Scholarly article on topic 'Clinical vascular imaging in the brain at 7T'

Clinical vascular imaging in the brain at 7T Academic research paper on "Clinical medicine"

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Abstract of research paper on Clinical medicine, author of scientific article — Laurens JL De Cocker, Arjen Lindenholz, Jaco JM Zwanenburg, Anja G van der Kolk, Maarten Zwartbol, et al.

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.

Academic research paper on topic "Clinical vascular imaging in the brain at 7T"

Author's Accepted Manuscript

Clinical Vascular Imaging in the Brain at 7 T

Laurens JL De Cocker, Arjen Lindenholz, Jaco JM Zwanenburg, Anja van der Kolk, Maarten Zwartbol, Peter Luijten, Jeroen Hendrikse

PII: S1053-8119(16)30661-9

DOI: http ://dx. 10.1016/j. neuroimage .2016.11.044

Reference: YNIMG13592

To appear in: Neuroimage

Received date: 30 July 2016 Revised date: 30 S eptember 2016 Accepted date: 16 November 2016

Cite this article as: Laurens JL De Cocker, Arjen Lindenholz, Jaco JM Zwanenburg, Anja van der Kolk, Maarten Zwartbol, Peter Luijten and Jeroei Hendrikse, Clinical Vascular Imaging in the Brain at 7 T, Neuroimage

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Clinical Vascular Imaging in the Brain at 7T

12* 1 1 1 Laurens JL De Cocker, , Arjen Lindenholz , Jaco JM Zwanenburg , Anja van der Kolk , 1 1 1 Maarten Zwartbol , Peter Luijten , Jeroen Hendrikse

1 Department of Radiology, University Medical Center Utrecht, the Netherlands

2 Department of Radiology, Kliniek Sint-Jan, Brussels, Belgium

^Corresponding author: Laurens J L De Cocker, Kliniek Sint-Jan, Department of Radiology, Kruidtuinlaan 32, 1000 Brussels, Belgium. Phone +32479539570; Fax +3222219117. E-Mail:


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

* Invited Review Article for 'Neuroimaging with Ultra-High Field MRI: Present and Future'

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.

1. Introduction

Vascular disorders of the brain, including stroke, are a major cause of death in addition to physical and cognitive disability. During the past decades, imaging has become an indispensable tool in the work-up, treatment planning and follow-up of ischemic and hemorrhagic stroke, as well as in the identification of cerebrovascular anomalies predisposing to stroke. Also, imaging may record the burden of incidental cerebrovascular lesions that may lead to pathologic brain aging. Compared to CT and other imaging modalities, brain magnetic resonance imaging (MRI) is by far the best technique to assess the total extent of cerebrovascular diseases in individual patients, as it allows for the accurate visualization of acute and chronic manifestations of large- and small-vessel disease in both the supra- and infra-tentorial regions. Although routine clinical practice is currently still limited to standard (1.5T) and high-field (3T) MRI, cerebrovascular disease evaluation at ultra-high-field (7T) MRI may benefit from a high signal to noise ratio (SNR) which can be transferred into a high resolution, as well as a high contrast to noise ratio (CNR). By enabling

the evaluation of the brain parenchyma on a submillimeter scale, very small cerebrovascular lesions, such as cortical microinfarcts, have come within the detection limit of 7T and to a lesser degree 3T MRI.[1] Also, compared to 1.5T arterial MR angiography (MRA), the use of high-field (3T) and even more so ultra-high field MRI (7T), has enabled the visualization of the lumen of much more peripheral intracranial vessels, and of the intracranial vessel walls of the circle of Willis (CoW) and beyond.[2, 3] Finally, MR perfusion weighted imaging (PWI) may benefit from 7T, for instance by the increased susceptibility effects and the lower amount of contrast agent required for dynamic susceptibility contrast (DSC) perfusion at 7T. Thus, the advent of 7T has during the past decade resulted in a wave of research exploring new developments in cerebrovascular imaging, which are now increasingly finding their way into clinical practice. In the current article, we will review the emerging clinical applications and future directions of vascular imaging in the brain at 7T.

2. Clinical Applications

A clinically feasible stroke imaging protocol at 7T has already been proposed and investigated for subacute and chronic stroke patients.[4] This imaging protocol includes T1-weighted 3D Magnetization-Prepared Rapid-Acquired Gradient-Echo (3D-MPRAGE), T2-weighted 2D Fluid Attenuated Inversion Recovery (2D-FLAIR), T2-weighted 2D Fluid Attenuated Inversion Recovery (2D-T2-TSE), T2* weighted 2D Fast Low Angle Shot Gradient Echo (2D-HemoFLASH) and 3D arterial Time-of-Flight (TOF) MRA, however, the imaging protocol excludes diffusion weighted imaging (DWI), the most sensitive imaging technique to detect acute infarctions.[4] With improvements being made to DWI at 7T, it may be expected that clinical stroke protocols at 7T imaging will be extended to include acute stroke patients as well.

