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At least 19 recordsLinked to original sources
PubMed2002

[Gene therapy for cerebral infarction (cerebral ischemia)].

The treatment strategies of cerebral infarction have been studied in order to prevent neuronal cell death. Gene therapy is one of the most promising therapy and has several advantage over classical drug therapies. There has been a problem that drug proteins are unable or difficult to pass through blood brain barrier. In gene therapy, however, drug proteins are expressed in the brain with transgene transfer technique. Ischemic neural death proceeds with a complex series of pathophysiological events in the neurons. But molecular mechanism of ischemic neuronal cell death gradually understood. It has been known that a number of genes can be potent candidates for treatment factors of cerebral infarction. Actually, many investigators have been studied treatment strategies of cerebral infarction using a variety of neurotrophic factors such as bcl-2, heat shock protein 72, glial cell line-derived neurotrophic factor (GDNF), and hepatocyte growth factor (HGF). Moreover, the development of new vectors and gene delivery systems have been studied. Gene therapy would be a strong strategy for treatment of cerebral infarction in the future.

Animals↗
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↗
PubMed1990

[Cerebral blood flow and event-related potential in patients with cerebral infarction].

Cerebral blood flow (CBF) and P 300, a long-latency positive component of the scalp-recorded event-related potential (ERP) associated with cognitive processing were investigated in patients with cerebral infarction to elucidate the relationship between CBF and cognitive function. Twenty-five patients with cerebral infarction with a mean age of 66.8 years were studied. ERP was recorded during auditory discrimination tasks. The latency of the P 300 from Pz region was recorded. The regional CBF was measured by the 133Xe inhalation method. The F1 (cortical gray matter flow) values were calculated using the Obrist's method. The mean F1 values in patients with cerebral infarction were significantly lower compared to the values obtained for the 15 control subjects (mean age, 68.4 years) (p less than 0.01). Patients with cerebral infarction showed significant prolongation of the P 300 latency compared to the 20 control subjects (mean age, 64.4 years) (p less than 0.02). There was a significant correlation between the P 300 latency and the mean F1 values in patients with cerebral infarction (p less than 0.01). Present results suggest that the cognitive impairment with respect to ERP may be related to the reduction of cortical blood flow in patients with cerebral infarction.

Aged↗
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↗
PubMed2007

A nonsynonymous SNP in PRKCH (protein kinase C eta) increases the risk of cerebral infarction.

Cerebral infarction is the most common type of stroke and often causes long-term disability. To investigate the genetic contribution to cerebral infarction, we conducted a case-control study using 52,608 gene-based tag SNPs selected from the JSNP database. Here we report that a nonsynonymous SNP in a member of protein kinase C (PKC) family, PRKCH, was significantly associated with lacunar infarction in two independent Japanese samples (P = 5.1 x 10(-7), crude odds ratio of 1.40). This SNP is likely to affect PKC activity. Furthermore, a 14-year follow-up cohort study in Hisayama (Fukuoka, Japan) supported involvement of this SNP in the development of cerebral infarction (P = 0.03, age- and sex-adjusted hazard ratio of 2.83). We also found that PKCeta was expressed mainly in vascular endothelial cells and foamy macrophages in human atherosclerotic lesions, and its expression increased as the lesion type progressed. Our results support a role for PRKCH in the pathogenesis of cerebral infarction.

Case-Control Studies↗
PubMedDate not supplied

Index of lipid peroxidation and glucose utilization in the cerebrospinal fluid in patients with cerebral infarction.

Cerebral ischemia could be observed as acute metabolic crisis, when oxygen and glucose supply is compromised and synthesis of energy is insufficient. Apart from the excitotoxicity, increased production of reactive oxygen species with consequent lipid peroxidation is also included in neuronal cell damage. Furthermore, these toxic compounds could also be produced during the process of secondary inflammation of ischemic tissue. In the early stage of ischemia, as a systemic response to acute stress, there is an increase in glucose level in cerebrospinal fluid (CSF) and peripheral blood. According to the metabolic crisis and acidosis in ischemic brain tissue we investigated index of lipid peroxidation (ILP) and glucose utilization (IGU) in CSF of 53 patients of both sexes, aged 55-70 years with cerebral infarction. Control group comprised 15 patients with sudden onset of motor deficit subjected to diagnostic lumbar radiculography and suspected on discal genesis. ILP in CSF, as the indicator and sequela of neuronal cell membranes damage, was two fold increased in the acute period of cerebral infarction and maximal values (3.5 times) were noticed 24 hours after the ischemic episode compared to controls. Besides the increase in glucose concentration in peripheral blood and CSF of patients with cerebral infarction, IGU was decreased (37%) with minimal values (32%) 24 hours after the ischemia. These changes indicate that glucose is available but cells are incapable to metabolize it. We concluded that ILP and IGU in CSF of patients with cerebral infarction could be indicators of metabolic dysfunction and neuronal cell damage. Also, these results suggest the significance of polyvalent therapy including antioxidative and antiinflammatory agents in acute phase of cerebral ischemia.

