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PubMed1996

Reduced CD8+ T-cell concentration in peripheral blood of patients with carotid artery stenosis: relation to arteritis temporalis.

The percentage and numbers of CD8+ T cells are markedly decreased in peripheral blood from patients with arteritis temporalis. Transient cerebral ischaemic attacks (TIA) or brain infarctions have been frequently reported as the first and only clinical manifestation, and signs of carotid artery stenosis have been reported in 15-20% of patients with arteritis temporalis. We used a determination of the CD8+ T-cell subset to evaluate patients with TIA. Concentrations of CD8+ T cells were measured in the peripheral blood of 24 patients with TIA. The cohort investigated was consecutive, but adjusted to have a 50% a priori probability of carotid artery stenosis. An ultrasound Doppler investigation of the carotid arteries was performed in all patients. Controls were 24 healthy subjects of comparable age and sex. Median percentage and concentrations of CD8+ T cells were significantly lower in patients with TIA and carotid artery stenosis compared with (1) patients with TIA and no carotid stenosis (CD8+ %: 13.5 vs 26; CD8+ x 10(9)/1: 0.24 vs 0.44, P < 0.001) and (2) healthy controls (CD8+ %: 13.5 vs 22.5; CD8+ x 10(9)/1: 0.24 vs 0.52, P < 0.001). The prevalence of a carotid artery stenosis in the combined first and second quartile of CD8+ % (CD8+ % <or= 15) was 80% (95% CI: 44-97%) and in the combined third and fourth quartile 28.5% (95% CI: 8-58%) (P = 0.03). The positive predictive value for carotid artery stenosis was 80%, an incremental ruling in gain of 60%. The negative predictive value was 71%. In patients with TIA and carotid artery stenosis, a reduced percentage and numbers of the CD8+ T-cell subset were significantly more frequent than in patients with no stenosis. No other signs of arteritis temporalis were found.

Adult↗
PubMed1998

Alcohol consumption and stroke: benefits and risks.

The complex relationship between alcohol consumption and stroke includes both benefits and risks. Regular light-to-moderate consumption of alcohol seems to decrease the risk for ischemic stroke by reducing atherothrombotic events, but the underlying mechanism is still unclear. Recent and current (but not previous) heavy drinking increases the risk for both hemorrhagic and ischemic strokes. Young and middle-aged men are stricken more often than women or elderly persons, probably because they are more often current heavy drinkers. Alcoholic cardiomyopathy is a cause of cardioembolic brain infarction. Cardiac arrhythmias caused by regular heavy drinking or binge drinking can precipitate thrombus formation and propagate already existing thrombi from the heart. The maintenance of high blood pressure by heavy drinking may promote cerebral arterial degeneration, but the effect of drinking habits on aneurysm formation is not known. Acute increases in systolic blood pressure and/or alterations in cerebral arterial tone could serve as mechanisms triggering hemorrhagic strokes during alcoholic intoxication. We lack studies to show that prevention of heavy drinking can efficiently influence the occurrence of strokes.

Adult↗
PubMed1991

Lack of protection by the N-methyl-D-aspartate receptor blocker dizocilpine (MK-801) after transient severe cerebral ischemia in the rat.

Glutamate is an important factor in the mechanisms of neuronal damage following cerebral ischemia. Blockade of one type of glutamate receptor, the N-methyl-D-aspartate (NMDA) receptor, decreases brain infarct size in experimental models of permanent focal ischemia, but protection in models of transient reversible ischemia is ambiguous. We investigated the effect of the noncompetitive NMDA receptor antagonist dizocipiline (MK-801) on neuronal damage in the CA1 region of the rat hippocampus, using two models of reversible cerebral ischemia: 10 or 15 min of bilateral common carotid occlusion combined with hypotension, or 6-8.5 min of cardiac arrest. Histopathologic evaluation of neuronal damage was performed 7 days after the ischemic insults. Thirteen groups of rats (a total of 129 animals) were treated with saline or dizocilpine in single or multiple doses ranging from 0.1 to 5 mg.kg-1, given intravenously or intraperitoneally prior to and/or after the ischemic insult. In none of the dizocilpine-treated groups could neuronal protection be demonstrated in the CA1 region of the septal as well as dorsotemporal hippocampus, compared to a corresponding saline-treated group. We conclude that systemically administered noncompetitive NMDA receptor antagonists do not provide a marked protection against neuronal damage after a transient period of severe forebrain ischemia.

