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1
Bowler, John Vaughan. "Cerebral infarction and '9'9Tc'm HMPAO SPECT". Thesis, King's College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260983.
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2
Sibson, Nicola Ruth. "A magnetic resonance imaging study of experimental cerebral ischaemia". Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360825.
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3
Taylor, Deanna Lesley. "Alterations in interstitial acid-base homeostasis during cerebral ischaemia". Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267025.
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4
Greenhalgh, Andrew. "Actions of interleukin-1 receptor antagonist in cerebral ischaemia". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-receptor-antagonist-in-cerebral-ischaemia(50aacd97-68c1-4f91-90b5-8f8deff5d21d).html.
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Cerebral ischaemia, or stroke, is a leading cause of death and disability worldwide. Ischaemic stroke, as a result of arterial occlusion, and subarachnoid haemorrhage (SAH), as a consequence of arterial rupture in the subarachnoid space, are major subtypes of stroke. Treatment options for both are limited, and many therapeutic strategies have failed. In ischaemic stroke, lack of evidence of brain penetration of treatments has been cited as a major weakness and contributing factor to failed clinical trials. In SAH, animal models do not always mimic key pathophysiological hallmarks of the disease, hindering development of new therapeutics. Inflammation is strongly associated with brain injury after cerebral ischaemia and inhibition of the pro-inflammatory cytokine interleukin-1 (IL-1) represents apossible therapeutic target. Therefore, the key objectives of this thesis were; (1) to improve preclinical data on a promising stroke treatment, interleukin-1 receptor antagonist (IL-1Ra), by investigating its pharmacokinetic profile and brain penetration in a rat model of ischaemic stroke, (2) to investigate the endovascular perforation model of SAH in rat, as a tool for the investigation of neuroprotectants, and (3) to examine the role of the inflammatory response in the SAH model and the effects of IL-1Ra. The neuroprotective effect, pharmacokinetic profile and brain penetration of IL-1Ra were assessed after a single subcutaneous (s.c.) dose (100mg/kg) in rats, after transient (90 min) middle cerebral artery occlusion (MCAo). A single s.c. dose of IL-1Ra reduced neuronal damage, resulted in sustained, high concentrations of IL-1Ra in plasma and cerebrospinal fluid and also penetrated brain tissue exclusively in areas of blood brain-barrier (BBB) breakdown. An endovascular perforation model of SAH in rat was investigated and produced widespread multifocal infarcts. In this model, administration of IL-1Ra (s.c.) reduced BBB breakdown, which correlated with injury at 48 h. IL-1_ was expressed in the brain early after SAH in areas associated with haem oxygenase-1 (HO-1) expression, indicating the presence of free haem. Stimulation of primary mouse mixed glial cells in vitro with haem induced expression and release of IL-1 alpha but not IL-1 beta. These data, after MCAo in rat, are the first to show that a single s.c. dose of IL-1Ra rapidly reaches salvageable brain tissue and is neuroprotective. This allows confidence that IL-1Ra is able to confer its protective actions both peripherally and centrally. After experimental SAH, we suggest that haem, a breakdown product of haemoglobin, released from lysed red blood cells in the subarachnoid space, acts as a danger associated molecular pattern (DAMP) driving IL-1- dependent inflammation. These data provide new insights into inflammation after SAH-induced brain injury and suggest IL-1Ra as a candidate treatment for the disease. Overall, these findings strengthen preclinical data supporting IL-1Ra as a neuroprotective therapy for ischaemic stroke, and identify SAH as a new indication for treatment with IL-1Ra.
5
Marquardt, Lars. "Large artery disease in patients with cerebral ischaemia : frequency, investigation and management". Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:70b598c5-97ca-4567-ac32-ed5092972a16.
