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

Dysphagia in stroke is linked with increased risk of pneumonia, increased length of stay and poorer outcomes. This study followed a cohort of 88 acute ischaemic stroke patients admitted to hospitals in Perth, Western Australia, over 30 days. There were 8/88 deaths (9%). Infections were treated in 25/80 survivors (31%). Presence and severity of dysphagia were measured at 2 and 7 days post-stroke. Respiratory tract infections occurred at significantly higher rates for dysphagics (p<0.05). At 2 days post-stroke, the odds ratio (OR) of chest infection for dysphagics was 1.45 (95% CI=1.07-1.98). Survivors who were "nil by mouth" 2 days post-stroke were significantly more likely to develop pneumonia (p=0.01). At 7 days post-stroke, dysphagics were again more likely to develop pneumonia (p=0.014) with OR=1.77 (95% CI=1.26-2.49). The total anterior circulation infarcts demonstrated more severe and prolonged dysphagia than other stroke subtypes.
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PMID:Dysphagia in acute ischaemic stroke: severity, recovery and relationship to stroke subtype. 1743 10

Hereditary hemorrhagic telangiectasia (HHT) or Rendu-Osler-Weber disease is a genetic disorder with autosomal dominance and variable penetrance, characterized by epistaxis, telangiectasia and visceral manifestations of the disease. The estimated minimal prevalence is 1/10,000 inhabitants. The diagnosis is established on clinical criteria, and may be further confirmed by the identification of causative mutations in either the ENG or the ACVRL1 gene coding for endoglin and ALK1, respectively. Pulmonary vascular manifestations of HHT include pulmonary arteriovenous malformations (PAVMs; especially in patients with ENG mutations) and less frequently pulmonary hypertension (especially in patients with ACVRL1 mutations). In 15-33% of patients with HHT, PAVMs consist of abnormal communications between pulmonary arteries and pulmonary veins, causing right-to-left shunting, and thus, frequently hypoxemia and dyspnea on exertion, although PAVMs may remain asymptomatic and frequently undiagnosed unless complications occur. PAVMs result in severe and frequent complications often at a young age, which may reveal the diagnosis, e.g. transient ischemic attack and cerebral stroke (10-19% of patients), systemic severe infections and abscesses (including cerebral abscess in 5-19% of patients), and rarely massive hemoptysis or hemothorax. Infections in HHT are related to the right-to-left shunting that bypasses the pulmonary capillaries and facilitates the passage of septic or aseptic emboli into the systemic and especially cerebral circulation, and potentially to minor defects in innate immunity. Treatment of PAVMs based on transcatheter coil vaso-occlusion of the feeding artery significantly decreases right-to-left shunting, hypoxemia and dyspnea on exertion, and reduces the risk of systemic complications. Long-term follow-up is warranted after transcatheter vaso-occlusion of PAVMs due to frequent recanalization of treated PAVMs and development or growth of untreated PAVMs. Patients with HHT should be informed of the risk of PAVM and potentially severe complications occurring in heretofore asymptomatic subjects. All adult patients with HHT should be proposed systematic screening for PAVM, by contrast echocardiography (preceded by anteroposterior chest radiograph) or computed tomography of the chest. Pulmonary hypertension is rare in HHT, and may be due either to systemic arteriovenous shunting in the liver increasing cardiac output or be clinically and histologically indistinguishable from idiopathic pulmonary arterial hypertension. Pulmonary hypertension is detected by systematic examination of right cardiac cavities and tricuspid regurgitation flow at echocardiography, and the diagnosis is established by right heart catheterization.
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PMID:Pulmonary vascular manifestations of hereditary hemorrhagic telangiectasia (rendu-osler disease). 1764 82

