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Dissertations / Theses on the topic 'Transient Ischemia'
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Li, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia." Connect to resource online, 2009. http://hdl.handle.net/1805/2021.
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Thesis (Ph.D.)--Indiana University, 2009.Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).
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Nishijima, Kazuaki. "In vivo evaluation of platelet-endothelial interactions after transient retinal ischemia." Kyoto University, 2003. http://hdl.handle.net/2433/148702.
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Eriksson, Rolf. "The Utility of Manganese for Magnetic Resonance Imaging of Transient Myocardial Ischemia." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5817.
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Platholi, Jimcy. "Regulation of protein phosphatase-1I : in transient global cerebral ischemia and reperfusion /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528857081&sid=17&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Hirose, Fumitaka. "In vivo evaluation of retinal injury after transient ischemia in hypertensive rats." Kyoto University, 2006. http://hdl.handle.net/2433/143861.
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Tokime, Tomoo. "Neuroprotective effect of FK506, an immunosuppressant, on transient global ischemia in gerbil." Kyoto University, 1997. http://hdl.handle.net/2433/202178.
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Silva, Matthew S. "NMR characterization of changes in the apparent diffusion coefficient of water following transient cerebral ischemia." Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0327102-221251.
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Chapman, Courtney Myfanwy. "Novel pharmaceutical combination confers protection from delayed cell death following transient cerebral ischemia." Thesis, Montana State University, 2009. http://etd.lib.montana.edu/etd/2009/chapman/ChapmanC0509.pdf.
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Stroke is a leading cause of death and disability throughout the world; ischemia is the most common form of stroke. Medical procedures such as cardio-pulmonary bypass surgery can cause ischemic stroke can be caused. There are no treatments to limit neural impairment following stroke. The current research investigates neuroprotection offered by treatment with a novel drug combination consisting of Simvastatinâ„¢, Gemfibrozilâ„¢, Troglitazoneâ„¢, and Spironolactoneâ„¢. Animals were treated with the drug cocktail three weeks proceeding and one week subsequent to surgery. Ischemic insult was induced by clamping the carotid arteries for 5 min. Sham subjects underwent similar surgical procedures, but the carotids were not clamped. Twenty-four hrs following the surgical procedure locomotor activity was monitored in an open field for 5 min. Seven to fourteen days following ischemia or the sham procedure animals were sacrificed and sections containing the hippocampal CA1 region were mounted on slides and stained with cresyl violet. The CA1 region was rated on a 4-point scale for level of damage. Rodents generally show increased locomotor activity following transient global ischemia in an open field. In our study, ischemic animals that received vehicle demonstrated increased activity relative to the animals that received the drug treatment on all behavioral measures. Ischemic animals that received vehicle treatment had significantly more neural damage in the hippocampal CA1 region than ischemic animals receiving the drug. The appearance of neurons in the CA1 hippocampal regions of animals in the sham condition was not significantly different from ischemic animals in the drug treatment condition. It is concluded that the drug treatment is effective in offering neuroprotection during transient global ischemia. The next step is to characterize the biochemical mechanisms behind the neuroprotection conferred by the drug treatment. Contrasting the protein expression levels of animals receiving the vehicle treatment with animals receiving the drug treatment following an ischemic insult will assist in elucidating these pathways. Predictions are made regarding the biochemical mechanisms affected by the drug treatment based on previous research on the biochemical pathways affected by each pharmaceutical.
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Leung, Wai-chung. "Investigations into the role of endothelial endothelin-1 on transient focal cerebral ischemia." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634127.
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Leung, Wai-chung, and 梁偉聰. "Investigations into the role of endothelial endothelin-1 on transient focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634127.
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Hsu, Melissa M. "Immediate and long-term changes in the rat hippocampus after transient forebrain ischemia /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9835293.
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Hattotori, Itaro. "Intravenous Administration of Thioredoxin Decreases Brain Damage Following Transient Focal Cerebral Ischemia in Mice." Kyoto University, 2004. http://hdl.handle.net/2433/147483.
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McGahan, Lynda. "Expression of immediate-early gene proteins in the rat hippocampus following transient global ischemia." Thesis, University of Ottawa (Canada), 1996. http://hdl.handle.net/10393/10454.
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The temporospatial expression patterns of the immediate-early gene (IEG) proteins Fos, FosB, $\Delta$FosB, Jun, JunB, JunD, and NGFI-A were investigated in rat hippocampus by immunonohistochemistry 2 h, 12 h, 24 h, and 48 h after forebrain ischemia. Transient global ischemia (20 min), produced by four vessel occlusion (4-VO), elicited different patterns of IEG expression in vulnerable CA1 and more resilient CA3 neurons. Cell counts revealed that initially, ischemia elevated immunoreactivity in both CA1 and CA3 hippocampal subfields for all IEGs examined, with the exception of JunD and NGFI-A. However, distinct patterns of IEG expression became evident in these regions at later time points following recirculation of blood flow. The pivotal difference was the persistence of ischemia-induced elevations of FosB and Jun expression in the CA1 region of the hippocampus. Unlike CA3 neurons where IEG immunoreactivity had subsided to basal levels by 24 h-48 h after reperfusion, CA1 neurons continued to display increased FosB- and Jun-like immunoreactivity 48 h post-ischemia. In contrast to FosB and Jun, JunB expression declined significantly below basal levels in CA1 neurons at 48 h, while JunB-like immunoreactivity remained unaltered in CA3 neurons. Given that JunB has been shown to inhibit the transactivating properties of Jun, decreased JunB levels may contribute to the apoptotic death of CA1 neurons by enhancing the transcriptional regulating activity of Jun. Also notable at 48 h was the complete loss of constitutive NGFI-A expression from CA1 neurons of ischemic animals. In summary, these findings suggest that persistent elevations in FosB and Jun expression coupled with reductions in JunB and NGFI-A levels may play a role in the apoptotic death of CA1 neurons following transient global ischemia. (Abstract shortened by UMI.)
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Sicard, Kenneth M. "Multimodal MRI, Behavioral Testing, and Histology in a Rat Model of Transient Focal Cerebral Ischemia : A Dissertation." eScholarship@UMMS, 2006. http://escholarship.umassmed.edu/gsbs_diss/318.
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Cerebral ischemia is defined as a decrease in blood flow to the brain. It is most often caused by obstruction of a cerebral blood vessel, and is recognized by the World Health Organization as the leading cause of serious adult disability and one of the top three causes of adult death worldwide. Most survivors demonstrate partial restitution of function over time, but the underlying recovery mechanism(s) remain unclear especially in a subset of patients with persistent neurological morbidities despite normal-appearing brain on neuroimaging. The optimal way to understand any human disease state is via clinical studies. Unfortunately, well-controlled experiments in humans are difficult due to small patient populations, the presence of numerous confounding variables, and ethical issues associated with invasive or discomforting experimental procedures. Anesthetized animal models of cerebral ischemia afford a means of avoiding the above difficulties. However, anesthesia and physiological perturbations that occasionally follow brain ischemia may affect the reliability of certain tools used to study this disease, such as functional magnetic resonance imaging (fMRI). Therefore, the central goals of this thesis were: 1) to evaluate the feasibility of performing fMRI in anesthetized and awake animals, 2) to assess fMRI responses under various perturbations of cerebral perfusion and tissue oxygenation in order to identify key factors that may modulate functional signal changes following ischemia, and 3) to utilize fMRI, behavioral tests and histology in an anesthetized animal model of transient focal cerebral ischemia to explore postischemic changes in brain pathology/function and how they relate to changes in behavior.
In the first study of this dissertation, I report the evaluation of fMRI responses in anesthetized and awake animals. Anesthesia is frequently used in animal models of cerebral ischemia, but is known to alter brain perfusion and metabolism which may, in turn, affect fMRI responsivity. Perfusion-based fMRI was used to evaluate cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) responses to hypercapnia in awake and isoflurane-anesthetized rats. Hypercapnia produced significant CBF and BOLD fMRI signal changes throughout the cerebrum in awake and isoflurane-anesthetized groups. These results show that perfusion-based fMRI can successfully detect stimulus-evoked hemodynamic changes in the brains of both conscious and isoflurane-anesthetized animals.
The second study of this dissertation: 1) investigates the effects of alterations in cerebral perfusion and oxygenation on fMRI signal changes, and 2) examines the self-consistency of an imaging-based formalism for the calculation of the cerebral metabolic rate of oxygen (CMRO2). Functional MRI responses to a stimulus can be described in terms of relative or absolute signal change. A relative fMRI response is defined as a percent-change relative to its own respective baseline value. An absolute fMRI response is defined as a quantitative change relative to a single fixed baseline value that serves as a control. Thus, an absolute fMRI signal change is largely independent of the baseline state and may more accurately index brain activity when baseline fMRI signals change significantly over time due to, for example, hemodynamic-metabolic disturbances that occur during and/or after brain ischemia. To address these issues, the effects of inspired hypoxic, normoxic, hyperoxic, and hypercapnic gases on baseline and forepaw stimulation-evoked changes in BOLD and CBF fMRI signals were examined in isoflurane-anesthetized rats. Relative fMRI responses to forepaw stimulation varied-whereas. absolute responses were similar--across gas conditions. These results demonstrate that absolute measurements of fMRI signal change may lend a more accurate measure of brain activity during states of altered basal physiology as well as support the self-consistency of the imaging-based CMRO2 formalism under these conditions.
The third and last study of this dissertation utilized multimodal MRI, behavioral tests, and histology at acute to chronic periods following transient middle cerebral artery occlusion (tMCAO) in the rat to examine the evolution of pathological, functional, and behavioral parameters following transient focal cerebral ischemia. MRI was used to track the evolution of brain pathology and function following cerebral ischemia, and it was found that the cerebral sensorimotor network, critical for sensory and motor behavioral functions, showed profoundly abnormal signal changes that required up to one day to normalize. Adhesive removal, forepaw placement and beam-walk behavioral tests demonstrated sensorimotor dysfunctions that gradually improved but remained long after the recovery of MRI parameters. Postmortem histology confirmed the presence of selective neural cell death within the sensorimotor network at time points when behavior was abnormal. These results suggest that subtle postischemic pathological changes in the brain undetectable by MRI may be responsible for persistent behavioral deficits-a finding which may be relevant to a clinical subset of patients with persistent neurological morbidities despite negative MRI results following cerebral ischemia.
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Fan, Man-hin Michael, and 范文軒. "Endotoxin from porphyromonas gingivalis improves recovery of the electrically induced Ca2+ transient following ischemia andreperfusion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011205.
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Kostulas, Konstantinos. "Genetic analysis of ischemic stroke and predisposing carotid artery stenosis : a stroke carol /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-395-5/.
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Fan, Man-hin Michael. "Endotoxin from porphyromonas gingivalis improves recovery of the electrically induced Ca2+ transient following ischemia and reperfusion /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38347945.
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Xie, Yicheng. "Optogenetic investigation of neuronal excitability and sensory-motor function following a transient global ischemia in mice." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/55954.
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Global ischemia occurs during cardiac arrest and has been implicated as a complication that can occur during cardiac surgery. It induces delayed neuronal death in human and animal models, particularly in the hippocampus, while it also can affect the cortex. Other than morphology and measures of cell death, relatively few studies have examined neuronal networks and motor-sensory function following reversible global ischemia in vivo. Optogenetics allows the combination of genetics and optics to control or monitor cells in living tissues. Here, I adapted optogenetics to examine neuronal excitability and motor function in the mouse cortex following a transient global ischemia. Following optogenetic stimulation, I recorded electrical signals from direct stimulation to targeted neuronal populations before and after a 5 min transient global ischemia. I found that both excitatory and inhibitory neuronal network in the somatosensory cortex exhibited prolonged suppression of synaptic transmission despite reperfusion, while the excitability and morphology of neurons recovered rapidly and more completely. Next, I adapted optogenetic motor mapping to investigate the changes of motor processing, and compared to the changes of sensory processing following the transient global ischemia. I found that both sensory and motor processing showed prolonged impairments despite of the recovery of neuronal excitability following reperfusion, presumably due to the unrestored synaptic transmission. Interestingly, motor processing recovered faster and more completely than sensory processing. My results suggest a uniform suppression of synaptic transmission, both in excitatory and inhibitory network, despite the rapid recovery of neuronal excitability and morphology, following a global ischemia and reperfusion. This prolonged suppression of synaptic transmission might impede the recovery of sensory and motor processing with differential severity. Besides, I extended tools for mesoscopic imaging using novel optogenetic sensors, including genetically encoded Ca2+ indicators - GCaMPs, and extracellular glutamate sensor - iGluSnFR. I found that iGluSnFR has fastest kinetics for reporting both sensory and spontaneous activity in the cortex, which can resolve temporal features of sensory processing that were not readily observed with GECIs. I suggest that iGluSnFR tools have potential utility in normal physiology, and neurologic pathologies in which abnormalities in glutamatergic signaling are implicated, such as stroke.Medicine, Faculty of
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Wang, Huan. "The Reck tumor suppressor protein alleviates tissue damage and promotes functional recovery after transient cerebral ischemia in mice." Kyoto University, 2012. http://hdl.handle.net/2433/157418.
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Souza, Carolina Melo de. "Neuroprotective effect of curcumin on oxidative stress, inflammation, memory and neuronal damage in rats submitted to transient cerebral ischemia." Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=12162.