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Stroke is the third leading cause of death in the developed world and is the leading neurological cause of disability with a massive impact on personal life and society. Large artery atherosclerosis is one of the main causes of ischaemic stroke. However, in several aspects of this condition there is still a significant amount of uncertainty about its prevalence, appropriate investigation and possible treatment. Reliable data on epidemiology are therefore necessary to provide clinicians and researchers with crucial information to guide diagnostic and therapeutic management as well as further research. With this thesis I aimed to provide useful information about the prevalence of large artery disease in certain groups of patients, and to contribute to investigation- and managementstrategies using data from a large population based study, the Oxford Vascular Study (OXVASC). OXVASC is a prospective, population-based incidence study of vascular disease in Oxfordshire, UK, which started in 2002 and is ongoing. The study population comprises all 91,106 individuals registered with nine general practices and uses multiple methods of case ascertainment to identify all patients with vascular events. Firstly, I have shown that the prevalence of ≥50% vertebral or basilar artery stenosis in posterior circulation TIA or minor stroke is more than twice as high as the prevalence of ≥50% carotid stenosis in patients with carotid territory events, and is associated with a very high early risk of stroke of 22% and TIA of 46%. Furthermore, severe vertebral and/or basilar artery stenosis is associated with multiple TIAs at first presentation. Secondly, I have shown that early risk of stroke was higher after posterior circulation TIA, with a 1-year risk of 16%, than after carotid territory TIA, with a 1-year risk of 9%. In addition, I was able to show for the first time, that the ABCD2 score was predictive of early stroke not only in patients with carotid circulation TIA but also in patients with vertebrobasilar TIA. Thirdly, in a pilot feasibility study about arterial spin labelling magnetic resonance imaging in patients with large artery disease in the vertebrobasilar circulation I have shown that patients with severe large artery disease have significantly impaired occipital brain perfusion. My results suggest that this new technique might be a useful tool to identify suitable patients for interventional treatment of vertebrobasilar large artery disease. Fourthly, I was able to show that the risk of ipsilateral stroke and TIA in patients with an asymptomatic carotid stenosis is very low with contemporary best medical treatment alone, suggesting that routine carotid endarterectomy for asymptomatic carotid stenosis might not longer be feasible. Finally, I have clarified that lower rates of intervention for moderate to severe symptomatic carotid stenosis in women than in men can be explained by sex-differences in the populationbased incidence of carotid large artery disease and not due to under-investigation or reluctance amongst women to undergo investigation or treatment.
6
Calamante, Fernando. "Diffusion and perfusion MRI and applications in cerebral ischaemia". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314345.
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7
Ben-Yoseph, O. "Multinuclear magnetic resonance spectroscopy studies of perturbed cerebral metabolism in vitro". Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240078.
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Thomas, David Lee. "Magnetic resonance imaging of diffusion and perfusion : techniques and applications to cerebral ischaemia". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391829.
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9
Smith, Stuart Ernest. "Excitatory amino acid antagonists and related agents as potential therapies in focal cerebral ischaemia in the rat". Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281943.
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Milidonis, Xenios. "Multicentre evaluation of MRI variability in the quantification of infarct size in experimental focal cerebral ischaemia". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28877.
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Ischaemic stroke is a leading cause of death and disability in the developed world. Despite that considerable advances in experimental research enabled understanding of the pathophysiology of the disease and identified hundreds of potential neuroprotective drugs for treatment, no such drug has shown efficacy in humans. The failure in the translation from bench to bedside has been partially attributed to the poor quality and rigour of animal studies. Recently, it has been suggested that multicentre animal studies imitating the design of randomised clinical trials could improve the translation of experimental research. Magnetic resonance imaging (MRI) could be pivotal in such studies due to its non-invasive nature and its high sensitivity to ischaemic lesions, but its accuracy and concordance across centres has not yet been evaluated. This thesis focussed on the use of MRI for the assessment of late infarct size, the primary outcome used in stroke models. Initially, a systematic review revealed that a plethora of imaging protocols and data analysis methods are used for this purpose. Using meta-analysis techniques, it was determined that T2-weighted imaging (T2WI) was best correlated with gold standard histology for the measurement of infarctbased treatment effects. Then, geometric accuracy in six different preclinical MRI scanners was assessed using structural phantoms and automated data analysis tools developed in-house. It was found that geometric accuracy varies between scanners, particularly when centre-specific T2WI protocols are used instead of a standardised protocol, though longitudinal stability over six months is high. Finally, a simulation study suggested that the measured geometric errors and the different protocols are sufficient to render infarct volumes and related group comparisons across centres incomparable. The variability increases when both factors are taken into account and when infarct volume is expressed as a relative estimate. Data in this study were analysed using a custom-made semi-automated tool that was faster and more reliable in repeated analyses than manual analysis. Findings of this thesis support the implementation of standardised methods for the assessment and optimisation of geometric accuracy in MRI scanners, as well as image acquisition and analysis of in vivo data for the measurement of infarct size in multicentre animal studies. Tools and techniques developed as part of the thesis show great promise in the analysis of phantom and in vivo data and could be a step towards this endeavour.
