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

Closure of patent foramen ovale (PFO) is expected to prevent paradoxical emboli. In the absence of randomized trials, its efficacy has been assessed by comparing uncontrolled cohort studies of medically treated patients with those treated by PFO closure. The objective of this study was to highlight a confounder of such studies, namely, the variability in the duration of follow-up. We searched the literature for cohort studies of patients with ischaemic strokes, including those with PFO. During the first year of follow-up, recurrence hazards in patients younger than 55 years were 1-4% in those with any ischaemic stroke, 1-6% in medically treated patients with PFO and 0-5% in those after PFO closure. In most studies, the recurrence hazards were highest immediately after the index stroke and declined thereafter. Still, hazards were commonly reported in terms of annual averages over a wide range of follow-up periods for the various cohort studies, thereby ignoring the possibility that the duration of the follow-up may in and of itself affect the derived average recurrence hazards. A disregard of the time variance of stroke recurrence may confound the conclusions from comparisons between uncontrolled studies of patients with stroke and PFO.
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PMID:Variability in duration of follow up may bias the conclusions of cohort studies of patients with patent foramen ovale. 1863 21

Surgery of a high-grade carotid stenosis is evidence-based stroke prevention. Also cognitive effects are reported after carotid endarterectomy (CEA): both deterioration and improvement, the former attributed to perioperative complications and the latter often to learning effect. By imaging, brain perfusion and diffusion changes were shown in subjects with a high-grade stenosis undergoing CEA. We wanted to find out if the cognition of patients undergoing CEA display postoperative worsening or true improvement in association with findings in serial MR imaging. The patients had a poorer overall cognition than healthy matched controls. The cerebral hemisphere ipsilateral to the stenosis had higher diffusion and more sluggish perfusion leading to perfusion deficits. These asymmetries were abolished by CEA. Postoperatively, the patients showed a trend for cognitive worsening, most often attentional, but over months, the group performance improved similarly to the controls. Still, lower baseline perfusion was associated with a greater cognitive improvement, most clearly in executive functions. Consequently, despite the risk for transient decline, true cognitive benefit by CEA seems possible.
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PMID:The effect of severe carotid occlusive disease and its surgical treatment on cognitive functions of the brain. 1882 89

Blood glucose is often elevated in acute stroke, and higher admission glucose levels are associated with larger lesions, greater mortality and poorer functional outcome. In patients treated with thrombolysis, hyperglycemia is associated with an increased risk of hemorrhagic transformation of infarcts. For a number of years, tight glycemic control has been regarded as beneficial in critically illness, but recent research has been unable to support this notion. The only completed randomized study on glucose-lowering therapy in stroke has failed to demonstrate effect, and concerns relating to the risk of inducing potentially harmful hypoglycemia has been raised. Still, basic and observational research is overwhelmingly in support of a causal relationship between blood glucose and stroke outcome and further research on glucose-lowering therapy in acute stroke is highly warranted.
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PMID:Blood glucose in acute stroke. 1927 49

Stroke and transient ischemic attack (TIA) arise from identical etiologies and many fatal or disabling strokes are preceded by a TIA. Ten percent of patients presenting with a TIA will suffer a stroke within 3 months with half occurring in the first 48 hours. Still, many patients with a TIA do not receive timely evaluation or therapy. Hospitalization offers the opportunity for rapid evaluation and secondary prevention, reduced time to thrombolysis for early second strokes, and can be cost effective for high risk patients. Stratification tools are now available which allow individualized assessment of risk for early second strokes based on patient characteristics on presentation. The use of scoring systems such as the ABCD(2) score to predict risk of stroke after TIA are useful in making an evidence-based judgment regarding need for hospitalization. High-risk patients have an 8.1% risk for stroke in the 48 hours after a TIA and warrant hospital admission. Intermediate-risk patients have a 4.1% risk of early second stroke and may be considered for admission, observation, or expedited clinic evaluation. Low-risk patients have a 2-day stroke risk of only 1% and are likely appropriate for prompt outpatient evaluation. TIA is a medical emergency, similar to unstable angina, and high risk patients should receive treatment and prevention measures instituted with comparable urgency.
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PMID:Risk stratification tools for transient ischemic attack: which patients require hospital admission? 1938 66

