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Tesi sul tema "Cerebrovascular disease"
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1
Holt, Jim, e Gregg Mitchell. "Cerebrovascular Disease KSA". Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etsu-works/6458.
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2
Murphy, Jeremy James. "Clinical trials in cerebrovascular disease". Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293328.
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3
Man, Lai-mei. "An exploratory study for the health seeking pattern of stroke survivors on alternative medicine". Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20133236.
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4
Williams, David James. "Near infrared spectroscopy in cerebrovascular disease". Thesis, University of Bath, 2002. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426180.
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5
Hoffmann, Tammy Coral. "Development and evaluation of a computer-generated individualised written education package for patients following stroke and their carers /". [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18924.pdf.
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6
Wan, Wai-kuen Christina. "An exploratory design of an empowerment group for the stroke survivors". Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19469937.
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7
Li, Sijian. "Evaluating the effectiveness of a stroke education programme in Wuhan City of China /". Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20793224.
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8
Fung, Mei-ling. "Stroke rehabilitation : predicting LOS and discharge placement /". Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25101298.
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9
Gibbs, Richard Geoffrey James. "The aetiology and epidemiology of cerebrovascular disease". Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405270.
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10
Chan, Chi-wing Martin. "Is bilateral isokinematic training (BIT) more effective than unilateral limb training in improving the hemiplegic upper-limb function /". View the Table of Contents & Abstract, 2004. http://sunzi.lib.hku.hk/hkuto/record/B30469697.
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11
Adomaitis, Laura G. "An intensive massed practice approach to retraining balance post-stroke /". view abstract or download file of text, 2002. http://wwwlib.umi.com/cr/uoregon/fullcit?p3055664.
Testo completoAbstract (sommario):
Thesis (Ph. D.)--University of Oregon, 2002.Typescript. Includes vita and abstract. Includes bibliographical references (leaves 183-193). Also available for download via the World Wide Web; free to University of Oregon users.
12
Vattanasilp, Wantana. "The contribution of neural and peripheral factors to muscle stiffness and function following stroke". Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/26242.
Testo completoAbstract (sommario):
The aim of these studies was to investigate the contributions of neural and peripheral factors to the increased resistance to movement and loss of function commonly observed following stroke. Three studies were undertaken to investigate the stiffness of the calf muscles in stroke subjects. Under relaxed conditions, neural factors such as spasticity and peripheral factors such as contracture and thixotropy were investigated. Under active conditions, the contribution of the tonic stretch reflex to functional movement, in this case walking, was investigated. These findings were compared to results retained from neurologically-normal subjects.
The clinical measurements of spasticity (Ashworth Scale and tendon jerk) were collected and the laboratory measurement (tonic stretch reflex) was measured in all studies. Clinical measurements of spasticity were performed to describe the stroke subjects clinically, whereas the laboratory measurement, ie, the measurement of the tonic stretch reflex recording EMG during sinusoidal stretching, was performed to provide a quantitative benchmark of spasticity in the gastrocnemius muscle. Measurement of the tonic stretch reflex was chosen because EMG can differentiate the neural and the peripheral contributions.
Under relaxed conditions, it was found that most stroke subjects exhibited resting tonic stretch reflexes, indicating the presence of spasticity. Stroke subjects also exhibited a thixotropic response which was within the range of normal responses. Some stroke subjects displayed muscle contracture. When the contributions of these various factors to stiffness were examined, contracture appeared to make the most significant contribution to the increased resistance to movement.
Under active conditions, the contribution of spasticity to walking dysfunction following stroke was investigated in a group of ambulant stroke subjects. The tonic stretch reflex was investigated under active conditions which mimicked the movement of the ankle joint during walking. Stroke subjects exhibited a smaller action tonic stretch reflex compared with normal subjects, and this finding was not statistically different. It was suggested that rather than exhibiting an ‘out of control’ tonic stretch reflex, stroke subjects had an impaired modulation of the tonic stretch reflex. Also, the action tonic stretch reflex of stroke subjects did not contribute as much as that of normal subjects to the resistance of calf muscles under active conditions. Therefore, it is suggested that an abnormal tonic stretch reflex does not routinely contribute to walking dysfunction following stroke. Furthermore, when the modulation of the tonic stretch reflex was measured at pre-ambulatory and ambulatory stages after early stroke, it was found that an improvement in function of the ankle joint was not accompanied by an ability to modulate the tonic stretch reflex in the gastrocnemius muscle.
Finally, a relation between the clinical and laboratory measurements of spasticity was found only for the tests of resistance to movement, but not for the tests of reflex activity. These findings suggested that clinical tests cannot adequately quantify spasticity, and that the resistance felt during passive movement cannot be differentiated using a clinical grading test such as the Ashworth Scale.
These studies add to the growing body of evidence that spasticity is not the major problem interfering with functional tasks after stroke. Therefore, it is not important to routinely reduce spasticity for the purpose of improvement in function. However, the need to prevent and/or minimise muscle contracture is essential in order to avoid the increase in passive stiffness which accompanies the contracture.
13
Fernández-Andújar, Marina. "Neuroimaging correlates of cognitive functioning in cerebrovascular disease". Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/290852.