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Young, Christopher Cheng. "The adult neural stem cell niche in ischaemic stroke". Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:86e6e236-047c-46d8-96e5-449a3f0505a8.
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Ischaemic stroke is a major cause of mortality and chronic disability for which there is no effective treatment. The subventricular zone (SVZ) is an adult neurogenic niche which mediates limited endogenous repair following stroke. To harness this phenomenon for therapy, it is important to understand how the SVZ niche is altered in stroke, and the processes that recruit neural precursors to the site of injury, which becomes a de facto neurogenic niche. Galectin-3 (Gal-3) is a β-galactoside binding protein involved in cellular adhesion, inflammation and tumour metastasis. Gal-3 is specifically expressed in the SVZ and maintains neuroblast migration to the olfactory bulb, although its role in post-stroke neurogenesis is not well-understood. Therefore, this project aimed to (1) characterise the cytoarchitecture of the SVZ in response to stroke, and (2) examine the role of Gal-3 in stroke outcome and tissue remodelling, and test the hypothesis that Gal-3 is required for neuroblast ectopic migration into the ischaemic striatum. Using the intraluminal filament model of middle cerebral artery occlusion (MCAO) in mice, and whole mounts of the lateral ventricular wall, significant SVZ reactive astrocytosis and increased vascular branching were observed, thereby disrupting the neuroblast migratory scaffold. Stroke increased SVZ cell proliferation without increase in cell death. Post-stroke ependymal cells were enlarged and non-proliferative, and assumed a reactive astroglial phenotype, expressing de novo high levels of glial fibrillary acidic protein. This was associated with focal planar cell polarity misalignment, and turbulent and decreased rate of cerebrospinal fluid flow. These findings demonstrate significant changes in multiple SVZ cell types which are positioned to influence post-stroke neurogenesis and regulation of the neural stem cell niche Gal-3 was up-regulated in the ischaemic brain and ipsilateral SVZ. To elucidate the role of Gal-3 after stroke, MCAO was performed in wildtype and Gal-3 null (Gal-3-/-) mice, and parameters of stroke outcome and post-stroke neurogenesis compared. The deletion of Gal-3 did not affect infarct volumes or neurological outcomes, although neuroblast migration into the ischaemic striatum was increased in Gal-3-/- brains. Gal-3-/- mice failed to mount an angiogenic response in the ischaemic striatum, and this was associated with lower levels of vascular endothelial growth factor (VEGF) and increased anti-angiogenic protein levels. Loss of Gal-3 further disrupted the pro-proliferative neural-vascular interaction at the basement membrane. The current data indicate that Gal-3 is a pleiotropic molecule which has distinct roles in both the SVZ and the post-stroke striatum as niches of adult neurogenesis.
12
Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.