CTP has a growing role in evaluating stroke. It can be performed immediately following NCCT and has advantages of accessibility and speed. Differentiation of salvageable ischemic penumbra from unsalvageable core infarct may help identify patients most likely to benefit from thrombectomy or thrombolysis. Still, CTP interpretation can be complex. We review normal and ischemic perfusion patterns followed by an illustrative series of technical/diagnostic challenges of CTP interpretation in the setting of acute stroke syndromes.
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PMID:Evaluation of CT perfusion in the setting of cerebral ischemia: patterns and pitfalls. 2019 Feb 8

Ischemic and hemorrhagic strokes are established etiological factors for recurrent seizures. Still, only few prospective data are available to predict post-stroke epilepsy and to choose the best point in time and anticonvulsive agent for treatment. In a prospective study we evaluated 264 consecutive stroke patients and assessed their post-stroke epilepsy risk within a follow-up of 1 year. Data on ten risk items concerning the stroke localisation, persisting neurological deficit, stroke subtype, established diagnosis of vascular encephalopathy, early- and late-onset seizures were collected using a post-stroke epilepsy risk scale (PoSERS). All patients underwent brain imaging with either CT, MRI or both and 148 patients underwent electroencephalography. The overall frequency of early-onset seizures within 14 days was 4.5%, of at least one late seizure 6.4% and of epilepsy 3.8%. Chi-Square tests showed significantly higher relative frequencies of seven of the ten clinical characteristics in post-stroke epilepsy patients. The total scale showed moderate sensitivity (70%) and positive predictive value (87.5%) while specificity (99.6%) and negative predictive value (98.8%) were relatively high. The EEG showed little value in predicting post-stroke epilepsy. The PoSERS appears to be a valuable tool to predict the risk for post-stroke epilepsy within the first few days after a stroke.
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PMID:Prospective evaluation of a post-stroke epilepsy risk scale. 2030 71

We and others have previously demonstrated that nitric oxide (NO)-induced inhibition of platelet shape change is important in regulating platelet adhesion and aggregation, and therapeutic intervention of this pathway is clinically relevant for secondary prevention of stroke with dipyridamole. In the present study, we investigated whether dipyridamole affected the shape change of aspirinated platelets. Platelet shape change was inhibited using both authentic NO and sodium nitroprusside, as monitored by light scattering and mean platelet volume measurements. Dipyridamole synergized with NO, even at supra-therapeutic levels, to inhibit thrombin-induced shape change and further potentiated cAMP dependent protein kinase (PKA) mediated phosphorylation of vasodilator stimulated phosphoprotein (VASP) Ser157, even without altered levels of platelet cAMP. The effect of dipyridamole on NO-inhibited shape change depended on cGMP synthesis as evaluated by inhibition of soluble guanylyl cyclase. Measured increases in cGMP levels by dipyridamole and NO was assessed by mathematical modeling and found to be consistent with inhibition of phosphodiesterase 5 (PDE5). The model could explain the unexpected efficiency of dipyridamole in inhibiting PDE5 at the measured cGMP levels, by the majority of cGMP being bound to cGMP-dependent protein kinase (PKG). Still, selective activators of PKG failed to extend NO-mediated inhibition of the thrombin-induced platelet shape change, suggesting that PKG was not responsible for the inhibitory effect of NO and dipyridamole on shape change. The effects of dipyridamole were independent of the prostanoid and ADP pathways. Thus, the effect of dipyridamole on NO-mediated inhibition of platelet shape change may be an important and additional beneficial therapeutic effect of dipyridamole, which we suggest, is acting though localized amplification of the NO/cGMP/Phosphodiesterase3/cAMP/PKA-pathway. Probably, the efficiency of dipyridamole could be amplified clinically with NO donors.
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PMID:Dipyridamole synergizes with nitric oxide to prolong inhibition of thrombin-induced platelet shape change. 2095 17