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CoordenaÃÃo de AperfeÃoamento de Pessoal de NÃvel SuperiorThe pathophysiology of cerebral ischemia involves a complex cascade of events which includes excitotoxicity, inflammation, oxidative stress and apoptosis. Curcumin is a polyphenol extracted from the rhizome of Curcuma longa. It has anti-inflammatory and antioxidant properties. In this study, we investigated the effects of curcumin on memory deficits, oxidative stress, inflammation and neuronal damage induced by transient cerebral ischemia (TCI). The TCI was induced by bilateral common carotid artery occlusion for 30 min followed by reperfusion. Vehicle or curcumin (6% DMSO in phosphate buffer) were orally administered 60 min before and daily after TCI. Cognitive evaluation was performed by using Y-maze, passive avoidance and water maze tests to assess working, spatial and aversive memories, respectively. To assess neuronal injury histological sections from hippocampus were stained with cresyl violet or FluoroJade C. The interleukin-1β and myeloperoxidase (MPO) contents from hippocampus were used for inflammatory evaluation. Oxidative stress was assessed by quantification of malondialdehyde (MDA), nitrite/nitrate, reduced glutathione (GSH) and superoxide dismutase (SOD) hippocampal. There were no changes in locomotor activity, neither in working memory. Curcumin prevented the TCI-induced early and late aversive memory deficits. The TCI impair spatial learning and memory. Curcumin treatment did not affect spatial learning, but showed a tendency to prevent the impairment on spatial memory. TCI promoted the increase in MPO activity and a tendency to increased concentrations of IL-1β and this effect was prevented by curcumin treatment. Curcumin treatment did not prevent the TCI-induced MDA increases 6h after surgery. Four days after surgery TCI showed a tendency to increase MDA contents and curcumin treatment lowered it. Curcumin prevented TCI- induced nitrite formation 6h after surgery and GSH depletion 24 hours after surgery. Curcumin protected the neurons from death 4d but not 7 days after TCI. Our results demonstrated that curcumin neuroprotection effects may be due to its anti-inflammatory and antioxidant properties.
A fisiopatologia da isquemia cerebral envolve uma complexa cascata de eventos dentre eles excitotoxicidade, inflamaÃÃo, estresse oxidativo e apoptose. A curcumina à um polifenol presente no rizoma da Curcuma longa e que apresenta propriedades antiinflamatÃria e antioxidante. No presente estudo, foram investigados os efeitos da curcumina sobre os dÃficits de memÃria, estresse oxidativo, inflamaÃÃo e dano neuronal induzidos por isquemia cerebral transitÃria (ICT). A ICT foi induzida por oclusÃo das artÃrias carÃtidas, por 30min, seguida de reperfusÃo. Os animais receberam curcumina ou veÃculo (6% de DMSO em tampÃo fosfato) por via oral 60 min antes e diariamente apÃs a ICT. A avaliaÃÃo dos dÃficits cognitivos foi realizada atravÃs dos testes do labirinto em Y, da esquiva passiva e do labirinto aquÃtico que avaliam as memÃrias de trabalho, aversiva e espacial, respectivamente. A integridade neuronal foi avaliada atravÃs de anÃlise histolÃgica do hipocampo utilizando as tÃcnicas de violeta de cresil e Fluoro Jade C. As dosagens de IL-1β e mieloperoxidase (MPO) em homogenatos hipocampais foram utilizadas para a avaliaÃÃo da inflamaÃÃo. O estresse oxidativo foi analisado atravÃs da quantificaÃÃo de malondialdeÃdo (MDA), nitrito/nitrato, glutationa reduzida (GSH) e atividade da superÃxido dismutase (SOD) hipocampais. NÃo foram observadas alteraÃÃes na atividade locomotora e nem na memÃria de trabalho. A curcumina preveniu dÃficits nas memÃrias aversiva recente e tardia induzidas por ICT. A ICT promoveu dÃficits no aprendizado e memÃria espacial. A curcumina nÃo alterou a aprendizagem, mas apresentou uma tendÃncia estatÃstica na prevenÃÃo do dÃficit de memÃria espacial. A ICT promoveu o aumento na atividade de MPO e tendÃncia a aumento nas concentraÃÃes de IL-1β e esse efeito foi prevenido pelo tratamento com curcumina. A ICT promoveu o aumento significativo nas concentraÃÃes de MDA. O tratamento com a curcumina nÃo alterou esse efeito 6h, mas preveniu o aumento 4 dias apÃs a ICT. A curcumina preveniu o aumento de nitrito e a depleÃÃo de GSH induzidos por ICT. A curcumina protegeu os neurÃnios da morte 4 mas nÃo 7 dias apÃs a ICT. Os efeitos neuroprotetores da curcumina parecem estar relacionados com suas propriedades anti-inflamatÃrias e antioxidante.
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Chin, Reiko. "Effects of Exercise Training on Myocardial Fatty Acid Metabolism in Rats with Depressed Cardiac Function Induced by Transient Ischemia." Kyoto University, 2001. http://hdl.handle.net/2433/150165.
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Kundrotienė, Jurgita. "Ischemic brain damage following transient and moderate compression of sensorimotor cortex in Sprague-Dawley and diabetic Goto-Kakizaki rats /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-819-X/.
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Xu, Kui. "The Central Nervous System Aspects of Cardiac Arrest and Resuscitation in a Rat Model of Global Ischemia." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270689501.
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Lennmyr, Fredrik. "Signal Transduction in Focal Cerebral Ischemia : Experimental Studies on VEGF, MAPK and Src family kinases." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5267-1/.
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Wang, Yachao [Verfasser], and Dirk [Akademischer Betreuer] Hermann. "Post-acute delivery of NMDA or GABAA α5 receptor antagonists promotes neurological recovery and peri-infarct brain remodeling after transient focal cerebral ischemia in mice / Yachao Wang ; Betreuer: Dirk Hermann." Duisburg, 2019. http://d-nb.info/1191692272/34.
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Maia, FlÃvio Damasceno. "L-deprenil previne alteraÃÃes neuroquÃmicas e comportamentais induzidas pela isquemia cerebral transitÃria." Universidade Federal do CearÃ, 2004. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=406.
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FundaÃÃo de Amparo à Pesquisa do Estado do CearÃCoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
O trabalho mostra o tratamento e os efeitos do l-deprenil (DEP), no aprendizado, na memÃria e na peroxidaÃÃo lipÃdica em cÃrebros de ratos submetidos à isquemia cerebral transitÃria (ICT). Os animais (ratos Wistar, fÃmeas, 200-250g) foram submetidos à isquemia cerebral transitÃria pela oclusÃo de ambas as artÃrias carÃtidas durante 20 minutos e tratados durante 5 dias com DEP (5 e 10 mg/kg). A temperatura retal foi monitorada e mantida em torno de 37ÂC atravÃs de uma luz incandescente. O mesmo procedimento foi feito no grupo controle + salina, Falso-operado + salina (FO) com exceÃÃo do clampeamento das artÃrias carÃtidas. No 6 dia apÃs a induÃÃo da isquemia, os animais foram submetidos aos testes de atividade locomotora e memÃria (esquiva passiva, labirinto em T elevado e labirinto aquÃtico de Morris), a seguir foram sacrificados e os cÃrebros dissecados sobre gelo (hipocampo e cÃrtex temporal) para as determinaÃÃes de MDA, nitrito/nitrato e atividade da catalase e atividade da protease caspase-3. No protocolo de avaliaÃÃo da Ãrea total do infarto encontramos apÃs 1 hora de ICT uma Ãrea de infarto 38,01  3,44% da Ãrea total do cÃrebro, e apÃs 24 horas de ICT uma Ãrea de infarto 22,00  2,90% da Ãrea total do cÃrebro. Os parÃmetros fisiolÃgicos estudados nÃo mostraram alteraÃÃes entre os grupos ICT e FO. Nenhuma alteraÃÃo na atividade locomotora foi detectada nos grupos FO, ICT, Dep 10 + ICT. PorÃm, um aumento na atividade locomotora foi observado no grupo Dep 5 + ICT (7,37  1, 77, p< 0,02) quando comparado com o grupo FO, tratado com salina, (4,66  1,54). No teste do Labirinto em T elevado (T Maze) a ICT afetou os processos de aquisiÃÃo e retenÃÃo de memÃria quando os animais foram testados no mesmo dia (esquiva 1 e 2) quando comparados com o grupo controle (FO). O teste de Kruskall-Wallis mostrou alteraÃÃo significativa na latÃncia da esquiva inibitÃria (esquiva 1 e 2 quando comparados com o treino) no falso-operado (FO - treino: 20,34  3,43 s; esquiva 1 - 231,6  34,81 s; esquiva 2 â 247,8  27,25 s; KW = 19,62, p< 0,001), e no grupo l-deprenil (5 e 10 mg/kg) + isquemia (Dep 5 â treino: 110,8  56,16 s; esquiva 1 - 299,8  0,16 s; esquiva 2 â 260  40,00 s; KW = 9,16, p< 0,01. Dep 10 â treino: 29,15  8,64 s; esquiva 1 â 299,80  0,25 s; esquiva 2 299,8  0,25 s; KW = 6,98, p< 0,05). Isto indica uma boa aquisiÃÃo de memÃria. Portanto, o resultado do grupo ICT + salina indicou um dÃficit da memÃria (ICT â treino: 37,75  11,52 s; esquiva 1 â 116,30  65,46 s; treino 2 â 195,00  64,10 s; KW = 3,90, p< 0,141). AlÃm disso, existiu uma diferenÃa significativa (Teste Mann-Whitney) entre os grupos na esquiva 3 (retenÃÃo) quando comparados com o grupo ICT (Dep 5, MW (3) = 18,483, p< 0,0003, Dep 10, MW (3) = 18,483, p< 0,003) significando que a retenÃÃo da memÃria foi aumentada pelo tratamento com a droga. No teste da esquiva passiva os animais do grupo controle (FO + salina) apresentaram uma boa retenÃÃo da memÃria, tanto na fase imediata (memÃria recente - MR), quanto na fase de consolidaÃÃo (memÃria tardia - MT), quando comparadas ao treino (ANOVA) (FO + salina (n-7)- treino - 15,94  4,40 s, MR - 138,84  34,60 s, MT - 196,32  34, 71, p< 0,006). Por outro lado, os animais que sofreram ICT nÃo apresentaram diferenÃa no tempo de latÃncia de entrada no lado escuro quando comparado com o treino, significando um dÃficit na aprendizagem e memÃria (ICT (n-7)- treino - 34,37  10,16 s, MR - 105,54  35,21 s, MT - 96,20  33, 44, p< 0,33), e, portanto dano na aquisiÃÃo e retenÃÃo da memÃria. Comparando os tratamentos observamos um aumento significativo, no tempo de latÃncia de entrada no lado escuro do aparelho, nos ratos tratados com l-deprenil 5 mg/kg quando avaliados na MR (FO + salina- 138,84  34,60s; ICT - 105,54  35,21; ICT + Dep 5- 198,88  38,42s; ICT + Dep 10- 188,06  34,60s; Kruskall-Wallis, KW-9,66, p<0,05, Mann-Whitney, Dep 5 vs ICT, p<0,05), enquanto na MT foi observada uma diminuiÃÃo significativa, no tempo de latÃncia de entrada no lado escuro do aparelho, nos ratos tratados com l-deprenil (5 e 10 mg/kg) (FO + salina- 196,32  34,71s; ICT - 96,20  33,44s; ICT + Dep 5- 299,83  0,16s; ICT + Dep 10- 264,70  35,28 s; Kruskall-Wallis, KW-14,57, p<0,05, Mann-Whitney, Dep 5 e Dep 10 vs ICT, p<0,05), significando melhora no aprendizado do animal fazendo-o lembrar o choque recebido durante o treino e indicando uma reversÃo da lesÃo sofrida com a ICT. No teste do Labirinto AquÃtico (Water Maze) a ICT promoveu um dano da retenÃÃo na memÃria dos animais em relaÃÃo ao grupo controle (FO), porÃm o l-deprenil conseguiu reverter o dano na aquisiÃÃo da memÃria induzida pela ICT em ambas as doses (5 e 10 mg/kg), observamos tambÃm que o grupo Dep 5 obteve um melhor desempenho na aquisiÃÃo da memÃria quando comparado com o grupo Dep 10. (FO (n-10): 5,4  0,84s; FO + DEP 10 (n-10): 9,7  2,28s; ICT (n-9): 32,44  2,95s; ICT + DEP 5 (n-8): 12,88  1,4s; ICT + DEP 10 (n-8): 4,5  0,70s; Kruskall-Wallis, KW-29,07, p<0,05, Mann-Whitney, FO + DEP 10, Dep 5 e Dep 10 vs ICT, p<0,05). Os ratos submetidos a ICT mostraram um aumento de 71% nos nÃveis de MDA no hipocampo quando comparados com o grupo controle (FO), e o tratamento com l-deprenil reverteu significativamente este efeito (p<0,05). Os valores dos nÃveis de MDA foram trazidos prÃximos aqueles valores do grupo controle (FO) em relaÃÃo aos grupos (ICT + DEP 5 e ICT + DEP 10, 34 e 38%, respectivamente) com ambas as doses de l-deprenil mais ICT (Hipocampo - FO (n-7): 45,4  4,45; ICT (n-7): 77,6  8,97; ICT + DEP 5 (n-7): 51,2  1,68; ICT + DEP 10 (n-7): 48,5  6,70 nmoles/g; p<0,05, ANOVA e Teste de Tukey). No cÃrtex temporal, a ICT nÃo aumentou os nÃveis de MDA quando comparados com o grupo controle. Portanto, os ratos submetidos a ICT e tratados com altas doses de l-deprenil (10 mg/kg) apresentaram nÃveis de MDA 30% menor que aqueles mostrados por ambos os grupos FO e ICT (CÃrtex temporal - FO (n-7): 46,8  4,36; ICT (n-7): 48,7  1,33; ICT + DEP 5 (n-7): 52,5  3,74; ICT + DEP 10 (n-7): 33,4  2,98 nmoles/g; p<0,05, ANOVA e Teste de Tukey). No hipocampo, os nÃveis de nitrito foram significativamente aumentados apÃs a ICT quando comparados com o grupo controle FO (82% aumento). O DEP 10 reverteu este efeito e os valores foram trazidos para aqueles do controle. Por outro lado, a isquemia nÃo afetou os nÃveis de nitrito no cÃrtex, entretanto o DEP 5 diminui significativamente os nÃveis de nitrito quando comparados com os grupos controle e ICT. A ICT mostrou um aumento em 50 % da atividade da protease caspase-3 no hipocampo; e o tratamento com l-deprenil (10 mg/kg) reverteu este efeito trazendo os valores prÃximos aos do grupo controle (FO), porÃm o tratamento com DEP 5 nÃo mostrou o mesmo (Valor da AbsorbÃncia: FO â 0,083  0,006; ICT - 0,124  0,017; ICT + DEP 10 â 0,080  0,007; ICT + DEP 5 â 0,125  0,007), porÃm nos animais controle que receberam tratamento com DEP 10 (FO + DEP 10) a atividade da caspase â 3 diminui em 99% em relaÃÃo ao grupo ICT. Em conclusÃo mostramos que a administraÃÃo do l-deprenil diariamente por 5 dias melhorou os danos da memÃria observados apÃs a isquemia cerebral transitÃria em ratos. A droga protegeu o cÃrebro contra a hiperperoxidaÃÃo e formaÃÃo de radicais livres observados apÃs o dano isquÃmico, como diminui a atividade da caspase â 3. Pelo menos parte desses efeitos à devido ao efeito antioxidante e conseqÃentemente inibiÃÃo da ativaÃÃo da produÃÃo de radicais livres pelo l-deprenil.