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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain damage following cerebral ischaemia is associated with disturbances in intracellular calcium homeostasis, the sodium-calcium exchanger (NCX) is a potential therapeutic target due to its ability to regulate intracellular calcium. Currently, however there is uncertainty as to whether the plasma membrane NCX has a neuroprotective or neurodamaging role following cerebral ischemia. To address this issue I compared hippocampal neuronal injury in NCX3 knockout mice (Ncx3-/-) and wild-type mice (Ncx3+/+) following global cerebral ischaemia. In order to perform this study I first established a bilateral common carotid occlusion (BCCAO) model of global ischaemia in wild-type C57/BlHsnD mice using controlled ventilation. After trials of several ischaemic time points, 17 minutes was established as the optimum duration of ischaemia to produce selective hippocampal CA1 neuronal loss in the wild-type mice. I then subjected NCX3 knockout and wild-type mice to 17 minutes of ischaemia. Following the 17 minute period of ischaemia, wild-type mice exhibited 80% CA1 neuronal loss and 40% CA2 neuronal loss. In contrast, NCX3 knockout mice displayed > 95% CA1 neuronal loss and 95% CA2 neuronal loss. Following experiments using a 17 minute duration of global ischaemia, a 15 minute duration of ischaemia was also evaluated. Wild-type mice exposed to a 15 minute period of ischaemia, did not exhibit any significant hippocampal neuronal loss. In contrast, NCX3 knockout mice displayed 45% CA1 neuronal loss and 25% CA2 neuronal loss. The results clearly demonstrate that mice deficient for the NCX3 protein are more susceptible to global cerebral ischaemia than wild-type mice. My findings showing a neuroprotective role for NCX3 following ischaemia, suggest that the exchanger has a positive role in maintaining neuronal intracellular calcium homeostasis. When this function is disrupted, neurons are more susceptible to calcium deregulation, with resultant cell death via calcium mediated pathways. Therefore, improving NCX activity following cerebral ischaemia may provide a therapeutic strategy to reduce neuronal death.
13
von, Sarnowski Bettina, Ulf Schminke, Ulrike Grittner, Franz Fazekas, Christian Tanislav, Manfred Kaps, Turgut Tatlisumak et al. "Cervical Artery Dissection in Young Adults in the Stroke in Young Fabry Patients (sifap1) Study". Karger, 2015. https://tud.qucosa.de/id/qucosa%3A70584.
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Background: Patients with carotid artery dissection (CAD) have been reported to have different vascular risk factor profiles and clinical outcomes to those with vertebral artery dissection (VAD). However, there are limited data from recent, large international studies comparing risk factors and clinical features in patients with cervical artery dissection (CeAD) with other TIA or ischemic stroke (IS) patients of similar age and sex.
Methods: We analysed demographic, clinical and risk factor profiles in TIA and IS patients ≤ 55 years of age with and without CeAD in the large European, multi-centre, Stroke In young FAbry Patients 1 (sifap1) study. Patients were further categorised according to age (younger: 18–44 years; middle-aged: 45–55 years), sex, and site of dissection.
Results: Data on the presence of dissection were available in 4,208 TIA and IS patients of whom 439 (10.4%) had CeAD: 196 (50.1%) had CAD, 195 (49.9%) had VAD, and 48 had multiple artery dissections or no information regarding the dissected artery. The prevalence of CAD was higher in women than in men (5.9 vs. 3.8%, p < 0.01), whereas the prevalence of VAD was similar in women and men (4.6 vs. 4.7%, n.s.). Patients with VAD were younger than patients with CAD (median = 41 years (IQR = 35–47 years) versus median = 45 years (IQR = 39–49 years); p < 0.01). At stroke onset, about twice as many patients with either CAD (54.0 vs. 23.1%, p < 0.001) or VAD (63.4 vs. 36.6%, p < 0.001) had headache than patients without CeAD and stroke in the anterior or posterior circulation, respectively. Compared to patients without CeAD, hypertension, concomitant cardiovascular diseases and a patent foramen ovale were significantly less prevalent in both CAD and VAD patients, whereas tobacco smoking, physical inactivity, obesity and a family history of cerebrovascular diseases were found less frequently in CAD patients, but not in VAD patients. A history of migraine was observed at a similar frequency in patients with CAD (31%), VAD (27.8%) and in those without CeAD (25.8%).
Conclusions: We identified clinical features and risk factor profiles that are specific to young patients with CeAD, and to subgroups with either CAD or VAD compared to patients without CeAD. Therefore, our data support the concept that certain vascular risk factors differentially affect the risk of CAD and VAD.
14
Gubern, Mérida M. Carme. "Nuevos determinantes moleculares en la respuesta a isquemia cerebral". Doctoral thesis, Universitat de Girona, 2015. http://hdl.handle.net/10803/362102.