Several large-scale clinical trials have assessed the efficacy of atorvastatin in the primary and secondary prevention of cardiovascular events in patients with diabetes mellitus and/or metabolic syndrome. In primary prevention, CARDS (Collaborative Atorvastatin Diabetes Study) showed that atorvastatin 10 mg/day (vs placebo) reduced relative risk of the composite primary endpoint (acute coronary heart disease [CHD] events, coronary revascularisation, or stroke) by 37% (p = 0.001). This decrease was similar to decreases in major cardiovascular events in the ASCOT-LLA (Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm) trial and HPS (Heart Protection Study). However, in CARDS, atorvastatin efficacy was evident as early as 6 months after starting treatment, whereas in HPS, simvastatin efficacy was noticeable only from about 15-18 months after starting treatment. In the ASCOT-LLA trial, in 2226 hypertensive diabetic patients without previous cardiovascular disease, atorvastatin (vs placebo) reduced the relative risk of all cardiovascular events and procedures by 25% (p = 0.038). In secondary prevention, substudies of the GREACE (GREek Atorvastatin and Coronary-heart-disease Evaluation), TNT (Treating to New Targets) and PROVE-IT (PRavastatin Or atorVastatin Evaluation and Infection Therapy) trials reported results for the approximately 15-25% of study participants who had diabetes. In the GREACE substudy, atorvastatin (vs physicians' standard care) significantly reduced the relative risk of total mortality by 52% (p = 0.049), coronary mortality by 62% (p = 0.042), coronary morbidity by 59% (p < 0.002) and stroke by 68% (p = 0.046). In the TNT substudy, incidence of the primary endpoint was significantly lower in diabetic patients treated with atorvastatin 80 mg/day rather than 10 mg/day (13.8% vs 17.9%; relative risk 0.75; p = 0.026). In the PROVE-IT substudy, a significantly lower incidence of acute cardiac events was reported for atorvastatin versus pravastatin recipients (21.1% vs 26.6%; p = 0.03) and, therefore, an absolute risk reduction of 5.5% was associated with atorvastatin therapy. ASPEN (Atorvastatin Study for Prevention of coronary heart disease Endpoints in Non-insulin-dependent diabetes mellitus) - a mixed primary and secondary prevention trial in diabetic patients - found that a 29% lower low-density lipoprotein-cholesterol level was seen with atorvastatin than placebo at endpoint (p < 0.0001); however, the reduction in composite primary endpoint of major cardiovascular events (cardiovascular mortality, nonfatal major cardiovascular event or stroke, and unstable angina requiring hospitalisation) with atorvastatin (13.7% vs 15.0% with placebo), and reduction in acute myocardial infarction relative risk of 27% with atorvastatin were not statistically significant. In CHD patients with metabolic syndrome (n = 5584) in a sub-analysis of the TNT trial, intensive versus lower-dosage atorvastatin therapy reduced the relative risk of major cardiovascular and cerebrovascular events by 29% (p < 0.0001). The analysis also revealed that CHD patients with, rather than those without, metabolic syndrome had a 44% greater level of absolute cardiovascular risk, thus clearly underscoring the clinical feasibility of administering intensive lipid-lowering therapy to CHD patients with metabolic syndrome. In summary, several patient populations, from definitive, large-scale studies, are now available to corroborate the integral place of atorvastatin--in line with various regional and internationally accepted disease management guidelines--in the primary and secondary prevention of cardiovascular events in patients with diabetes and/or metabolic syndrome.
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PMID:Atorvastatin efficacy in the prevention of cardiovascular events in patients with diabetes mellitus and/or metabolic syndrome. 1791 May 20