2.1. Ischemic stroke

About 80% of strokes are ischemic and about 20% hemorrhagic in origin. Hemorrhagic transformation is a not infrequent complication of ischemic stroke and figure 1 shows an axial 7T FLAIR image of a patient with ischemic stroke undergoing hemorrhagic transformation in the territory of the right middle cerebral artery. The figure displays the high degree of detail discernible with 7T in stroke patients.[4] Most ischemic strokes have an extracranial origin and result either from cardio-embolism or artery-to-artery embolism from the carotid or vertebrobasilar arteries. Screening for cardiac arrhythmia and evaluation of the neck vessels may point towards the correct stroke origin in most of these patients. In case of artery-to-artery embolism from the neck, luminal imaging may reveal arterial stenosis, most frequently at the level of the carotid bifurcation.

In a considerable proportion of patients, however, the origin of stroke may be related to intracranial arterial lesions, evaluation of which may especially benefit from high-resolution MR imaging. Not unlike arterial lesions in the neck, intracranial arterial lesions include atherosclerotic plaques, and, more rarely, dissection or vasculitis.

2.1.1. Intracranial atherosclerosis

Arterial TOF MRA is routinely performed in stroke patients to detect intracranial arterial stenosis, and is usually preferred above angiographic techniques (CTA and DSA) because of its non-invasiveness, the lack of ionizing radiation, and no need to administer a contrast medium (figure 2). Also, it can be acquired in the same imaging session as DWI, the most sensitive technique to detect acute infarction. Compared to 1.5T and 3T, arterial TOF MRA at 7T allows the visualization of much smaller intracranial arteries, such as the lenticulostriate arteries (figure 2), while adding a contrast agent may enable the visualization of even more distal arteries in addition to veins and venules.[2, 4, 5] The presence of intracranial arterial narrowing alone, however, does not necessarily correspond to a stroke origin; arterial stenosis may already have been present a long time before the onset of stroke, and may be compensated by adequate primary (circle of Willis) or secondary (leptomeningeal)

collaterals.[6, 7] Also, atherosclerotic plaques may be present without luminal narrowing due to arterial remodeling.[8] Because of the shortcomings of lumenography, there is a need for intracranial vessel wall imaging to link cerebral infarction with intracranial arterial lesions, such as symptomatic plaques, dissection or vasculitis. Because of the small caliber of intracranial arteries, a high SNR which can be transferred into a high resolution, as well as a high CNR are required for visualization of the pathologic vessel wall, and even more so for the healthy vessel wall (figure 3).[3] Since spatial resolution increases with field strength, (ultra-)high field imaging techniques are required to visualize wall thickening of arteries of the circle of Willis and beyond.[3] Also, for optimal vessel wall visualization, signal suppression of the arterial lumen (black blood imaging techniques including double inversion recovery and techniques based on motion-sensitizing prepulses) is required for delineation of the inner vessel wall (figure 3A and 3B), while cerebrospinal fluid (CSF) suppression facilitates the demarcation of the outer vessel wall (figure 3B), especially for the more peripheral vessels surrounded by subarachnoid (CSF) spaces in case of cerebral atrophy.[3] However, acquisition of 3D isotropic sequences with high resolution and sufficient brain coverage result in relatively long scan times (figure 3).[3, 9] Compared to 3T imaging, the increased signal-to-noise ratio (SNR) of 7T leads to an overall better vessel wall visibility, visualizes more atherosclerotic plaques, and thus offers the highest potential to identify the total burden of intracranial atherosclerosis.[10, 11] Recently, several studies investigating the relationship between intracranial vessel wall changes on 3T and 7T and brain infarction have been published.[12-14] Although most studies have so far only been performed in a limited number of patients, the following preliminary conclusions may be drawn. Eccentric atherosclerotic lesions are most frequently detected and seem to be associated with a focal (short-segment) thickening pattern, while concentric plaques usually show a more diffuse (long-segment) thickening.[14] Although contrast-enhancement of intracranial atherosclerotic plaques is frequently observed and has been linked to the vessels supplying the area of ischemic injury, it may as well appear in asymptomatic lesions.[10, 14-16] Since atherosclerotic lesions of the intracranial vasculature cannot be correlated with histopathology in living patients (unlike the carotid plaques which may be surgically removed by endarterectomy), only post-mortem quantitative MRI-pathologic correlation studies have been performed to compare plaque contents with plaque signal intensities on 3T and 7T on CoW specimens.[17-20] These have shown the promising result that different tissue components of advanced intracranial plaques have distinguishable relaxation times on ultra-high-resolution quantitative MR imaging. T2 and T2* relaxation times at 3T, and T1 relaxation times at 7T, have shown the most differences among individual tissue components of intracranial plaques, including lipid, fibrous tissue, fibrous cap, calcifications, and the healthy vessel wall.[17, 18] Hence, the most promising method for distinguishing intracranial plaque components at 7T is T1-weighted imaging.