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Cerebral ischaemia is a potent inducer of gene expression, however, little is known about the mechanisms that regulate this expression. Studies of gene expression and the study of the mechanisms regulating this expression allow identifying new molecules regulated by ischaemia and possibly involved in the physiopathology of stroke. This thesis shows, (1) the importance of validating suitable endogenous controls for the studies of gene expression for each experimental condition; (2)that Gcf2/Lrrfip1 presents as a gene with diverse isoforms that are differentially expressed in response to stroke and that rLrrfip1, which has a possible protector role, is the main isoform; and (3) that the differential expression of the microRNAs remains from the acute to the chronic phase of ischaemia, having determined that miR-347 promotes neuronal apoptosis and Acsl4 and Arf3, potential targets of microRNAs differentially expressed in response to ischaemia, are new proteins to study in the physiopathology of stroke.La isquèmia cerebral és un potent inductor de l’expressió gènica, en canvi, poc es coneix sobre els mecanismes que regulen aquesta expressió. Els estudis d’expressió gènica i l’estudi dels mecanismes reguladors d’aquesta expressió permeten identificar noves molècules regulades per la isquèmia i possiblement implicades en la fisiopatologia de l’ictus. Aquesta tesi mostra, (1) la importància de validar els controls endògens idonis per als estudis d’expressió gènica per cada condició experimental; (2) que Gcf2/Lrrfip1 és un gen amb diverses isoformes diferencialment expressades en resposta a la isquèmia, sent rLrrfip1 la isoforma principal amb un possible rol protector; i (3) que l’expressió diferencial dels microRNAs es manté des de la fase aguda fins la fase crònica de la isquèmia, havent determinat que el miR-347 promou l’apoptosis neuronal i que Acsl4 i Arf3, potencials dianes de microRNAs diferencialment expressats en resposta a la isquèmia, són noves proteïnes d’estudi en la fisiopatologia de l’ictus.
15
Overell, James Richard. "Vascular investigation and management of ischaemic stroke". Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394761.
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Pogoryelova, Oksana. "A study of epigenetics in ischaemic stroke". Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=201969.
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Ischaemic stroke rates are expected to rise significantly in the next decades due to an aging population. This increases the demand for new stroke biomarkers for early detection of patients at risk and new targets for treatment. It has been hypothesized that epigenetics may be important in the aetiology of stroke. The study consisted of three types of investigation: analysis of candidate gene polymorphism, candidate gene methylation analysis and epigenome-wide methylation analysis (EWAS) of pooled stroke and control samples. The stroke types studied were large vessel disease (LVD), small vessel disease (SVD) and cardioembolic stroke (CE). DNA from peripheral blood samples was used for EWAS and methylation analysis. Significant increases in rare allele frequency were observed in the EHMT2 and DNMT3B genes for all stroke cases; MBD2, DNMT3B and DNMT3L polymorphisms were associated with LVD. IL10, SOD3, LINE1 and PITX2 were significantly hypomethylated in LVD. IL10 and ALOX15 were hypomethylated in CE compared to controls. Methylation levels of following genes were associated with age (LINE1, IL10, MTHFR, TNFα, and PITX2), gender (SOD3 and LINE1), total cholesterol level (SOD3) and systolic blood pressure (IL10). HDAC9 genetic polymorphism was associated with the MTHFR methylation level. A distinctive methylation pattern for each stroke subtype was found by EWAS. The CE pool was hypomethylated at genome, chromosome and gene level, while LVD and SVD pools had regions with higher and lower methylation levels compared to the controls. GNAS was identified as new candidate gene by EWAS. The results suggested that genetic polymorphism and DNA methylation levels of candidate genes were associated with ischaemic stroke. Stroke subtypes had distinct methylation profiles suggesting differences in underlying aetiology. Variations in methylation levels detected in this study could lead to identification of specific biomarkers. Replication on a large number of subjects is required before final conclusions can be drawn.
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Dawson, Suzanne L. "Blood pressure variability and cerebral autoregulation in acute ischaemic stroke". Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29609.