The present work shows the effects of l-deprenyl (DEP, 5 and 10 mg/kg, po) on memory, as well as on rat brain free radical formation after transient cerebral ischemia (TCI). Wistar rats were anesthetized and submitted to TCI by occlusion of both carotid arteries for 20 minutes. In another experiment, animals were submitted to surgery without ischemia (sham-operated). After surgery, ischaemic rats were treated with DEP (DEP, 5 and 10 mg/kg, po) once and daily for 5 days. One group of animals was left untreated (controls). The parameters studied were, memory acquisition and memory retention, locomotor activity and tiobarbituric acid reactive substances, as an index of lipid peroxidation. After treatment all, animals were submitted to passive avoidance test, water maze test and elevated T maze test, and 24 h later sacrificed and their hippocampi and temporal cortex dissected for evaluation of lipid peroxidation and used for catalase activity determinations. The protein concentration was measured according to the method described by Lowry (1951). In another set of experiments the animals were sacrificied forty eight hours after ischemia for caspase activity evaluation. Results show that DEP significantly reversed ischaemia-induced memory deficits. l-Deprenyl treatment significantly improved memory deficits as compared to ischemic group as measured by The elevated T maze and Water maze tests. A similar result was observed on the passive avoidance test where l-deprenyl improved late but not early memory as compared to the ischemic group. Except for an increased locomotor activity observed in the group treated with 5 mg/kg, no other alteration was detected in this behavioral test. Rats submitted to transient cerebral ischemia (and without l-deprenyl) showed an increase im MDA levels in the hippocampus and the treatment with l-deprenyl (5 and 10 mg/kg) significantly reversed this effect bringing values close to those of the sham-operated controls. A similar profile was observed with nitrite levels. Rats submitted to transient cerebral ischemia show an increase in caspase activity in the hippocampus and the treatment with l-deprenil (10 mg/kg) significantly reversed this effect bringing values close to those of the sham-operated controls. Moreover catalase activity in the hippocampi was not altered by ischemia. In conclusion, the work showed a signifant protective effect of l-deprenyl on memory deficits and lipid hyperperoxidation observed after cerebral ischemia. Possibly, the drug is acting at least in part through its antioxidant and antiapoptotic activities.
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Tucker, Jessica Janice. "Predictors of Admission for Stroke or Transient Ischemic Attack Patients." ScholarWorks, 2019. https://scholarworks.waldenu.edu/dissertations/7257.
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Approximately 11% of patients diagnosed with a stroke or a transient ischemic attack are readmitted to the hospital, creating a cost burden of nearly $2 billion per year for Medicare beneficiaries. Because researchers and policy makers consider hospital readmission for patients with strokes or transient ischemic attack to be an indicator for the delivery of quality care, the Centers for Medicare and Medicaid Services has imposed financial penalties of up to 3% of a hospital's Medicare reimbursement in 1 year for excessive readmissions, potentially impacting the financial sustainability of various healthcare organizations. The ecological systems theory allows for the understanding of how microsystems, mesosystems, exosystems, macrosystems, and chronosystems impact the development, influence, and predictability characteristics of a specific population serviced in a healthcare setting. This quantitative study analyzed cross-sectional data from the 2016 National Hospital Ambulatory Care Survey, using cross-tabulations with chi-square followed by multiple regression analyses. Overall, this study addressed the gap in the existing literature by examining admission rates for patients with the diagnoses of strokes or TIA and the association between ancillary service use, insurance status, and provider level evaluation. The study concluded that few predictors that exist between the independent and dependent variables, with the exception of the amount of laboratory tests ordered. Maintaining the financial reasonability by avoiding penalties for stroke or transient ischemic attack unnecessary admission from value-based purchasing, the implication for social change is maintaining access to care for patients by avoiding hospital closures.
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Guan, Ling. "Autonomic nervous system parameters to predict the occurrence of ischemic events after transient ischemic attack or minor stroke." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/63274.
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The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate
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Haynes, Helena. "A Doctor of Nursing Practice-Led Transitions of Care Model for Stroke and Transient Ischemic Attack." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/293391.
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Background/Objectives: Gaps in care due to the movement of patients between health settings and/or practitioners, known as transitions of care (TOC), may contribute to second stroke or TIA events. The elements that impact TOC in the stroke/TIA population have not been fully elucidated. The purpose of this study is to identify key elements of a Doctor of Nursing Practice-led TOC model that could be used to develop and evaluate a TOC program for the stroke/TIA population. Design: A descriptive study was performed to 1) identify elements that may affect transitions of care using a stroke database and post-discharge phone surveys and 2) based on information from Aim 1, propose a DNP-led TOC model specific to the stroke/TIA. Setting: An urban primary stroke center in the southwest United States. Participants: All patients in the GWTG®-stroke database from May 1 - December 31st, 2012 and patients who consented at discharge from the stroke unit following a stroke or TIA. Measurements: Patient demographics including: length of stay (LOS), age, race, ethnicity, comorbidities, insurance, discharge status, thirty-day readmission rate, and follow up survey. Results: Patient data (n=276) from GWTG®-stroke database was obtained. Average LOS was 7.81 +/- 11.15 days. The majority of patients were greater than age 65 (59%); 53% relied on Medicare support; those age 50-59 (21%) were most likely to be uninsured (47%). Fifty-one percent were discharged directly home, 48% of those were referred to outpatient rehab services. Two-thirds received rehabilitation services during hospitalization. Eight patients experienced a subsequent hospital readmission; two of those had a repeat stroke event. Although patients reported understanding their discharge instructions, their perception of ongoing care was poor. Conclusion: Key elements of a TOC model specific to the stroke and TIA patient population could include: patient surveillance, comprehensive care planning, follow-up, stroke education and point of contact. Advanced practice nurses have been successful in leading such programs, and a DNP-led model providing continuity of care would support the transition of an effective model into clinical practice.
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Skogmo, Emelie, and Emelie Nyblom. "Uppföljning av patienter med Transitorisk Ischemisk Attack (TIA)- och minor stroke som medverkat i TIA-skolan på Enköpings lasarett." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-154017.
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The purpose of this study was to investigate how patients who had undergone Hallberg's TIA-school at Enköpings Lasarett rate their physical and mental health 18 months after participation. Another purpose was to examine whether they re-diagnosed with a TIA or suffered a stroke. The design of the quantitative study was longitudinal and descriptive. In the study 16 patients participated and to measure their mental and physical health the questionnaire SF36 was used. The results showed that none of the participants suffered a new TIA or stroke since participation in the TIA-school. The participants' self-rated health measured with SF36 showed the highest values in the areas of social function, emotional role function and physical role function. Which indicates a good self-rated health in these areas. Participants were asked how their physical and mental health limited them in everyday life. The majority of participants was not limited at all during the day, either physically (50%) or psychologically (62.5%). Our results demonstrate that a TIA-school like the one at Enköpings Lasarett may have long-term effects on an individual basis, but this effect can not be demonstrated in all off the patients.
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Filho, Ailton Teles Fontenele. "Efeito neuroprotetor do prÃ-condicionamento por estresse de contensÃo sobre a lesÃo induzida por breve mudanÃa subcrÃtica isquÃmica: papel dos receptores A1 da adenosina." Universidade Federal do CearÃ, 2009. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=3315.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel SuperiorO acidente vascular cerebral, doenÃa incapacitante e terceira causa de morte em paÃses desenvolvidos à caracterizada pela interrupÃÃo ou reduÃÃo do fluxo sangÃÃneo para o cÃrebro capaz de causar alteraÃÃo na funÃÃo cerebral. Sabe-se que o receptor A1 da adenosina possui um papel chave na neuroproteÃÃo devido à diminuiÃÃo da liberaÃÃo de glutamato e hiperpolarizaÃÃo neuronal. O objetivo desse trabalho foi determinar os efeitos do prÃ-condicionamento por estresse de contensÃo em ratos submetidos à isquemia cerebral transitÃria (ICT) por oclusÃo bilateral das carÃtidas e a participaÃÃo dos receptores A1 da adenosina nesse processo. Inicialmente, ratos Wistar machos, entre 200-240g, foram submetidos ao estresse de contensÃo (ST) em cilindros por 2h e imediatamente depois submetidos à ICT pela oclusÃo de ambas as artÃrias carÃtidas durante 30min. Um dos grupos dos animais foi prÃ-tratado com o antagonista do receptor A1 da adenosina, DPCPX, antes do estresse de contensÃo nas doses de 0,1mg/kg ou 1mg/kg. A temperatura retal foi monitorada e mantida a 37ÂC atravÃs de uma luz incandescente. Vinte e quatro horas depois do tÃrmino da ICT os animais foram sacrificados, tiveram seus cÃrebros dissecados, seccionados e imersos em soluÃÃo de Cloreto de 2,3,5-Trifeniltetrazol (TTC) a 1% por 30 min. para analise da viabilidade do tecido cerebral. Os testes comportamentais foram efetuados 72h apÃs a ICT e consistiram em Teste do Campo Aberto para a atividade locomotora, Labirinto em Y para a memÃria operacional ou de procedimento e Esquiva Passiva para aferiÃÃo da memÃria aversiva de curta e longa duraÃÃo. Os animais submetidos à ICT tiveram dano no tecido cerebral (FO= 10,36  0,75%; ISQ= 18,52  2,62%) alÃm de diminuiÃÃo no comportamento exploratÃrio de rearing (no de eventos: FO= 5,00 1,23; ISQ= 1,50  0,72) e dÃficit da memÃria aversiva de longa duraÃÃo (FO= 271,2  17,61s; ISQ= 108,4 67,64s). Nenhuma diferenÃa significativa foi encontrada no nÃmero de cruzamentos em Campo Aberto (FO= 15,71 2,02; ISQ= 11,00 2,13), na memÃria de procedimento (FO= 70,16  5,77; ISQ= 71,37  7,94), ou na memÃria aversiva de curta duraÃÃo (FO= 145,9  42,75; ISQ= 113,1  64,97).Os animais prÃ-condicionados por estresse tiveram uma reduÃÃo na taxa de infarto cerebral (FO= 10,36  0,75%; ISQ= 18,52  2,62%; ISQ+ST= 12,59  0,87%) e um retorno aos nÃveis normais do comportamento de rearing observado no teste do campo aberto (FO= 5,00 1,23; ISQ= 1,50 0,72; ISQ+ST= 6,091 1,443). No teste de esquiva passiva, observamos uma tendÃncia à melhora da memÃria aversiva de longa duraÃÃo (FO= 271,2  17,61s; ISQ= 108,4 67,64s; ISQ+ST= 156,1Â45,81s). Quando tratados com o DPCPX na dose de 1mg/kg, os animais tiveram um bloqueio da neuroproteÃÃo obtida com o prÃ-condicionamento (ISQ= 18,52  2,62%; ISQ+ST= 12,59  0,87%; ISQ+ST+DPCPX 1= 19,95  3,38%), aumento no nÃmero de rearings que havia sido normalizada pela contensÃo (ISQ= 1,50 0,72; ISQ+ST= 6,091 1,443; ISQ+ST+DPCPX 1= 3,20 0,90) e uma tendÃncia à reversÃo dos efeitos do prÃ-condicionamento na memÃria aversiva de longa duraÃÃo (ISQ= 108,4 67,64s; ISQ+ST= 156,1Â45,81s; ISQ+ST+DPCPX 1= 88,61 38,83s). O estresse de contensÃo conferiu neuroproteÃÃo aos animais submetidos à ICT e tal neuroproteÃÃo foi perdida pelo tratamento prÃvio com DPCPX. Esses achados apontam para a participaÃÃo do receptor A1 da adenosina na proteÃÃo conferida por estresse de contensÃo por mecanismos que ainda precisam ser esclarecidos.