Aged↗
PubMed2002

[Relation of pentanucleotide repeat polymorphism of apolipoprotein (a) gene to plasma lipoprotein (a) level among Chinese patients with myocardial infarction and cerebral infarction].

OBJECTIVE: Investigate the distribution and characteristics of 5'pentanucleotide TTTTA repeat (PNTR) polymorphism of apolipoprotein (a) [apo (a)] gene among Chinese patients with myocardial infarction (MI) and cerebral infarction, and its relationship to plasma lipoprotein (a) [Lp (a)] level. METHODS: DNA was extracted from the peripheral blood of 438 patients with myocardial infarction (MI, documented angiographically) and 218 controls, and 809 patients with cerebral infarction (documented by CT) and 1 817 controls. Plasma Lp (a) level was measured by ELISA. PNTR polymorphism of apo (a) gene was determined by polymerase chain reaction (PCR) and subsequent polyacrylamide gel electrophoresis. RESULTS: Eight alleles and 29 genotypes in apo (a) PNTR were detected in the four groups. The frequency of (TTTTA)(4 - 7) allele in the cerebral infarction group was 7.0%, significantly higher than that in control group (5.4%, P < 0.05). The frequency of genotype (TTTTA)(5/8) in MI group was 13.2%, significantly higher than that in the control group (7.8%, P < 0.05). No significant difference was seen in other alleles and genotypes among different groups (all P > 0.05). The level of triglyceride (TG) in patients with MI was 5.13 mmol/L +/- 1.15 mmol/L, significantly higher than that in controls (4.90 mmol/L +/- 0.99 mmol/L, P < 0.05). The level of TG in patients with cerebral infarction was 1.84 mmol/L +/- 1.36 mmol/L, not significantly different from that in controls (1.83 mmol/L +/- 1.51 mmol/L). The level of total cholesterol (TC) in patients with MI was 4.85 mmol/L +/- 1.04 mmol/L, significantly lower than that in controls (4.97 mmol/L +/- 1.00 mmol/L, P < 0.001). The level of TC in patients with cerebral infarction was 1.97 +/- 1.11 mmol/L, not significantly different from that in controls (1.79 mmol/L +/- 1.23 mmol/L). A negative correlation between the number of PNTR and Lp (a) level was observed in both MI group (P < 0.001) and cerebral infarction group (P < 0.01), and not in the control group. Small fragment repeat of apo (a) PNTR was correlated with cerebral infarction (OR = 1.4, 95% CI: 1.040 approximately 1.910), not significantly with MI (P > 0.05). Multiple logistic regression analysis showed that individuals with plasma Lp (a) > 300 mg/L had higher risk of MI (OR = 2.4, 95% CI: 1.630 - 3.594), and a higher risk of cerebral infarction (OR = 1.6, 95% CI: 1.013 - 2.021) after adjustment for age, sex, SBP, DBP, BMI, smoking, TC, TG, HDL-C, LDL-C and Glu. CONCLUSION: Plasma Lp (a) is an independent risk factor for MI and cerebral infarction. PNTR of apo (a) gene was negatively correlated with Lp (a) levels both in MI group and cerebral infarction group. Association with PNTR genotype was only found in cerebral infarction, but not in MI.

Adult↗
PubMed2005

Changes in cerebral glucose metabolism in newborn infants with cerebral infarction.

Cerebral infarction in infants is not uncommon, and it differs in many important ways from cerebral infarction in older children and adults. Computed tomography, ultrasound, and conventional and diffusion-weighted magnetic resonance imaging are useful for diagnosing cerebral infarction, but these imaging techniques cannot be used to measure cerebral blood flow and metabolic activity. Abnormality in those parameters seems to follow a different pattern and time course than those in older patients. In this study, the rapid changes in regional cerebral blood flow and metabolic rate of glucose were estimated by single-photon emission computed tomography and positron emission tomography during the acute and subacute phases of neonatal infarction. Subacute increases in blood flow and metabolic rate in the infarcted area of a term infant with multiple apneic episodes within 2 days after birth were observed, as well as acute increases in both in the infarcted area of a term infant with acute clonic seizures within 24 hours after birth. Follow-up studies at 4 months for the first infant and at 10 days for the second infant demonstrated that both the blood flow and metabolic rate in the infarcted region decreased. The results of this study should contribute to an understanding of the relationship between blood flow and metabolic rate changes after neonatal infarction as well as to improvement of diagnosis of neurologic impairments in neonates.

Cerebral Infarction↗
PubMed1993

Infection as a risk factor for cerebral infarction.

Cerebral infarction is a common complication in severe bacteraemic infections, such as endocarditis and meningitis, but it also occurs in other more common, milder infections. Febrile infections, mostly of the respiratory tract, and of probable bacterial origin, have been found as a risk factor for cerebral infarction. There are many mechanisms that could link a preceding infection to cerebral infarction, including septic emboli, arteritis, activation of the coagulation system and changes in blood rheology.

