During each cardiac cycle pulsatile arterial blood inflates the vascular bed of the brain, forcing cerebrospinal fluid (CSF) and venous blood out of the cranium. Excessive arterial pulsatility may be part of a harmful mechanism causing cognitive decline among elderly. Additionally, restricted venous flow from the brain is suggested as the cause of multiple sclerosis. Addressing hypotheses derived from these observations requires accurate and reliable investigational methods. This work focused on assessing the pulsatile waveform of cerebral arterial, venous and CSF flows. The overall aim of this dissertation was to explore cerebral blood flow and intracranial pulsatility using MRI, with respect to measurement, physiological and pathophysiological aspects. Two-dimensional phase contrast magnetic resonance imaging (2D PCMRI) was used to assess the pulsatile waveforms of cerebral arterial, venous and CSF flow. The repeatability was assessed in healthy young subjects. The 2D PCMRI measurements of cerebral arterial, venous and CSF pulsatility were generally repeatable but the pulsatility decreased systematically during the investigation. A method combining 2D PCMRI measurements with invasive CSF infusion tests to determine the magnitude and distribution of compliance within the craniospinal system was developed and applied in a group of healthy elderly. The intracranial space contained approximately two thirds of the total craniospinal compliance. The magnitude of craniospinal compliance was less than suggested in previous studies. The vascular hypothesis for multiple sclerosis was tested. Venous drainage in the internal jugular veins was compared between healthy controls and multiple sclerosis patients using 2D PCMRI. For both groups, a great variability in the internal jugular flow was observed but no pattern specific to multiple sclerosis could be found. Relationships between regional brain volumes and potential biomarkers of intracranial cardiac-related pulsatile stress were assessed in healthy elderly. The biomarkers were extracted from invasive CSF pressure measurements as well as 2D PCMRI acquisitions. The volumes of temporal cortex, frontal cortex and hippocampus were negatively related to the magnitude of cardiac-related intracranial pulsatility. Finally, a potentially improved workflow to assess the volume of arterial pulsatility using time resolved, four-dimensional phase contrast MRI measurements (4D PCMRI) was evaluated. The measurements showed good agreement with 2D PCMRI acquisitions. In conclusion, this work showed that 2D PCMRI is a feasible tool to study the pulsatile waveforms of cerebral blood and CSF flow. Conventional views regarding the magnitude and distribution of craniospinal compliance was challenged, with important implications regarding the understanding of how intracranial vascular pulsatility is absorbed. A first counterpoint to previous near-uniform observations of obstructions in the internal jugular veins in multiple sclerosis was provided. It was demonstrated that large cardiac- related intracranial pulsatility were related to smaller volumes of brain regions that are important in neurodegenerative diseases among elderly. This represents a strong rationale to further investigate the role of excessive intracranial pulsatility in cognitive impairment and dementia. For that work, 4D PCMRI will facilitate an effective analysis of cerebral blood flow and pulsatility.

Microvascular lesions of the brain are observed in numerous pathological conditions including Alzheimer's disease (AD). Regional patterns of microvascular abnormality can be characterized using current neuroimaging technologies. When applied to mouse models of human disease, these technologies reveal cerebral vascular patterns and help uncover genotype-to-phenotype relationships. This thesis focuses on the development and testing of techniques for measuring two perfusion-related metrics in mouse brain regions, namely, cerebral blood volume (CBV) and cerebral blood flow (CBF) using micro-computed tomography (micro-CT) and arterial spin labeling (ASL), respectively. The main developments for measurement of CBV have included: refinements to micro-CT specimen preparation; registration of micro-CT images to an MRI anatomical brain atlas; and masking of major vessels to calculate small-vessel CBV (sv-CBV). The development of this micro-CT technique provided reference values of CBV over neuroanatomical brain regions in wildtype mice. A separate study was conducted to assess regional sv-CBV in a mouse model of AD; this study was motivated by the prevalence of microvascular lesions in patients who suffer from AD. Significant regional differences in sv-CBV were found between AD-afflicted mice and controls. The main developments for measurement of CBF have included: design and implementation of accurate ASL slice positioning and optimization of inversion efficiency parameters. The development of this ASL technique provided reference values of CBF over neuroanatomical brain regions in wildtype mice. These techniques for measuring CBV and CBF over mouse brain regions could lead to improved characterization of vascularity in models of neurological diseases.