Testo completoAbstract (sommario):
Cerebrovascular diseases (CD) are the third most common cause of death and the leading cause of disability in adults in developed countries (Carmichael, 2012; World Health Organization, 2004). Specifically, ischemic stroke and white matter lesions (WML) often result in multiple neurological, cognitive impairment and behavioral and emotional disorders (Gorelick et al., 2011; Troncoso et al., 2008). Strokes are responsible for damage in the core of the ischemic lesion but may also cause alterations in remote areas from the primary ischemic lesion. The thalamus is a key structure in the cortico-subcortical circuits (Alexander et al., 1986; Byne et al., 2009) and is involved in multiple cognitive functions (Herrero et al., 2002; Sherman, 2005) especially in functions executive, one of the most affected cognitive domains after suffering a stroke. Although it is known that the cortico- subcortical circuits are involved in cognitive functions, to date their neuroimage correlates are unknown. The overall objective of this thesis was to study the effects of a disruption in the cortico-subcortical circuits, due to a direct or remote damage, in executive functions. For the study of remote thalamic abnormalities we use the technique of diffusion tensor image (DTI) for both ischemic stroke and WML. Moreover, due to attention and cognitive inhibition are one of the most important functions of executive domain, we studied the relationship between a specific white matter (WM) tract -called Front aslant Tract (FAT)- and these functions. The study results showed that remote thalamic microstructural abnormalities secondary to a cerebrovascular lesion can occur in both ipsilateral and contralateral thalamus, in healthy subjects with WML and in patients with cerebral ischemic stroke. These thalamic abnormalities may be related to a disruption in the cortico-subcortical circuits associated with executive dysfunction. In addition, the right FAT is involved in attention and response inhibition functions in community-dwelling subjects and participants with ischemic stroke. In conclusion, the results obtained in this thesis suggest that stroke can affect the cortico-subcortical circuits through thalamic microstructural abnormalities and these could be related to cognitive dysfunction. Finally, the novel technique of DTI can play an important role in understanding the cognitive functioning in both ischemic stroke and WML.Los accidentes cerebrovasculares (ACV) son la tercera causa más común de muerte y la causa principal de discapacidad en adultos en los países desarrollados (Carmichael, 2012; Organización Mundial de la Salud, 2004). Concretamente, el ictus isquémico y las lesiones de sustancia blanca (LSB) frecuentemente dan lugar a múltiples secuelas neurológicas, deterioro cognitivo y alteraciones conductuales y emocionales (Gorelick et al., 2011; Troncoso et al., 2008). Los ACV son responsables de daño en la zona primaria de la lesión isquémica pero también pueden producir alteraciones en áreas remotas a ésta. El tálamo es una estructura clave en los circuitos cortico-subcorticales (Alexander et al., 1986; Byne et al., 2009) y está involucrado en múltiples funciones cognitivas (Herrero et al., 2002; Sherman, 2005) especialmente en las funciones ejecutivas, uno de los dominios cognitivos más afectados después de sufrir un ACV. Aunque se sabe que los circuitos cortico-subcorticales están implicados en las funciones cognitivas, hasta la fecha sus correlatos de neuroimagen se desconocen. El objetivo general de esta tesis ha sido estudiar los efectos de una interrupción en los circuitos cortico-subcorticales debido a una lesión directa o remota en las funciones ejecutivas. Para el estudio de las anomalías talámicas remotas usamos la técnica de la Imagen por Tensor de Difusión (ITD), tanto para el ictus isquémico como para las LSB. Además, dado que la atención y la inhibición cognitiva son una de las funciones más importantes de las funciones ejecutivas, estudiamos la relación entre un tracto de sustancia blanca (SB) -llamado Frontal Aslant Tract (FAT)- y estas funciones. Los resultados de los estudios mostraron que anomalías secundarias microestructurales talámicas remotas a la lesión cerebrovascular pueden ocurrir tanto en el tálamo ipsilateral como en el tálamo contralateral, en sujetos sanos con LSB y en pacientes con un ictus cerebral isquémico. Estas anomalías talámicas pueden estar relacionadas con una disrupción en los circuitos cortico-subcorticales asociado con disfunción ejecutiva. Además, en sujetos de la comunidad y con un ictus isquémico, el FAT derecho está implicado en atención e inhibición de respuesta. En conclusión, los resultados obtenidos en la presente tesis doctoral sugieren que los ACV puede afectar los circuitos cortico-subcortical a través de anomalías microstructurales talámicas y éstas podrían estar relacionadas con la disfunción cognitiva. Finalmente, la novedosa técnica de la ITD puede tener un papel relevante en el conocimiento del funcionamiento cognitivo tanto en el ictus isquémico como en las LSB.
14
Zhu, Li. "Cerebrovascular disease and dementia : a population-based study /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3810-5/.
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15
Perkins, Jeremy Michael Towers. "Changing cerebrovascular reactivity in occlusive carotid artery disease". Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245525.
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16
Wei, Jade Wei. "Disparities in the burden of stroke in China and its relevance to emerging economies". Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/28922.
