SEARCH · Search PubMed
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.
Explore the source record for details and available documents.
The role of serum cholesterol in predicting the risk of stroke is unclear and may depend on the subtype of the disease. In 1964 to 1965, 54,385 Swedish men and women participated in a health survey with serum cholesterol and diastolic blood pressure determinations. The Swedish mortality register was used to identify causes of death in this cohort during 20.5 years of follow-up (1964 to 1985). A person-year-based Poisson model was used for multivariate analysis. Relative risk increased with decreasing serum cholesterol level for subarachnoid hemorrhage in men and for cerebral hemorrhage in women but not for subarachnoid hemorrhage in women. For cerebral hemorrhage in men, the risk function was U-shaped. Adjustment for diastolic blood pressure did not significantly change the relation between the risk for any of the different stroke types and the cholesterol level. A low cholesterol level predicts death from intracranial bleeding, but the data suggest that there is differing risk pattern for men and women.
Explore the source record for details and available documents.
The relationship between recovery from aphasia and regional cerebral blood flow (CBF) was compared in 87 patients, 44 with cerebral hemorrhage and 43 with non-embolic cerebral infarction. CBF values correlated poorly with aphasia outcome in patients with cerebral hemorrhage whereas a tight correlation was demonstrated in patients with non-embolic cerebral infarction. A marked variability of CBF values in the acute and subacute stage might account for the poor correlation between CBF and aphasia outcome in patients with cerebral hemorrhage. On the other hand, a sharp discrimination was achieved between those with a good recovery from aphasia and those with a poor recovery by the dimensions of the hematoma on CT. In non-embolic cerebral infarction, a relative frontal ischemia was associated with motor aphasia while a relative temporal ischemia was associated with sensory aphasia. This dichotomy was not demonstrated in the regional CBF values in patients with cerebral hemorrhage.
A ten-year follow-up study of stroke among residents 40 years and older in a rural community located on Shikoku Island, Japan, was completed in 1977. The response rate for the initial examinations was 85% of 920 males and 90% of 1,012 females. Seven hundred and seventy-two males and 901 females who were initially free of stroke were followed from July 1967 through June 1977. The incidence of all strokes was 10.47 per thousand person-years for males and 6.41 per thousand person-years for females. The statistically significant risk factors for stroke were age, male sex, elevated blood pressure, ECG abnormalities, and funduscopic abnormalities. Elevated blood pressure was the strongest risk factor and mean arterial pressure was the best predictive measure. Twice as high a proportion of strokes were subclassified as cerebral hemorrhage (26%) in this study as have been reported in comparable studies in the United States (12-15%). An inverse relationship between serum cholesterol levels and cerebral hemorrhage incidence, but not cerebral infarct, was observed. High alcohol intake was a risk factor for cerebral hemorrhage but not for cerebral infarct. No relationship between stroke and weight was observed despite the relationship of stroke to blood pressure and of weight to blood pressure.
Cerebral hemorrhage associated with antithrombotic and thrombolytic therapy in acute stroke continues to present a major clinical problem. Rupture of the cerebral microvasculature involves the degradation and remodeling of extracellular matrix. Here we demonstrated that the delayed administration of heparin 3 hours after photothrombotic middle cerebral artery occlusion (MCAO) caused cerebral hemorrhage in wild-type (WT) mice but not in tissue plasminogen activator (tPA)-deficient knockout (KO) mice. Heparin administration increased tPA activity and its mRNA expression at 6 and 12 hours after MCAO in the ischemic hemispheres of WT mice. The expression of tPA was enhanced in microglial cells in the ischemic border zone. We also observed an exacerbation of matrix metalloproteinase (MMP) 9 expression at the mRNA level and its conversion to an active form after heparin administration in the ischemic hemisphere in WT mice but not in tPA KO mice. The increased MMP 9 expression was localized in microglial cells and endothelial cells. These findings suggest that endogenous tPA, through the enhancement of MMP 9 expression and proteolytic activation, plays an essential role in the pathogenesis of heparin-produced cerebral hemorrhage. Targeting tPA, MMP 9, or both may provide a new approach for preventing cerebral hemorrhage associated with antithrombotic therapy for stroke in humans.
To compare cerebral circulation in aphasic patients who had cerebral hemorrhage against those who with cerebral thrombosis, we studies 50 patients with hypertensive intracranial (putaminal) hemorrhage and 20 patients with cerebral thrombosis whose diagnoses were confirmed on repeated CT scan and cerebral angiography. The measurements of regional cerebral blood flow (rCBF) by the 133Xe intraarterial injection method was carried out in 40 patients. The evolution of the aphasic syndrome was analyzed according to Hirano's classification and the patients were divided into two groups: those having a favorable recovery from aphasia; those with a poor recovery. Twelve out of 20 patients with cerebral hemorrhage showed a favorable recovery from aphasia, whose left hemispheric mean blood flow (mCBF) was 33.1 +/- 9.7 ml/100 g/min. The mCBF was 30.8 +/- 10.3 ml/100 g/min in 8 patients with a poor recovery. There was no significant difference in mCBF values between the two groups. The favorable recovery group showed slightly higher regional values in the left frontal and temporal lobes than did the poor recovery group, but no significant difference was found between the two group. Here, rCBF values failed to correlate between the two kinds of recovery from aphasia in patients with cerebral hemorrhage. The marked variability in rCBF values in the acute stage might partly account for the poor correlation in cerebral hemorrhage. In contrast, a series of rCBF studies demonstrated that rCBF values stabilized in the acute and subacute stage in cerebral thrombosis. Nine out of 20 patients with cerebral thrombosis had a favorable recovery from aphasia.(ABSTRACT TRUNCATED AT 250 WORDS)
We determined the effect of hemodilution and hypertension on cerebral hemorrhage and brain injury in 32 rats subjected to 180 minutes of middle cerebral artery occlusion and 120 minutes of reperfusion. We divided the rats into four groups. In the control group (n = 8) neither hematocrit nor blood pressure was manipulated during occlusion, in the hemodilution group (n = 8) 5% albumin was administered to maintain a hematocrit of 30% during occlusion, in the hypertension group (n = 8) mean arterial blood pressure was increased to 30 mm Hg above baseline during occlusion with phenylephrine, and in the hemodilution/hypertension group (n = 8) albumin and phenylephrine were employed simultaneously during occlusion. We assessed the amount of cerebral hemorrhage (as concentration of extravasated hemoglobin) spectrophotometrically and the extent of ischemic injury (as percentage of the hemisphere with deficient staining) histochemically using 2,3,5-triphenyltetrazolium chloride. Mean +/- SD hemoglobin concentration in the hemisphere ipsilateral to the occlusion in the hemodilution/hypertension group (71 +/- 14 micrograms/g brain tissue) was significantly (p less than 0.05) greater than that in the hemodilution and hypertension groups (25 +/- 5 and 29 +/- 7 micrograms/g, respectively), hemoglobin concentrations in these two groups were in turn significantly (p less than 0.05) greater than that in the control group (2 +/- 3 micrograms/g). Mean +/- SD percentage of the ipsilateral hemisphere with deficient staining was significantly (p less than 0.05) less in the hypertension and hemodilution hypertension groups (8 +/- 3% and 11 +/- 6%, respectively) than in the control and hemodilution groups (26 +/- 8% and 26 +/- 7%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.