Stroke,as disabling disease and as third cause death in developed countries, is characterized for the interruption of cerebral blood flow capable to cause alteration on brain functions. It is well established that the activation of A1 adenosine receptor confers neuroprotection against acute noxious brains stimuli. The aim of this study was to investigate the effects of preconditionnement by restraint stress on rats subjected to transient cerebral ischemia (TCI) and the participation of A1 receptor in this process. Firstly, Wistar male rats weighing 200-240g were exposed to immobilisation stress for 2 hours followed to TCI by occlusion of both carotid arteries for 30 minutes. Group of animals were pretreated with A1 receptor antagonist DPCPX (0,1mg/kg or 1 mg/kg. i.p.) before immobilisation stress. Retal temperature was monitored and 37ÂC were maintened during cirurgical procedure using a heating light. Infarct size was determined by TTC staining 24h after TCI and the behavioral tests were performed after 72 hours. Open field test were used to assess locomotor activity, Y-maze test for working memory and passive avoidance test to aversive short and long term memory evaluation. Our results showed that TCI caused damage on brain tissue (sham operated= 10.36 Â 0.75%; ISC= 18.52 Â 2.62%), decreased the vertical exploratory behavior (number of events: sham= 5.00 Â 1.23; ISC= 1.50 Â 0.72) and deficit on long term aversive memory (sham= 271.2 Â 17.61s; ISC= 108.4 Â 67.64s). No differences were found on the crossing behavior (sham= 15.71 Â 2.02; ISC= 11.00 Â 2.13), working memory (sham= 70.16 Â 5.77; ISC= 71.37 Â 7.94) neither short term memory (sham= 145.9 Â 42.75; ISC= 113.1 Â 64.97). The infarct volume rates on restraint stress (RS) group were significantly less than ischemic (ISC) group (sham= 10.36 Â 0.75%; ISC= 18.52 Â 2.62%; RS= 12.59 Â 0.87%) while the number of rearing were significantly higher (sham= 5.00Â 1.23; ISC= 1.50Â 0.72; RS= 6.091Â 1.443). On the passive avoidance test, restraint stress tend to impair the ischemic damage on the long term memory (sham= 271.2 Â 17.61s; ISC= 108.4 Â 67.64s; RS= 156.1 Â 45.81s). When treated with DPCPX (1mg/kg) the infarct size show an increase (ISC= 18.52 Â 2.62%; RS = 12.59 Â 0.87%; DPCPX= 19.95 Â 3.38%) suggesting a blockade of neuroprotection action achieved by restraint stress. DPCPX also decreased the number of rearing on the open field test (ISC= 1.50 Â 0.72; RS= 6.091Â 1.443; DPCPX = 3.20 Â 0.90) and tend to reverse the improvement of long term aversive memory accessed by restraint stress (ISC= 108.4 Â 67.64s; RS= 156.1 Â 45.81s; DPCPX 1= 88.61Â 38.83s). This work showed a neuroprotection of pre conditioning restraint stress against cerebral ischemia and the blockade of this action by a previously administration of DPCPX, A1 adenosine antagonist. These findings point to the involvement of the A1 adenosine receptor in the protection conferred by restraint stress by mechanisms that still need to be clarified.
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Alsadoon, Abdulaziz. "Clinical Prediction Rule for Treatment Change Based on Echocardiogram Findings in Transient Ischemic Attack and Non-Disabling Stroke." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32406.
Full textAbstract:
The goal of this study was to derive a clinical prediction rule for transient ischemic attack (TIA) and non-disabling stroke to predict a treatment change based on echocardiogram.
Methods: We conducted a cohort sub-study for TIA and non-disabling stroke patients collected over five years from 8 Emergency Departments. We compiled a list of 27 potential predictors to look for treatment change based on echocardiogram findings. We used a univariate, logistic regression and recursive partitioning analysis to develop the final prediction model.
Results: The frequency of treatment change was seen in 87 (3.1%) of 2804 cases. The final model contains six predictors: age less than 50 years old, coronary artery disease history, history of heart failure, any language deficit, posterior circulation infarct and middle cerebral artery infarct on neuroimaging.
Conclusions: We have developed a highly sensitive clinic prediction rule to guide in the use of echocardiogram in TIA and non-disabling stroke.
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Graber, Taylor. "Imaging for Chest Pain Assessment: An Algorithmic Approach Using Noninvasive Modalities to Define Medical vs. Interventional Treatment." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/623439.
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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.To analyze the roles of CCTA, MPI, and CC to formulate a sequential clinical algorithm to use in patients with chest pain, risk factors for CAD, and an abnormal EKG. The goals of the study are to streamline and refine workup, to decrease radiation exposure to patients, and to contain costs. 39 patients underwent CCTA, MPI, and CC within 30 months of each other. CCTA was used to categorize mild, moderate, or severe CAD. MPI used SSS, SDS, TID, and formal reading to define mild, moderate, or severe physiologic ischemia. CC and coronary intervention cine films were analyzed to define and treat anatomical CAD medically or by intervention. Results: There was strong correlation between CCTA, CC, and treatment type (p<0.0001). CCTA was able to stratify all patients with mild or severe ischemia to appropriate treatment groups, and to reduce the need for MPI. With moderate ischemia from CCTA, the additional use of MPI could have reduced the need for 16/18 (89%) patients who underwent CC to undergo further testing. No patients with mild or moderate CAD by CCTA, followed by mild to moderate physiologic ischemia by MPI, needed CC or intervention. 37/39 patients (95%) could have avoided one or more tests using our algorithm. CCTA followed by MPI may be used in symptomatic patients with risk factors for CAD and an abnormal EKG to stratify mild and moderate CAD, and to thereby avoid cardiac catheterization. Our algorithm could lead to savings in healthcare expenditures, save patients from unnecessary invasive procedures, decrease radiation exposure, and total cost.
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Edwards, Jodi Dawn. "The utilization and timing of neuroimaging and the role of neurophysiological techniques in the diagnostic evaluation of transient ischemic attack." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46437.
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Background: Transient ischemic attack (TIA) is an episode of transient focal neurological deficit with an ischemic vascular cause. Neuroimaging can detect ischemia, determine etiologic mechanisms, and identify stroke risk after TIA, and early assessment reduces stroke risk. Despite guidelines recommending imaging, Canadian hospital-based studies have reported underutilization and delays in the use of imaging procedures after TIA. However, as many TIA patients are not evaluated in hospital, population-based studies are required to determine whether imaging use increased after guideline implementation and characterize trends in imaging timing after TIA. Although administrative databases enable population-based studies of procedure utilization and timing, previous studies have been restricted to hospital-based cohorts, as physician claims data lack validity for TIA ascertainment. Further, as many patients are not evaluated acutely, the assessment of alternative techniques may inform the subacute effects of transient ischemia.
Methods: In Chapter 2, sensitivity, specificity, and positive predictive value were used to evaluate the validity of multiple algorithms for TIA case ascertainment from physician claims data. Chapters 3 and 4 provided estimates of imaging utilization before and after guideline implementation and trends in imaging timing in population-based TIA cohorts. Chapter 5 used transcranial magnetic stimulation to measure thresholds for intracortical inhibition and facilitation subacutely after TIA and assessed the relationship of these thresholds with clinical features of TIA.
Summary of Findings: The algorithms for TIA ascertainment using physicians claims data evaluated in Chapter 2 were not valid, informing the case definition for subsequent population-based analyses. Chapter 3 showed increases in neuroimaging use but overall poor utilization after the implementation of practice guidelines, with differences by modality and diagnostic setting. In Chapter 4, no changes in imaging timing after TIA were observed over the study period. In Chapter 5, alterations in intracortical thresholds after TIA on transcranial magnetic stimulation were observed and correlated with clinical risk scores.
Conclusions: This dissertation contributes new knowledge of population-based practices of the use and timing of neuroimaging after TIA and has implications for future research examining barriers for timely access to imaging techniques and the utility of alternative techniques in the diagnostic evaluation of individuals with TIA
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Irewall, Anna-Lotta. "Recurrent events and secondary prevention after acute cerebrovascular disease." Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-130505.
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Background Patients who experience a stroke or transient ischemic attack (TIA) are at high risk of recurrent stroke, but little is known about temporal trends in unselected populations. Reports of low adherence to recommended treatments indicate a need for enhanced secondary preventive follow-up to achieve the full potential of evidence-based treatments. In addition, socioeconomic factors have been associated with poor health outcomes in a variety of contexts. Therefore, it is important to assess the implementation and results of secondary prevention in different socioeconomic groups. Aims The aims of this thesis were to assess temporal trends in ischemic stroke recurrence and evaluate the implementation and results of a nurse-led, telephone-based follow-up program to improve blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C) levels after stroke/TIA. Methods In study I, we collected baseline data for unique patients with an ischemic stroke event between 1998 and 2009 (n=196 765) from the Swedish Stroke Register (Riksstroke). Recurrent ischemic stroke events within 1 year were collected from the Swedish National Inpatient Register (IPR) and the cumulative incidence was compared between four time periods using the Kaplan-Meier survival analysis and the logrank test. Implementation (study II) and 1-year results (study III-IV) for the secondary preventive follow-up were studied in the NAILED (Nurse-based Age-independent Intervention to Limit Evolution of Disease) study. Between 1 Jan 2010 and 31 Dec 2013, the baseline characteristics of consecutive patients admitted to Östersund Hospital for acute stroke or TIA were collected prospectively (n=1776). Consenting patients in a condition permitting telephone-based follow-up were randomized to nurse-led, telephone-based follow-up or follow-up according to usual care. Follow-up was cunducted at 1 and 12 months after discharge and the intervention included BP and LDL-C measurements, titration of medication, and lifestyle counseling. In study II, we analyzed factors associated with non-participation in the randomized phase of the NAILED study, including association with education level. In addition, we compared the 1-year prognosis in terms of cumulative survival between participants and non-participants. In study III, we compared differences in BP and LDL-C levels between the intervention and control groups during the first year of follow-up and, in study IV, in relation to level of education (low, ≤10 years; high, >10 years). Results The cumulative 1-year incidence of recurrent ischemic stroke decreased from 15.0% to 12.0%. Among surviving stroke and TIA patients, 53.1% were included for randomization, 35.7% were excluded mainly due to physical or cognitive disability, and 11.2% declined participation in the randomized phase. A low level of education was independently associated with exclusion, as well as the patient’s decision to abstain from randomization. Excluded patients had a more than 12-times higher risk of death within 1 year than patients who were randomized. After 1 year of follow-up, the mean systolic BP, diastolic BP, and LDL-C levels were 3.3 mmHg (95% CI 0.3 to 6.3), 2.3 mmHg (95% CI 0.5 to 4.2), and 0.3 mmol/L (95% CI 0.1 to 0.4) lower in the intervention group than among controls. Among participants with values above the treatment goal at baseline, the differences in systolic BP and LDL-C levels were more pronounced (8.0 mmHg, 95% CI 4.0 to 12.1; 0.6 mmol/L, 95% CI 0.4 to 0.9). In the intervention group, participants with a low level of education achieved similar or larger improvements in BP and LDL-C than participants with a high level of education. In the control group, BP remained unaltered and the LDL-C levels increased among participants with a low level of education. Conclusion The 1-year risk of ischemic stroke recurrence decreased in Sweden between 1998 and 2010. Nurse-led, telephone-based secondary preventive follow-up is feasible in just over half of the survivors of acute stroke and TIA and achieve better than usual care in terms of BP and LDL-C levels, and equality in BP improvements across groups defined by education level. However, a large proportion of stroke survivors are in a general condition precluding this form of follow-up, and their prognosis in terms of 1-year survival is poor. Patients with a low education level are over-represented within this group and among patients declining randomization for secondary preventive follow-up.
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Barton, Andrew Charles. "Towards the development of an electrochemical immunosensor for the identification of transient ischemic attack via the labeless detection of biomedical markers." Thesis, Cranfield University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443734.
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Ingvoldstad, Christopher T. "Transient Ischemic Attack (tia) Guideline Knowledge And Perceived Barriers To Implementation Amongst Emergency Department Health Care Providers In A Rural State." ScholarWorks @ UVM, 2015. http://scholarworks.uvm.edu/graddis/335.
Full textAbstract:
Transient Ischemic Attack (TIA) is a prominent risk factor for subsequent stroke, and its associated morbidity, mortality, and health care costs. Studies have demonstrated up to 80% reductions in subsequent stroke rate with prompt, optimized protocols for rapid TIA evaluation and treatment. National Stroke Association (NSA) and American Heart Association (AHA) guidelines have recommended institution of protocols assuring timely completion of the recommended testing, and evaluation by a stroke expert within 48 hours. However, limited literature exists on the implementation of guideline-based care in rural regions, and the few studies related to TIA suggest that barriers including difficulty accessing services and poorly updated TIA knowledge amongst rural, non-neurologist providers exist despite national guidelines.
Behavior change theories have suggested that evaluating factors hindering or motivating behavior change may aid in tailoring implementation of guideline-based practices. This descriptive study sought to understand ED health care providers' perceived barriers to implementation of NSA/AHA TIA guidelines in a rural state. All healthcare providers in each of the state's emergency departments were invited by email to complete an online anonymous survey assessing knowledge of present TIA guidelines and perceived barriers to implementation of these guidelines in their practice setting using a modified Barriers and Facilitators Assessment Instrument (BFAI). After completing the knowledge based questions, respondents were presented a brief educational overview of the guidelines to ensure adequate familiarity with the TIA guidelines to complete the BFAI.
Thirty-nine respondents completed the survey. Twenty-seven worked at regional or academic medical centers, and 12 worked at critical access hospitals representing the more rural regions of the state. Consistent with prior work, the most notable finding of this study was a low awareness of the present TIA guidelines amongst ED providers, with none of the survey respondents correctly identifying all items consistent with the evaluation guidelines for TIA. In addition to a low awareness of the guidelines, a number of perceived barriers to implementation were identified, which may inform efforts at implementation, and/or offer a model for similar barrier assessment elsewhere.
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Weih, Markus Karl. "Einfluß vontransitorisch-ischämischen Attacken auf darauf folgenden ischämische Hirninfarkte." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/13765.