Testo completoAbstract (sommario):
With an estimated 5.7 million deaths from stroke each year, stroke is the second leading
cause of mortality worldwide. However, there are significant disparities in the burden
of chronic, non-communicable diseases such as stroke across the world. Whilst rates of
stroke and cardiovascular disease have remained relatively stable or have been
declining over the past 10 years in developed countries, recent demographic transitions
and economic developments have resulted in developing countries witnessing an
escalation in the rates of these diseases that now top lists of leading causes of death and
disability along with historic communicable diseases. Of the developing countries,
Brazil, Russia, India, Indonesia, China, and the Republic of South Africa — the star
performing emerging economies, are projected to have the highest potential for
economic grth in the coming decades. Much of the success witnessed in these
countries has been attributable to trade liberalisation and market opening reforms;
however, these reforms have also inadvertently triggered extensive demographic, social
and health transitions in the vast, heterogeneous populations of these countries.
Notably, the people in these countries have been increasingly exposed to unhealthy
diets and sedentary lifestyles, typical of urban metropolises, ways of life that have
inflamed the progression of atheromatous and ischaemic disease.
With one-fifth of the world’s population, China experiences nearly 60% of all the
stroke deaths from the 6 major emerging economies, one third of stroke deaths
worldwide, and has stroke listed as a leading cause of death and disability, making it an
optimal candidate for examination of the evolving epidemiology of stroke in these
countries. As in many developing nations, limited epidemiological data exist on stroke
in China. The aim of this thesis was therefore firstly to examine the burden of stroke in
China in relation to the changing epidemiology of its two predominant subtypes:
ischaemic stroke and intracerebral haemorrhage (ICH); secondly to explore disease
burden in terms of mortality, morbidity and cost by type of stroke; and thirdly, to
identify points of disparity in the management of stroke, in order to facilitate the
appropriate design and implementation of future interventions aimed at reducing this
burden.
The majority of this work is based on analyses of the ChinaQUEST (QUality
Evaluation of Stroke Care and Treatment) study which used a multi-centre, prospective,
hospital registry design to collect data from 62 hospitals in 37 cities across mainland
China. Chinese hospitals are classified as Level 1 (community hospitals with only the
most basic facilities and very limited inpatient capacity), Level 2 (hospitals with at least
100 inpatient beds providing acute medical care and preventative care services to
populations of at least 100,000), and Level 3 (major tertiary referral centres in
provincial capitals and major cities). Statistical analyses as appropriate to each section
of work were undertaken using STATA (StataCorp LP, College Station, TX).
17
Cheung, Ching-ying Crystal. "Facial emotion recognition after subcortical cerebrovascular diseases /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23425027.
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18
Farr, Tracy Deanne, e University of Lethbridge Faculty of Arts and Science. "A mouse model for studying stroke induced impairments, recovery, and compensation in the motor cortex". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2003, 2003. http://hdl.handle.net/10133/156.
Testo completoAbstract (sommario):
Stroke is the third leading cause of death and survivors suffer motor impairments. The rodent sensorimotor system is similar to the human's, making rodents a good model to study the effects of stroke. Transgenic technology makes the mouse a desirable stroke model, however, there are few behavioural tests to assess behavioural outcome. This thesis evaluates mice subjected to permanent or temporary occlusion focal motor cortex strokes in a skilled reaching task. The first experiment documents changes in skilled movements in mice with a permanent occlusion focal motor cortex stroke. The second experiment is identical but uses a temporary occlusion focal motor cortex stroke. The third experiment compares the two strokes. The results indicate permanent occlusion mice suffer great impairments, and a larger injury, than temporarily occluded animals. The mice with the largest insults were most impaired. Mice make an excellent behavioural and genetic model for studying motor system stroke.viii, 115 leaves : ill. ; 29 cm.
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Foroud, Afra, e University of Lethbridge Faculty of Arts and Science. "Moving from stroke to development : a deconstruction of skilled reaching in humans". Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2008, 2008. http://hdl.handle.net/10133/1307.
Testo completoAbstract (sommario):
The purpose of this thesis is to describe the organization of the movements of skilled
reaching. Our knowledge of reaching behaviour has been limited to an understanding of
specific actions. Results from this thesis describe how reaching is the product of
interactions of various parameters that assemble in an integrative way in ontogeny, yet
can become dismantled on one level, or generally, throughout multiple levels of what
constitutes the behaviour after stroke in adults. These findings demonstrate that skilled
reaching constitutes motor parameters that may not be visible in a healthy adult, but that
function through development, and by inhibitory systems in adults, to create a smooth
and finely articulated action. An examination of the movement patterns of reaching
within the full context of the behaviour can be applied to therapeutic strategies for motor
disorders and, most importantly, deepen our understanding of the relations between
reaching and cognition.xiii, 254 leaves : ill. (some col.) ; 29 cm
20
張晶凝 e Ching-ying Crystal Cheung. "Facial emotion recognition after subcortical cerebrovascular diseases". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31224155.
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Shenkin, Susan Deborah. "Life course influences on cognitive ability and cerebrovascular disease". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/25179.
