Clinical vascular imaging in the brain at 7T

Abstract

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.

Fig. 1

Ultra-high resolution imaging of ischemic stroke. Axial 7 T contrast-enhanced 3D-FLAIR image of 50-year-old female with a recent right-sided ischemic stroke with hemorrhagic transformation, repetition time 8000ms, echo time 300ms, inversion time 2200 ms, acquired voxel size 0.8×0.8×0.8 mm³, reconstructed voxel size 0.5×0.5×0.5 mm³, field-of-view 250x250×190 mm³, scan duration 10:48 min. A hyperintense border is seen to surround the lentiform nucleus (putamen and globus pallidus, arrowheads), which appears hypointense due to blood components. A smaller infarct is also seen in the insular region (black arrow), and multiple hyperintense dots are also seen along the ventricular border of the head of the caudate nucleus (white arrow), all of which are compatible with satellite infarctions.

Fig. 2

MR Angiography of the intracranial perforating arteries. MR Angiography of the intracranial perforating arteries. Coronal Maximum Intensity Projection (MIP) of a 7 T Time-of-Flight (TOF) MRA, repetition time 16ms, echo time 3.3 ms, acquired voxel size 0.25×0.3×0.4 mm³, reconstructed voxel size 0.2×0.2×0.2 mm³, field-of-view 200x190×50 mm³, scan duration 9:54 min, performed in a 51-year-old male. Perforating lenticulostriate arteries (arrowheads) branching off from the middle cerebral arteries are clearly seen in both cerebral hemispheres.

Fig. 3

Intracranial vessel wall imaging at 3 T and 7 T. Intracranial vessel wall imaging at 3 T and 7 T. Intracranial vessel wall imaging of a 71 year-old-male with a recent left sided ischemic infarction in the anterior circulation (not shown) resulting from symptomatic carotid artery disease. (A) A transverse 3 T contrast-enhanced T1 Volume Isotropically Reconstructed Turbo Spin Echo Acquisition (VIRTA), repetition time 1500 ms, echo time 36 ms, acquired voxel size 0.6×0.6×1.0 mm³, reconstructed voxel size 0.5×0.5×0.5 mm³, field-of-view 200x167×45 mm³, scan duration 6:42 min (Dieleman et al., 2016b). Most of the arterial vessel walls of the circle of Willis are visible and appear to be normal (arrowheads). Blood is more suppressed than cerebrospinal fluid. (B) A transverse 7 T post-contrast T1 Magnetization Preparation Inversion Recovery (MPIR) TSE acquisition, repetition time 3952ms, echo time 37ms, inversion time 1375, acquired voxel size 0.8×0.8×0.8mm³, reconstructed voxel size 0.5×0.5×0.5 mm³, field-of-view 250x250×190 mm³, scan time 10:40 min (van der Kolk et al., 2011, The arterial vessel walls (arrowheads) are better seen due to an improved contrast with blood and cerebrospinal fluid, which is almost completely suppressed.

Fig. 4

Cortical microinfarcts. 7 T contrast-enhanced 3D-FLAIR imaging of a 68- year-old man with a large right-sided temporoparietal ischemic infarction (A), repetition time 8000ms, echo time 300ms, inversion time 2200 ms, acquired voxel size 0.8×0.8×0.8 mm³, reconstructed voxel size 0.5×0.5×0.5 mm³, field-of-view 250x250×190 mm³, scan duration 10:48 min. (A) Sagittal and (B) axial reconstruction shows multiple tiny cortical hyperintensities, compatible with cortical microinfarcts. Most cortical microinfarcts seen involve all cortical layers, compatible with type I microinfarcts according to De Reuck et al., (2014).

Fig. 5

Perivascular Spaces and Lacunar Infarcts. An example of a juxtacortical, enlarged perivascular space (PVS) mimicking a cerebral microinfarct (CMI), in a post-mortem brain of a 68-year-old female with Alzheimer's Disease pathology (BB VI) and severe cerebral amyloid angiopathy, identified on (A) T2-weighted ex vivo MR-imaging (repetition time 3500 ms, echo time 164 ms, acquired voxel size 0.4×0.4×0.4 mm³, no SENSE acceleration, scan duration 112 min) and with (B) histopathological correlation, Hematoxylin & Eosin (H&E) staining. (A) The small hyperintense enlarged PVS is located in juxtaposition to the cortex (white arrow). (B) No evidence of neuronal death or gliosis is seen on H&E (black arrow). (images courtesy of S.J. van Veluw).

Fig. 6

Cerebellar cortical infarct cavity on 7 T post-mortem MRI. Cerebellar cortical infarct cavity (white arrow) in the left cerebellar hemisphere on T2-weighted 7 T post-mortem MRI; 3D TSE; TR 3000 ms; TE 207 ms; reduced focusing angle of 40°; acquired voxel size 0.70 × 0.70 × 0.70 mm³; matrix size 284×169; FOV 200 × 119 x 120 mm³; SENSE: 2×2; scan duration 8:39 min. The cavity and the surroundings of the cerebellum are black due to Fomblin, a proton-free fluid without MR signal. Notice the sharp demarcation of the cavity and surrounding hyperintense gliosis (white arrow) from the intact subjacent white matter (black arrows), which proved to be characteristic imaging features of cerebellar cortical infarct cavities and enabled the translation to clinical 1.5 T MRI scans (De Cocker et al., 2014;.

Fig. 7

B1-inhomogeneity artifacts on a 7 T MR FLAIR images of a 42-year-old female with a recent left-sided ischemic stroke. (A) A transverse 3 T FLAIR image, repetition time 10000ms, echo time 120ms, inversion time 2800 ms, acquired voxel size 0.75×1.27×4.00 mm³, reconstructed voxel size 0.4×0.4×4.0 mm³, field-of-view 230x182×129 mm³, scan duration 2:00 min. No B0- or B1-inhomogeneity artifacts are seen on the image. Some patient motion is present in the image. Two hyperintense lesions are present; along the posterior margin of the left putamen and in the left insular region (white arrowheads). (B) A transverse 7 T FLAIR image, repetition time 8000ms, echo time 300 ms, inversion time 2200 ms, acquired voxel size 0.8×0.8×0.8 mm³, reconstructed voxel size 0.5×0.5×0.5 mm³, field-of-view 250x250×190 mm³, scan time 10:48 min. The image is affected by B1-imhomogeniteity artefacts, best seen in both temporal lobes (white arrows). The two hyperintense lesions are seen in much more detail compared to the 3 T MR image in (A) (white arrowheads).