13 research outputs found

    Inter-patient variations in flow boundary conditions at middle cerebral artery from 7T PC-MRI and influence on Computational Fluid Dynamics of intracranial aneurysms

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    Background: Computational fluid dynamics(CFD) of intracranial aneurysms requires flow boundary conditions(BCs) as inputs. Patient-specific BCs are usually unavailable and substituted by literature-derived generic BCs. Therefore, we investigated inter-patient BC variations and their influence on middle cerebral artery aneurysmal hemodynamics. Method: We retrospectively collected CT angiography and 7-T Phase-Contrast(PC)-MRI data from eight middle-cerebral-artery bifurcation aneurysms to reconstruct the geometry and measure the arterial flowrates, respectively. The coefficient of variation(CoV) was calculated for the inlet flowrate and the pulsatility index(PI). The outflow split estimated by Murray's law was compared with PC-MRI measurements. For each aneurysm, we performed seven simulations: “baseline” using PC-MRI-derived BCs and the other six with changing BCs to explore the influence of BC variations on hemodynamics. Results: From PC-MRI, the inlet flowrate was 1.94 ± 0.71 cm3/s(CoV = 36%) and PI was 0.37 ± 0.13(CoV = 34%). The outflow split estimated by Murray's law deviated by 15.3% compared to PC-MRI. Comparing to “baseline” models, ±36% variations in inlet flowrate caused −61% to +89% changes in time-averaged wall shear stress(WSS), −37% to +32% in normalized WSS(NWSS; by parent-artery), and −42% to +126% in oscillatory shear index(OSI). The ±34% variations in PI caused, −46% to +67% in OSI. Applying ±15% variations in outflow split led to inflow jet deflection and −41% to +52% changes in WSS, −41% to +47% in NWSS, and −44% to +144% in OSI. Conclusion: Inflow rate and outflow split have a drastic impact on hemodynamics of intracranial aneurysms. Inlet waveform has a negligible impact on WSS and NWSS but major impact on OSI. CFD-based models need to consider such sensitivity

    Inter-patient variations in flow boundary conditions at middle cerebral artery from 7T PC-MRI and influence on Computational Fluid Dynamics of intracranial aneurysms

    No full text
    Background: Computational fluid dynamics(CFD) of intracranial aneurysms requires flow boundary conditions(BCs) as inputs. Patient-specific BCs are usually unavailable and substituted by literature-derived generic BCs. Therefore, we investigated inter-patient BC variations and their influence on middle cerebral artery aneurysmal hemodynamics. Method: We retrospectively collected CT angiography and 7-T Phase-Contrast(PC)-MRI data from eight middle-cerebral-artery bifurcation aneurysms to reconstruct the geometry and measure the arterial flowrates, respectively. The coefficient of variation(CoV) was calculated for the inlet flowrate and the pulsatility index(PI). The outflow split estimated by Murray's law was compared with PC-MRI measurements. For each aneurysm, we performed seven simulations: “baseline” using PC-MRI-derived BCs and the other six with changing BCs to explore the influence of BC variations on hemodynamics. Results: From PC-MRI, the inlet flowrate was 1.94 ± 0.71 cm3/s(CoV = 36%) and PI was 0.37 ± 0.13(CoV = 34%). The outflow split estimated by Murray's law deviated by 15.3% compared to PC-MRI. Comparing to “baseline” models, ±36% variations in inlet flowrate caused −61% to +89% changes in time-averaged wall shear stress(WSS), −37% to +32% in normalized WSS(NWSS; by parent-artery), and −42% to +126% in oscillatory shear index(OSI). The ±34% variations in PI caused, −46% to +67% in OSI. Applying ±15% variations in outflow split led to inflow jet deflection and −41% to +52% changes in WSS, −41% to +47% in NWSS, and −44% to +144% in OSI. Conclusion: Inflow rate and outflow split have a drastic impact on hemodynamics of intracranial aneurysms. Inlet waveform has a negligible impact on WSS and NWSS but major impact on OSI. CFD-based models need to consider such sensitivity

    Clinical Vascular Imaging in the Brain at 7 T

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    Stroke and related cerebrovascular diseases are a major cause of mortality and disability. Even at standard-field-strengths (1.5T), MRI is by far the most sensitive imaging technique to detect acute brain infarctions and to characterize incidental cerebrovascular lesions, such as white matter hyperintensities, lacunes and microbleeds. Arterial time-of-flight (TOF) MR angiography (MRA) can depict luminal narrowing or occlusion of the major brain feeding arteries, and this without the need for contrast administration. Compared to 1.5T MRA, the use of high-field strength (3T) and even more so ultra-high-field strengths (7T), enables the visualization of the lumen of much smaller intracranial vessels, while adding a contrast agent to TOF MRA at 7T may enable the visualization of even more distal arteries in addition to veins and venules. Moreover, with 3T and 7T, the arterial vessel walls beyond the circle of Willis become visible with high-resolution vessel wall imaging. Also, with 7T MRI, the brain parenchyma can now be visualized on a submillimeter scale. As a result, high-resolution imaging studies of the brain and its blood supply at 7T have generated new concepts of different cerebrovascular diseases. In the current article, we will discuss emerging clinical applications and future directions of vascular imaging in the brain at 7T MRI

