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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence and characteristics of atrial septal aneurysm were identified by transesophageal echocardiography (TEE) in a multicenter prospective study. One hundred and seventy-seven consecutive patients were evaluated in 2 years and 2 groups were compared: Group 1, 51 patients with documented cerebral ischemia event; Group 2, 126 patients affected by cardiac disease referred for other reasons. Group 1 included patients selected among 352 patients admitted to the Neurological and Geriatric Division of our Hospital in the period of this study. Patients with stroke-related carotid lesions and patients with a negative TC scan were excluded from this study. Atrial septal aneurysm was identified in 15 patients: 8 in Group 1 (16%), and 7 in Group 2 (5%), with a significant statistical difference between the groups (p = 0.02). All patients with atrial septal aneurysm underwent before TEE transthoracic echocardiography, leading to a correct diagnosis in 10 of 15 cases (66%); all patients underwent 24-hours ECG monitoring. A right to left shunt was detected by contrast echocardiography in 9 patients, 6 in Group 1 and 3 in Group 2, (NS). A more pronounced shunt was evident in Group 1. There was no difference between the 2 groups with regard to associated cardiac disease, arrhythmias and type of atrial septal aneurysm. The thickness of the septum was greater in Group 1, with significant statistical difference (p = 0.002). It is concluded that atrial septal aneurysm, diagnosed by TEE, is a potential source of embolic events.
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PMID:[Evaluation of atrial septum aneurysm with transesophageal echocardiography in cardioembolic cerebral ischemia]. 130 2

Anticardiolipin antibody (ACA) has been associated with cerebral ischemia, suggesting an important role in the pathogenesis of vascular thrombosis and a marker for increased thrombotic risk. Its prevalence and significance in stroke are unknown. In this study, consecutively admitted patients diagnosed as having stroke were studied. A total of 246 patients, 141 men and 105 women, aged 34 to 91 years (mean age, 63.5 years), were screened for the presence of ACA. Elevated concentration of circulating ACA was present in 4 out of 170 patients with infarct, and in 1 out of 76 patients with hemorrhage. They were 4 men and 1 woman, aged 49 to 84 years (mean age, 66.8 years). The prevalence of ACA in stroke was 2% (2.3% for infarction and 1.3% for hemorrhage). All the elevated ACA were of IgG isotype. No strong association between antibody positivity and stroke was found in this study. The routine screen of ACA in stroke is of questionable value.
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PMID:Anticardiolipin antibody in stroke. 131 98

Formation of free radicals and subsequent lipid peroxidation may have an important role in tissue injury and neuronal cell death after cerebral ischaemia. We conducted a prospective, controlled study to determine whether the endogenous antioxidant vitamins A and E had a protective function in acute ischaemic stroke. The study population consisted of 80 patients seen at the Free University Hospital in Brussels. Entry criteria were occurrence of sudden focal neurological deficit lasting more than 3 h; deficit due to acute ischaemia in the territory of the middle cerebral artery; and investigation within 24 h of onset of the episode. Outcome was assessed within the first 21 days. 80 controls matched for age and sex had various neurological disorders other than acute ischaemia. Serum concentrations of vitamins A and E were similar in the study and control groups. In the study population a serum vitamin A concentration higher than the mean of 2.27 mumol/l was associated with a higher frequency of complete recovery within the first 24 h (p less than 0.05), decreased mortality (p = 0.038), and a better outcome as assessed by the Mathew scale of neurological deficit (p less than 0.03) and the Barthel index. There was no significant difference in outcome between patients with vitamin E concentrations above or below the mean of 35.3 mumol/l. Our results suggest a beneficial effect of a high serum vitamin A concentration on early outcome in ischaemic stroke.
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PMID:Serum concentrations of vitamins A and E and early outcome after ischaemic stroke. 135 49