Testo completoAbstract (sommario):
This thesis aimed to investigate life coarse influences on cognitive ability and cerebrovascular disease (CVD) in older people. 110 community-dwelling subjects (70.0% female, mean age 78.2 (SD 1.4) years) born in Edinburgh hospitals between 1921 and 1926 had birth parameters (weight, length, placental weight) extracted from archives, underwent physical and neuropsychological tests, and imaging of brain volume, white matter lesions (WML) and diffusion tensor imaging (DTI). (1) Relationship between cognitive ability and structural brain indices. Cognitive ability (g) was associated with both whole brain volume (r = .24, P <.05) and intracranial area (r = .27, P <.01), suggesting the relationship between brain size and cognitive ability in old age is due to the persistence of this relationship from earlier life. (2) Relationships among early life factors (birth parameters, social class, the Apolipoprotein E (APOE) gene) and cognitive ability. There was an association between birth weight and cognitive ability in old age (Raven’s r = .20, P = .04; MMSE ρ = .23, P = .02), partly but not fully explained by this association in earlier life. Therefore, the prenatal environment may influence cognitive ability into old age. Social class correlated negatively with cognitive ability in childhood (ρ = .21, P = .02) but not later life (Raven’s ρ = -.09, P = .36): the influence of the shared environment decreases with time. APOEe4 was associated with worse performance on logical memory only. (3) Relationship among early life factors and CVD. Birth parameters, particularly placental weight, were associated with a history of CVD (t = -2.2, P = .04), WML load (ρ = -.23, P = .04), and DTI (
22
Willats, Lisa. "Improved quantification of perfusion in patients with cerebrovascular disease". Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1445148/.
Testo completoAbstract (sommario):
In recent years measurements of cerebral perfusion using bolus-tracking MRI have become common clinical practice in the diagnosis and management of patients with stroke and cerebrovascular disease. An active area of research is the development of methods to identify brain tissue that is at risk of irreversible damage, but amenable to salvage using reperfusion treatments, such as thrombolysis. However, the specificity and sensitivity of these methods are limited by the inaccuracies in the perfusion data. Accurate measurements of perfusion are difficult to obtain, especially in patients with cerebrovascular diseases. In particular, if the bolus of MR contrast is delayed and/or dispersed due to cerebral arterial abnormalities, perfusion is likely to be underestimated using the standard analysis techniques. The potential for such underestimation is often overlooked when using the perfusion maps to assess stroke patients. Since thrombolysis can increase the risk of haemorrhage, a misidentification of 'at-risk' tissue has potentially dangerous clinical implications. This thesis presents several methodologies which aim to improve the accuracy and interpretation of the analysed bolus-tracking data. Two novel data analysis techniques are proposed, which enable the identification of brain regions where delay and dispersion of the bolus are likely to bias the perfusion measurements. In this way true hypoperfusion can be distinguished from erroneously low perfusion estimates. The size of the perfusion measurement errors are investigated in vivo, and a parameterised characterisation of the bolus delay and dispersion is obtained. Such information is valuable for the interpretation of in vivo data, and for further investigation into the effects of abnormal vasculature on perfusion estimates. Finally, methodology is presented to minimise the perfusion measurement errors prevalent in patients with cerebrovascular diseases. The in vivo application of this method highlights the dangers of interpreting perfusion values independently of the bolus delay and dispersion.
23
Bamford, John Michael. "The classification and natural history of acute cerebrovascular disease". Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292663.
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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.
Testo completoAbstract (sommario):
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.
25
Power, Albert. "Dysregulated coagulation in haemodialysis : vascular access and cerebrovascular disease". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9607.
Testo completoAbstract (sommario):
Uraemia confers a prothrombotic tendency in tandem with a bleeding diathesis through platelet dysfunction that is most evident in patients with renal failure who are dependent on haemodialysis. This form of renal replacement therapy accentuates this clinical paradox by its procoagulant nature and the use of regular anticoagulation to prevent dialysis circuit and vascular access thrombotic dysfunction. This thesis evaluates such dysregulated coagulation in the extracorporeal circuit, the central venous catheter and dialyser, and in the twin substrates of cerebrovascular disease, thromboembolism and haemorrhage. Firstly the comparative effect of catheter site on thrombosis is evaluated by the jugular and translumbar routes before examining catheter type as a determinant in a randomised, controlled clinical trial. Subsequently novel use of catheter flow monitoring as a predictive tool for thrombotic dysfunction is presented and the efficacy of thrombolytic therapies assessed. Lastly a prospective pharmacokinetic evaluation of tinzaparin in dialysis circuit anticoagulation which revealed a novel influence of gender on anti-factor Xa activity. Stroke incidence and risk is examined in one of the largest studies to date before two specific risk factors for thromboembolic stroke are examined, intracranial arterial calcification and transient ischaemic attack. A potential association between intracranial arterial calcification and this stroke subtype is described for the first time in haemodialysis and results from the first prospective screening study for transient ischaemic attack in haemodialysis are presented. Finally renal dysfunction is shown to be a determinant of thrombolytic efficacy in acute ischaemic stroke. All these studies advance our understanding of thrombotic catheter dysfunction, its thrombolytic management and the behaviour of tinzaparin in haemodialysis. In addition they afford unique insights into cerebrovascular disease in haemodialysis that challenge traditional paradigms of a pathology with high incidence in these patients.
26
Ellis, Graham. "Stroke liaison workers for patients and carers". Thesis, Connect to e-thesis, 2008. http://theses.gla.ac.uk/288/.
Testo completoAbstract (sommario):
Thesis (MD.) - University of Glasgow, 2007.MD. thesis submitted to the Division of Cardiovascular and Medical Sciences, Faculty of Medicine, University of Glasgow, 2007. Includes bibliographical references. Print version also available.
27
Adomaitis, Laura G. "An intensive massed practice approach to re-training balance post-stroke". view abstract; pdf file available for purchase, 2002. http://wwwlib.umi.com/cr/uoregon/fullcit?p3055664.