Microvascular lesions of the brain are observed in numerous pathological conditions including Alzheimer's disease (AD). Regional patterns of microvascular abnormality can be characterized using current neuroimaging technologies. When applied to mouse models of human disease, these technologies reveal cerebral vascular patterns and help uncover genotype-to-phenotype relationships. This thesis focuses on the development and testing of techniques for measuring two perfusion-related metrics in mouse brain regions, namely, cerebral blood volume (CBV) and cerebral blood flow (CBF) using micro-computed tomography (micro-CT) and arterial spin labeling (ASL), respectively. The main developments for measurement of CBV have included: refinements to micro-CT specimen preparation; registration of micro-CT images to an MRI anatomical brain atlas; and masking of major vessels to calculate small-vessel CBV (sv-CBV). The development of this micro-CT technique provided reference values of CBV over neuroanatomical brain regions in wildtype mice. A separate study was conducted to assess regional sv-CBV in a mouse model of AD; this study was motivated by the prevalence of microvascular lesions in patients who suffer from AD. Significant regional differences in sv-CBV were found between AD-afflicted mice and controls. The main developments for measurement of CBF have included: design and implementation of accurate ASL slice positioning and optimization of inversion efficiency parameters. The development of this ASL technique provided reference values of CBF over neuroanatomical brain regions in wildtype mice. These techniques for measuring CBV and CBF over mouse brain regions could lead to improved characterization of vascularity in models of neurological diseases.

A endarterectomia de carótida tem um papel bem estabelecido na prevenção de AVC ipsilateral em pacientes com mais de 50% de estenose sintomática da artéria carótida interna. No entanto, o dano cerebral isquêmico contribui significativamente para a morbidade e mortalidade perioperatórias aumentadas na endarterectomia de carótida com clampeamento intra-operatório temporário. Portanto a relação entre a gravidade do dano isquêmico neuronal durante o procedimento e o sistema de auto-regulação do funcionamento da relação oferta/consumo de oxigênio cerebral precisa ser explorado. Esta avaliação poderia ser feita usando-se um marcador sensível de estresse hipóxico, tal como a proteína S-100ß, que é liberada das células da astroglia que sofreram dano estrutural, para o interior da circulação sangüínea quando a permeabilidade da barreira hemato-encefálica está alterada. Isto é especialmente verdadeiro porque uma baixa pressão no coto distal ao clampeamento continua a ser o critério principal para shunt, embora ela possa estar normal em 6% a 30% dos pacientes que subseqüentemente desenvolvem sinais neurológicos, e anormal em 3% a 11% daqueles que não desenvolvem sinais de isquemia. Então, faz sentido investigar outros métodos para detectar dano cerebral isquêmico em endarterectomia de carótida, tais como a taxa de extração de oxigênio cerebral (ECO2) para permitir a otimização de variáveis acessíveis à intervenção médica, como: shunt, parâmetros ventilatórios e parâmetros hemodinâmicos. O objetivo deste trabalho foi avaliar a correlação entre um marcador de dano cerebral isquêmico, a proteína S-100ß sérica, com a fração de extração de oxigênio cerebral (ECO2) e com a pressão arterial de dióxido de carbono (PaCO2) em pacientes submetidos à endarterectomia de carótida para estenose sintomática, com clampeamento temporário. Este estudo transversal avaliou 33 pacientes, estado físico II e III e média de idade de 70 ± 8 anos que