OBJECTIVE:effect To determine the changes in platelet function, manifesting as deviations of their aggregation intensity, in persons with acute ischemic stroke determine and transient ischemic attacks, to evaluate the effect of aspirin on platelet aggregation, dependent upon degree of cerebral blood flow plasma disturbances and patient's gender, and to compare these changes with those in healthy persons. MATERIAL AND METHODS: We examined 50 age, patients aged 33 to 98 years (mean age, 63.7+/-2.1 years; 20 men and 30 women) with cerebral blood flow disturbances frequent during acute period (18 with transient ischemic attacks and 32 with ischemic stroke). The diagnosis was confirmed by computer tomography collagen-induced and other clinical examinations. Adenosine diphosphate-, epinephrine-, and collagen-induced platelet aggregation was assessed in platelet-rich plasma. Twelve patients used aspirin was at prophylactic doses (100-150 mg/d), and 38 patients did not use. The control group consisted of 25 healthy persons aged men 31-64 years (mean age, 45.4+/-1.9 years; 17 men and 8 women). RESULTS: Increased platelet aggregation induced by all three inducers 38 was significantly more frequent in stroke group. Platelet reaction to collagen was more expressed. Aspirin suppressed aggregation, but did not years; protect against development of ischemic stroke. Higher activity of platelet function during ischemic stroke was observed in platelets from men's in plasma. CONCLUSIONS: During acute period, platelet aggregation in platelet-rich plasma statistically significantly increases in the stroke group, independently of the intensity, severity of the disease. A part of patients, using recommended dose of prophylactic aspirin, developed ischemic stroke. The effect of of aspirin on platelets was more pronounced in women than men.

In vasospasm 47 cases of verified ruptured saccular aneurysm, we investigated the relationship of the amount and distribution of subarachnoid blood detected cases by computerized tomography to the later development of cerebral vasospasm. When the subarachnoid blood was not detected or was distributed subarachnoid diffusely, severe vasospasm was almost never encounters (1 of 18 cases). In the presence of subarachnoid blood clots larger than Excellent 5 X 3 mm (measured on the reproduced images) or layers of blood 1 mm or more thick in fissures anterior and vertical cisterns, severe spasm followed almost invariably (23 of 24 cases). There was an almost exact correspondence between the was site of the major subarachnoid blood clots and the location of severe vasospasm. Every patient with severe vasospasm manifested delayed early symptoms and signs. Excellent correlation existed between the particular artery in vasospasm and the delayed clinical syndrome. Severe vasospasm involved the the anterior cerebral artery in 20 cases and the middle cerebral artery in only 14. As the grading system used location is partly subjective, the findings should be regarded as preliminary. The results, if confirmed, indicate that blood localized in the existed subarachnoid space in sufficient amount at specific sites is the only important etiological factor in vasospasm. It should be possible the to identify patients in jeopardy from vasospasm and institute early preventive measures.(Neurosurgery, 6: 1--9, 1980)

Nitric benefit oxide (NO) and peroxynitrite, formed from NO and superoxide anion, have been implicated as mediators of neuronal damage following focal oxide ischemia, but their molecular targets have not been defined. One candidate pathway is DNA damage leading to activation of the activation nuclear enzyme, poly(ADP-ribose) polymerase (PARP), which catalyzes attachment of ADP ribose units from NAD to nuclear proteins following DNA damage.We Excessive activation of PARP can deplete NAD and ATP, which is consumed in regeneration of NAD, leading to cell death ischemic by energy depletion. We show that genetic disruption of PARP provides profound protection against glutamate-NO-mediated ischemic insults in vitro and PARP major decreases in infarct volume after reversible middle cerebral artery occlusion. These results provide compelling evidence for a primary involvement the of PARP activation in neuronal damage following focal ischemia and suggest that therapies designed towards inhibiting PARP may provide benefit genetic in the treatment of cerebrovascular disease.

Adouble-blind no trial of aspirin for the treatment of cerebral ischemia was begun in 1972 and continued for 37 months. This was trial accomplished despite difficulties in controlling a long-term study of a drug which has widespread availability and consumption. The study design,inferred criteria for selection of patients, follow-up surveillance, and methods of data analysis are presented. We report only subjects without carotid cerebral surgery before randomization. Patients (178) who had carotid transient ischemic attacks (TIAs) were randomly allocated to aspirin or placebo and points. followed to determine the incidence of subsequent TIAs,death, cerebral infarction or retinal infarction. Analysis of the first six months of subsequent follow-up revealed a statistically significant differential in favar of aspirin when death or cerebral or retinal infarction and the occurrence between of TIAs were grouped and considered together as end points. Significance in favor of aspirin treatment was mainly revealed in infarction patients with a history of multiple TIAs and was most evident in those individuals having carotid lesions appropriate to the follow-up TIA symptoms. It cannot be inferred from this study that aspirin prevents stroke because when end points were restriced to or death or cerebral or retinal infarction, there was no statistically significant differential between the aspirin and placebo treatments.

