blacks and 0.82 (95% confidence interval, 0.29 to 2.33) in older blacks after adjustment for age, sex, education, history of heart disease, diabetes, systolic blood pressure, treatment for hypertension, Quetelet index, and serum hemoglobin and magnesium levels. CONCLUSIONS: These results indicate that much of the increased risk for cerebral infarction experienced by blacks can be explained by their higher prevalence of stroke risk factors, especially diabetes, hypertension, and lower educational attainment. Younger blacks, however, may still be at increased risk after adjusting for stroke risk factors.

Adult↗
PubMed1998

Survival and recurrence after first cerebral infarction: a population-based study in Rochester, Minnesota, 1975 through 1989.

We used the Kaplan-Meier product limit method to estimate rates and Cox proportional hazards regression analysis with bootstrap validation to model significant independent predictors of and temporal trends in survival and recurrent stroke among 1,111 residents of Rochester, MN, who had a first cerebral infarction from 1975 through 1989. The risk of death after first cerebral infarction was 7% +/- 0.7% at 7 days, 14% +/- 1.0% at 30 days, 27% +/- 1.3% at 1 year, and 53% +/- 1.5% at 5 years. Independent risk factors for death after first cerebral infarction were age (p < 0.0001), congestive heart failure (p < 0.0001), persistent atrial fibrillation (p < 0.0001), recurrent stroke (p < 0.0001), and ischemic heart disease (p < 0.0001 for age < or =70, p > 0.05 for age >70). The risk of recurrent stroke after first cerebral infarction was 2% +/- 0.4% at 7 days, 4% +/- 0.6% at 30 days, 12% +/- 1.1% at 1 year, and 29% +/- 1.7% at 5 years. Age (p = 0.0002) and diabetes mellitus (p = 0.0004) were the only significant independent predictors of recurrent stroke. Neither the year nor the quinquennium of the first cerebral infarction was a significant determinant of survival or recurrence. The temporal trend toward improving survival after first cerebral infarction documented in Rochester, MN, in the decades before 1975 has ended.

Aged↗
PubMed1994

[Therapeutic effectiveness of zuzhongping on patients with arteriosclerostic cerebral infarction].

Forty-six patients with acute arteriosclerostic cerebral infarction were randomly divided into two groups: control group and treatment group. Each of them included 23 patients respectively. The patients in the control group were given Dextran-40 but the ones in the treatment group were given the mixture of Zuzhongping. The course of treatment was 3 weeks. It was found that there was a significant difference (P < 0.01) in the score percentage, before and after treatment of neurological defects, between the control group and the treatment group, and the former (29.70 +/- 33.52) was much lower than the latter (45.40 +/- 27.60). The total curative rate of the treatment group (87.0%, 20/23) was significantly higher than that of the control group (60.9%, 14/23). There was an obviously prolonged KPTT (kaolin partial thromboplastin time) value and a decreased Fb (fibrinogen) level in the treatment group. Before treatment they were 32.43 +/- 4.03 sec and 6.18 +/- 1.77 g/L respectively, but after treatment, 52.96 +/- 10.50 sec and 4.5 +/- 0.95 g/L respectively. The authors suggest that the significant therapeutic efficacy of Zuzhongping in the patients with acute arteriosclerostic cerebral infarction is related to its action of anticoagulation, modification of PGI2 and TXA2 level in the body, decreased blood Fb level, hyperglycemia, etc.

Aged↗
PubMed1998

Change in bladder contractility associated with bladder overactivity in rats with cerebral infarction.

PURPOSE: To evaluate the contractile properties of overactive bladder from rats in the chronic stage of experimental cerebral infarction. MATERIALS AND METHODS: Cystometry was performed in conscious male S-D rats after inducing occlusion of the left middle cerebral artery. Bladder muscle strips were evaluated for force development in response to field stimulation, acetylcholine and KCl. By measuring the contractile response to field stimulation after adding atropine and alpha,beta-methylene-ATP, contributions of cholinergic and purinergic transmission were determined. RESULTS: Bladder capacity of cerebral-infarcted rats was <50% of the capacity of sham-operated rats and significantly less than that of sham-operated rats even 4 months after surgery. There was no significant difference in bladder weight between sham-operated rats and cerebral-infarcted rats. No differences in the contractile response of detrusor strips to field stimulation and acetylcholine, or in the relative contribution of cholinergic and purinergic transmission to the contractile response, were observed over time or between strips from sham-operated rats and cerebral-infarcted rats. KCl induced significantly less contraction in strips from 4 month infarcted rats than in strips from 4 month sham-operated rats, 2 week infarcted rats and 2 month infarcted rats. CONCLUSIONS: This animal model will be useful for chronic studies on the mechanism of detrusor hyperactivity (DH).

Animals↗
PubMedDate not supplied

Frequency of cerebral infarction in patients with inherited neuromuscular diseases.

We evaluated the frequency of cerebral infarction in 131 patients with Duchenne's muscular dystrophy, myotonic dystrophy, Becker's muscular dystrophy, or Friedreich's ataxia. Electrocardiographic abnormalities were found in 83% of patients with Duchenne's muscular dystrophy, 56% with myotonic dystrophy, 50% with Becker's muscular dystrophy, and 25% with Friedreich's ataxia. Atrial flutter occurred in 2.3% of the patients, and atrial fibrillation in only 0.9%. Evidence of cerebral infarction was found in only 2 patients (1.5%). Both patients had cardiomyopathy and either atrial fibrillation or flutter. Despite frequent cardiac involvement, cerebral infarction is an uncommon occurrence in patients with inherited neuromuscular diseases.

Adolescent↗
PubMed1987

CSF beta-endorphin and leu-enkephalin levels in the acute and chronic stages of cerebral infarction.

To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive beta-endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF beta-endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.

Acute Disease↗