Clinical vascular imaging in the brain at 7T.

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. In addition, 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.

Enlarged perivascular spaces in the basal ganglia are associated with arteries not veins.

Enlarged perivascular spaces (EPVS) are common in cerebral small vessel disease (CSVD) and have been identified as a marker of dysfunctional brain clearance. However, it remains unknown if the enlargement occurs predominantly around arteries or veins. We combined in vivo ultra-high-resolution MRI and histopathology to investigate the spatial relationship of veins and arteries with EPVS within the basal ganglia (BG). Furthermore, we assessed the relationship between the EPVS and measures of blood-flow (blood-flow velocity, pulsatility index) in the small arteries of the BG. Twenty-four healthy controls, twelve non-CAA CSVD patients, and five probable CAA patients underwent a 3 tesla [T] and 7T MRI-scan, and EPVS, arteries, and veins within the BG were manually segmented. Furthermore, the scans were co-registered. Six autopsy-cases were also assessed. In the BG, EPVS were significantly closer to and overlapped more frequently with arteries than with veins. Histological analysis showed a higher proportion of BG EPVS surrounding arteries than veins. Finally, the pulsatility index of BG arteries correlated with EPVS volume. Our results are in line with previous works and establish a pathophysiological relationship between arteries and EPVS, contributing to elucidating perivascular clearance routes in the human brain.

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

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.

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

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 cm around each cortical CMBs was compared with a similar reference site (no CMB) in the contralateral hemisphere, using a 4-point scale. Also, jPVS dilatation was compared between patients with and without cortical CMBs. Eleven patients (24%) had cortical CMBs [total=35, median=1, range=1-14] of whom five had >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.

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

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 ß. 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.