Testo completo
28
Chow, Esther Oi-wah. "Resilience among stroke survivors : the experience of Hong Kong women /". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B34861439.
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29
Kwok, Wing-yee Eunice. "Early supported discharge program for stroke patients". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40720883.
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30
Luque, Gómez Ana. "Paper de "Chlamydia pneumoniae" en la generació de respostes immunes implicades en la malaltia cerebrovascular". Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/80091.
Testo completoAbstract (sommario):
L’aterosclerosi carotídia és una de les principals causes del ictus isquèmic, el qual és una de les principals causes de mort i morbiditat als països desenvolupats. Avui dia es considera l’aterosclerosi una malaltia multifactorial en la que intervenen des d’un component genètic fins a diferents factors de risc clàssics com la hipertensió, l’edat, la diabetis, etc. Aquests factors de risc clàssics només són capaços d’explicar el 90% dels cassos, de forma que nous factors de risc, encara desconeguts, deuen estar implicats en el inici i progressió de l’arteriosclerosi. S’ha proposat que la infecció per virus o bactèries, com Cytomegalovirus o Herpes simplex virus, pot ser un d’aquests factors. Tanmateix, el microorganisme més estudiat ha estat Chlamydia pneumoniae, ja que es tracta d’una bactèria de vida intracel•lular obligada, capaç de causar estats d’infecció crònics. S’ha realitzat un estudi pilot amb l’objectiu de la determinació de marcadors d’hipòxia, inflamació i angiogènesi en plaques carotídies amb estenosi lleu o moderada (<50%). Posteriorment, s’ha analitzat la relació entre presència d’infecció per C. pneumoniae y aterosclerosi analitzant la presència d’infecció en plaques carotídies de baix a elevat grau, i en sèrum de pacients sotmesos a endarterectomia. Finalment, s’ha realitzat un estudi de genoma complet mitjançant microarrays en cèl•lules endotelials de caròtida humana per tal de determinar les vies de senyalització claus activades per la infecció d’aquestes cèl•lules amb C. pneumoniae i veure quins processos proaterogènics s’activen. S’ha comprovat l’activació de plaques carotídies arterioscleròtiques en estats inicials per la presència de marcadors d’hipòxia, inflamació, angiogènesi i respostes immunes. S’ha detectat presència d’ADN de C. pneumoniae per PCR en lesions carotídies inicials suggerint que C. pneumoniae pot jugar un paper clau en el inici i progressió de la lesió arterioscleròtica. Mitjançant un model in vitro d’infecció de cèl•lules endotelials de caròtida humana hem pogut establir vies metabòliques claus en la propagació d’inflamació, generació de respostes immunes i d’apoptosi. Per tant, suggerim la possible implicació de la infecció per C. pneumoniae en el inici i progressió de l’aterosclerosi carotídia.ROLE OF CHLAMYDIA PNEUMONIAE IN THE GENERATION OF IMMUNE RESPONSES INVOLVED IN THE CEREBROVASCULAR DISEASE Carotid atherosclerosis is one of the main causes of ischemic brain stroke which is one of the most common causes of death and morbidity in developed countries. Nowadays atherosclerosis is considered a multi-factorial disease in which take part a genetic component and different classic risk factors such as hypertension, age, diabetes, etc. These classic risk factors are only able to explain the 90% of cases, so new risk factors, still unknown, should be involved in initial stages and development of atherosclerosis. Infectious agents, like Cytomegalovirus or Herpes simplex virus, have been related to the development of cardiovascular disease. However, Chlamydia pneumoniae is the most studied microorganism because it is bound intracellular Gram-negative bacterium able to cause chronic infection stages. A pilot study had been performed to identified hypoxia, inflammation and angiogenesis markers in atherosclerotic carotid plaques with low to moderate stenosis (<50%). We investigated the presence of C. pneumoniae infection in different vascular territories related with risk of ischemic stroke and we also identified any differences between early and advanced lesions. Furthermore, we studied the relationship between the presence of C. pneumoniae and over-expression of the HIF-1α in carotid lesions to confirm an association between hypoxic tissue environment and bacterial infection in our specimen. A whole genome microarrays study was performed in human carotid artery endothelial cells infected with C. pneumoniae in order to identified important pathways and proatherogenic processes activated by the infection. There was an activation of initial carotid atherosclerotic plaques due to the presence of hypoxia, inflammation, angiogenesis and immune responses markers. DNA of C. pneumoniae was detected by PCR in early lesions. Using an in vitro human carotid artery endothelial cells infection model we defined important metabolic pathways in inflammation progress, immune responses generation and apoptosis. Therefore, we suggest that C. pneumoniae might play an important role in activation and development of the initial stages of carotid atherosclerosis.
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Cvetkovic, ́. Jasmina. "Immune mechanisms in atherosclerotic vascular disease /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-268-X.
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Salas, Perdomo Angélica María. "Estudio de la lesión por reperfusión en la isquemia cerebral experimental y su tratamiento". Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667982.
Testo completoAbstract (sommario):
El ictus es un fenómeno agudo que causa una interrupción del aporte sanguíneo al cerebro, causando muerte de las células por la falta de oxígeno. El ictus es la segunda causa de muerte para personas mayores de 60 años y la causa más frecuente de discapacidad permanente. Debido al creciente envejecimiento de la población y al gran impacto que tiene el ictus, existe una gran necesidad de investigar sobre esta enfermedad, los factores de riesgo, sus consecuencias y por supuesto, nuevos tratamientos.