Full textAbstract:
Ischämietoleranz bezeichnet das Phänomen, dass ein kurzer ischämischer, metabolischer oder physikalischer Stimulus das Gehirn paradoxerweise "resistent" macht gegenüber einer darauffolgenden, längerdauernden Ischämie. In einer retrospektiven Studie versuchten wir die Hypothese zu untermauern, dass transiente ischämische Attacken (als kurzdauernde ischämische Stimuli) vor einem Infarkt (prodromale TIAs) protektiv sind gegen eine nachfolgende zerebrale Ischämie. Es zeigte sich dabei, dass Patienten mit prodromalen TIAs ein geringeres Defizit und einen günstigeren Verlauf zeigten und im CT seltener Infarktfrühzeichen hatten. Somit könnten transiente ischämische Attacken, vor einem Schlaganfall, analog zu der Situation am Herzen und wie in zahlreichen in vivo Modellen gezeigt, ein klinisches Korrelat zur hypoxischen Präkonditionierung darstellen. Im experimentellen Teil der vorliegenden Arbeit wird gezeigt, dass sich hypoxische Präkonditionierung in vitro in neuronalen Kulturen modellieren lässt. Eine kurzzeitige Sauerstoff-Glucose-Deprivation (OGD) 1-3 Tage vor einer längeren OGD führt zu einem signifikanten Schutz von Neuronen, bis zu 90%. Hypoxietoleranz kann auch durch andere metabolische Stimuli, wie Inhibition von Atmungskettenenzymen durch 3-NPA im gleichen Zeitrahmen simuliert werden. Eine genaue Kenntnis der endogenen Neuroprotektion durch Ischämietoleranz könnte in Zukunft helfen, den Schaden durch ischämische Infarkte und ischämische Enzephalopathien zu minimieren.Ischemic tolerance is a phenomenon where a brief episode of ischemia renders the brain resistant against a subsequent, longerlasting ischemic event. In a retrospective study we tested the hypothesis that transient ischemic attacks (as brief ischemic stimuli) before cerebral ischemia (prodromal TIA's) may have a protective effect. Here we show that patients with prodromal TIA's have less severe neurologic impairment, a better clinical course and have less early infarct signs. Therefore we siggest that TIA's, before stroke could represent a clinical correlate to hypoxic preconditioning, as shown in the heart. Experimentally we were able to model hypoxic preconditioning in vitro using neuronal cultures. Brief oxygen-glucose deprivation (OGD) 1-3 days before longer lasting OGD protects neurons, up to 90%. Hypoxic tolerance was also simulated by metabolic stimuli like inhibition of the respiratory chain by 3-NPA. Increasing knowledge of this endogenous neuroprotection by ischemic tolerance might help to minimize neuronal damage following ischemic strokes and hypoxic encephalopathy.
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Neves, Celso Ricardo Bregalda. "Resultados em longo prazo do tratamento de pacientes com suboclusão carotídea com sinal do barbante." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-23082017-113800/.
Full textAbstract:
INTRODUÇÃO: Pacientes com suboclusão da carótida com sinal do barbante podem ser incorretamente classificados como portadores de oclusão total, por meio de exames não invasivos. A história natural e o tratamento desta condição são controversos na literatura médica. OBJETIVOS: 1. Avaliar a evolução, em longo prazo, de pacientes com suboclusão carotídea com sinal do barbante assintomáticos, quando submetidos a tratamento clínico exclusivo; 2. Avaliar os resultados imediatos e em longo prazo do tratamento intervencionista de pacientes com suboclusão carotídea com sinal do barbante sintomáticos. MÉTODOS: Foram inclusos 195 pacientes que apresentavam ultrassonografia Doppler convencional prévia com oclusão completa de, pelo menos, uma das carótidas internas, totalizando 204 carótidas ocluídas (9 oclusões bilaterais). Após a realização de angiotomografia computadorizada e ultrassonografia com contraste de microbolhas, 46 pacientes (46 carótidas) apresentavam, na realidade, placas suboclusivas com fluxo filiforme na carótida interna, sendo acompanhados prospectivamente. Desses, 22 eram assintomáticos e foram tratados clinicamente; e 24 eram sintomáticos e foram submetidos à tentativa de angioplastia com implante de stent. O seguimento foi executado com consultas periódicas e ultrassonografia Doppler realizadas com 14 dias, 3 meses, 6 meses e, posteriormente, a cada 12 meses, após a intervenção. Angiotomografia computadorizada era realizada em até 2 meses após o procedimento. RESULTADOS: O seguimento médio foi de 63,9 meses. Os pacientes assintomáticos tiveram sobrevida cumulativa de 81,8%, sem quaisquer eventos neurológicos em 60 meses. Os pacientes sintomáticos tiveram taxa de sucesso no implante de stent de 79,1% (19 de 24). Não houve isquemia miocárdica ou morte em até 30 dias após a cirurgia. Um dos pacientes com sucesso no implante do stent apresentou paresia de membro superior com recuperação em 3 meses, portanto, a taxa de desfecho primário (acidente vascular cerebral, infarto agudo do miocárdio e morte), foi 4,2%. A taxa de perviedade para os procedimentos com sucesso foi de 89,4%, em 60 meses. Os pacientes sintomáticos com sucesso na angioplastia tiveram taxa de sobrevida livre de eventos neurológicos de 84,2%, em 60 meses, com sobrevida total de 89,4% nesse período. Todos os 5 pacientes sintomáticos nos quais a angioplastia não foi factível evoluíram com eventos neurológicos no acompanhamento, com sobrevida de 40,0%, em 60 meses. CONCLUSÕES: 1. Pacientes com suboclusão carotídea com sinal do barbante assintomáticos são favorecidos, em longo prazo, pelo tratamento medicamentoso exclusivo. 2. Pacientes com suboclusão carotídea com sinal do barbante sintomáticos beneficiam-se, em longo prazo, da angioplastia com implante de stentINTRODUCTION: Patients with carotid near-occlusion with string sign may be incorrectly classified as total occlusion through non-invasive tests. The natural history and treatment of such condition are controversial in medical literature. OBJECTIVES: 1. Monitor the natural long-term outcome of asymptomatic patients with carotid near-occlusion with string sign treated medically; 2. Evaluate the short and long-term results of interventional treatment in symptomatic patients with carotid near-occlusion with string sign. METHODS: 195 patients, who had previous Doppler ultrasound with complete occlusion of at least one internal carotid, were included. 9 had bilateral occlusion, totaling 204 occluded arteries. After conducting computed tomography angiography and contrast-enhanced ultrasound, 46 patients (46 carotid arteries) had near-occlusion with string sign and were prospectively analyzed. Asymptomatic patients (22) received best medical therapy while symptomatic individuals (24) were referred to carotid artery stenting. After the procedure follow-up was made with clinical surveillance and Doppler ultrasound performed at 14 days, 3 months, 6 months and then every 12 months thereafter. A computed tomographic angiography was performed within 2 months. RESULTS: Mean follow-up was of 63.9 months. Asymptomatic patients had a cumulative survival rate of 81.8%, in 60 months, without any neurologic events. Symptomatic patients had intraoperative success rate of 79.1% (19/24 procedures). No intraoperative or 30-day events of myocardial infarction or death occurred. One of the successful carotid artery stenting patients evolved with a mild upper limb monoparesis, with total recovery in 3 months. The rate of primary end point (stroke, myocardial infarction or death) was 4.2%. Cumulative patency rate for the 19 successful procedures was 89.4%, in 60 months. Symptomatic individuals with successful angioplasty had a neurologic event-free survival rate of 84.2%, in 60 months, with overall survival rate of 89.4%, in the same period. All 5 symptomatic patients to whom string angioplasty procedure was not feasible evolved with neurological events, with a cumulative survival rate of 40.0%, in 60 months. CONCLUSIONS: 1. Asymptomatic patients with carotid near-occlusion with string sign evolve well with best medical therapy in long-term follow-up; 2. Symptomatic patients with carotid near-occlusion with string sign have good outcomes with carotid artery stenting in long-term follow-up
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Boyle, Brian William. "Evaluation of the Extent to Which Massachusetts General Hospital Emergency Department Triage of Transient Ischemic Attack Patients Aligns With Virtual TIA Clinic Protocol: A Pilot Cross-Sectional Medical Record-Review to Inform Care Redesign Efforts." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295888.
Full textAbstract:
The Virtual TIA Clinic Protocol was developed as part of the Partners Care Redesign
effort to reduce costs and increase quality in the care of patients presenting with symptoms of
transient ischemic attack, through risk stratification, triage, and follow-up based on factors
including the ABCD2 score. The work presented here is a small N, pilot cross-sectional study
which compares actual practice in the MGH ED to what the protocol would suggest, in an effort
both to validate the components of the protocol and to better understand further opportunities to
create value in the care of this patient population. It was found that actual practice resulted in
triage patterns similar to what would have been dictated by the protocol in question. This
suggests that full implementation of the protocol – with the costs associated – may not be
justified. Further work could involve refinement of the protocol to achieve the desired effect on
triage, with future, similar studies made more effective by a code to designate patients in whom
TIA is possible but who do not ultimately receive the code for such under the current
documentation system.
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Israelsson, Larsen Hanna. "Comorbidity and vascular risk factors associated with idiopathic normal pressure hydrocephalus : the INPH-CRasH Study." Doctoral thesis, Umeå universitet, Institutionen för farmakologi och klinisk neurovetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-120175.
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Idiopathic normal pressure hydrocephalus (INPH) is a dementia treatable by insertion of a cerebrospinal fluid shunt. It has been suggested that INPH has similar pathophysiological mechanisms as cerebrovascular disease, but the vascular risk factor (VRF) profile of INPH patients has not been assessed using a modern epidemiological approach. The cognitive symptoms of INPH resemble the symptoms of depression, but the prevalence of depression among INPH patients is unknown. In addition, few studies investigate the impact of shunting on the quality of life (QoL), and no study has investigated the impact of comorbidity on QoL in INPH patients. The objective of this dissertation was to present the VRF profile of INPH and to investigate the hypothesis that INPH may be a subgroup of vascular dementia. Additional objectives were to assess the prevalence of depression in INPH patients and to investigate the impact of shunting and comorbidities on QoL in INPH. In the first cohort, the prevalence of possible INPH was assessed through clinical and radiological examinations in patients with a transient ischemic attack (TIA), consecutively admitted to the same hospital during 2006-2008. In the second cohort, VRFs, vascular disease and QoL were analysed in INPH patients consecutively shunted 2008-2010 in five out of six neurosurgical centres in Sweden. Patients remaining after inclusion (n=176, within the age-span 60-85 years and not having dementia) were compared to population-based age- and gender-matched controls (n=368, same inclusion criteria as for the INPH patients). Assessed VRFs were: hypertension, diabetes, obesity, hyperlipidemia, psychosocial factors (stress and depression), smoking, alcohol intake, physical activity and, dietary pattern. Cardiovascular, cerebrovascular and peripheral vascular disease as well as QoL were also assessed. Parameters were assessed through questionnaires, clinical examinations, measurements, ECG and, blood samples. In the first cohort, 4% of the TIA patients had clinically and radiologically verified INPH. In the second cohort, VRFs were overrepresented among the INPH patients compared with the controls. The VRFs independently associated with INPH were: hyperlipidemia (Odds ratio (OR): 2.4, 95%CI: 1.4-4.0), diabetes (OR: 2.2, 95%CI: 1.2-3.9), obesity (OR: 5.4, 95%CI: 2.5-11.8) and, psychosocial factors (OR: 5.3, 95%CI: 3.2-8.9). When adding the VRFs that were overrepresented in INPH, although not independently (physical inactivity and hypertension), these six VRFs accounted for 24% of the INPH cases in the elderly population (population attributable risk %: 24). Depression was overrepresented in shunted INPH patients compared to the controls (46% vs. 13%, p<0.001) and the main predictor for low QoL was a coexisting depression (p<0.001). In conclusion, the results of the INPH-CRasH study are consistent with a vascular pathophysiological component of INPH and indicate that INPH may be subgroup of vascular dementia. In clinical care and research, a complete risk factor analysis as well as screening for depression and a measurement for quality of life should be included in the work-up of INPH patients. The effect of targeted interventions against modifiable VRFs and anti-depressant treatment in INPH patients should be evaluated.Idiopatisk normaltryckshydrocefalus (INPH, från engelskans ”idiopathic normal pressure hydrocephalus”) är en neurokirurgiskt behandlingsbar demens. Behandlingen är att operera in en shunt som dränerar cerebrospinalvätska från ventriklarna. Det har föreslagits att INPH skulle kunna orsakas av liknande patofysiologiska mekanismer som vid cerebrovaskulär sjukdom, men den vaskulära riskfaktorprofilen hos INPH-patienter har aldrig undersökts i en modern epidemiologisk studie. De kognitiva symtomen vid INPH påminner om symtomen vid depression, men prevalensen av depression hos INPH-patienter är okänd. Få studier undersöker hur shuntning påverkar livskvalitet och ingen studie har undersökt hur komorbiditet påverkar livskvaliteten vid INPH. Syftet med den här avhandlingen var att undersöka den vaskulära riskfaktorprofilen hos INPH-patienter samt att utforska hypotesen att INPH skulle kunna vara en undergrupp till vaskulär demens. Ytterligare ett syfte med avhandlingen var att undersöka hur många INPH-patienter som har depression samt undersöka hur shunting och komorbiditet påverkar livskvalitet vid INPH. I den första kohorten undersöktes kliniska och radiologiska fynd som tydde på INPH hos de patienter som blivit diagnostiserade med en TIA (från engelskans: transient ischemic attack) 2006-2008 på Norrlands Universitetssjukhus i Umeå. I den andra kohorten undersöktes konsekutivt shuntade INPH-patienter 2008-2010 från fem av sex neurokirurgiska kliniker i Sverige. De patienter som inkluderades i studien (n=176, ålder: 60-85 år, ej dementa) jämfördes med köns- och åldersmatchade kontroller från normalpopulationen (n=368, samma inklusionskriterier som för INPH-patienterna). De riskfaktorer som undersöktes var: hypertension, hyperlipidemi, diabetes, fetma, psykosociala faktorer (stress och depression), rökning, alkohol, fysisk aktivitet och diet. Även kardiovaskulära och cerebrovaskulära sjukdomar undersöktes, liksom perifer vaskulär sjukdom samt livskvalitet. Datainsamling skedde genom frågeformulär, kliniska undersökningar, mätningar, EKG och blodprov. I den första kohorten hade 4% av TIA-patienterna kliniskt och radiologiskt verifierad INPH. I den andra kohorten var vaskulära riskfaktorer överrepresenterade hos INPH-patienterna jämfört med iv normalpopulationen. Hyperlipidemi (OR: 2.4, 95%CI: 1.4-4.0), diabetes (OR: 2.2, 95%CI: 1.2-3.9), fetma (OR: 5.4, 95%CI: 2.5-11.8) och psykosociala faktorer (OR: 5.3, 95%CI: 3.2-8.9) var associerade med INPH oberoende av kön, ålder och de andra riskfaktorerna. Hypertension och fysisk inaktivitet var också associerade med INPH, dock inte oberoende av övriga riskfaktorer. Sammanlagd PAR% (från engelskans: population attributable risk %) för de här sex riskfaktorerna var 24%. INPH-patienterna hade depression i högre utsträckning än kontrollerna (46% vs. 13%, p<0.001), och depression var den viktigaste prediktorn för låg livskvalitet. Resultaten tyder på att vaskulär sjukdom och vaskulära riskfaktorer är involverade i den patofysiologiska mekanismen vid INPH. INPH kan vara en undergrupp till vaskulär demens. En fullständig riskfaktoranalys och screening för depression bör ingå i den preoperativa utvärderingen såväl som i forskning på INPH-patienter, och ett mått på livskvalitet bör införas. Effekten av riktade insatser mot såväl vaskulära riskfaktorer som depression vid INPH bör utvärderas.