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This thesis examines the haemodynamic changes that occur following acute ischaemic stroke with reference to beat-to-beat blood pressure (BP) levels and variability as well as static and dynamic cerebral autoregulation (CA). Elevated 24h BP levels following acute stroke are associated with a poor outcome, but whether shorter durations of recording using beat-to-beat measurements or other BP parameters such as variability have the same prognostic significance is unknown. A single 10 minute non-invasive beat-to-beat BP monitoring period following acute cerebral infarction showed that increasing BP levels and beat-to-beat beat variability of mean arterial and diastolic BP were associated with a worse prognosis in terms of post ictal death/disability. These initial prognostic findings for BP variability might be explained if CA responses to rapid changes in systemic BP were impaired post stroke. The second part of the thesis set out to measure dynamic and static CA using novel non-invasive techniques employing transcranial Doppler ultrasonography to measure cerebral blood flow velocity in response to non-pharmacologically induced pressor and depressor BP stimuli. The initial study found that in normal controls, the reproducibility and actual values obtained for the autoregulatory indices for both static and dynamic tests varied according to the BP stimulus used. As a result of these initial studies thigh cuff release was used as the stimulus for dynamic CA, and isometric hand grip and thigh cuff inflation as the stimuli for static CA. When the CA results for a study group of acute ischaemic stroke patients were compared to an age and sex matched control group dynamic CA was significantly reduced in the patients' affected and non-affected hemispheres, whereas static CA was unimpaired.
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Schulz, Ursula Gabriele Renate. "Risk factors for specific subtypes of ischaemic stroke". Thesis, University of Oxford, 2004. http://ora.ox.ac.uk/objects/uuid:43200f6f-abe0-4b1e-84a2-31df49707b6f.
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Ischaemic stroke is a complex disorder with many different aetiologies, but previous studies of stroke often did not differentiate aetiological subtypes of ischaemic stroke. However, different stroke subtypes may have different risk factors, and to target preventive treatments more effectively, we need to understand these associations. I studied the association of established vascular risk factors with different aetiological stroke subtypes in population-based cohorts of stroke patients. I studied Diffusion Weighted Magnetic Resonance Imaging (DWI) in patients with subacute minor stroke and TIA to determine whether DWI may be a useful addition to the management of such patients, and whether it may be a useful tool in future epidemiological studies of stroke. To determine whether carotid anatomy may be a risk factor for large vessel atheroma I studied angiographical data from the European Carotid Surgery Trial. My main findings are that the prevalence of risk factors differs between stroke subtypes. It also differs between hospitalised and non-hospitalised patients, highlighting that risk factor studies should be performed in population-based cohorts. Analysis of family history data suggests that future genetic studies may best be targeted at non-cardioembolic stroke and at younger patients, and that genetic studies of hypertension may help to unravel some of the genetic factors contributing to stroke risk. DWI is sensitive in subacute minor stroke, and inter- and intra-observer reproducibility are high. DWI frequently adds useful information and may influence patient management. More widespread use of DWI in patients with subacute stroke and TIA should be considered, and DWI may also be a useful tool in future epidemiological studies of stroke. Carotid anatomy varies considerably between individuals, is very asymmetrical within individuals, and it differs between men and women. These findings may partly explain differences in plaque development between individuals, asymmetrical plaque formation within individuals, and sex differences in the distribution of carotid plaque and in the prevalence of carotid atheroma in the general population. Carotid anatomy may be a risk factor for local plaque development. Although not amenable to treatment, knowing which anatomical configuration is associated with atheroma formation could help to identify high-risk individuals in whom other risk factors should be treated aggressively.
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Arroja, Mariana Moreira. "Cerebral damage following ischaemic stroke : the role of Angiotensin-(1-7)". Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/9010/.