El principal objetivo del tratamiento del ictus es el retorno del FSC al tejido. Aunque la reperfusión es indispensable para salvar el tejido cerebral hipoperfundido, esta puede tener efectos nocivos que se conocen como daño por reperfusión. Diversos estudios han demostrado las alteraciones provocadas por la reperfusión, como el aumento de la producción de ROS y RNS, aumento de expresión de moléculas de adhesión intercelular, inflamación, disminución de la función y ruptura de la BHE, transformación hemorrágica del infarto y desarrollo de un fenotipo procoagulante/protrombótico de la pared vascular.
Esta tesis se ha enfocado en el estudio de dos principales consecuencias del daño por reperfusión como son el estrés oxidativo y la transformación hemorrágica (TH) del infarto en modelos animales. Sin embargo, los seres humanos que sufren un ictus suelen presentar enfermedades concomitantes que exacerban el daño por isquemia/reperfusión y es importante que en los modelos animales también se evalúen estos factores de riesgo o situaciones clínicas relacionadas con el ictus isquémico humano. Teniendo en cuenta estas circunstancias, este trabajo de tesis se ha centrado en el estudio del estrés oxidativo aumentado por hiperglucemia y en la trasformación hemorrágica del infarto en condiciones de linfopenia. Así mismo, estudiamos la posibilidad de modular el estrés oxidativo y la respuesta inflamatoria como métodos para potenciar el tratamiento del ictus y minimizar los daños por reperfusión.
En el primer trabajo mostramos que los ratones a los que se les indujo hiperglucemia previamente a la I/R podían beneficiarse del tratamiento con el antioxidante natural ácido úrico (AU). Este estudio ha demostrado que las altas concentraciones sanguíneas de glucosa exacerban el daño por isquemia/reperfusión. Y que el AU puede contribuir a reducir el volumen de infarto en los ratones hiperglucémicos a través de su efecto antioxidante con una gran eficacia en la limpieza de radicales libres derivados del peroxinitrito y sus efectos vasculoprotectores limitando la toxicidad de la glucosa y la muerte celular secundaria.
El segundo trabajo se centra en el estudio de las células T y su relación con la TH. Este estudio demuestra que los linfocitos T reducen el riesgo de TH. Confirma la relevancia del volumen del infarto como un factor crítico que incrementa el riesgo de TH. A su vez, los resultados de este estudio resaltan la comunicación bidireccional que existe entre las células T y las plaquetas creando un puente entre la inmunidad y la hemostasia para prevenir la TH tras un ictus isquémico agudo. Estos resultados pueden determinar nuevas dianas celulares y moleculares para la prevención de la TH secundaria al ictus isquémico.
En el tercer trabajo, hemos intentado reducir la TH mediante un tratamiento farmacológico con el inmunomodulador Fingolimod. Los resultados de este estudio muestran una activación de la vía de señalización S1P en el cerebro después de la I/R, esta activación sugiere que los fármacos moduladores del receptor S1P pueden desempeñar un papel en el parénquima independiente de los efectos del fármaco sobre el sistema inmune. También demostró que el Fingolimod puede atenuar la TH del infarto cerebral por una vía independiente de los linfocitos, pero el tratamiento no es efectivo en condiciones de trombocitopenia.Stroke is an acute phenomenon caused by the interruption of the blood supply to the brain. Stroke is one of the leading causes of death and permanent disability in the world. Due to the huge impact of stroke in our society, there is a great need to investigate this disease, the risk factors, their consequences and, of course, new treatments. The main objective of stroke treatment is the return of cerebral blood flow to the brain tissue. Although reperfusion is essential to save hypoperfused brain tissue, it may have unwanted complications that are known as reperfusion damage. This thesis has focused on the study of two negative consequences of reperfusion, such as oxidative stress and hemorrhagic transformation (HT) of infarction in animal models. Likewise, we studied the possibility of modulating oxidative stress and the inflammatory response in order to minimize reperfusion damage. In the first work we showed that mice that had hyperglycemia induced before ischemia/reperfusion could benefit from treatment with uric acid (AU) through its antioxidant effect, limiting glucose toxicity and secondary cell death. The second work focuses on the study of T cells and their relationship with HT. The results of this study highlight the bidirectional communication that exists between T cells and platelets, creating a bridge between immunity and hemostasis to prevent HT after an acute ischemic stroke. These results can determine new cellular and molecular targets for the prevention of HT secondary to ischemic stroke. In the third work, we have tried to reduce HT through a pharmacological treatment with Fingolimod. It also showed that Fingolimod can attenuate the HT of cerebral infarction through a lymphocyte-independent pathway, but the treatment is not effective in thrombocytopenia conditions. Overall this thesis identifies cellular and molecular mechanisms underlying complications of reperfusion therapies following ischemic stroke, and suggests pharmacological therapies to increase the benefits of reperfusion treatments.
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Mara, Prengler. "Magnetic resonance perfusion and cerebrovascular studies in sickle cell disease". Thesis, University College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418098.
Testo completo
34
Gale, Catherine Rose. "Antioxidant vitamins, cerebrovascular disease and cognitive function in elderly people". Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264648.