A variety of human disorders, e.g., ischemic heart disease, stroke, kidney disease, eventually share the deleterious consequences of a common, hypoxic and oxidative stress pathway. In this review, we utilize recent information on the cellular defense mechanisms against hypoxia and oxidative stress with the hope to propose new therapeutic tools. The hypoxia-inducible factor (HIF) is a key player as it activates a broad range of genes protecting cells against hypoxia. Its level is determined by its degradation rate by intracellular oxygen sensors prolyl hydroxylases (PHDs). There are three different PHD isoforms (PHD1-3). Small molecule PHD inhibitors improve hypoxic injury in experimental animals but, unfortunately, may induce adverse effects associated with PHD2 inhibition, e.g., angiogenesis. As yet, no inhibitor specific for a distinct PHD isoform is currently available. Still, the specific disruption of the PHD1 gene is known to induce hypoxic tolerance, without angiogenesis and erythrocytosis, by reprogramming basal oxygen metabolism with an attendant decreased oxidative stress in hypoxic mitochondria. A specific PHD1 inhibitor might therefore offer a novel therapy against hypoxia. The nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) regulates the basal and inducible expression of numerous antioxidant stress genes. Disruption of its gene exacerbates oxidative tissue injury. Nrf2 activity is modulated by Kelch-like ECH-associated protein 1 (Keap1), an intracellular sensor for oxidative stress. Inhibitors of Keap 1 may prove therapeutic against oxidative tissue injury.
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PMID:Hypoxia. 1. Intracellular sensors for oxygen and oxidative stress: novel therapeutic targets. 2098 May 51

Stroke is a life-threatening or life-changing disease that is expensive in health care costs and lost productivity. Stroke also is a leading cause of human suffering. While the risk of stroke may be reduced with advances in prevention, recent advances in acute care can limit the consequences of stroke. In particular, the success of reperfusion therapies including intra-arterial interventions and intravenous administration of thrombolytic agents means that some patients with stroke may be cured. Still, the time window for effective treatment of stroke is relatively short. As a result, modern stroke management requires the close collaboration of the public, health care providers, administrators, insurance companies, and the government. Potential strategies to extend modern stroke care to as many patients as possible include 1) educational programs to train community emergency medical service personnel and physicians, 2) development of stroke care plans at community hospitals, 3) an integrated community-comprehensive stroke center program based on consultation, and telemedicine. The goal is to have a highly integrated approach to provide emergency treatment of the stroke that provides key emergency treatment, including intravenous administration of thrombolytic medications, at a community hospital (primary stroke center) with evacuation to a comprehensive stroke center that has resources and expertise that are not available in the primary stroke center. Taiwan is an ideal location for the development of such regional stroke programs.
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PMID:Management of acute stroke: impact of registration studies. 2104 14

Patients with systolic heart failure are thought to be at increased risk for thromboembolic events. Although these patients may have increased hypercoaguable markers, the incidence of stroke is thought to be relatively low. Still, oral anticoagulation with warfarin is sometimes prescribed in these patients to prevent potential thromboembolic events. Current guidelines do not recommend warfarin use in patients with systolic heart failure unless indicated for other cardiovascular conditions. Several studies that have attempted to address this controversy have, as a whole, demonstrated that the rates of thromboembolic events in patients with systolic heart failure taking warfarin are similar to those in patients taking placebo, basically showing no additional protective benefit of warfarin. In addition, these studies have shown an increased risk of bleeding with warfarin. However, these trials are of poor quality to date. The 4 post hoc analyses in this article had warfarin added at the investigators' discretion and included patients with indications for warfarin, such as atrial fibrillation. The 3 randomized trials in this article did not attain enrollment numbers to reach any calculated power and were stopped early; thus, they were unable to detect a difference. Since warfarin has shown benefit in patients with atrial fibrillation and in mechanical heart valves to decrease the risk of thromboembolism, it might stand to reason that warfarin would have the same benefit in systolic heart failure patients without the above indications. However, given the current available data, warfarin is not supported in patients with systolic heart failure in the absence of an indication for this drug.
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PMID:Oral anticoagulation with warfarin for patients with left ventricular systolic dysfunction. 2113 1


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