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Muus, Ingrid. "Helbredsrelateret livskvalitet efter apopleks : Validering og anvendelse af SSQOL-DK, et diagnosespecifikt instrument til måling af helbredsrelateret livskvalitet blandt danske apopleksipatienter." Doctoral thesis, Nordic School of Public Health NHV, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:norden:org:diva-3500.
Full textAbstract:
Sammenfatning Baggrund og formål: Apopleksisygdommen er ansvarlig for flest tilfælde af invalidering blandt voksne i eget hjem. I Danmark alene lever godt 50.000 mennesker med følgerne efter apopleksi. En følge kan være reduceret evne til at kommunikere, afasi. Forebyggelse kan reducere antallet af nye tilfælde og følgerne efter sygdommen. Livskvalitet ved kronisk sygdom har voksende bevågenhed. Rehabilitering medvirker til at patienten kan blive fysisk, psykisk og socialt fungerende på et niveau, men sygdommens indvirken på oplevelsen af helbredsrelateret livskvalitet er i Danmark ikke undersøgt med sygdomsspecifikke instrumenter. Patienter med afasi udelukkes som regel fra undersøgelser, der kræver intakt tale og forståelse. Afhandlingens overordnede mål er at tilvejebringe et instrument, som kan anvendes til at måle helbredsrelateret livskvalitet efter apopleksi inkl. afasi. Metode og materiale: Afhandlingen har en kvantitativ tilgang. Et nordamerikansk instrument, Stroke Specific Quality of Life Scale, version 2.0, SSQOL © (copyright Linda S. Williams), er blevet oversat og kulturelt bearbejdet til dansk i overensstemmelse med anerkendt systematik i studie I. Instrumentet dækker med 49 items 12 domæner med fysisk, socialt og mentalt fokus samt 13 items, der dækker en vurdering af domænerne og livskvaliteten sammenlignet med før apopleksien. Instrumentets psykometriske egenskaber er blevet testet ved hjælp af tre studiepopulationer rekrutteret dels retrospektivt, dels konsekutivt. I studie II blev reliabilitet og validitet undersøgt, og i studie III responsivitet og sensitivitet. Afprøvningerne er foretaget med referenceformularer som eksterne kriterier i form af etablerede generiske skalaer. I studie IV er afprøvet en proxy-version tiltænkt patienter, som er ude af stand til selv at udfylde skemaet eller som ikke er i stand til at kommunikere tilstrækkeligt. Afprøvningen blev udført af en nærtstående udpeget af patienten. I studie V blev en gruppe let ramte patienter beskrevet, og variabler med betydningsfuld sammenhæng med oplevelsen af forringet helbredsrelateret livskvalitet blev undersøgt. Data er blevet testet ved hjælp af gennemsnit og standarddeviationer, median og range, proportioner, korrelationer og logistisk regression. Resultater: Den danske version af SSQOL, SSQOL-DK, har god face- og indholdsvaliditet. Det udfyldes på 10-20 minutter. Stabilitet, undersøgt med test-retest metode, viste korrelationer i området rs 0.65-0.99. Intern konsistens undersøgt med Cronbach’s alfa viste værdier i områderne 0.81-0.94 i studie II, 0.75-0.96 i studie III og 0.64-0.87 i studie V. Der blev set en ceiling effekt, 24-52%, men beskeden floor effekt. Begrebsvaliditet viste moderat delte varianser med de eksterne kriterier, r2 0.03-0.62. Konvergent validitet var (r) > 0.40 med undtagelse af et enkelt item. SSQOL-DK var i stand til at klassificere retning af ændring i livskvalitet over tid i overensstemmelse med eksterne kriterier i 43-58 % af tilfældene. Proxy-versionen viste god overensstemmelse mellem patient- og proxy data. I en gruppe af let ramte patienter med apopleksi og transcerebral iskæmi, TCI, et år efter sygdommen vurderede 57 % deres livskvalitet som uændret i forhold til før apopleksien. Det mandlige køn (OR 3.77), erhvervsaktivitet (OR 2.84), og lavere scores på domænerne Mood og Work ved tre måneder var covariater, som var signifikant relateret til sandsynligheden for at vurdere livskvaliteten forringet efter sygdommen. Konklusion: Der foreligger nu et dansksproget instrument, SSQOL-DK, som har demonstreret tilfredsstillende reliabilitet og validitet, og som kan anvendes på gruppeniveau til dansktalende patienter med let til moderat apopleksi. Apopleksipatienten med større kommunikationsproblemer har dog stadig begrænsede muligheder med dette instrument, idet de foreliggende resultater fra proxy-afprøvningen fordrer yderligere undersøgelse af datas validitetAbstract Background and aim: Stroke is most frequently the cause of adult disability. In Denmark more than 50.000 people suffer from the sequels of stroke. One of them may be aphasia, i.e. reduced ability to communicate. Primary and secondary prevention may reduce the incidence and the severity of stroke. The interest in quality of life with a chronic disease is increasing. Rehabilitation efforts are targeted for physical, mental and social function but the impact on health related quality of life after stroke has not been studied with stroke specific instruments. Aphasic patients are normally excluded from studies where communicative skills are required. The aim of this thesis is to develop an instrument suitable for measuring health related quality of life after stroke. Methods and material: The design of the thesis is quantitative. In study I Stroke Specific Quality of Life Scale, version 2.0, SSQOL © (copyright Linda S. Williams), an American instrument recently developed, was translated and culturally adapted to Danish according to established guidelines. With 49 items SSQOL covers 12 domains comprising physical and mental issues. Thirteen items covers an appraisal of each domain compared to pre stroke status and overall quality of life. Psychometric properties was examined by studying three samples of stroke survivors. Study II and III examined reliability, validity and responsiveness. Established generic scales were used as external criteria. Study IV tested a proxy-version meant for stroke patients with language impairment or patients who are unable to fill in a questionnaire. The patients chose the proxies. Study V provided health related quality of life in a group of mildly affected patients after stroke or transient ischemic attack, TIA. Significant covariates with deteriorated health related quality of life were studied. Data were analyzed with mean and standard deviations, median and range, proportions correlations and logistic regression. Results: The Danish version of SSQOL, SSQOL-DK, showed good face- and content validity. It can be completed in less than 25 minutes. Test-retest showed correlations rs 0.65-0.99. Internal consistency showed Cronbach’s alpha from 0.81-0.94 in study II, 0.75-0.96 in study III and 0.64-0.87 in study V. Ceiling effect was 24-52%, floor-effect was modest. Construct validity showed shared variance with external criteria, r2 0.03-0.62. Convergent validity showed (r) >0.40 for 48 out of 49 items. SSQOL-DK classified direction of change in over all quality of life concordantly from 43-58% with external criteria. The agreement between patient- and proxy data was good. Fifty seven (57) percent of mildly affected patients after stroke or TIA rated their overall quality of life unchanged one year after stroke compared to pre stroke status. In the regression model male sex OR 3.77), working outside home (OR 2.84), and less than 5.00 (maximum score) on the domains Mood and Work/productivity at three months were significant predictors for rating over all quality of life deteriorated at 12 months. Conclusion: The SSQOL-DK has demonstrated satisfactory reliability and validity and can be used on group level measuring health related quality of life among Danish survivors after mild to moderate stroke and TIA. Stroke survivors with severe communication problems are still limited as validity of the proxy data should be further tested
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Svetlana, Ružička Kaloci. "Procena značaja cerebralnih mikroembolusa u akutnom ishemijskom cerebrovaskularnom događaju." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2015. http://www.cris.uns.ac.rs/record.jsf?recordId=94481&source=NDLTD&language=en.
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Otkrivanje embolusa u cerebralnoj cirkulaciji na egzaktan način moguće je samo upotrebom transkranijalnog doplera. Istraživanje je obuhvatilo 150 ispitanika, obolelih od akutnog ishemijskog cerebrovaskularnog događaja (ishemijskog moždanog udara i tranzitornog ishemijskog ataka) u zoni vaskularizacije a. cerebri medie (ACM), a lečenih na Klinici za neurologiju, Kliničkog centra Vojvodine. Ciljevi istraživanja su obuhvatili određivanje prevalence i frekvence MES kod bolesnika sa akutnim ishemijskim cerebrovaskularnim događajem (TIA, IMU) tokom serijskog monitoringa, utvrđivanje povezanost pojave MES u odnosu na etiologiju ishemijske epizode, procenjivanje efekata terapije (antiagregacione i antikoagulantne) na pojavu MES tokom serijskog monitoringa, i utvrđivanje prediktivnog značaja MES na dalji tok bolesti tj, rani povratni embolizam unutra tri meseca. Utvrdili smo da se mikroembolusi kao markeri aktivne embolizacije mogu registrovati primenom transkranijalnog doplera u akutnoj fazi moždanog udara u određenoj meri. U ispitivanom uzorku metodom transkranijalne detekcije kod 52 (34,7%) bolesnika je registrovana pojava cerebralnih mikroembolusa. Ovi ispitanici su činili MES (+) grupu pacijenata. Kod 98 (65,3%) bolesnika nisu registrovani ES, oni su činili MES (-) grupu pacijenata. Detekcija je vršena u prvih 72h od vremena nastanka IMU ili TIA. Zaključili smo da se serijskim monitoringom registruje smanjenje prevalence i frekvence embolijskih signala. Utvrdili smo da su starija životna dob, hipertenzija i dijabetes statistički značajno povezani sa pojavom mikroembolusnih signala. Najveća zastupljenost mikroembolusa registrovana je u aterotrombotičnom podtipu ishemijskog moždanog udara. Utvrđen je prediktivni značaj aterosklerotske bolesti velikih krvnih sudova na pojavu MES. Registrovana je statistički značajno češća pojava MES kod simptomatske karotidne stenoze, visokog stepena (70-90%), neravne i ulcerisane površine plaka. Nije utvrđena statistički značajna povezanost pojave MES, kliničkih manifestacija bolesti i neuroradiološkog nalaza. Nije registrovan uticaj antitrombotičke terapije na pojavu mikroembolusnih signala. Zabeležena je veća stopa recidiva IMU i TIA kod bolesnika sa registrovanim cerebralnim mikroembolusima. Utvrđen je prediktivni značaj MES na pojavu recidiva IMU ali ne i prediktivni značaj na pojavu letalnog ishoda.Detection of emboli in the cerebral circulation to the exact way it is possible only by using transcranial doppler. The study included 150 patients of acute ischemic cerebrovascular events (ischemic stroke and TIA) in a zone of vascularization a. cerebri media (ACM), and treated at the Clinic of Neurology, Clinical Center of Vojvodina Research objectives included the determination of the prevalence and frequency of MES in patients with acute ischemic cerebrovascular accident (TIA, IMU) during serial monitoring, establishing the link between the appearance MES in relation to the etiology of ischemic episodes, assessing the effects of therapy(antiplatelet and anticoagulant) on the occurrence of MES during serial monitoring and determine the predictive value MES in the further course of the disease, ie. return early embolism within three months. We have found that microemboli as markers of active embolization can register by using transcranial Doppler in the acute phase of stroke in certain extent. In the examined sample using transcranial detection with 52 (34.7%) patients the occurrence of cerebral microemboli is registered. These respondents are accounted for MES (+) group of patients. With 98 patients (65.3%) is not registered EC, they account for MES (-) group of patients. Detection was performed during 72 hours from the time of occurrence of ischemic stroke or TIA. We concluded that serial monitoring registers decrease in prevalence and frequency of embolic signals. We found that older age, hypertension, and diabetes are significantly associated with the appearance of microembolic signals. The highest incidence of microemboli was registered in atherothrombotic ischemic stroke subtype. It is determined the predictive significance of atherosclerotic disease of large blood vessels on the occurrence of MES. More common MES is significantly registered with symptomatic carotid stenosis, greater degree (70-90%), uneven surfaces and ulcerated plaque. There was no statistically significant correlation between the occurrence of MES, clinical manifestations and neuroradiological findings. It is not registered impact of antithrombotic therapy on the incidence of microembolic signals. We are noticed thet the higher rate of recurrence of ischemic stroke and TIA patients with cerebral microemboli is registered. The predictive significance of MES in recurrence of ischemic stroke is determined, but not predictive significance of the occurrence of a lethal outcome.
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Barbosa, Carlos José Dornas Gonçalves. "Mecanismos envolvidos no aumento do risco de sangramento em pacientes com acidente vascular cerebral ou ataque isquêmico transitório prévios em uso de antiagregante plaquetário." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-09042018-082518/.
