994 resultados para Acidente cerebral vascular : Idoso
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Few studies have addressed early cerebrovascular lethality in Brazil. Objective: To evaluate 10 and 28-day stroke case-fatality rates in three hospitals in three Brazilian cities. Methods: We described the stroke registries in Sao Paulo, Joao Pessoa, and Natal. Results: Out of a total of 962 first-ever events (mean age, 68.1 years-old; 53% men), 83.6% (804 cases) were classified as ischemic and 16.4% (158) as hemorrhagic stroke. Overall, the case-fatality rates and 95% confidence intervals (95% CI) for hemorrhagic stroke events were higher than for ischemic events, both at 10 (12.3%; 95% CI 7.2-17.4 versus 7.0%; 95% CI 5.3-8.8) and at 28 days (19.8%; 95% CI 13.6-26.0 versus 11.1%; 95% CI 8.9-13.3). Conclusions: We did not find any substantial differences in early case-fatality rates according to stroke subtypes, when comparing the three centers.
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Cerebral amyloid angiopathy (CAA) is an age-associated disease characterized by amyloid deposition in cerebral and meningeal vessel walls. CAA is detected in the majority of the individuals with dementia and also in a large number of non-demented elderly individuals. In addition, CAA is strongly associated with Alzheimer's disease (AD) pathology. Mechanical consequences including intra-cerebral or subarachnoid hemorrhage remains CAA most feared complication, but only a small fraction of CAA results in severe bleeding. On the hand the non-mechanical consequences in cerebrovascular regulation are prevalent and may be even more deleterious. Studies of animal models have provided strong evidence linking the vasoactive A beta 1-40, the main species found in CAA, to disturbances in endothelial-dependent factors, disrupting cerebrovascular regulation Here, we aimed to review experimental findings regarding the non-mechanical consequences of CAA for cerebrovascular regulation and discuss the implications of these results to clinical practice. (C) 2012 Elsevier Inc. All rights reserved.
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Collateral circulation, defined as the supplementary vascular network that maintains cerebral blood flow (CBF) when the main vessels fail, constitutes one important defense mechanism of the brain against ischemic stroke. In the present study, continuous arterial spin labeling (CASL) was used to quantify CBF and obtain perfusion territory maps of the major cerebral arteries in spontaneously hypertensive rats (SHRs) and their normotensive Wistar-Kyoto (WKY) controls. Results show that both WKY and SHR have complementary, yet significantly asymmetric perfusion territories. Right or left dominances were observed in territories of the anterior (ACA), middle and posterior cerebral arteries, and the thalamic artery. Magnetic resonance angiography showed that some of the asymmetries were correlated with variations of the ACA. The leptomeningeal circulation perfusing the outer layers of the cortex was observed as well. Significant and permanent changes in perfusion territories were obtained after temporary occlusion of the right middle cerebral artery in both SHR and WKY, regardless of their particular dominance. However, animals with right dominance presented a larger volume change of the left perfusion territory (23 +/- 9%) than animals with left dominance (7 +/- 5%, P<0.002). The data suggest that animals with contralesional dominance primarily safeguard local CBF values with small changes in contralesional perfusion territory, while animals with ipsilesional dominance show a reversal of dominance and a substantial increase in contralesional perfusion territory. These findings show the usefulness of CASL to probe the collateral circulation.
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We evaluated the functional dependence of stroke survivors from the Study of Stroke Mortality and Morbidity, using the Rankin Scale. Out of 355 ischemic stroke survivors (with a mean age of 67.9 years), 40% had some functional dependence at 28 days and 34.4% had some functional dependence at 6 months. Most predictors of physical dependence were identified at 28 days. These predictors were: low levels of education [illiterate vs. >= 8 years of education, multivariate odds ratio (OR) = 3.7; 95% confidence interval (95%CI): 1.60-8.54] and anatomical stroke location (total anterior circulation infarct, OR = 16.9; 95%CI: 2.93-97.49). Low levels of education and ischemic brain injury influenced functional dependence in these stroke survivors. Our findings reinforce the necessity of developing strategies for the rehabilitation of stroke patients, more especially in formulating specific strategies for care and treatment of stroke survivors with low socioeconomic status.