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35
Gatenby, Paul, Gytis Danta, Roger Tuck, Colin Andrews e Carolyn Hawkins. "Cerebrovascular disease associated with antiphospholipid antibodies: more questions than answers". Master's thesis, BioMed Central, 2006. http://hdl.handle.net/10440/104.
Testo completoAbstract (sommario):
Neurological syndromes occur in a significant number of patients with antiphospholipid antibodies. The
optimal management for these patients however remains uncertain.
Our study is a descriptive analysis looking retrospectively at 45 patients who presented to the principal
tertiary referral centre in the Australian Capital Territory, with either cerebral arterial or venous
thrombosis for which there was no obvious cause for their presentation when initially reviewed. The
diagnosis was based on the clinical findings made by one of three neurologists attached to our centre.
Radiological findings and the presence of either IgM or IgG anticardiolipin antibodies, IgG anti-beta-2
glycoprotein 1 antibodies or a lupus anticoagulant were then documented.
In this group of patients three subgroups were identified:
1. Individuals that fulfilled the Sapporo Classification Criteria
2. Individuals with transiently positive antiphospholipid antibodies and
3. Individuals with persistently low positive antiphospholipid antibodies.
The most interesting of these three groups are those individuals with transiently positive antiphospholipid
antibodies. A potential cause for presentation was identified in only one patient of this group with
documented infective endocarditis and bacteraemia. Comparison with the other two groups suggested
that there was little in terms of clinical presentation, radiological findings or intercurrent risk factors for
thrombotic disease to distinguish between them. With disappearance of antiphospholipid antibodies, the
individuals within this group have not had further thrombotic events.
Our observations emphasise the problems that continue to exist in relation to the occurrence of
cerebrovascular disease in the context of antiphospholipid antibodies and the optimal management of
these stratified groups. Our findings also raise an as yet unanswered question as to the signficance of these
transiently positive antiphospholipid antibodies. In the absence of significant intercurrent risk factors our
findings would suggest that in the group we describe that they are likely to be of clinical significance.
36
Gan, Rui. "Robust multimodal medical image registration and statistical cerebrovascular segmentation /". View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?COMP%202006%20GAN.
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Rau, Marie Therese. "Elderly stroke patients and their partners: a longitudinal study of social support and well-being changes associated with a disabling stroke". PDXScholar, 1986. https://pdxscholar.library.pdx.edu/open_access_etds/478.
Testo completoAbstract (sommario):
This investigation explored the relationship of demographic, social network, social support, and stroke-related factors to depressive symptomatology and well-being in 50 elderly individuals who had recently suffered a first, completed stroke and their partners. Data were gathered at two points in time, with interviews scheduled six months apart. Outcome measures included the CES-D depression scale and the Index of Psychological Well-Being. Data were analyzed using descriptive statistics, correlational procedures, multiple regression, and change-focused regression analyses. For the caregivers, lower depression levels at Time 1 were associated with better subjective health, less concern about being able to care for the patient in the future, higher levels of patient ADL functioning, greater perceived pre-stroke instrumental support, and greater patient optimism. At Time 2, lower caregiver depression scores were associated with lower levels of perceived burden, fewer health problems or negative changes in health status, fewer negative network interactions, greater network density, greater frequency of network contacts, and fewer perceived personality and behavior changes in the patient. Best predictors of depression score for the caregivers at Time 1 were subjective health rating, the patient's level of ADL functioning, degree of concern about ability to care for the patient in the future, the proportion of the network providing instrumental support, and the percent of reciprocal confiding relationships reported. At Time 2, best predictors of depression were level of perceived caregiver burden, objective health score, and network density. The best predictor of caregiver depression level over time was Time 1 depression level. Perceived caregiver burden was also a strong predictor of depression score. For the patients, higher depression scores at Time 1 were associated with whether they felt they could have done anything to prevent the stroke, higher levels of concern about their partner's ability to care for them in the future, and greater reported frequency of pre-stroke disagreement with their partners. At Time 2, higher levels of depressive symptomatology were associated with decreased satisfaction with amount of social contact, a greater proportion of friends in the post-stroke network, a greater degree of perceived negative health change, and change in employment status.
38
Man, Lai-mei, e 文麗媚. "An exploratory study for the health seeking pattern of stroke survivors on alternative medicine". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31978617.
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39
Wan, Wai-kuen Christina, e 尹慧娟. "An exploratory design of an empowerment group for the strokesurvivors". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31978228.
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40
Tam, Lai-yin Ann. "Study of the strain and needs of adult children caregivers of elderly stroke patients /". Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19470265.
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Fung, Shuk-man Wendy. "A study of medical social services and stroke patients : an application of the unitary approach /". [Hong Kong : University of Hong Kong], 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13418014.
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42
Wu, Chiung-man Skemp Lisa. "Learning to be a family caregiver for severely debilitated stroke survivors during the first year in Taiwan". [Iowa City, Iowa] : University of Iowa, 2009. http://ir.uiowa.edu/etd/451.
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43
Ahmed, Tahir. "Selective neuronal loss, microglial activation and adult neurogenesis after stroke : an in vitro and in vivo analysis of the SDF-1alpha/CXCR4 axis in focal ischaemia and endogenous mechanisms of neural repair". Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610788.
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44
Cotter, Paul Eoin. "Cardiac parameters in young patients with cryptogenic stroke". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648802.