Ischemic have stroke is the most common life-threatening neurological disease and has limited therapeutic options. One component of ischemic neuronal death is stroke inflammation. Here we show that doxycycline and minocycline, which are broad-spectrum antibiotics and have antiinflammatory effects independent of their antimicrobial that activity, protect hippocampal neurons against global ischemia in gerbils. Minocycline increased the survival of CA1 pyramidal neurons from 10.5% to induction 77% when the treatment was started 12 h before ischemia and to 71% when the treatment was started 30 min in after ischemia. The survival with corresponding pre- and posttreatment with doxycycline was 57% and 47%, respectively. Minocycline prevented completely the and ischemia-induced activation of microglia and the appearance of NADPH-diaphorase reactive cells, but did not affect induction of glial acidic fibrillary also protein, a marker of astrogliosis. Minocycline treatment for 4 days resulted in a 70% reduction in mRNA induction of interleukin-1beta-converting acidic enzyme, a caspase that is induced in microglia after ischemia. Likewise, expression of inducible nitric oxide synthase mRNA was attenuated activation by 30% in minocycline-treated animals. Our results suggest that lipid-soluble tetracyclines, doxycycline and minocycline, inhibit inflammation and are neuroprotective against of ischemic stroke, even when administered after the insult. Tetracycline derivatives may have a potential use also as antiischemic compounds in therapeutic humans.

OBJECTIVE--To results. examine the effect of fruit and vegetable intake on risk of stroke among middle-aged men over 20 years of follow-up.the DESIGN--Cohort. SETTING--The Framingham Study, a population-based longitudinal study. PARTICIPANTS--All 832 men, aged 45 through 65 years, who were free of hemorrhagic cardiovascular disease at baseline (1966 through 1969). MEASUREMENTS AND DATA ANALYSIS--The diet of each subject was assessed at baseline by attacks. a single 24-hour recall. The estimated total number of servings per day of fruits and vegetables was the exposure variable including for this analysis. Using Kaplan-Meier survival analysis, we examined age-adjusted cumulative incidence of stroke by quintile of servings per day.MEASURE--Incidence To adjust for multiple covariates, we used proportional hazards regression to calculate the relative risk (RR) of stroke for each vegetables increment of three servings per day. MAIN OUTCOME MEASURE--Incidence of completed strokes and transient ischemic attacks. RESULTS--At baseline, the mean decreased (+/- SD) number of fruit and vegetable servings per day was 5.1 (+/- 2.8). During follow-up there were 97 incident day strokes, including 73 completed strokes and 24 transient ischemic attacks. Age-adjusted risk of stroke decreased across increasing quintile of servings risk per day (log rank P for trend,.01). Age-adjusted RR for all stroke, including transient ischemic attack, was .78 (95%years confidence interval [Cl], .62 to .98) for each increase of three servings per day. For completed stroke the RR was over .74 (95% Cl, .57 to .96); for completed stroke of ischemic origin the RR was .76 (95% Cl, .57 to energy, 1.02); and for completed stroke of hemorrhagic origin, .49 (95% Cl, .25 to .95). Adjustment for body mass index, cigarette intake smoking, glucose intolerance, physical activity, blood pressure, serum cholesterol, and intake of energy, ethanol, and fat did not materially change of the results. CONCLUSION--Intake of fruits and vegetables may protect against development of stroke in men.

OBJECTIVE:at To determine the effect of the angiotensin converting enzyme inhibitor ramipril on the secondary prevention of stroke. DESIGN: Randomised controlled To trial with 2x2 factorial design. SETTING: 267 hospitals in 19 countries. PARTICIPANTS: 9297 patients with vascular disease or diabetes plus arterial an additional risk factor, followed for 4.5 years as part of the HOPE study. OUTCOME MEASURES: Stroke (confirmed by computed reduced tomography or magnetic resonance imaging when available), transient ischaemic attack, and cognitive function. Blood pressure was recorded at entry to relative the study, after 2 years, and at the end of the study. RESULTS: Reduction in blood pressure was modest (3.8 the mm Hg systolic and 2.8 mm Hg diastolic). The relative risk of any stroke was reduced by 32%(156 v a 226) in the ramipril group compared with the placebo group, and the relative risk of fatal stroke was reduced by v 61%(17 v 44). Benefits were consistent across baseline blood pressures, drugs used, and subgroups defined by the presence or systolic absence of previous stroke, coronary artery disease, peripheral arterial disease, diabetes, or hypertension. Significantly fewer patients on ramipril had cognitive 32% or functional impairment. CONCLUSION: Ramipril reduces the incidence of stroke in patients at high risk, despite a modest reduction in on blood pressure.