Animals↗
PubMed1995

Risk factors for cerebrovascular disease and the role of coagulation and fibrinolysis.

Cerebrovascular disease is one of the major causes of morbidity and mortality in the developed world. A number of important risk factors have been identified with the occurrence of stroke, including advancing age, hypertension, smoking and diabetes mellitus, but the mechanisms that link these risk factors to the development of cerebrovascular disease are unclear. The pathogenesis of cerebrovascular disease includes syndromes of atherothrombotic brain infarction and intracerebral hemorrhage. The role of abnormalities of the coagulation and fibrinolytic systems in these processes has not been properly evaluated with regard to clinical outcome, although there is evidence that raised concentrations of fibrinogen are associated with an increased risk of stroke. Smaller studies have identified increases in FVIII/vWF in association with acute stroke and raised levels of tissue plasminogen activator. Although factor VII is considered a risk factor for coronary artery disease, little is known regarding its role in the development of cerebrovascular disease. Improved understanding of the pathogenesis of stroke and the potential to predict patients at risk of stroke should herald the beginning of new approaches in stroke management.

Blood Coagulation↗
PubMed1998

Association between carotid atherosclerosis and hemostatic markers in patients with cerebral small artery disease.

The purposes of this study were to investigate the association between carotid atherosclerosis and hemostatic markers, and to elucidate the difference in hemostatic markers between intima-media thickening and plaque formation in patients with cerebral small artery disease. We investigated carotid atherosclerosis by assessing diffuse intima-media thickness measurements and localized plaque using B-mode ultrasonography, and we measured the concentrations of plasma fibrinogen, beta-thromboglobulin and platelet factor 4 as markers for platelet activation, and the activity of plasma von Willebrand factor as a marker for endothelial damage. The intima-media thickness was significantly associated with age, male sex, the concentrations of plasma beta-thromboglobulin and platelet factor 4, and the activity of plasma von Willebrand factor. The plaque score showed a significant association with male sex, the concentration of fibrinogen, and the activity of plasma von Willebrand factor. These results may indicate that underlying mechanisms are not the same between the intima-media thickness and plaque formation. We suggest that hemostatic markers could reflect the severity of carotid atherosclerosis in patients with cerebral small artery disease, and that preventive antiplatelet therapies against brain infarction might be necessary for patients with severe carotid atherosclerosis.

Adult↗
PubMed2001

Prophylactic therapy with enoxaparin during L-asparaginase treatment in children with acute lymphoblastic leukemia.

Forty-one consecutive children with acute lymphoblastic leukemia (ALL) received prophylaxis therapy with the low molecular weight heparin (LMWH) enoxaparin during L-asparaginase treatment. Enoxaparin was given every 24 h subcutaneously at a median dose of 0.84 mg/kg per day (range, 0.45-1.33 mg/kg per day) starting at the first dose of L-asparaginase until 1 week after the last dose. Molecular analysis for thrombophilic polymorphisms documented prothrombin G20210A mutation in 3/27 (11%), homozygosity for MTHFR C677T mutation in 5/27 (18.5%, and heterozygosity for factor V Leiden mutation in 5/27 (18.5%) children. There were no thrombotic events during 76 courses of L-asparaginase in 41 patients who had received enoxaparin. One patient suffered brain infarct 7 days after enoxaparin was stopped. There were no bleeding episodes. In a historical control group of 50 ALL children who had not received prophylactic enoxaparin during L-asparaginase treatment, two had thromboembolisms (one deep vein thrombosis and one pulmonary embolism). Enoxaparin is safe and seems to be effective in prevention of thromboembolism in ALL patients during L-asparaginase therapy. This study provides pilot data for a future randomized trial of the use of LMWH during ALL therapy for the prevention of asparaginase-associated thrombotic events.