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Introdução: O antecedente de AVCI e/ou AIT está presente em 5% dos pacientes com coronariopatia aguda e em até 17% dos pacientes com coronariopatia crônica. Esta população apresenta elevado risco para eventos cardiovasculares, assim como para desfechos hemorrágicos maiores (principalmente quando em uso de tratamento antitrombótico). A agregabilidade plaquetária apresenta papel fundamental no balanço isquêmico/hemorrágico; entretanto, esse mecanismo é pouco estudado em pacientes com evento cérebro vascular isquêmico prévio. O principal objetivo desse estudo é avaliar se pacientes com DAC e AVCI/ AIT prévio exibem alterações na agregabilidade plaquetária que justifiquem o risco aumentado para sangramento nesses indivíduos. Casuística e Métodos: Entre janeiro de 2013 e abril de 2015, 140 pacientes foram selecionados nos bancos de dados da unidade coronária e do serviço de cirurgia cardíaca do InCor- HCFMUSP. Critérios de inclusão: coronariopatia aguda prévia (há mais de 12 meses), antecedente de AVCI/AIT (anterior ao episódio de coronariopatia aguda), uso crônico de AAS e assinatura do Termo de Consentimento Livre e Esclarecido. Critérios de exclusão: AVCH prévio, uso de antiagregação plaquetária dupla ou anti-inflamatórios não esteroidais, trombofilia ou coagulopatia conhecida, trombocitopenia ou trombocitose, angioplastia ou cirurgia cardíaca nos últimos 6 meses, disfunção renal grave ou qualquer doença terminal. Desenho do estudo: Estudo de caso e controle (1:1), com os grupos caso (AVCI/AIT prévio) e controle (sem AVCI/AIT prévio) pareados por sexo, idade, tipo de coronariopatia aguda e tempo entre a coronariopatia aguda e a inclusão no estudo. A agregabilidade plaquetária foi mensurada pelo VerifyNow Aspirin®, VerifyNow P2Y12®, Agregometria óptica com agonista ADP, Agregometria óptica com agonista adrenalina e tromboelastrografia (Reorox®). Resultados: Os grupos controle (n=70) e caso (n=70), estavam bem pareados em relação à maioria das variáveis analisadas. A idade média da população global foi de 66 anos, 73% apresentavam IAM prévio, e o tempo médio entre o episódio de coronariopatia aguda e a inclusão no presente estudo foi de 5,31 anos. No momento da avaliação os pacientes do grupo caso apresentavam valores mais elevados de pressão arterial sistólica (135,84 ± 16,09 vs 123,68 ± 16,11mmHg, p < 0,001), embora esse grupo utilizasse maior número de antihipertensivos (2,37 ± 1,09 vs 3,0 ± 1,23, p=0,006). Em relação a variáveis metabólicas, o perfil lipídico não presentou diferença significativa entre os grupos, entretanto o grupo caso apresentou maiores valores de creatinina (1,24 ± 0,35 vs 1,11 ± 0,27 mg/dL, p=0,037) e também de glicemia de jejum (116,16 ± 32,03 vs 134,88 ± 57,58 mg/dL, p=0,031). No que se refere à meta principal do estudo, a agregabilidade plaquetária foi similar nos dois grupos por todos os métodos utilizados: VerifyNow Aspirin® (525,00 ± 79,78 vs 530,35 ± 83,81 ARU nos grupos caso e controle, respectivamente, p=0,7), VerifyNow P2Y12® (262,14 ± 43,03 vs 251,74 ± 43,72 PRU, p=0,21), Agregometria óptica com agonista ADP (78,34 ± 9,02 vs 77,55 ± 9,70%, p=0,82), Agregometria óptica com agonista adrenalina (49,01± 23,93% vs 49,34 ± 21,7, p=0,77), e tromboelastografia (Firmeza máxima do coágulo: 2,136,00 ± 569,97 vs 2.001,27 ± 635,68 Pa, p=0,19). Conclusão: Em pacientes com doença arterial coronária crônica a agregabilidade plaquetária foi similar nos indivíduos com ou sem AVCI/AIT. Esses resultados apontam para que outros mecanismos sejam responsáveis pelo elevado risco hemorrágico dessa populaçãoBackground: Ischemic stroke (IS) or transient ischemic attack (TIA) history is present in 5% of patients with acute coronary syndrome (ACS) and in 17% of patients with stable atherosclerotic disease (CAD). This population has a higher risk for major cardiovascular events and an increased incidence of major hemorrhagic outcomes when subjected to modern antithrombotic regimens, Platelet aggregability have key role in \"ischemic-hemorrhagic\" balance, however, these factors are little known in the population with prior cerebrovascular event. The aim of this study is to evaluate whether patients with coronary artery disease and previous IS/ TIA exhibit alterations in platelet aggregation, justifying the increased bleeding risk of these individuals. Methods: Between January 2013 and April 2015, 140 participants were selected in the coronary care unit and cardiac surgery service databank. Inclusion criteria: prior ACS (over 12 months), history of IS/ TIA previous to ACS, chronic use of aspirin since ACS and agreement to the consent form. Exclusion criteria: prior hemorrhagic stroke, current dual antiplatelet therapy or anti-inflammatory non-steroidal, any thrombophilia or coagulopathy, thrombocytopenia, thrombocytosis, PCI or CABG in the last 6 months, severe renal impairment and any terminal illness. Study design: Case-control study (1:1), case group (previous IS/TIA) and control group (without previous IS/TIA) matched for sex, age, type of previous ACS, time between ACS and inclusion in the study. Platelet aggregation was assessed by VerifyNow Aspirin®, VerifyNow P2Y12®, Light transmission aggregometry aggonist with agonists adrenaline, Light transmission aggregometry aggonist with ADP, and thromboelastography (Reorox®). Results: The control group (n=70) and case group (n=70), were well matched. The mean age was 63 years, about 73% presented previous AMI and the index ACS occurred 5,31 years before study inclusion. At the evaluation day patients in the case group presented higher SBP levels (135.84 ± 16.09 vs 123.68 ± 16.11 mmHg, p < 0,001), although this group were using more antihypertensive medications (2.37 ± 1.09 vs 3.0 ± 1.23, p=0,006). In relation to metabolic profile, lipid profile did not presented diferences, however, case group presented higher values for creatinine (1.24 ± 0.35 vs 1.11 ± 0.27 mg/dL, p=0.037) and also presented higher values for fasting glucose.(116.16 ± 32.03 vs 134.88 ± 57.58 mg/dL, p=0.031) Platelet aggregation was statistically similar in both groups: VerifyNow Aspirin® (525.00 ± 79.78 vs 530.35 ± 83.81 ARU, p=0.7), VerifyNow P2Y12® (262.14 ± 43.03 vs 251.74 ± 43.72 PRU, p=0.21), Light transmission aggregometry aggonist with agonists ADP (78,34 ± 9,02 vs 77,55 ± 9,70%, p=0,82), Light transmission aggregometry aggonist with adrenaline (49,01 ± 23,93% vs 49,34 ± 21,7, p=0,77) and thromboelastography (maximum clot firmness: 2.136,00 ± 569,97 vs 2.001,27 ± 635,68 Pa, p=0,19). Conclusion: Platlet aggregability is similar in CAD patients with or without previous IS/TIA and this results point at other reasons to justify the high risk for bleeding in this patients
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Radenko, Koprivica. "Rana karotidna endarterektomija nakon akutnog neurološkog deficita." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2016. http://www.cris.uns.ac.rs/record.jsf?recordId=100762&source=NDLTD&language=en.
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Ciljevi: Cilj ove studije je da ispita bezbednost rane karotidne endarterektomije (CEA) u odnosu na odložene CEA nakon akutnog ishemijskog neurološkog deficita (TIA/CVI). Drugi cilj je da istražimo da li postoji razlika u brzini neurološkog oporavka između navedenih grupa. Metode: Ukupno 157 ispitanika u prospektivnoj studiji je praćeno 30 dana postoperativno. Grupa I ili rana CEA, je imala 50 ispitanika operisanih od 3. do 14. dana po TIA/CVI događaju. Grupa II ili odložena CEA, je imala 107 ispitanika operisanih od 15. do 180. dana nakon TIA/CVI. Praćen je proceduralni opšti i specifični morbiditet i mortalitet u 30-dnevnom postoperativnom periodu. Rankin skor (mRS) smo koristili za procenu neurološkog invaliditeta. U odnosu na vrednost mRS skora smo formirali dve podgrupe mRS<3 i mRS3. U statističkoj analizi koristili smo Pirsonov hi test, Studentov test, ANOVU analizu varijanse, Boniferonijev test i multiplu analizu varijanse za ponovljena merenja (GLM- general line model), kao i parametarsku i neparametarsku korelaciju i regresiju. Nivo značajnosti je bio 0,05. Rezultati: Prosečna starost ispitanika je bila 66,72 godine uz 66,2% osoba muškog pola. U grupi I je prosečno vreme do intervencije bilo 9,5 dana, a u grupi II 72,22 dana. Grupe su homogene u odnosu na faktore rizika i komorbiditet. Grupa I je imala 54% nestabilnih aterosklerotskih plakova u poređenju sa grupom II gde ih je bilo 31,8% (χ2 = 7.084; p < 0.01). U grupi I TIA je imalo 50% ispitanika, a u grupi II CVI nalaza je bilo 68,2% (χ2 =4.825; p <0.05). CVI do 1 cm veličine je statistički značajno više zastupljen u grupi I , a CVI do 2 cm u grupi II (χ2 = 6.913; p <0.05). Stopa CVI je u grupi I bila 2.0% a u grupi II je 2.8% (F = 0.083; p > 0.05). Stopa postoperativnog infarkta miokarda (IM) je u grupi I je 2.0% a u grupi II je 1.9%. Stopa specifičnog hirurškog morbiditeta je u grupi I 4.0% a u grupi II 3.7%. U grupi I ukupni morbiditet bio 6.0% a u grupi II 7.5%, razlika nije bila statistički značajna (F =0.921; p > 0.05). Mortaliteta u obe grupe nije bilo. CVI/IM/smrt stopa je u grupi I bio 4.0% a u grupi II je bio 4.7% (F = 0.122; p >0.05). Hiperlipidemija je signifikantan faktor rizika za CVI/IM/smrt (χ2 = 4.083; p < 0.05). Poboljšanje mRS je u grupi I imalo 52%, a u grupi II 31,8% pacijenata (χ2 = 5.903; p <0.01). Relativni rizik je 2,4 odnosno toliko puta je veća šansa da kod bolesnika dođe do promene mRS ako je bolesnik u grupi I. Pad mRS koji nastupa između trećeg i desetog dana nakon CEA je statistički visoko značajno izraženiji u grupi ranih CEA ( F 3,701 df 1 p=0,029). Kod bolesnika sa TIA u preko 60% slučajeva došlo je do pada mRS, a kod onih koji su imali CVI u oko 25.5% (χ2 = 18.050; p < 0.01). Kod Rankin skora podgrupe mRS<3 i mRS3 je pad bio značajan i po vremenu (F 18,774; df 6; p=0,000) i po podgrupi ali je daleko brži pad zapažen u podgrupi mRS<3(F 6,010; df 1; p=0,003). Zaključak: Rana CEA je jednako bezbedna kao i odložena CEA u pogledu incidence perioperativnog morbiditeta i mortaliteta. Ranom CEA se postiže znatno brži neurološki oporavak pacijenata, naročito onih sa TIA i mRS<3 skorom.Objectives: The aim of this study was to investigate the safety of early carotid endarterectomy (CEA) in relation to the delayed CEA after acute ischemic neurological events (TIA / CVI). The second objective was to investigate whether there is a difference in speed of neurological recovery between these groups. Methods: A total of 157 patients in the prospective study followed 30 days postoperatively. Group I or early CEA, had 50 patients operated from 3 to 14 days after TIA / CVI event. Group II or delayed CEA, had 107 patients operated from 15 to 180 days after the TIA / CVI. Accompanied by the general and specific procedural morbidity and mortality in 30-day postoperative folow up. Rankin score (mRS) were used for evaluation of neurologic disability. In relation to the value of mRS score we formed two subgroups mRS <3 i mRS3. In the statistical analysis we used the Pearson chi test, Student's test, ANOVA analysis of variance, Boniferony test and multiple analysis of variance for repeated measures (GLM- general line model), as well parametric and nonparametric correlation and regression. The significance level was 0.05. Results: The mean age was 66.72 years with 66.2% of males. In Group I is the average time to intervention was 9.5 days, and in group II 72.22 days. The groups were homogeneous in relation to risk factors and comorbidities. Group I had 54% of unstable atherosclerotic plaques compared with group II, where it was 31.8% (χ2 = 7.084; p <0.01). In the group I TIA had 50% of respondents, while in group II CVI was 68.2% (χ2 = 4.825; p <0.05). CVI to 1 cm in size were significantly more frequent in the group I, a CVI to 2 cm in group II (χ2 = 6.913; p <0.05). CVI rate in the group I was 2.0%, and in group II was 2.8% (F = 0.083, p> 0.05). Postoperative myocardial infarction (MI) in the group I is 2.0%, and in group II was 1.9%. Specific surgical morbidity rate in the group I and 4.0% in the group II 3.7%. In group I total morbidity was 6.0% in group II 7.5%, the difference was not statistically significant (F = 0.921; p> 0.05). Mortality in both groups was not. CVI/IM/death rate in group I was 4.0% in group II was 4.7% (F = 0.122; p> 0.05). Hyperlipidemia is a significant risk factor for CVI/IM/death (χ2 = 4.083; p<0.05). Improving mRS in the group I had 52% and in group II 31.8% of patients (χ2 = 5.903; p <0.01). The relative risk was 2.4 times as much and is more likely to occur in patients mRS changes if the patient in group I. Improving mRS that occurs between the third and tenth days after CEA was highly statistically significantly greater in the group of early CEA (F 3,701 df 1 p = 0.029). In patients with TIA in 60% of cases there was a decline mRS, and those had CVI in about 25.5% (χ2 = 18.050; p <0.01). In Rankin score subgroups mRS <3 i mRS 3 the decline was significant and time (F 18,774; df 6; p =0.000) and in the subgroup but it is far more rapid decline observed in the subgroup mRS <3 (F 6.010; df 1; p = 0.003). Conclusions: Early CEA is as safe as the delayed CEA in respect incidence of perioperative morbidity and mortality. Early CEA is achieved significantly faster recovery of neurological patients, especially those with TIA and mRS <3 compared with delayed CEA.
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Grieser, Christian. "Erkennung zerebraler Ischämie mittels computertomographischer Perfusionskartographie und CT-Angiographie." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2006. http://dx.doi.org/10.18452/15429.