foram submetidos à anestesia geral endovenosa e inalatória . PaCO2 (mmHg) e % ECO2 foram medidas antes do clampeamento da carótida (T1), 5 minutos após o clampeamento (T2) e 5 minutos após o desclampeamento (T3) a partir de amostras sangüíneas retiradas da veia jugular interna. S-100ß foi determinada nos seguintes momentos: antes do clampeamento da carótida (T1), imediatamente antes do desclampeamento (T2) e 6 horas após o desclampeamento (T3). O tempo médio de isquemia cerebral foi de 16 minutos [(IQ25-75) 11,05 a 19,00]. Os coeficientes de correlação de Spearman (rs) para a relação entre os níveis de S-100β em 6 horas após a cirurgia e os níveis de ECO2 e PaCO2 durante o período do estudo foram rs = 0,59 (P = 0,00) e rs = -0,36 (P = 0,00) respectivamente. Em conclusão, os presentes achados sugerem que o dano neuronal isquêmico avaliado pela ECO2 durante o período isquêmico podem predizer um aumento de S-100ß. Contudo, futuros estudos são necessários para determinar o impacto clínico de tais achados. / Carotid endarterectomy (CED) is a well established procedure to prevent ipsilateral stroke in patients with more than 50% symptomatic internal carotid artery (ICA) stenosis. However, ischemic brain injury persists as a significant contributing factor to increased perioperative morbidity and mortality in carotid endarterectomy with temporary intraoperative clamping. Hence, the relationship between the severity of neuronal ischemic damage during carotid endarterectomy (CED) and the autoregulation system of the functioning brain oxygen supply/consumption ratio needs to be further explored. This appraisal could be made using a sensitive marker of hypoxic stress, such as S-100ß released into de bloodstream when structural damage to astroglial cells alter the permeability of the blood-brain barrier. This methodological resource can be valuable since a low stump pressure is generally the main criterion for shunting, although normal in about 6-30% of patients who subsequently develop neurological signs and abnormal in 3-11% in those without signs of ischemia. Thus, it makes sense to search for additional subsidies to detect ischemic brain damage during carotid endarterectomy, such as the rate of brain oxygen extraction (ECO2). This earlier accessible variable at low cost could help medical decision-making such as shunt or changes in hemodynamic and ventilatory parameters. The aim of this study was, therefore, assess the correlation between a marker of neuronal ischemic damage, serum S-100ß, and brain oxygen extraction fraction (ECO2) and PaCO2 (arterial carbon dioxide tension) in patients undergoing carotid endarterectomy for symptomatic stenosis with temporary clamping. This cross-sectional study assessed 33 patients, physical status II-III, and mean age of 70 ± 8 years, who undergoing intravenous general anesthesia. PaCO2 (mmHg) and %ECO2 were measured prior to carotid clamping (T1), 5 min after carotid clamping (T2) and 5 min after carotid unclamping (T3) with blood drawn from the internal jugular vein. Serum S-100β was determined at T1 - prior to carotid clamping, T2 - immediately before carotid unclamping, and T3 - 6 h after carotid unclamping. The median time of brain ischemia was 16 min [(IQ25-75) 11.05 to 19.00]. Spearman correlation coefficients (rs) for the relationship between S-100ß level at 6 h after surgery and PaCO2 and ECO2 levels during the study period were rs = -0.36 (P < 0.01) and rs = 0.59 (P < 0.01), respectively. To conclude, the present findings suggest that brain ischemic neural damage monitored by ECO2 during the ischemic time may predict an increase in S-100ß. Further studies are warranted to assess the clinical impact of these results.