Adolescent↗
PubMed1998

Effect of glutamate transporter on neuronal damage induced by photochemical thrombotic brain ischemia.

To study the effects of glutamate transporters on the pathogenesis of brain infarct, pharmacological and histological analyses were carried out on the thrombotic focal ischemic model. Expression of mRNA coding for the glutamate transporter GLAST increased significantly in the penumbra at 72 h following the ischemia. Combined with confocal laser scanning microscopic analysis, double staining showed expression of GLAST mRNA in both neurons and glial cells in the penumbra. L-trans-Pyrrolidine-2,4-dicarboxylate (L-trans-PDC), a glutamate uptake inhibitor, dose-dependently enhanced the volume of the infarct induced by the ischemia. The results suggest that a compensatory increase in the activity of glutamate transporter may accompany pathological changes after ischemic injury.

ATP-Binding Cassette Transporters↗
PubMed2001

Protective effects of pamiteplase, a modified t-PA, in a rat model of embolic stroke.

The effects of alteplase (tissue plasminogen activator, t-PA) and pamiteplase (a modified t-PA with longer half-life and increased potency) were compared in a clinically relevant model of embolic stroke. Rats were treated with pamiteplase (0.5 mg/kg or 1 mg/kg bolus), alteplase (10 mg/kg infusion) or normal saline. Pamiteplase (1 mg/kg) was as effective as alteplase in reducing 24 h brain infarct volumes, neurological deficit scores and residual clot grades. Cerebral blood flow recovery at 30 min after thrombolytic treatment was partial and did not correlate with 24 h infarct volumes or neurological deficits. However, there was good correlation between 24 h residual clot grades and infarct volumes, suggesting a delayed timeframe for pamiteplase- and alteplase-induced reperfusion.

Animals↗
PubMedDate not supplied

Sudden death in the dysphagic stroke patient--a case of airway obstruction caused by a food bolus: a brief report.

The clinical events leading up to the sudden death of a dysphagic stroke patient with dementia is described. A 63-yr-old man sustained right thalamic and mid-brain infarctions. On the inpatient stroke rehabilitation ward, he exhibited significant impulsivity and dementia, the latter felt to be premorbid. The patient frequently coughed, and modified barium swallow testing showed dysphagia, with aspiration occurring only when consuming greater than teaspoon amounts of liquid. He subsequently died at home while eating a meal. Autopsy showed an intact large cheese ball (bocconcini) occluding the airway. Sudden death in the impulsive stroke patient secondary to airway occlusion by a food bolus has not previously been reported, although such patients seem to be at greater risk. New eating-related interventions are warranted for dysphagic patients who exhibit impulsivity. It is proposed that food particle size be limited to 1 cm2 and that such patients be closely monitored while eating.

Airway Obstruction↗
PubMed2002

Dynamic cardiophysiologic variables correlate with lesion location and FIMTM in patients with ischemic stroke.

OBJECTIVE: To examine the correlation between a clinical measure of function in patients undergoing rehabilitation who had recently had an ischemic stroke and to examine cardiophysiologic measures registered during effort. DESIGN: A cohort study comprising a sample of consecutive patients, without a history of cardiac disease or rhythm disturbances, admitted for rehabilitation after an ischemic supratentorial stroke. All patients were examined for the FIM trade mark score and dynamic cardiophysiologic variables. Results were analyzed in relation to stroke location. Thirty-eight patients participated in the study. Ten patients had a superficial lesion, 20 had a deep brain lesion, and eight had no noticeable lesion by computed tomographic imaging. Function was measured with the FIM instrument 48-72 hr after admission and repeated at 1 wk before discharge. Electrocardiographic activity was recorded during physiotherapy treatment. The relationship between the RR and QT intervals in the electrocardiographic waveforms was found to estimate two cardiophysiologic variables, the constant (a) and the slope (b) values, reflecting the dynamic change of QT during physiotherapy effort. RESULTS: Only for the subgroup of patients who sustained a deep brain lesion did the motor items in the FIM instrument on admission and discharge scores have a statistically significant relationship with the slope variable (b) and an inverse statistically significant relationship with the constant variable (a). CONCLUSIONS: Deep brain infarction seems to result in a significant dysfunction of the autonomic nervous system, manifesting itself as distorted dynamic behavior of the QT interval and with impaired functional performance.