To investigate the pathophysiological process of transient ischaemic events in a clinically relevant model, we produced transient focal cerebral ischaemia in five baboons using endogenously generated platelet microemboli. Thrombogenic segments of Dacron vascular graft were incorporated as unilateral carotid arterio-arterial shunts to produce endogenous platelet microemboli. The embolized microparticles were quantified by isotopic imaging using 111In-platelets and by transcranial Doppler ultrasonography. Platelet microemboli accumulated rapidly in the shunted carotid territory and reached a maximum value of 3.2 +/- 0.8 x 10(9) in the embolized hemisphere 20 min after initiating blood flow through the graft segment. Sixty min after removing the grafts 111In-platelets were largely cleared from hemispheric vasculature. Recovered animals exhibited mild contralateral hemiparesis which disappeared completely within 24 h. We conclude that endogenously generated platelet microemboli accumulate transiently in the dependent cerebral circulation and produce corresponding transient focal neurological dysfunction. This model may be useful in the evaluation of new therapeutic strategies in acute stroke.
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PMID:Production of transient ischaemic events by platelet emboli in baboons. 135 85

Focal cerebral ischaemia was induced in rats by occlusion of the left middle cerebral artery. Two days later, infarct volume was determined by magnetic resonance imaging and the concentrations of the polyamines putrescine (PU), spermine and spermidine by HPLC. In control (occluded) animals, PU levels were elevated in infarcted and non-infarcted areas of the left hemisphere. Treatment with the ornithine decarboxylase (ODC) inhibitor alpha-difluoromethylornithine, prevented the ischaemia-induced increase in tissue PU without affecting infarct volume. Conversely, administration of the N-methyl-D-aspartate (NMDA) receptor antagonist CGP 40116 decreased cortical infarction without changing the tissue content of PU. We conclude that there is no direct link between NMDA receptor activation and brain PU, or PU and post-ischaemic tissue damage, and that inhibitors of ODC are not cerebroprotective in this animal model of stroke.
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PMID:Differing effects of alpha-difluoromethylornithine and CGP 40116 on polyamine levels and infarct volume in a rat model of focal cerebral ischaemia. 135 66

Conditions causing a reduction of oxygen availability (anoxia), such as stroke or diabetes, result in drastic changes in ion movements, levels of neurotransmitters and metabolites and subsequent neural death. Currently, there is no clinically available treatment for anoxia induced neural cell death resulting in drastic and permanent central nervous system dysfunction. However, there have been some exciting developments in experimentally induced anoxic conditions where several classes of drugs appear to significantly reduce neural cell death. This report aims to provide the foundations for understanding both the basic mechanisms involved in retinal ischaemic damage and experimental treatments used to prevent such damage. We discuss the normal release, actions and uptake of the fast retinal neurotransmitters, glutamate and GABA, in the vertebrate retina. Immunocytochemistry is used to demonstrate that both glutamate and GABA are found in the macaque retina. Following this is a discussion on how ischaemia may enhance neurotransmitter release or disrupt its uptake, thus causing an increase in extracellular concentration of these neurotransmitters and subsequent neuronal damage. The mechanisms involved in glutamate neurotoxicity are reviewed, because excess glutamate is the likely cause of retinal ischaemic damage. Finally, the mechanisms behind four possible modes of treatment of neurotransmitter toxicity and their advantages and disadvantages are discussed. Hopefully, further research in this area will lead to the development of a rational therapy for retinal, as well as cerebral ischaemia.
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PMID:Interrelationship between retinal ischaemic damage and turnover and metabolism of putative amino acid neurotransmitters, glutamate and GABA. 136 7

Thromboembolic phenomena and transient ischaemic attacks (TIA) are considered the basis of ischaemic pathologies. The aim of the present research is to investigate the involvement of k-opioid receptors in cerebral blood flow (CBF) impairment which results in experimental stroke or dietary atherosclerosis in rabbits. CBF measurement showed a significant decrease in rabbits submitted to embolization and/or atherosclerosis. Binding studies showed that massive cerebral ischaemia and atherosclerosis produced a significant increase in the number of k-opioid receptors (Bmax), without changing (KD) affinity values. In conclusion, the results obtained seem to indicate that the increase in k-opioid receptors might play a crucial role in a common cerebral biochemical mechanism both in ischaemic and atherosclerotic pathologies.
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PMID:K-opioid receptor changes in experimental models of cerebral ischaemia and atherosclerosis in the rabbit. 136 91