A endarterectomia de carótida tem um papel bem estabelecido na prevenção de AVC ipsilateral em pacientes com mais de 50% de estenose sintomática da artéria carótida interna. No entanto, o dano cerebral isquêmico contribui significativamente para a morbidade e mortalidade perioperatórias aumentadas na endarterectomia de carótida com clampeamento intra-operatório temporário. Portanto a relação entre a gravidade do dano isquêmico neuronal durante o procedimento e o sistema de auto-regulação do funcionamento da relação oferta/consumo de oxigênio cerebral precisa ser explorado. Esta avaliação poderia ser feita usando-se um marcador sensível de estresse hipóxico, tal como a proteína S-100ß, que é liberada das células da astroglia que sofreram dano estrutural, para o interior da circulação sangüínea quando a permeabilidade da barreira hemato-encefálica está alterada. Isto é especialmente verdadeiro porque uma baixa pressão no coto distal ao clampeamento continua a ser o critério principal para shunt, embora ela possa estar normal em 6% a 30% dos pacientes que subseqüentemente desenvolvem sinais neurológicos, e anormal em 3% a 11% daqueles que não desenvolvem sinais de isquemia. Então, faz sentido investigar outros métodos para detectar dano cerebral isquêmico em endarterectomia de carótida, tais como a taxa de extração de oxigênio cerebral (ECO2) para permitir a otimização de variáveis acessíveis à intervenção médica, como: shunt, parâmetros ventilatórios e parâmetros hemodinâmicos. O objetivo deste trabalho foi avaliar a correlação entre um marcador de dano cerebral isquêmico, a proteína S-100ß sérica, com a fração de extração de oxigênio cerebral (ECO2) e com a pressão arterial de dióxido de carbono (PaCO2) em pacientes submetidos à endarterectomia de carótida para estenose sintomática, com clampeamento temporário. Este estudo transversal avaliou 33 pacientes, estado físico II e III e média de idade de 70 ± 8 anos que foram submetidos à anestesia geral endovenosa e inalatória . PaCO2 (mmHg) e % ECO2 foram medidas antes do clampeamento da carótida (T1), 5 minutos após o clampeamento (T2) e 5 minutos após o desclampeamento (T3) a partir de amostras sangüíneas retiradas da veia jugular interna. S-100ß foi determinada nos seguintes momentos: antes do clampeamento da carótida (T1), imediatamente antes do desclampeamento (T2) e 6 horas após o desclampeamento (T3). O tempo médio de isquemia cerebral foi de 16 minutos [(IQ25-75) 11,05 a 19,00]. Os coeficientes de correlação de Spearman (rs) para a relação entre os níveis de S-100β em 6 horas após a cirurgia e os níveis de ECO2 e PaCO2 durante o período do estudo foram rs = 0,59 (P = 0,00) e rs = -0,36 (P = 0,00) respectivamente. Em conclusão, os presentes achados sugerem que o dano neuronal isquêmico avaliado pela ECO2 durante o período isquêmico podem predizer um aumento de S-100ß. Contudo, futuros estudos são necessários para determinar o impacto clínico de tais achados. / Carotid endarterectomy (CED) is a well established procedure to prevent ipsilateral stroke in patients with more than 50% symptomatic internal carotid artery (ICA) stenosis. However, ischemic brain injury persists as a significant contributing factor to increased perioperative morbidity and mortality in carotid endarterectomy with temporary intraoperative clamping. Hence, the relationship between the severity of neuronal ischemic damage during carotid endarterectomy (CED) and the autoregulation system of the functioning brain oxygen supply/consumption ratio needs to be further explored. This appraisal could be made using a sensitive marker of hypoxic stress, such as S-100ß released into de bloodstream when structural damage to astroglial cells alter the permeability of the blood-brain barrier. This methodological resource can be valuable since a low stump pressure is generally the main criterion for shunting, although normal in about 6-30% of patients who subsequently develop neurological signs and abnormal in 3-11% in those without signs of ischemia. Thus, it makes sense to search for additional