Infection is a risk factor for adult stroke and neonatal encephalopathy. We investigated whether exposure to bacterial endotoxin increases hypoxia-induced brain cell death and impairs cerebral metabolic compensatory responses to hypoxia. Prehatching chicken embryos (incubation day 19) were exposed to bacterial lipopolysaccharide (LPS) (3 mg Salmonella typhimurium LPS per egg) or hypoxia (4% ambient O(2) for 1 h), alone or in combination with LPS, followed 4 h later by hypoxia. Cerebral cell death and glial activation were assessed histologically. Further, chicken embryo brains were studied by magnetic resonance imaging (MRI) and spectroscopy (MRS) to assess haemodynamic and metabolic responses. In most brain areas, combined LPS/hypoxia resulted in a 30- to 100-fold increase in terminal deoxynucleotidyl transferase dUTP nick end labelling -positive cells, compared to control and single-insult groups. Glial activation correlated with the severity of cell death and was significantly greater in the combined-insult group (P<0.05). Hypoxia was associated with a 10-fold increase in lactate/N-acetyl-aspartate (NAA), an approximately 20% increase in total creatine/NAA, rapid decreases in T2 and T2(*), and a reduction in direction-averaged brain-water diffusion (D(av)) by approximately 15%. Liposaccharide pretreatment did not alter the magnitude or timing of these responses, but engendered baseline shifts (increased Cho/NAA, Cr/NAA, and Dav, and reduced T2(*)). In conclusion, LPS greatly increased hypoxia-induced brain damage in this model and induced changes in baseline haemodynamics and metabolism but did not affect the magnitude of the glycolytic response to hypoxia. The damage-enhancing effects of LPS are not because of additional energy depletion but because of a synergistic toxic component.
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PMID:Greater hypoxia-induced cell death in prenatal brain after bacterial-endotoxin pretreatment is not because of enhanced cerebral energy depletion: a chicken embryo model of the intrapartum response to hypoxia and infection. 1803 Mar 3

The relation between acute ischaemic stroke and infection is complex. Infection appears to be an important trigger that precedes up to a third of ischaemic strokes and can bring about stroke through a range of potential mechanisms. Infections that present subsequent to stroke also complicate up to a third of cases of stroke and might worsen outcome. Inflammatory responses, which are a defence mechanism against infection but can also be a pathogenic mechanism that precipitates stroke and neurological sequelae, are important features. Although factors such as stroke severity and dysphagia are important predictors of poststroke infection, there is evidence from experimental and clinical settings of impaired immunity or brain-induced immunodepression after stroke. Greater understanding of the relation between inflammation and both infection and ischaemic mechanisms is needed. This might be particularly important because new treatment strategies for acute ischaemic stroke are being investigated, including those that modulate cytokines and the immune system.
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PMID:Acute ischaemic stroke and infection: recent and emerging concepts. 1833 49

In this retrospective study, we collected clinical and radiographic data on children (age range, 1 month to 18 years) with symptoms and radiographic confirmation of seizure after ischemic stroke for the period of January 1996 to July 2006. Thirty-nine out of 94 children with ischemic stroke had poststroke seizures. Thirty-three out of 39 children with poststroke seizures had new onset seizures but only data of 28 were available. Infection was the most common etiology in the early poststroke seizure group (52.4%) but not in the late poststroke seizure group (0%). Infarction involving arterial ischemic stroke of anterior circulation were the most common in both the early poststroke seizure (61.9%) and the late poststroke seizure group (57.1%). Epilepsy was the most common sequelae in both the early poststroke seizure (38.1%) and late poststroke seizure group (100%). Children who had initial focal neurological sign (100% vs. 38.1%; P=0.007) or the focal cortical dysfunction on EEG (85.7% vs. 33.3%; P=0.029) were prone to develop late poststroke seizures. Late poststroke seizures had a high risk of developing poststroke epilepsy (100% vs. 38.1%; P=0.007). We conclude that seizures commonly occur in childhood ischemic stroke. Most poststroke seizures developed at an early stage. Infection was the most common etiology that caused early poststroke seizures in childhood ischemic stroke. Initial focal neurological signs and focal cortical dysfunction on EEG are risk factors for developing epilepsy. Poststroke seizures did not affect mortality, but there was a significant difference in normal outcome and epilepsy between those with or without poststroke seizures.
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PMID:Seizures in childhood ischemic stroke in Taiwan. 1865 41

Basic and animal research implicate inflammatory mechanisms in the pathogenesis and progression of atherosclerosis, plaque rupture, thrombosis, and stroke. Inflammatory biomarkers, particularly high-sensitivity C-reactive protein and lipoprotein-associated phospholipase A2, have been identified as potential predictors of stroke risk and prognosis. Infections may also precipitate stroke. Medications, especially hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), reduce inflammatory marker levels independently of lipid effects, and the ability of statins to reduce coronary events and stroke correlates with their effect on inflammatory biomarkers. Vaccination against influenza may also reduce stroke risk. Determining whether reduction of biomarkers reduces risk of recurrent stroke, however, requires further study before inflammatory markers become a routine part of the evaluation of stroke patients.
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PMID:Inflammatory markers and stroke. 1909 Nov 70