Blood pressure and clinical status of 1,736 patients with cerebrovascular disease were observed during 12 months of treatment with nicardipine. The most common diagnoses were chronic cerebral ischemia (53.2%), transient ischemic attacks (TIA; 25.1%), and cerebral infarct (8.7%); 50.1% of patients were classed as hypertensive [systolic blood pressure (SBP) > or = 160 mm Hg or diastolic blood pressure (DBP) > or = 90 mm Hg]. Most patients (91.2%) received a daily dose of 60 mg nicardipine. Additional treatments included diuretics (37%), beta-blockers (11.5%), other antihypertensive drugs (15.8%), platelet antiaggregants (25.1%), and cardiotonic drugs (15.1%). A total of 282 patients (16.2%) were lost to follow-up, 21 (1.2%) patients withdrew due to side effects, 32 (1.8%) died, and 9 (0.5%) patients had treatment interrupted due to concomitant illness. In the hypertensive subgroup, blood pressure (SBP/DBP) was reduced from a mean baseline value of 175 +/- 22/97 +/- 14 mm Hg to 152 +/- 17/85 +/- 11 mm Hg at 3 months and 149 +/- 23/81 +/- 11 mm Hg after 12 months of treatment. The incidence of TIA or stroke among these patients was reduced from 29 cases (3.5%) during the first 3 months to 11 cases (1.54%) during months 4-12 (p < 0.01). In normotensive patients there were 18 (2.15%) cases during months 1-3 and 13 (1.55%) cases during months 4-12 (difference not significant). In the 280 patients treated with nicardipine alone, the most frequent side effects during the first month were facial flushing (6.8%), gastrointestinal problems (5%), dizziness (3.2%), headache (3.2%), drowsiness (3.2%), and hypotension (1.1%). Most of these side effects were transient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of nicardipine in patients with high risk of stroke. 136 3

A review is given of the normal regulation of cerebral blood flow (CBF) and its pathophysiology in hypertension and stroke. In otherwise healthy hypertensive patients, the absolute level of CBF is the same as in normal subjects. CBF autoregulation, however, is shifted towards higher pressure, thus impairing the tolerance to hypotension. In most patients, this does not interfere with the beneficial effect of treatment, i.e., stroke prevention. Cerebral ischemia, however, may be provoked by overzealous pressure lowering in selected clinical settings: initial or intensified treatment of very severe hypertension, treatment of hypertension in the elderly, and treatment of hypertension in acute stroke. In the latter, a complicated sequence of brain ischemia and hyperemia makes antihypertensive intervention difficult in the early phase, when blood pressure is probably best allowed to decrease spontaneously.
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PMID:Regulation of cerebral blood flow in health and disease. 138 71

A cat stroke model was used to evaluate the efficacy of Dextran-40 (DEX) or Fluosol-DA 20% (FDA) in the treatment of focal cerebral ischemia. The animals were assigned randomly to one of three treatment groups: control, isovolemic hemodilution with DEX or isovolemic hemodilution with FDA. The oxidation state of cytochrome aa3 was measured in-vivo using near infrared reflectance spectrophotometry. The cerebral edema was measured by magnetic resonance imaging (MRI). The MRI edema indices for the three groups revealed that the FDA group had less edema (p less than 0.05), approaching that of non-stroke controls. The relative oxidation state of aa3 for the DEX group declined both during and after hemodilution. At the ninth hour post stroke the FDA group was better (aa3 more oxidized. p less than 0.025). Changes in blood and plasma components were reflective of the extent of hemodilution. Whole blood viscosity analysis revealed a difference (p less than 0.05) at the lower shear rates comparing DEX to FDA with FDA being higher than DEX. Two animals in each of the groups were allowed to awaken at the end of the procedure for functional assessment. These observations suggest that hemodilution with FDA following stroke significantly reduces early post-ischemic cerebral edema, improves oxidation in the peri-infarct area and appears to minimize functional deficits.
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PMID:Treatment of cerebral ischemia with Dextran-40 or Fluosol DA 20%. 138 45


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