subsidies to detect ischemic brain damage during carotid endarterectomy, such as the rate of brain oxygen extraction (ECO2). This earlier accessible variable at low cost could help medical decision-making such as shunt or changes in hemodynamic and ventilatory parameters. The aim of this study was, therefore, assess the correlation between a marker of neuronal ischemic damage, serum S-100ß, and brain oxygen extraction fraction (ECO2) and PaCO2 (arterial carbon dioxide tension) in patients undergoing carotid endarterectomy for symptomatic stenosis with temporary clamping. This cross-sectional study assessed 33 patients, physical status II-III, and mean age of 70 ± 8 years, who undergoing intravenous general anesthesia. PaCO2 (mmHg) and %ECO2 were measured prior to carotid clamping (T1), 5 min after carotid clamping (T2) and 5 min after carotid unclamping (T3) with blood drawn from the internal jugular vein. Serum S-100β was determined at T1 - prior to carotid clamping, T2 - immediately before carotid unclamping, and T3 - 6 h after carotid unclamping. The median time of brain ischemia was 16 min [(IQ25-75) 11.05 to 19.00]. Spearman correlation coefficients (rs) for the relationship between S-100ß level at 6 h after surgery and PaCO2 and ECO2 levels during the study period were rs = -0.36 (P < 0.01) and rs = 0.59 (P < 0.01), respectively. To conclude, the present findings suggest that brain ischemic neural damage monitored by ECO2 during the ischemic time may predict an increase in S-100ß. Further studies are warranted to assess the clinical impact of these results.

Imagem por ressonância magnética tem sido um dos principais métodos para a aquisição de imagens para diagnósticos na medicina, em especial para a obtenção de medidas do cérebro. Apesar de se mostrar muito eficiente, o método atualmente utilizado para a realização da ressonância em hospitais e centros de diagnósticos, em alguns casos, necessita da aplicação de um contraste de gadolínio intravenoso. Essa injeção do contraste pode mostrar-se um tanto quanto invasivo, podendo em alguns casos resultar em algumas reações indesejadas nos pacientes. Em vista disso, um método que tem sido bastante estudado recentemente e muito promissor é o de Arterial Spin Labeling (ASL). Este método tem como sua principal vantagem o fato de não ser invasivo e de possibilitar a quantificação da perfusão sanguínea cerebral (CBF). No presente trabalho, foi feita uma otimização do contraste na aquisição das fases mais tardias da metodologia de ASL em múltiplas fases. Isso foi feito através de uma modulação do angulo de flip e é particularmente importante para a análise das imagens de pacientes com problemas neurovasculares, principalmente aqueles associados ao retardo nos tempos de trânsito do sangue arterial. Também, foi realizada toda a obtenção e processamento de dados para a avaliação da perfusão sanguínea cerebral utilizando o método proposto. / Magnetic resonance imaging has been one of the major methods to acquire images for medical diagnoses, specially, for obtaining brain images. Although the major method using magnetic resonance used today has high efficiency, in some cases it needs an injection of intravascular contrast agent, like gadolinium. This contrast agent application can be a lot invasive for the patient, in extremes cases resulting to allergic reactions the patient. Therefore, a method that has been studied recently and is very promising is the Arterial Spin Labeling (ASL). This method has the major advantage the feature that it is completely non invasive for the patient and it allows to quantify the perfusion value. In this work, it was implemented an optimization of the contrast in the late phases of ASL multiphase acquisition. It was made using a modulation of the flip angle and it is critical to analyze images from patients with some neurovascular disease, especially those associated with arterial blood transit time delay. Besides that, it was made all data acquisition and data processing for the brain perfusion evaluation using the proposed method.