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↗
PubMed2001

Cerebral blood flow velocity in two patients with neonatal cerebral infarction.

Cerebral blood flow velocity was measured in the middle cerebral artery of two patients who exhibited unilateral neonatal cerebral infarction during the neonatal period. Doppler studies demonstrated increases in cerebral blood flow velocity but decreases in the resistance index on the affected side of the middle cerebral artery in the neonate who developed hemiplegia with cystic encephalomalacia, although the neonate with normal neurologic outcome exhibited symmetric cerebral blood flow velocity and resistance index. The asymmetry in cerebral blood flow velocity measurements of both middle cerebral arteries may be useful to evaluate the severity of brain damage and predict the neurodevelopmental prognosis of unilateral neonatal cerebral infarction.

Blood Flow Velocity↗
PubMed1989

[A 3 to 6-year follow-up study of 414 cases of cerebral infarction and cerebral hemorrhage].

To study the long-term prognosis, we performed annual follow-up examinations on 414 patients who had survived cerebrovascular accidents, including 334 cases of cerebral infarction and 80 cases of cerebral hemorrhage. All patients had been admitted to the Neurological Service of our hospital from January 1, 1976 to December 31, 1980, and were followed up for 3-6 years. The life-table method, the log rank test, and the rank sum test were used to determine the cumulative marked improvement rate, the cumulative recovery rate of pathological reflexes, the cumulative survival rate, and the cumulative recurrence rate. The results revealed the marked improvement rate in cerebral infarction was 81.98%, while in cerebral hemorrhage 89.87% at the end of 3 years after discharge. The recovery rate of pathological reflexes was 52.59% in cerebral infarction, 54.75% in cerebral hemorrhage at the end of 4 years. The cumulative survival rate was 58.67% in cerebral infarction, 53.36% in cerebral hemorrhage at the end of 6 years. The cumulative recurrence rate was 49.39% in cerebral infarction, 49.81% in cerebral hemorrhage at the end of 6 years.

Adult↗
PubMed1993

Secular trend of mortality from cerebral infarction and cerebral hemorrhage in Taiwan, 1974-1988.

BACKGROUND AND PURPOSE: Pathological patterns of stroke are different in various races, with the predominant stroke type in the Chinese being intracerebral hemorrhage. A total of 31,078 deaths from cerebral infarction and 77,773 deaths from cerebral hemorrhage in Taiwan were reported for groups of subjects aged 40-79 years during the period 1974-1988 to elucidate their secular trends. METHODS: Vital statistics and demographic data were collected for analyzing the truncated age-adjusted mortality rates. Poisson regression analysis was used to estimate the relative risk and 95% confidence interval. RESULTS: The mortality rates for cerebral hemorrhage were greater than those for cerebral infarction. The mortality rates increased exponentially with age for both subtypes. The decline in age-specific mortality for the period 1974-1983 was much more striking for cerebral hemorrhage than for cerebral infarction. Mortality from cerebral infarction and hemorrhage increased with age for all birth cohorts except the cerebral hemorrhage mortality of the oldest cohort. Male/female ratios for both cerebral infarction and hemorrhage were greater in the younger age groups. The cerebral hemorrhage/infarction ratio during the period 1984-1988 was highest for the younger age groups and lowest for the oldest age groups. CONCLUSIONS: The different secular trends of mortality from cerebral infarction and hemorrhage imply that these two patterns of stroke may be associated with some different risk factors.

Adult↗
PubMed1997

[Acute myocardial infarction and cerebral infarction at Kusatsu-spa].

From January 1989 to June 1995, 31 patients were admitted to our hospital with acute myocardial infarction (15 were tourists and 16 were Kusatsu residents) and 40 were admitted with cerebral infarction (15 tourists and 25 Kusatsu residents). We examined the possibility that hot hot-spring bathing was related to the occurrence of their illness. Fifteen patients with acute myocardial infarction (9 tourists and 6 Kusatsu residents) and 27 patients with cerebral infarction (11 tourists and 16 Kusatsu residents) had a hot hot-spring bath within 24 hours before the onset of symptoms. In 12 of the 15 with acute myocardial infarction (6 tourists and 6 Kusatsu residents) and in 15 of the 27 with cerebral infarction (9 tourists and 6 Kusatsu residents), symptoms began within 3 hours after they began bathing. In 2 of the remaining 3 patients with acute myocardial infarction and in 8 of the remaining 12 patients with cerebral infarction, bathing at night was followed by the onset of symptoms the next morning (more than 3 hour later). Acute myocardial infarction and cerebral infarction within 3 hours after hot hot-spring bathing may be attributable to transient change in blood pressure, heart rate, blood viscosity, fibrinolytic activity, and platelet function. We described previously that hot hot-spring bathing at night can accentuate the nocturnal decrease in blood pressure and can make the early morning increase in blood viscosity more abrupt. These phenomena may account for the occurrence of acute myocardial infarction and cerebral infarction early in the morning.

Aged↗