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Objective: To identify and compare perceptions of pain and how it is faced between men and women with central post-stroke pain. Methods: The participants were 25 men and 25 women of minimum age 30 years-old and minimum schooling level of four years, presenting central post-stroke pain for at least three months. The instruments used were: Mini-Mental State Examination; structured interview for the Brief Psychiatric Scale; Survey of Sociodemographic and Clinical Data; Visual Analogue Scale (VAS); Ways of Coping with Problems Scale (WCPS) in Scale; Revised Illness Perception Questionnaire (IPQ-R); and Beck Depression Inventory (BD). Results: A significantly greater number of women used the coping strategy "Turn to spiritual and religious activities" in WCPS. They associated their emotional state with the cause of pain in IPQ-R. "Distraction of attention" was the strategy most used by the subjects. Conclusion: Women used spiritual and religious activities more as a coping strategy and perceived their emotional state as the cause of pain.
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CONTEXT: Stroke is a frequent cause of dysphagia. OBJECTIVE: To evaluate in a tertiary care hospital the prevalence of swallowing dysfunction in stroke patients, to analyze factors associated with the dysfunction and to relate swallowing dysfunction to mortality 3 months after the stroke. METHODS: Clinical evaluation of deglutition was performed in 212 consecutive patients with a medical and radiologic diagnosis of stroke. The occurrence of death was determined 3 months after the stroke. RESULTS: It was observed that 63% of the patients had swallowing dysfunction. The variables gender and specific location of the lesion were not associated with the presence or absence of swallowing dysfunction. The patients with swallowing dysfunction had more frequently a previous stroke, had a stroke in the left hemisphere, motor and/or sensitivity alterations, difficulty in oral comprehension, alteration of oral expression, alteration of the level of consciousness, complications such as fever and pneumonia, high indexes on the Rankin scale, and low indexes on the Barthel scale. These patients had a higher mortality rate. CONCLUSIONS: Swallowing evaluation should be done in all patients with stroke, since swallowing dysfunction is associated with complications and an increased risk of death.
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Stroke affects mainly people aged over 65 years, and atherosclerosis predominates as the main etiopathogenic factor in ischemic stroke (IS). On the other hand, cardiac embolism and arterial dissection are the most frequent causes of IS in patients aged less than 45 years. However, inappropriate control of traditional vascular risk factors in young people may be causing a significant increase of atherosclerosis-related IS in this population. Furthermore, a variety of etiologies, many of them uncommon, must be investigated. In endemic regions, neurocysticercosis and Chagas' disease deserve consideration. Undetermined cause has been still reported in as many as one third of young stroke patients.
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There is evidence that the explicit lexical-semantic processing deficits which characterize aphasia may be observed in the absence of implicit semantic impairment. The aim of this article was to critically review the international literature on lexical-semantic processing in aphasia, as tested through the semantic priming paradigm. Specifically, this review focused on aphasia and lexical-semantic processing, the methodological strengths and weaknesses of the semantic paradigms used, and recent evidence from neuroimaging studies on lexical-semantic processing. Furthermore, evidence on dissociations between implicit and explicit lexical-semantic processing reported in the literature will be discussed and interpreted by referring to functional neuroimaging evidence from healthy populations. There is evidence that semantic priming effects can be found both in fluent and in non-fluent aphasias, and that these effects are related to an extensive network which includes the temporal lobe, the pre-frontal cortex, the left frontal gyrus, the left temporal gyrus and the cingulated cortex.