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The renin angiotensin system (RAS), a homeostatic system involved in blood pressure and volume control, is implicated in the pathology of several risk factors for ischaemic stroke. Mounting evidence now suggests that the RAS may play a role in the pathophysiology of ischaemic stroke. This is thought to be due to an imbalance between the classical RAS axis, Angiotensin converting enzyme/Angiotensin II/Angiotensin II receptor type I (ACE/Ang II/AT1R), and the counter-regulatory RAS axis, Angiotensin converting enzyme 2/Angiotensin-(1-7)/Mas receptor [ACE2/Ang-(1-7)/MasR]. The counter- regulatory axis has been shown to provide neuroprotection in ischaemic stroke animal models. Therefore, the studies conducted in this thesis aimed to test the neuroprotective potential of Ang-(1-7) as a post-stroke therapy following transient focal cerebral ischaemia. Furthermore, experiments were conducted to test a potential synergistic effect between MasR and alternative Ang II receptor, Angiotensin II receptor type II (AT2R), agonism following stroke.
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Shrewsbury-Gee, Joanne. "An investigation of compounds of potential value in experimental cerebral ischaemia". Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329110.
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Hassan, Ahmad. "The genetics of ischaemic stroke and the cerebral small vessel disease subtype". Thesis, St George's, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407965.
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Hamilton-Bruce, Monica Anne. "Conventional and topographic electroencephalography and somatosensory evoked potential studies in ischaemic stroke". Adelaide, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phh222.pdf.
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Copies of author's previously published articles inserted. Bibliography: leaves I-LXIV. Assesses the diagnostic and prognostic value of early electroencephalography (EEG) and somatosensory evoked potential studies in cortical and non-cortical ischaemic stroke. Both conventional and topographic/quantitative studies were performed. A parallel study was carried out on healthy volunteers to provide an effective control. Equipment and quantitative EEG (qEEG) variability was also assessed.
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Salomão, Macedo Salinet Angela. "The natural history of the cerebral blood flow regulation after acute ischaemic stroke". Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/28578.
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Acute stroke is known to lead to impairment of cerebral blood flow (CBF) regulation, but its natural history and techniques for its comprehensive assessment have not been previously reported. Noninvasive measurements of blood pressure (BP), end-tidal CO2 and CBF velocity (CBFv, using transcranial Doppler ultrasound) during active, passive and motor imagery paradigms were performed in healthy older controls (n=27) and in stroke patients (n=27). Two innovative analytical techniques were firstly used in stroke studies: subcomponent analysis and multivariate dynamic modeling. In controls, significant increase in CBFv during the paradigms with no significant difference in the response amplitude was found. A reproducibility study, not previously reported, was also performed. Following acute stroke, subcomponents analysis revealed a decrease of CBFv response to the passive paradigm and impairment of the myogenic pathways of CBF regulation. Multivariate dynamic modeling removed the influences of BP and PaCO[subscript 2] showing that the reduced CBFv response to neural activation was directly related and better expressed by the contribution of the stimulation component, instead of the CBFv raw change. The contribution of motor imagery in the CBFv increase was lower compared to the other two paradigms. Impairment of cerebrovascular reactivity to CO[subscript 2] was also detected by the model, without the need of performing specific tests for this purpose. The natural history of CBF regulation revealed a deterioration of control mechanisms in both the acute (< 72h) and subacute (2 weeks) phases, reaching the controls’ levels in the chronic phases (1 and 3 months). It has been demonstrated in this thesis that CBF regulation changes significantly over time after stroke (particularly in the first weeks after onset), having potential impact not only immediately post ictus but also during the subsequent rehabilitation phase.
24
Aspey, Benjamin Steven. "Studies of an ischaemic stroke model (middle cerebral artery occlusion in the rat) and modifications to improve its consistency". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392357.
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Msayib, Yunus. "Quantifying impaired metabolism following acute ischaemic stroke using chemical exchange saturation transfer magnetic resonance imaging". Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:a98323ce-5998-436d-bca4-09df549cf191.