    Relations between location and type of intracranial atherosclerosis and parenchymal damage

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    The aim of this study was to assess the relation between location and type of intracranial atherosclerosis (ICAS) and cortical microinfarcts (CMIs) and macroinfarcts in 18 patients presenting with ischemic stroke (n = 12) or transient ischemic attack (TIA) (n = 6) using 7 tesla MR imaging. The protocol included: 3D T2-weighted FLAIR and 3D T1-weighted Magnetization-Preparation Inversion Recovery Turbo Spin Echo sequence. ICAS lesions and infarcts were scored by two raters. The relation between ICAS lesions, calculated ratios of ICAS lesion characteristics, location, and infarcts were examined using linear regression analyses. A total number of 75 ICAS lesions (all patients), 101 CMIs (78% of patients), and 31 macroinfarcts (67% of patients) were found. Seventy-six and sixty-five percent of the CMIs and macroinfarcts, respectively, were found in the same vascular territory as the ICAS lesions (p = 0.977, p = 0.167, respectively). A positive correlation existed between the number of macroinfarcts and CMIs (p < 0.05). In patients with macroinfarcts, we found more concentric (p < 0.01) and diffuse (p < 0.05) type of ICAS lesions. A high prevalence of brain tissue lesions, both macroinfarcts and CMIs, were found in patients with ICAS. Macroinfarcts were found to be related to specific ICAS lesion types. The type of ICAS lesion seems to be promising as a marker for ICAS patients at higher risk of future infarcts

    Cerebral amyloid angiopathy severity is linked to dilation of juxtacortical perivascular spaces

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    Perivascular spaces are an emerging marker of small vessel disease. Perivascular spaces in the centrum semiovale have been associated with cerebral amyloid angiopathy. However, a direct topographical relationship between dilated perivascular spaces and cerebral amyloid angiopathy severity has not been established. We examined this association using post-mortem magnetic resonance imaging in five cases with evidence of cerebral amyloid angiopathy pathology. Juxtacortical perivascular spaces dilation was evaluated on T2 images and related to cerebral amyloid angiopathy severity in overlying cortical areas on 34 tissue sections stained for Amyloid β. Degree of perivascular spaces dilation was significantly associated with cerebral amyloid angiopathy severity (odds ratio = 3.3, 95% confidence interval 1.3-7.9, p = 0.011). Thus, dilated juxtacortical perivascular spaces are a promising neuroimaging marker of cerebral amyloid angiopathy severity

    Microbleeds colocalize with enlarged juxtacortical perivascular spaces in amnestic mild cognitive impairment and early Alzheimer's disease : A 7 Tesla MRI study

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    MRI-visible perivascular spaces (PVS) in the semioval centre are associated with cerebral amyloid angiopathy (CAA), but it is unknown if PVS co-localize with MRI markers of CAA. To examine this, we assessed the topographical association between cortical cerebral microbleeds (CMBs) - as an indirect marker of CAA - and dilatation of juxtacortical perivascular spaces (jPVS) in 46 patients with amnestic mild cognitive impairment (aMCI) or early Alzheimer's disease (eAD). The degree of dilatation of jPVS 1 cortical CMBs. The degree of jPVS dilatation was higher around CMBs than at the reference sites [Wilcoxon signed rank test, Z = 2.2, p = 0.03]. Patients with >1 cortical CMBs had a higher degree of jPVS dilation [median=2.2, IQR = 1.8-2.3] than patients without cortical CMBs [median=1.4, IQR = 1.0-1.8], p = 0.02. We found a topographical association between a high degree of jPVS dilatation and cortical CMBs, supporting a common underlying pathophysiology - most likely CAA

    Microbleeds colocalize with enlarged juxtacortical perivascular spaces in amnestic mild cognitive impairment and early Alzheimer's disease : A 7 Tesla MRI study

    No full text
    MRI-visible perivascular spaces (PVS) in the semioval centre are associated with cerebral amyloid angiopathy (CAA), but it is unknown if PVS co-localize with MRI markers of CAA. To examine this, we assessed the topographical association between cortical cerebral microbleeds (CMBs) - as an indirect marker of CAA - and dilatation of juxtacortical perivascular spaces (jPVS) in 46 patients with amnestic mild cognitive impairment (aMCI) or early Alzheimer's disease (eAD). The degree of dilatation of jPVS 1 cortical CMBs. The degree of jPVS dilatation was higher around CMBs than at the reference sites [Wilcoxon signed rank test, Z = 2.2, p = 0.03]. Patients with >1 cortical CMBs had a higher degree of jPVS dilation [median=2.2, IQR = 1.8-2.3] than patients without cortical CMBs [median=1.4, IQR = 1.0-1.8], p = 0.02. We found a topographical association between a high degree of jPVS dilatation and cortical CMBs, supporting a common underlying pathophysiology - most likely CAA
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