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Zielsetzung In den Industrieländern stellt der Schlaganfall nach kardiovaskulären und Krebs – erkrankungen die dritthäufigste Krankheitsgruppe dar. Im Hinblick auf die Therapie des akuten Schlaganfalls muss die bildgebende Diagnostik schnell und einfach das Ausmaß der zerebralen Ischämie beschreiben können. Ziel dieser Studie war die Einführung und die Validierung eines CT – Protokolls, welches die Diagnostik des akuten Schlaganfalls verbessern soll. Zu diesem CT – Protokoll gehören ein Nativ – CT des Schädels, eine CT – Perfusionsuntersuchung und eine CT – Angiographie. Zusätzlich wollte diese Arbeit herausfinden, ob es physiologische Unterschiede zwischen der grauen Substanz und der weißen Substanz gibt, deren Kenntnis entscheidend für die Auswertung von computertomographischen Perfusionsuntersuchungen sind. Material und Methoden Insgesamt wurden 101 Patienten (Alter von 14 – 94 Jahre, mittleres Alter 69 Jahre) mit einem 8 – bzw. 16 – Zeilen – MSCT (Light Speed Ultra oder Light Speed pro 16, GE Healthcare), die zur Abklärung einer zerebralen Ischämie zum CT vorgestellt wurden, untersucht. Zuerst wurde eine native CT – Serie akquiriert. In der Untersuchung der zerebralen Perfusion wurde eine 2 cm breite Schicht über 60 sec mit 20 intermittierenden Aufnahmen während einer Injektion von 40 ml Kontrastmittel (Iopromid, Jodgehalt von 370 mg) aufgezeichnet. Daran an schloss sich eine CT – Angiographie Untersuchung. Zur Bestimmung des regionalen zerebralen Blutflusses, des regionalen zerebralen Blutvolumens und der mittleren Verweildauer wurden definierte Messfelder (Regions of Interests, ROIs) bestimmt und mit der kontralateralen Hemisphäre verglichen. Ergebnisse Es konnte gezeigt werden, dass der regionale zerebrale Blutfluss und das Blutvolumen im Bereich der Hirnrinde höher sind als im Hirnmark. Insgesamt wurden 66 Patienten mit einer zerebralen Ischämie wurden gefunden. Bei 22 dieser Patienten konnte ein Infarktgeschehen in der Nativ – CT diagnostiziert werden. Diese Ischämien ließen sich auch in der CT – Perfusion mit reduziertem regionalem zerebralem Blutfluss und verlängerter mittlerer Verweildauer nachweisen. Zusätzlich fanden sich 44 Patienten von 101 Untersuchten, die in der CT – Perfusion ein Perfusionsdefizit aufwiesen. Bei diesen Patienten ließ sich kein entsprechendes Korrelat in der Nativ – CT nachweisen. Für 38 dieser 44 Patienten konnte eine CTA durchgeführt werden, wovon für 35 Patienten ein Korrelat zwischen der CT – Perfusion und der CTA gefunden werden konnte. Schlussfolgerung Die Ergebnisse dieser Arbeit zeigen, dass es physiologische Unterschiede zwischen der Hirnrinde und dem Hirnmark gibt, deren Kenntnis für die Bewertung computertomographischer Perfusionsuntersuchungen eine wesentliche Interpretationshilfe darstellt. In Bezug auf die Diagnostik des akuten Schlaganfalls mit der Nativ – CT konnte diese Arbeit zeigen, dass der Nachweis von Infarktfrühzeichen eingeschränkt ist. Mit Hilfe der CT – Perfusion ist es möglich, anhand von zerebralen Perfusionswerten den Schweregrad und die Ausdehnung der zerebralen Ischämie zu bestimmen. Die CT – Angiographie zeigt eine gute Korrelation zur CT – Perfusion, es lassen sich zuverlässig Gefäßverschlüsse darstellen. Im Hinblick auf das weitere Therapievorgehen geben diese Methoden eine wichtige Hilfestellung, etwa zur Überlegung, ob man eine Lysetherapie durchführen sollte oder nicht.Purpose Stroke is the third – leading cause of death in developed countries, following cardiovascular disease and cancer. There is a need for an easily and rapidly performed technique to detect cerebral ischemia in the first hours after its occurrence. The purpose of this study was the introduction and validation of a Stroke protocol which includes an unenhanced CT scan, a CT Perfusion and a CT Angiography. Furthermore, the purpose of this study was to determine if there is a difference between Perfusion parameters in gray and white matter, which are necessary to know while performing perfusion maps. Data and Methodology A total of 101 patients (age range 14 – 94, average age 69 years) were examined using multiple row CT (8 / 16 row multiple detector, light ultra speed or light speed 16, GE medical systems) for diagnosing cerebral ischemia. First a series of native images was acquired. During the examination of cerebral perfusion a 2 cm wide slab was recorded for 60 sec with 20 intermittent scans following injection of 40 ml of contrast medium with an iodine content of 370 mg / ml. By defining Regions of Interests (ROIs) regional cerebral blood flow (CBF), regional cerebral blood volume (CBV) and mean transit time (MTT) were calculated. Results Physiological regional cerebral blood flow and cerebral blood volume in gray matter were higher than in white matter. In total 66 patients with a cerebral ischemia were found. The unenhanced CT detected 22 patients with cerebral ischemia, which were confirmed by CT Perfusion in all cases. These ischemic areas revealed reduced regional CBF and extended MTT. Furthermore an ischemia correlative was discovered by perfusion analysis for 44 patients (out of 101 investigated) where the extent of the cerebral ischemia had not been visible by unenhanced CT. For 38 out of 44 patients with cerebral ischemia we were able to perform a CTA. For 35 out of these 38 patients, we found a sizable correlation between perfusion maps and CTA. Conclusion There are physiological differences for CT Perfusion parameters between gray and white matter, which are necessary to know for the interpretation of perfusion maps. However, this examination was able to show that unenhanced CT is not always capable of showing early CT signs. With the help of CT perfusion it is possible to detect the extent of acute cerebral ischemia. Furthermore, CT Angiography shows a sizable correlation compared to CT Perfusion. In conjunction, these methods give important Information for the early diagnosis and the therapeutic strategy of ischemic brain injury.
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Yu, Chou Hsin, and 周心語. "Study of apoptotic signaling pathway after transient cerebral ischemia." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/19755187296645864759.
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碩士東海大學
食品科學系
98
Stroke, also known as cerebral ischemia, is one common disease of humans. In studying the pathophysiological alterations of stroke, an animal model of transient focal cerebral ischemia in rat was established. Through this animal model of stroke, we were interested to investigate potential post-ischemic brain alterations, particular in the regulation of post-ischemic apoptosis. Global examination found that ischemia/reperfusion caused a significant loss in body weight and deficits in neurobehavior and motor coordination. Ischemia/reperfusion insult caused brain infarction. Histological examination revealed a remarkable atrophy of neuronal nuclei, cell apoptosis, neurofilament loss, and microglia and astrocyte activation. To further elicit the inflammatory response, the activation of resident microglia, the infiltration of neutrophils, macrophages, and B lymphcytes, and the expression of pro-inflammatory mediator cyclooxygenase-2 were detected in ischemic brain tissues. Using TUNEL staining to detect apoptosis-related chromosome breakage, a significant TUNEL-positive signal was detected in cerebral cortex, hippocampus, and striatum after cerebral ischemia/reperfusion. An elevation of protein expression in extrinsic apoptosis pathway-associated molecules such as TNF-α receptor 1, Fas, TNF-α, FADD, and Bid was detected by western blot after cerebral ischemia/reperfusion. Intriguingly, cerebral ischemia/reperfusion also increased the expression of FLIP, a natural antagonist against extrinsic apoptosis. Regarding the intrinsic apoptosis pathway, cerebral ischemia/reperfusion decreased anti-apoptotic Bcl-2 and Bcl-xL expression but increased pro-apoptotic Bad, PUMA, and Bax expression. The apparent expression of p53, a transcription factor critical to apoptosis induction, was detected in ischemic tissues. In addition to caspase-dependent apoptotic cascades, the expression of caspase-independent apoptotic molecule AIF was elevated after cerebral ischemia/reperfusion. Enzymatic measurement further showed the activation of caspase-3, caspase-8, and caspase-9 after cerebral ischemia/reperfusion. These findings suggest that cerebral ischemia/reperfusion triggers caspase-independent and caspase-dependent apoptotic cascades leading to post-ischemic apoptosis.
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Chou, Ya-Shuan, and 鄒亞璇. "Electrophysiological diaschisis-transient and permanent focal cerebral ischemia in rats." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/03324329145812716700.
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碩士國立成功大學
醫學工程研究所碩博士班
97
Ischemia stroke is the most common type of stroke. The remote changes in blood flow, metabolism and electric activity resulted from focal cerebral injury were called diaschisis. Ischemic models were evaluated electrophysiological diaschisis and benefits of reperfusion in this research. Diaschisis is often seen clinically after brain injury. We designed several different models to evaluate the phenomena of electrophysiological diaschisis. This study included three transient models (occlusion of the MCA for 30, 90 and 150 min) and two permanent models (occluded proximal MCA without reperfusion and electrocoagulation of the distal MCA). SSEP was recorded prior to MCAo and 24 hours, 7 days after reperfusion. Brain infarction was assessed by Nissle staining and quantified by MCID program. We measured the Fluoro-Jade positive cells which quantification of degenerate neuron. SSEP stimuli were recorded in the somatosensory cortex after stimulating the fore- and hind-limb with 3.0 mA DC potential. The amplitude between the first positive (P1) and the first negative (N1) peaks and the P1 latency were analyzed. The suppressed SSEP amplitude was significantly different between permanent and transient groups. The suppressed amplitude was recorded not only from ischemic but also non-ischemic hemispheres. Interestingly, diaschisis is a common consequence after brain damages especially those with cortical infarction. Reperfusion ameliorated neuron degeneration, electrophysiological function and diaschisis. In conclusion, our results suggest that cortical lesion leads to diaschisis, which can be reversed by reperfusion.
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Ratilal, Bernardo Oliveira 1975. "Neuroprotective strategies for transient focal cerebral ischemia : an experimental model." Doctoral thesis, 2014. http://hdl.handle.net/10451/18264.
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Tese de doutoramento, Medicina (Neurocirurgia), Universidade de Lisboa, Faculdade de Medicina, 2015Object: The aim of this research was to explore the effects of single pretreatment dose of potential neuroprotective drugs in a focal cerebral ischemia-reperfusion (I-R) model. Methods: After the setting up and establisment of the selected animal model, forty-two Wistar male adult rats were subjected to right middle cerebral artery (MCA) intraluminal occlusion for 60 minutes, under continuously cortical perfusion monitoring. Rats were randomly divided into three groups: control (saline), recombinant human erythropoietin (rhEPO, 1.000 IU/kg)-treated and 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD- 8, 5 mg/kg) -treated. Saline or drugs were administered 10 minutes before the onset of ischemia. At 24-hour reperfusion, animals were examined for neurological deficits, blood samples were collected and animals euthanized. The following parameters were blindly evaluated: brain infarct volume, ipsilateral hemispheric edema, neuron specific enolase (NSE) plasma levels, parenchyma histology, Fluoro-Jade positive neurons, p-Akt and total Akt expression, and p-Akt-positive nuclei. Results: Data demonstrated that for rhEPO-treated group severity of neurological deficits (p<0.001), brain edema (p<0.001), and NSE plasma levels (p<0.001) were significantly reduced when compared to control group. Infarct volume and counting number of degenerating neurons in the interest area were similar between these groups, however, perivascular edema was less marked following treatment. No variations on the expression or localization of p-Akt were seen. TDZD-8-treated group compared to control group had: reduced infarct volume (p<0.001) and hemispheric edema (p<0.001), diminished number of dying neurons (p<0.001), decreased serum rise of NSE (p<0.001), and improved neurological performance (p<0.001). Fewer signs of perivascular edema and increased p-Akt nucleus translocation (p<0.05) were found. Conclusions: Results suggest that TDZD-8 has neuroprotective effects due to a complex and mixed synergic interaction between direct neuronal GSK-3β inhibition and Akt modulation, but further research is required before this drug may become clinically available. Additionally, it is presented first evidence that prophylactic rhEPO administration at the considered dose, which has its safety profile well-described in humans, reduced brain edema xi and preserved the neuronal pool of the penumbra area following I-R-injury. These benefits appear to be the result of an indirect effect in brain swelling as a consequence of diminished blood-brain barrier disruption and not due to a direct rhEPO neuronal action in the infarct area. Erythropoietin is a potential therapy to prevent neuronal injury induced by intraoperative transient artery occlusion. A translational study is supported and a summary protocol for a putative clinical trial is proposed.
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Bourdage, Carl J. A. "Age-dependent memory impairments following transient global ischemia : relationship to hippocampal pathology." Thesis, 2009. http://spectrum.library.concordia.ca/976602/1/MR63119.pdf.
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Most human stroke victims are part of an older population while most animal models of ischemia employ young adult rodents. To add generalizability to rodent models of global ischemia, and its associated neuropathology and memory impairments, to the human stroke population, this thesis examines the effect of a IS-minute global ischemia via four vessel occlusion (4VO) in rats that were 8-weeks, 20-weeks, and SO-weeks of age. Rats were tested for object-location memory, using a 24-hour retention delay and object-recognition memory, using IS-minute and 24-hour delays. Rats with sham-ischemia in all age groups showed a preference for the moved object during the novel-object-in-place (NOIP) test of spatial memory, and for the novel object during the IS-minute novel-object- preference (NOP) test and with the exception of the 20-week group, during the 24-hour NOP test. However, rats that received ischemia displayed impairments in all age groups in the NOIP, in the 20-week group during the IS-minute NOP test, and in the 20and SO-week groups in the 24-hour NOP test of object recognition. Ischemic rats in all age groups had significantly fewer cells in the CA1, CA2, and hilus subfields of the hippocampus, than did sham-ischemia controls. Only the SO-week ischemia group had significant damage in CA3 and the dentate gyrus. Performance in the NOIP test was correlated with cell counts in CA1, CA2, and the dentate gyrus, and with CA1 and CA2 in the IS-minute NOP test. These findings indicate that the severity of memory impairments and neuropathology due to ischemia are influenced by the age of the brain.