This prospective study was done to determine the predisposing factors and outcome of stroke in Bangladeshi children. It was carried out in Khulna Medical College Hospital from July 2002 to June 2007. Admitted children with acute neurological deficit attributable to a vascular cause were included in the study. Forty two children were finally diagnosed with stroke; 73.8% were male. Apart from paresis/paralysis in 35 (83.3%) cases, headache/vomiting/convulsion was the presenting problem in 28 (66.7%) cases at the onset. Infection in 17 (40.5%) children and trauma in 11 (26.2%) were the important predisposing factors. CT scan revealed ischemia and hemorrhage in 18 (42.8% and 8 (19.1%) cases, respectively. Twenty two (52.4%) of the children recovered fully and 3 (7.2%) expired.
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PMID:Predisposing factors and outcome of stroke in childhood. 1917 36

The aim of this study was to identify the influence of diabetes mellitus on patients with atherosclerosis obliterans (ASO) of the lower extremities. A prospective study was designed to compare differences between ASO patients with and without diabetes mellitus in regard to clinical characteristics and outcomes of management. Two hundred fifty-three consecutive (61.1%) diabetic and 161 (38.9%) nondiabetic patients were included in this study. Crural artery occlusion occurred more frequently in diabetic patients (tibioperoneal segment 26.5% vs 14.3%; p = .003). Diabetic patients had higher comorbidities, such as ischemic heart disease, disabling stroke, and renal failure. Infection requiring urgent surgical intervention was higher in diabetic patients (39.1% vs 24.2%; p = .001). This required primary major amputation in limb-threatening ischemia superimposed with infection (27.6% vs 17.7%; p = .037). The feasibility (67.2% vs 69.8%; p = .651) and success (74.4% vs 79.0%; p = .481) of revascularization between the two groups were comparable. Diabetic patients often needed more distal revascularization for limb salvage (34.4% vs 18.5%; p = .019). The mortality rate after revascularization was higher in diabetic patients (13.3% vs 2.5%; p = .009). Diabetes mellitus per se has no direct impact on limb salvageability in limb-threatening ischemia. The parity of feasibility and success in revascularization between the two groups should encourage attempts at limb salvage revascularization in diabetic patients.
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PMID:Comparative study of the management of diabetic versus nondiabetic patients with atherosclerosis obliterans of the lower extremities. 1934 91

The objective of this study is to evaluate the clinical and radiological characteristics and the outcome of status epilepticus (SE). 117 consecutive patients with SE were evaluated including their demographics, history of epilepsy, antiepileptic drug (AED) default, comorbidities, SE type and duration. The study included 22 children, 77 adults and 18 elderly patients with SE. Blood counts, serum chemistry, ECG, cranial MRI, cerebrospinal fluid and EEG were done. Patients were treated with IV phenytoin, valproate, lorazepam or diazepam as per a fixed protocol and responses to first and second drugs were noted. Death during hospital was recorded. The etiology of SE was infection in 53.8%, drug default in 7.9%, metabolic in 14.5%, stroke in 12.8% and miscellaneous in 11% of patients. 92.3% of patients had convulsive and 7.7% nonconvulsive SE. Cranial MRI was abnormal in 62%. Infection as an etiology was more common in children, drug default and metabolic causes in adults and stroke in adults and elderly. Following first AED, SE was controlled in 50%. 30% of patients remained refractory to second AED which was related to duration of SE and mortality. 29% patients died and death was higher in elderly (44%) compared to children (14%). Acute symptomatic SE is more common in developing countries. Refractory SE is associated with SE duration and mortality.
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PMID:A clinical, radiological and outcome study of status epilepticus from India. 1973 Sep 28


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