Texto completo da fonteResumo:
In ischaemic stroke a disruption of cerebral blood flow leads to impaired metabolism and the formation of an ischaemic penumbra in which tissue at risk of infarction is sought for clinical intervention. In stroke trials, therapeutic intervention has largely been based on perfusion-weighted measures, but these have not been shown to be good predictors of tissue outcome. The aim of this thesis was to develop analysis techniques for magnetic resonance imaging (MRI) of chemical exchange saturation transfer (CEST) in order to quantify metabolic signals associated with tissue fate in patients with acute ischaemic stroke. This included addressing robustness for clinical application, and developing quantitative tools that allow exploration of the in-vivo complexity. Tissue-level analyses were performed on a dataset of 12 patients who had been admitted to the John Radcliffe Hospital in Oxford with acute ischaemic stroke and recruited into a clinical imaging study. Further characterisation of signals was performed on stroke models and tissue phantoms. A comparative study of CEST analysis techniques established a model-based approach, Bloch-McConnell model analysis, as the most robust for measuring pH-weighted signals in a clinical setting. Repeatability was improved by isolating non-CEST effects which attenuate signals of interest. The Bloch-McConnell model was developed further to explore whether more biologically-precise quantification of CEST effects was both possible and necessary. The additional model complexity, whilst more reflective of tissue biology, diminished contrast that distinguishes tissue fate, implying the biology is more complex than pH alone. The same model complexity could be used reveal signal patterns associated with tissue outcome that were otherwise obscured by competing CEST processes when observed through simpler models. Improved quantification techniques were demonstrated which were sufficiently robust to be used on clinical data, but also provided insight into the different biological processes at work in ischaemic tissue in the early stages of the disease. The complex array of competing processes in pathological tissue has underscored a need for analysis tools adequate for investigating these effects in the context of human imaging. The trends herein identified at the tissue level support the use of quantitative CEST MRI analysis as a clinical metabolic imaging tool in the investigation of ischaemic stroke.
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Turner, Renée Jade. "Characterising the role of substance P in acute ischaemic stroke". 2007. http://hdl.handle.net/2440/56839.
Texto completo da fonteResumo:
More than 15 million people worldwide will suffer a stroke each year two thirds will die or be left permanently disabled. Accordingly, stroke represents an enormous financial burden on the community, due to the cost of hospitalisation, treatment and rehabilitation of stroke patients. Despite the significance of this public health problem, a safe and widely applicable stroke therapeutic remains elusive. Cerebral oedema is widely recognised as a common and often fatal complication of stroke that is associated with worsened outcome. However, the exact mechanisms of oedema formation remain unclear, with current therapies largely ineffective in addressing the mechanisms of cerebral swelling, and also being associated with their own negative side-effect profile. This thesis characterises the role of neurogenic inflammation and the neuropeptide, substance P (SP), in mediating the development of blood brain barrier breakdown, cerebral oedema and resultant functional deficits following stroke, using a rodent model of reversible cerebral ischaemia. The findings of this thesis demonstrate that increased SP immunoreactivity, particularly of the penumbral tissue vasculature, is a feature of tissue perfusion following stroke, but not in non-reperfused infarcts. The central role for SP in the breakdown of the BBB following stroke and the associated deleterious effects of such breakdown was confirmed by studies using an NK₁ receptor antagonist. These antagonists conferred a profound attenuation of BBB breakdown, cerebral oedema formation, neuronal death and injury, and the associated development of functional deficits following reversible stroke. Similarly, depletion of all neuropeptides by capsaicin pre-treatment also reduced both histological abnormalities and functional deficits following stroke, confirming the central role of neuropeptides in the secondary injury process after stroke. The NK₁ receptor antagonist was able to be safely combined with the currently approved treatment for stroke, tPA, producing a synergistic effect of greater protection from the ischaemic insult. In particular, histological and functional outcome were markedly improved, as well as a reduction in the risk of intracerebral haemorrhage and death. Furthermore, the NK₁ receptor antagonist was effective even when administered up to 8 h following the onset of ischaemia, and in a variety of stroke severities. We conclude that SP plays a central role in the secondary injury that occurs following stroke, in particular, the genesis of BBB breakdown and cerebral oedema. Accordingly, combination therapy of tPA and an NK₁ receptor antagonist may offer a novel therapeutic strategy for the clinical management of ischaemic stroke of varying severity.http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1298280
Thesis (Ph.D.) -- The University of Adelaide, School of Medical Sciences, 2007