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INTRODUÇÃO: A via de acesso transfemoral é preferencial para o implante por cateter de bioprótese valvar aórtica. Entretanto, algumas situações, como a presença de doença vascular periférica, impossibilitam a utilização desse acesso. Nesses casos, o acesso por dissecção da artéria subclávia é uma alternativa para a realização do procedimento. Nosso objetivo foi avaliar a experiência brasileira com a utilização da artéria subclávia como via de acesso para o implante por cateter da bioprótese CoreValve®. MÉTODOS: Foram requisitos para o procedimento área valvar aórtica < 1 cm², ânulo valvar aórtico ≥ 20 mm e ≤ 27 mm (CoreValve® de 26 mm e 29 mm), aorta ascendente ≤ 43 mm e artéria subclávia com diâmetro ≥ 6 mm, isenta de lesões obstrutivas significativas, tortuosidade acentuada e calcificação excessiva. O acesso pela artéria subclávia foi obtido por dissecção cirúrgica e, sob visão direta, punção da artéria subclávia. Obtido o acesso arterial, empregou-se a técnica padrão. RESULTADOS: Entre janeiro de 2008 e abril de 2012, 8 pacientes com doença vascular periférica foram submetidos a implante de prótese CoreValve® pela artéria subclávia em 4 instituições. O procedimento foi realizado com sucesso em todos os casos, com redução do gradiente transvalvar aórtico médio de 46,4 ± 17,5 mmHg para 9,3 ± 3,6 mmHg (P = 0,0018) e melhora dos sintomas. Aos 30 dias e no seguimento de 275 ± 231 dias, 87,5% e 62,5% dos pacientes, respectivamente, apresentavam-se livres de complicações maiores (óbito, infarto do miocárdio, acidente vascular cerebral e cirurgia cardíaca de urgência). CONCLUSÕES: Na experiência brasileira, o acesso pela artéria subclávia mostrou-se seguro e eficaz como via alternativa para o implante por cateter da bioprótese CoreValve®.
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OPINION STATEMENT: • In acute spinal cord ischemia syndrome (ASCIS), treatment recommendations are derived from data of cerebral ischemic stroke, atherosclerotic vascular disease and acute spinal cord injury. Besides acute management, secondary prevention is of major importance. Pathologies affecting the aorta as well as underlying cerebrovascular conditions should be treated whenever possible.• ASCIS may occur after aortic surgery, less often after thoracic endovascular aortic repair (TEVAR). Protocols are proposed.• Acute spinal cord hemorrhage can be treated surgically and/or pharmacologically.• Symptomatic treatment in patients with a spinal cord lesion is of major importance. Depending on level and extension of the lesion, there is a risk for systemic and neurological complications, which may be life-threatening.• Each spinal vascular malformation is a unique lesion that needs an individualized treatment algorithm. In case of a symptomatic vascular malformation, endovascular intervention is the primary treatment option.• Spinal dural Arteriovenous fistula (AVF) may be treated endovascularly or surgically. If preoperative localization of the fistula is possible, surgery is feasible with a low complication rate. In comparison, endovascular approaches are less invasive.• Spinal AVM are rather treated endovascularly than surgically or in a stepwise multidisciplinary approach.• Symptomatic and exophytic spinal cavernous angiomas should be treated surgically. Deep spinal cavernous angiomas that are asymptomatic or only show mild symptoms can be observed.
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Vascular endothelial growth factor (VEGF) has potent angiogenic and neuroprotective effects in the ischemic brain. Its effect on axonal plasticity and neurological recovery in the post-acute stroke phase was unknown. Using behavioral tests combined with anterograde tract tracing studies and with immunohistochemical and molecular biological experiments, we examined effects of a delayed i.c.v. delivery of recombinant human VEGF(165), starting 3 days after stroke, on functional neurological recovery, corticorubral plasticity and inflammatory brain responses in mice submitted to 30 min of middle cerebral artery occlusion. We herein show that the slowly progressive functional improvements of motor grip strength and coordination, which are induced by VEGF, are accompanied by enhanced sprouting of contralesional corticorubral fibres that branched off the pyramidal tract in order to cross the midline and innervate the ipsilesional parvocellular red nucleus. Infiltrates of CD45+ leukocytes were noticed in the ischemic striatum of vehicle-treated mice that closely corresponded to areas exhibiting Iba-1+ activated microglia. VEGF attenuated the CD45+ leukocyte infiltrates at 14 but not 30 days post ischemia and diminished the microglial activation. Notably, the VEGF-induced anti-inflammatory effect of VEGF was associated with a downregulation of a broad set of inflammatory cytokines and chemokines in both brain hemispheres. These data suggest a link between VEGF's immunosuppressive and plasticity-promoting actions that may be important for successful brain remodeling. Accordingly, growth factors with anti-inflammatory action may be promising therapeutics in the post-acute stroke phase.