Aged↗
PubMedDate not supplied

Endovascular stent graft placement for patients with aortic aneurysm and end-organ dysfunction.

Endovascular stent grafts (ESGs) for the treatment of aortic aneurysm is becoming popular because it is less invasiveness for the patient. This new modality seems to be especially useful for treating high risk patients, such as those with end-organ dysfunction. In this study we retrospectively analyzed the results of ESG placement for patients with renal or hepatic dysfunction. From January 1996 to December 1997, six patients with end-organ dysfunction (two with descending thoracic aneurysm and four with abdominal aneurysm) underwent ESG placement. Five of these patients had renal dysfunction, with serum creatinine levels of 2.0 mg/dl or greater, and the remaining patient had hepatic dysfunction with a prothrombin time less than 60%. One of the patients also had severe atherosclerotic disease with a history of multiple brain infarctions. All the patients received custom made endovascular spiral Z stents covered with a woven Dacron (DuPont Co., Wilmington, DE) graft, which was delivered via a femoral artery under local anesthesia. None of the patients showed significant changes in renal or hepatic function after the procedure. None of the five patients with renal dysfunction needed hemodialysis after ESG placement, although the mean preoperative level of serum creatinine and blood urea nitrogen was 3.4 mg/dl and 42.0 mg/ dl, respectively. All the patients left the recovery room on postoperative day 1. These results indicated that endovascular stent graft placement is extremely useful in the treatment of aortic aneurysm patients with end-organ dysfunction.

Aged↗
PubMed1989

N-isopropyl-p-[I-123]iodoamphetamine lung imaging in a patient with chronic pulmonary thromboembolism.

A patient with a brain infarct was found to have chronic pulmonary embolism associated with perfusion defects on blood flow imaging with N-isopropyl-p-[I-123]iodoamphetamine (I-123 IMP). However, gradually increasing uptake of I-123 IMP was seen in later images, in areas distal to the embolus. The increased uptake to the embolized lung seemed to be through the systemic collateral circulation.

Aged↗
PubMed1997

HCV hepatitis associated with anticardiolipin antibody and a cerebrovascular accident. Response to interferon therapy.

A 54-year-old man with chronic hepatitis C virus (HCV) developed quadrihemianopsia caused by lacunar brain infarction. Extensive evaluation revealed high titers of anticardiolipin antibodies (ACA). Following interferon treatment (6 x 10(6), three times a week for 2 months and 3 x 10(6) for another 7 months), liver transaminase levels decreased to normal, HCV RNA in blood was no longer detectable, concomitantly with the disappearance of the ACA. The patient remained clinically stable without evidence for either HCV activity (RNA) or ACA or further thromboembolic events.

Antibodies, Anticardiolipin↗
PubMed1993

Brain capillary density and cerebral blood flow after occlusion of the middle cerebral artery in normotensive Wistar-Kyoto rats and spontaneously hypertensive rats.

OBJECTIVE: In order to elucidate why spontaneously hypertensive rats (SHR) develop larger brain infarcts distal to an arterial occlusion than normotensive Wistar-Kyoto (WKY) rats, we determined the surface and volume densities of cerebral capillaries, and the regional cerebral blood flow distal to an arterial occlusion in SHR and WKY rats. DESIGN: Occlusion of the middle cerebral artery was chosen because the middle cerebral artery territory is most commonly affected by cerebral infarcts in man. METHODS: Surface and volume densities of capillaries in the neocortex of the middle cerebral artery territory were measured by stereological techniques on histological sections. Fifteen minutes after ligation of the right middle cerebral artery, regional cerebral blood flow was measured autoradiographically by the [14C]-iodoantipyrine method. RESULTS: The capillary density of the neocortex did not differ between the SHR and WKY rats. The blood flow was significantly lower within the middle cerebral artery territory in the SHR than in the WKY rats. CONCLUSIONS: The reduced blood flow distal to the occlusion in SHR is probably a consequence of structural adaptation of arterial resistance vessels, rather than being caused by reduced capillary density.