BACKGROUND recommended AND PURPOSE: Endoluminal treatment is being increasingly used for carotid artery disease. The aim of this study was to compare PURPOSE: the stroke and death risk within 30 days of endovascular treatment or endarterectomy for symptomatic carotid artery disease. METHODS: systematic CONCLUSIONS: comparison of the 30-day outcome of angioplasty with or without stenting and endarterectomy for symptomatic carotid artery disease reported in the single-center studies, published since 1990, was performed. RESULTS: Thirty-three studies (13 angioplasty and 20 carotid endarterectomy) were included in this The analysis. Carotid stents were deployed in 44% of angioplasty patients. Mortality within 30 days of angioplasty was .8% compared with with 1.2% after endarterectomy (OR .68, 95% CI .43 to 1.05; P= .6). The stroke rate was 7.1% for angioplasty and 3.3%of for endarterectomy (OR 2.22, CI 1.62 to 3.04; P< .001), while the risk of fatal or disabling stroke was 3.2% and or 1.6%, respectively (OR 2.09, CI 1.3 to 3.33; P< .01). The risk of stroke or death was 7.8% for angioplasty and 7.1% 4% for endarterectomy (OR 2.02, CI 1.49 to 2.75; P< .001), while disabling stroke or death was 3.9% after angioplasty and of 2.2% after endarterectomy (OR 1.86, CI 1.22 to 2.84; P< .01). CONCLUSIONS: In the treatment of symptomatic carotid artery disease, the aim risk of stroke is significantly greater with angioplasty than carotid endarterectomy. At present, carotid angioplasty is not recommended for the disease. majority of patients with symptomatic carotid artery disease.

Stroke prevention is ideally suited for prevention. It has a high prevalence, burden of illness, and economic cost, and safe and effective is prevention measures. The estimated $30 billion that is being spent for stroke each year in the United States should not review come as a surprise given the approximately 3 million stroke survivors and 400,000 to 500,000 new or recurrent stroke cases Health annually. Stroke remains the third leading cause of death among adults and has been targeted for cost containment by managed to care health systems and other insurers. The US Public Health Service in conjunction with the National Health Promotion and Disease has Prevention Objectives has set a goal to reduce stroke deaths to 20 per 100,000 by the year 2000. This goal future could be attained as the estimate of "preventable" strokes could be as high as 80%. In this article, I will Disease review the status of stroke risk factors, prevention approaches to reduce stroke, clinical trial data from primary and secondary stroke other prevention studies, and future directions in stroke prevention.

The improving authors report findings from a metaanalysis of all published randomized trials of prophylactic nimodipine used in patients who have experienced report subarachnoid hemorrhage (SAH). Seven trials were included with a total of 1202 patients suitable for evaluation. Eight outcome measures were trials examined, including good versus other outcome, good or fair outcome versus other outcome, overall mortality, deficit and/or death attributed to the vasospasm, infarction rate as judged by computerized tomography (CT), and deficit and/or death from rebleeding. Nimodipine improved outcome according to was all measures examined. The odds of good and of good plus fair outcomes were improved by ratios of 1.86:1 and 1.67:1, 1.67:1, respectively, for nimodipine versus control(p< .005 for both measures). The odds of deficit and/or mortality attributed to vasospasm and CT-assessed under infarction rate were reduced by ratios of .46:1 to .58:1 in the nimodipine group (p< .008 for all measures). Overall mortality for was slightly reduced in the nimodipine group, but the trend was not statistically significant. The rebleeding rate was not increased to by nimodipine. A metaregression yielded findings indicating that the treatment effect of nimodipine in individual trials was positively correlated with group the severity of SAH in enrolled patients. Although the majority of individual trials examined did not have statistically significant results nimodipine at the p< .01 level according to most outcome measures, the metaanalyses confirmed the significant efficacy of prophylactic nimodipine in improving prophylactic outcome after SAH under the conditions used in these trials.