A endarterectomia de carótida tem um papel bem estabelecido na prevenção de AVC ipsilateral em pacientes com mais de 50% de estenose sintomática da artéria carótida interna. No entanto, o dano cerebral isquêmico contribui significativamente para a morbidade e mortalidade perioperatórias aumentadas na endarterectomia de carótida com clampeamento intra-operatório temporário. Portanto a relação entre a gravidade do dano isquêmico neuronal durante o procedimento e o sistema de auto-regulação do funcionamento da relação oferta/consumo de oxigênio cerebral precisa ser explorado. Esta avaliação poderia ser feita usando-se um marcador sensível de estresse hipóxico, tal como a proteína S-100ß, que é liberada das células da astroglia que sofreram dano estrutural, para o interior da circulação sangüínea quando a permeabilidade da barreira hemato-encefálica está alterada. Isto é especialmente verdadeiro porque uma baixa pressão no coto distal ao clampeamento continua a ser o critério principal para shunt, embora ela possa estar normal em 6% a 30% dos pacientes que subseqüentemente desenvolvem sinais neurológicos, e anormal em 3% a 11% daqueles que não desenvolvem sinais de isquemia. Então, faz sentido investigar outros métodos para detectar dano cerebral isquêmico em endarterectomia de carótida, tais como a taxa de extração de oxigênio cerebral (ECO2) para permitir a otimização de variáveis acessíveis à intervenção médica, como: shunt, parâmetros ventilatórios e parâmetros hemodinâmicos. O objetivo deste trabalho foi avaliar a correlação entre um marcador de dano cerebral isquêmico, a proteína S-100ß sérica, com a fração de extração de oxigênio cerebral (ECO2) e com a pressão arterial de dióxido de carbono (PaCO2) em pacientes submetidos à endarterectomia de carótida para estenose sintomática, com clampeamento temporário. Este estudo transversal avaliou 33 pacientes, estado físico II e III e média de idade de 70 ± 8 anos que foram submetidos à anestesia geral endovenosa e inalatória . PaCO2 (mmHg) e % ECO2 foram medidas antes do clampeamento da carótida (T1), 5 minutos após o clampeamento (T2) e 5 minutos após o desclampeamento (T3) a partir de amostras sangüíneas retiradas da veia jugular interna. S-100ß foi determinada nos seguintes momentos: antes do clampeamento da carótida (T1), imediatamente antes do desclampeamento (T2) e 6 horas após o desclampeamento (T3). O tempo médio de isquemia cerebral foi de 16 minutos [(IQ25-75) 11,05 a 19,00]. Os coeficientes de correlação de Spearman (rs) para a relação entre os níveis de S-100β em 6 horas após a cirurgia e os níveis de ECO2 e PaCO2 durante o período do estudo foram rs = 0,59 (P = 0,00) e rs = -0,36 (P = 0,00) respectivamente. Em conclusão, os presentes achados sugerem que o dano neuronal isquêmico avaliado pela ECO2 durante o período isquêmico podem predizer um aumento de S-100ß. Contudo, futuros estudos são necessários para determinar o impacto clínico de tais achados. / Carotid endarterectomy (CED) is a well established procedure to prevent ipsilateral stroke in patients with more than 50% symptomatic internal carotid artery (ICA) stenosis. However, ischemic brain injury persists as a significant contributing factor to increased perioperative morbidity and mortality in carotid endarterectomy with temporary intraoperative clamping. Hence, the relationship between the severity of neuronal ischemic damage during carotid endarterectomy (CED) and the autoregulation system of the functioning brain oxygen supply/consumption ratio needs to be further explored. This appraisal could be made using a sensitive marker of hypoxic stress, such as S-100ß released into de bloodstream when structural damage to astroglial cells alter the permeability of the blood-brain barrier. This methodological resource can be valuable since a low stump pressure is generally the main criterion for shunting, although normal in about 6-30% of patients who subsequently develop neurological signs and abnormal in 3-11% in those without signs of ischemia. Thus, it makes sense to search for additional subsidies to detect ischemic brain damage during carotid endarterectomy, such as the rate of brain oxygen extraction (ECO2). This earlier accessible variable at low cost could help medical decision-making such as shunt or changes in hemodynamic and ventilatory parameters. The aim of this study was, therefore, assess the correlation between a marker of neuronal ischemic damage, serum S-100ß, and brain oxygen extraction fraction (ECO2) and PaCO2 (arterial carbon dioxide tension) in patients undergoing carotid endarterectomy for symptomatic stenosis with temporary clamping. This cross-sectional study assessed 33 patients, physical status II-III, and mean age of 70 ± 8 years, who undergoing intravenous general anesthesia. PaCO2 (mmHg) and %ECO2 were measured prior to carotid clamping (T1), 5 min after carotid clamping (T2) and 5 min after carotid unclamping (T3) with blood drawn from the internal jugular vein. Serum S-100β was determined at T1 - prior to carotid clamping, T2 - immediately before carotid unclamping, and T3 - 6 h after carotid unclamping. The median time of brain ischemia was 16 min [(IQ25-75) 11.05 to 19.00]. Spearman correlation coefficients (rs) for the relationship between S-100ß level at 6 h after surgery and PaCO2 and ECO2 levels during the study period were rs = -0.36 (P < 0.01) and rs = 0.59 (P < 0.01), respectively. To conclude, the present findings suggest that brain ischemic neural damage monitored by ECO2 during the ischemic time may predict an increase in S-100ß. Further studies are warranted to assess the clinical impact of these results.