Testo completo
45
Evans, Nicholas Richard. "Multimodal imaging of inflammation at the neurovascular interface in cerebrovascular disease". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275947.
Testo completoAbstract (sommario):
A carotid atherosclerotic plaque represents a nidus of inflammation mere centimetres below the blood-brain barrier. This inflammation, along with associated regions of microcalcification, are histopathological features of atheroma at risk of rupture (so-called “vulnerable plaques”) that trigger thromboembolic stroke. While conventional clinical imaging simply measures the degree of vessel stenosis, it is a crude measure that reveals little of the metabolic processes affecting plaque vulnerability. Our research demonstrates the utility of positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) and 18F-sodium fluoride (NaF), measuring inflammation and microcalcification respectively, to identify culprit carotid atheroma in vivo, and establish how these processes influence plaque vulnerability. Furthermore, for stroke care it is the downstream thromboembolic effects upon the brain that are key. While proinflammatory conditions may increase the risk of stroke, the relationship between atheroma inflammation and the peri-infarct inflammatory response following a stroke remains poorly defined. Our work demonstrates how inflammatory activity in symptomatic carotid atheroma, measured using PET, influences both chronic small vessel disease and the evolution of lesion volume in the post-stroke period. Using metabolic imaging we can both identify vulnerable atheroma in vivo and demonstrate how these processes affect infarct evolution. We show that whilst inflammation is a generalised process, microcalcification is a focal process that may represent a point of maximum vulnerability. These results also reveal the complexity of the atheroma-brain interaction that may simultaneously trigger events while also influencing stroke evolution in the early recovery period. This has important implications for understanding pathophysiology of both atherosclerosis and stroke evolution, advancing drug-discovery, and potential clinical applications to minimise the impact from this devastating disease.
46
馮美玲 e Mei-ling Fung. "Stroke rehabilitation: predicting LOS and discharge placement". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970515.
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47
Moloczij, Natasha. "Sustaining one's own health and wellness while supporting a stroke survivor spouses' and partners' perspectives : a thesis submitted to Auckland University of Technology in partial fulfilment of the requirements for the degree of Master of Health Science, 2009". Click here to access this resource online, 2009. http://hdl.handle.net/10292/654.
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48
Dawson, Jesse. "Prevention of stroke risk stratification and targeted and novel therapies /". Thesis, Connect to e-thesis, 2009. http://theses.gla.ac.uk/851/.
Testo completoAbstract (sommario):
Thesis (MD.) - University of Glasgow, 2009.MD. thesis submitted to Division of Cardiovascular and Medical Sciences, University of Glasgow, 2009. Includes bibliographical references. Print version also available.
49
Silasi, Gergely, e University of Lethbridge Faculty of Arts and Science. "Novel treatments for inducing cortical plasticity and functional restitution following motor cortex stroke". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2005, 2005. http://hdl.handle.net/10133/278.
Testo completoAbstract (sommario):
Stroke remains a leading cause of disability in the western world, with symptoms ranging in severity from mild congnitive or motor impairments, to severe impairments in both cognitive and motor domains. Despite ongoing research aimed at helping stroke patients the disease cannot be prevented or cured, therefore a large body of research has been aimed at identifying effective rehabilitative strategies. Based on our understanding of normal brain function, and the meachanisms mediating the limited spontaneous recovery that is observed following injury, factors that promote brain plasticity are likely to be effective treatments for stroke symptoms. The current thesis investigated three novel treatments (COX-2 inhibitor drug, vitamin supplement diet, and social experience) in a rat model of focal ischemia in the motor cortex. All three treatments have been previously shown to alter plasticity in the normal brain, however the current experiments show that the treatments have differential effects following stroke. The COX-2 inhibitors provided limited improvement in functional performance, whereas the vitamin supplement treatment had no effect. Social experience on the other hand was found to block the usually observed spontaneous improvements following the stroke. These results suggest that factors that alter dendritic plasticity may in fact serve as effective stroke treatments depending on the site and the mechanisms whereby the plastic changes are induced.ix, 149 leaves : ill. ; 29 cm.
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Gharbawie, Omar A., e University of Lethbridge Faculty of Arts and Science. "Modeling middle cerebral artery stroke in rats : an examination of the skilled reaching impairments". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2006, 2006. http://hdl.handle.net/10133/388.
Testo completoAbstract (sommario):
Middle cerebral artery (MCA) stroke can produce chronic incapacitating motor
impairments. Understanding the neural basis of the motor syndromes is complicated by
the diversity of neural structures damaged but the problem can be addressed in laboratory
rats by inducing selective infarcts. Nevertheless, the motor syndromes that ensue from
stroke in rats remain poorly understood and undermine its potential as a model for
clinical stroke. The objective of the present thesis was to document the skilled reaching
impairments from neocortical and subcortical MCA infarcts in rats. In addition, the
integrity of the motor system components spared by the infarct was assessed
neurophysiologically and neuroanatomically. Characteristic reaching impairments
emerged from each infarct but there were also some overlapping features that might be
explained by neural dysfunction extending beyond the boundaries of the infarct. The
present studies showed that the laboratory rat is an ideal animal model for studying
stroke, which should be of interest to both clinical and research scientists studying stroke.xiii, 345 leaves : ill. ; 29 cm. + 1 CD-ROM