Animals↗
PubMed1990

Cocaine in the cradle: a hidden epidemic.

Intrauterine exposure to cocaine is reaching epidemic proportions and is affecting the lives of an increasing number of infants and children. The toxic effects are manifested as microcephaly, growth retardation, brain infarcts, congenital malformations, and withdrawal symptoms lasting for several weeks. Preliminary long-term follow-up studies reveal worrisome psychologic alterations that may profoundly affect the personality of exposed individuals.

Child Behavior Disorders↗
PubMed1997

An update on aortic causes of ischemic stroke.

In the past few years evidence that atherosclerotic disease of the aortic arch is probably an underestimate source of emboli, particularly moving thrombi in the lumen, has accumulated. Pathological studies, and more recently transesophageal echocardiographic studies, have shown that atherosclerotic disease of the aortic arch is an independent risk factor for ischemic stroke and carries a high risk of recurrent vascular events. It could account for a more or less part of brain infarcts of unknown cause, with no carotid or cardiac source of emboli. This location of atherosclerotic disease is rare under 60 years of age. It mainly involves patients older than 60 years of age, and is frequent in patients in their eighties. Transesophageal echocardiography is accurate, safe and well tolerated for the examination of the aortic arch, even in elderly patients. Practical implications for patients and future clinical trials are important. As it is a strong marker for recurrent vascular events, the risks and benefits of different therapeutic options should now be evaluated in randomised trials.

Aorta, Thoracic↗
PubMed2004

Cervicocranial arterial dissections.

Cervicocranial dissections are an increasingly recognized cause of stroke in the young. When the dissections narrow the vascular lumen, they often alter blood flow enough to cause transient ischemic attacks in the brain. Alterations in the endothelium activate the coagulation cascade, leading to the formation of intramural clot that may embolize distally to cause brain infarction. Pain and neuro-ophthalmic symptoms and signs are common manifestations.

Carotid Artery, Internal↗
PubMed2005

Effect of statins in stroke prevention.

PURPOSE OF REVIEW: This paper reviews recent studies into the outcomes of clinical trials in which statin therapy has been used in the prevention and treatment of strokes. RECENT DEVELOPMENTS: Epidemiologic studies found no or little association between blood cholesterol levels and stroke. Randomized trials have confirmed that LDL lowering decreased the risk of stroke, in diabetic or hypertensive patients with 'normal' LDL cholesterol at baseline, and in patients with coronary artery disease, with respectively 48, 27 and 25% reduction in stroke incidence. A meta-analysis of trials showed that the greater the LDL cholesterol reduction, the greater the intima-media thickness and stroke risk reductions. Even if statins also have 'pleiotropic' effects, their main action seems to be through LDL reduction. The Heart Protection Study only included strokes that occurred 4.6 years before--a time when the stroke event rate is low and the cardiac event rate is high, and so may not have had the power to find a true effect of LDL cholesterol lowering in preventing recurrent stroke. The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial may give a definite answer because SPARCL investigators included 4732 patients with brain infarction or transient ischemic attacks and no history of myocardial infarction within 6 months of their stroke event, at a time when the expected stroke rate is very high and the myocardial infarction rate is very low. The results should be announced by mid-2006. SUMMARY: The positive effect of statins on stroke observed in trials of patients with coronary heart disease depended mainly on between-group LDL reduction, but other mechanisms could be involved. Though effective in prevention of major coronary events after a first stroke, statins have not yet been proven effective in prevention of recurrent stroke.

Humans↗