The Arterial Spin Labelling (ASL) method is a Magnetic Resonance technique used toquantify the cerebral perfusion. It has the big advantage to be non-invasive so doesn’tneed the injection of any contrast agent. But due to a relatively low Signal-to-NoiseRatio (SNR) of the signal acquired (only approximately 1% of the image intensity), ithas been hampered to be widely used in a clinical setting so far.The primary objective of this project is to make the method more robust by improvingthe quality of the images, the SNR, and by reducing the acquisition time. DifferentASL protocols with different sets of parameters have been investigated. The modificationsperformed on the protocol have been investigated by analyzing images acquired onhealthy volunteers. An optimized protocol leading to a good trade-off between the differentaspects of the method, has been suggested. It is characterized by a 3:43:44:0mm3with a two-segment acquisition.A more advanced ASL method implies the acquisition of images at different inversiontimes (TI), which is called the mutli-TI method. The influence of the range of TI used inthe method has been explored. An optimized TI range (from 410ms to 3860ms, sampledevery 150ms) has been suggested to make the ASL method as performant as possible.A numerical model and a fitting algorithm have been used to extract the informationon the perfusion from the images acquired. Different models have been investigated aswell as their influence on the reliability of the results.Finally, a criterion has been implemented to evaluate the reliability of the results sothat the clinician or the user of the method can figure out how much he can count onthe results provided by the method.

Patients who are treated in an intensive care unit need continuous monitoring in orderfor clinicians to be prepared to intervene should a secondary event occur. For patientstreated at the neurointensive care unit (NICU) who have suffered a subarachnoid hemorrhage (SAH) this secondary event could be ischemia, resulting in a lack of blood flow.Blood flow can be measured using magnetic resonance imaging (MRI). The process is facilitated with a software called NOVA. Repeated measurements can therefore be performedas a way to monitor the patients, which in this context would be referred to as longitudinalmeasurements. As more data can be collected ways of analyzing and visualizing the datain a comprehensible way is needed. The aim of this thesis was therefore to develop and implement a method for analyzing and visualizing the longitudinal MR measurement data.With this aim in mind two research questions were relevant. The first one was how NOVAflow longitudinal measurements can be visualized to simplify interpretation by cliniciansand the second one was in what ways the longitudinal data can be analyzed. A graphicaluser interface (GUI) was created to present the developed analysis and visualization tool.Development of the tool progressed using feedback from supervisors and neurosurgeons.Visualization and analysis was done through plots of blood velocity and blood flow as themain component as well as a 2D vessel map. The final implementation showed multipleexamples of how the longitudinal data could be both visualized and analyzed. The resultstherefore provided a tool to analyze and visualize NOVA flow longitudinal measurementsin a way which was easily interpreted. Further improvements of the tool is possible andan area of improvement could involve increasing the adaptability of the tool.

No description available.