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Vascular endothelial growth factor (VEGF) is a potent angiogenic factor, which also has neuroprotective activity. In view of these dual actions on vessels and neurons, we were interested whether VEGF promotes long distance axonal plasticity in the ischemic brain. Herein, we show that VEGF promotes neurological stroke recovery in mice when delivered in a delayed way starting 3 days after middle cerebral artery occlusion. Using anterograde tract-tracing experiments that we combined with histochemical and molecular biological studies, we demonstrate that although VEGF promoted angiogenesis predominantly in the ischemic hemisphere, pronounced axonal sprouting was induced by VEGF in the contralesional, but not the ipsilesional corticobulbar system. Corticobulbar plasticity was accompanied by the deactivation of the matrix metalloproteinase MMP9 in the lesioned hemisphere and the transient downregulation of the axonal growth inhibitors NG2 proteoglycan and brevican and the guidance molecules ephrin B1/2 in the contralesional hemisphere. The regulation of matrix proteinases, growth inhibitors, and guidance molecules offers insights how brain plasticity is controlled in the ischemic brain.
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Major progress has recently been made in the neuro-imaging of stroke as a result of improvements in imaging hardware and software. Imaging may be based on either magnetic resonance imaging (MRI) or computed tomography (CT) techniques. Imaging should provide information on the entire vascular cervical and intracranial network, from the aortic arch to the circle of Willis. Equally, it should also give information on the viability of brain tissue and brain hemodynamics. CT has the advantage in the detection of acute hemorrhage whereas MRI offers more accurate pathophysiological information in the follow-up of patients.
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Proton magnetic resonance spectroscopy (MRS) allows the assessment of various cerebral metabolites non-invasively in vivo. Among 1H MRS-detectable metabolites, N-acetyl-aspartate and N-acetyl-aspartyl-glutamate (tNAA), trimethylamines (TMA), creatine and creatine phosphate (tCr), inositol (Ins) and glutamate (Gla) are of particular interest, since these moieties can be assigned to specific neuronal and glial metabolic pathways, membrane constituents, and energy metabolism. In this study on 94 subjects from a memory clinic population, 1H MRS results (single voxel STEAM: TE 20 ms, TR 1500 ms) on the above metabolites were assessed for five different brain regions in probable vascular dementia (VD), probable Alzheimer's disease (AD), and age-matched healthy controls. In both VD and AD, ratios of tNAA/tCr were decreased, which may be attributed to neuronal atrophy and loss, and Ins/tCr-ratios were increased indicating either enhanced gliosis or alteration of the cerebral inositol metabolism. However, the topographical distribution of the metabolic alterations in both diseases differed, revealing a temporoparietal pattern for AD and a global, subcortically pronounced pattern for VD. Furthermore, patients suffering from vascular dementia (VD) had remarkably enhanced TMA/tCr ratios, potentially due to ongoing degradation of myelin. Thus, the metabolic alterations obtained by 1H MRS in vivo allow insights into the pathophysiology of the different dementias and may be useful for diagnostic classification.
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We have previously shown that antioxidants such as a-phenyl-tert-butyl nitrone or N-acetylcysteine attenuate cortical neuronal injury in infant rats with bacterial meningitis, suggesting that oxidative alterations play an important role in this disease. However, the precise mechanism(s) by which antioxidants inhibit this injury remain(s) unclear. We therefore studied the extent and location of protein oxidation in the brain using various biochemical and immunochemical methods. In cortical parenchyma, a trend for increased protein carbonyls was not evident until 21 hours after infection and the activity of glutamine synthetase (another index of protein oxidation) remained unchanged. Consistent with these results, there was no evidence for oxidative alterations in the cortex by various immunohistochemical methods even in cortical lesions. In contrast, there was a marked increase in carbonyls, 4-hydroxynonenal protein adducts and manganese superoxide dismutase in the cerebral vasculature. Elevated lipid peroxidation was also observed in cerebrospinal fluid and occasionally in the hippocampus. All of these oxidative alterations were inhibited by treatment of infected animals with N-acetylcysteine or alpha-phenyl-tert-butyl nitrone. Because N-acetylcysteine does not readily cross the blood-brain barrier and has no effect on the loss of endogenous brain antioxidants, its neuroprotective effect is likely based on extraparenchymal action such as inhibition of vascular oxidative alterations.