Intracranial dissection may be hard to diagnose due to the small caliber of the involved arteries, and thus its diagnosis may highly benefit from the spontaneous bright signal on T1 shown on high-resolution vessel wall imaging, as has already been investigated at 3T.[16, 21] In addition, dissection often shows wall enhancement, and may present a visible flap and dual lumen.[16, 21]

2.1.2. Vasculitis, reversible vasoconstriction syndrome and moyamoya

Central nervous system (CNS) vasculitis and reversible vasoconstriction syndrome (RCVS) often show clinical and lumenographic overlap, and at times only high-resolution vessel wall imaging with MRI may show distinguishing features between these two entities.[22, 23] CNS vasculitis is characterized by short segments of vessel wall thickening, which is concentric more often than eccentric, and is associated with vessel wall enhancement, which may resolve after healing.[16, 22-24] Compared to CNS vasculitis, RCVS shows longer segments of reversible wall thickening, continuous throughout the entire wall of the diseased vessel, with no or only mild enhancement.[23] Furthermore, high-resolution intracranial vessel wall imaging at 3T has been reported to be beneficial in differentiating moyamoya disease, atherosclerotic-moyamoya syndrome, and vasculitic-moyamoya syndrome.[25] Although vessel wall imaging studies at 7T for moyamoya are still lacking, MPRAGE has already been found superior to TOF MRA at 7T due to shorter scanning times and better brain coverage.[26]

2.2. Incidental or silent infarction and the aging brain

Apart from brain infarction presenting with stroke (figure 1), many (small) brain infarctions present with only few or non-specific clinical symptoms, or may even be clinically silent.[27-29] Still, these infarcts may present later on as an incidental finding on neuroimaging studies. They are associated with cognitive decline and worse physical functioning, and an increased risk of future stroke.[30-32] Traditionally, incidental cerebral infarctions include large and small cortical infarcts as well as subcortical infarcts, of which the latter includes lacunar infarcts.[33-36]

2.2.1. Lacunar infarcts, perivascular spaces and white matter hyperintensities

Due to the superior evaluation of small-caliber arteries in the brain on 7T arterial TOF MRA (figure 2), it has been found that the number of lenticulostriate arteries supplying the basal ganglia is reduced in patients with lacunes (of presumed vascular origin) compared to age-matched controls. This finding has later been translated to 1.5T with flow-sensitive black blood MRA, suggesting that occlusion of lenticulostriate arteries underlies lacunar infarction of the basal ganglia.[5, 36, 37] At times, lacunes may be difficult to distinguish from enlarged perivascular spaces (PVS), although the latter do not have a T2-hyperintense rim around the fluid-filled space on T2-weighted or FLAIR imaging, unless they traverse an area of white matter hyperintensity.[36] At high resolution, a central vessel can occasionally be seen in the center of a perivascular space, which may differentiate the spaces from lacunes.[36, 38] Also, optimized MRI parameters and segmentation methods have been developed for PVS at 7T, which have shown that PVS are much more abundant than previously reported in young patients.[38, 39] Despite the term lacunar infarction, it has been shown that only a small proportion of lacunar infarcts progress to lacunes,[40, 41] and non-cavitating lacunar infarcts often continue to resemble white matter lesions instead.[36, 40] Also, in non-vascular disease such as multiple sclerosis (MS), characterization of white matter lesions with high

resolution MR imaging has shown diagnostic benefits. With the increased SNR of 7T MRI, the typical localization of MS plaques around small venules can be demonstrated.[42-44]

2.2.2. Cortical microinfarcts

Another major clinical advancement of 7T MRI is its ability to detect cortical microinfarcts (CMIs) (figure 4). Historically being a strictly pathologic diagnosis recorded during autopsy in elderly people, high resolution MRI has made it possible to visualize some of these lesions in vivo at 7T (figure 4) [45-48] and to a lesser degree at 3T [1, 49]. Nevertheless, the majority of microinfarcts currently remain under the detection limits of clinical in vivo MRI.[50] On post-mortem 7T MRI studies, three types of CMIs have been distinguished based on the involvement of all three cortical layers (type 1), two cortical layers (type 2), or one (superficial, middle or deep) cortical layer only (type 3).[51] CMIs should be distinguished from enlarged or atypically shaped perivascular spaces, which can be CMI mimics but which are located juxtacortically (figure 5).[52] CMIs are associated with atherosclerosis, and are believed to be of microembolic origin.[53-55] Also, CMIs are a new marker of vascular dementia, especially if occurring in strategic locations, such as the inferior frontal and cingulate gyri.[49, 51, 56] Although CMIs have also been described in the cerebellum on post-mortem 7T MRI studies, the somewhat larger cortical infarct cavities (< 1.5 cm) are more frequently observed in that region (figure 6).[57-59] As originally found on postmortem 7T MRI, those cerebellar cortical infarct cavities demonstrate a characteristic sparing of juxtacortical white matter (figure 6), a finding which has recently allowed translation to lower field-strength MRI in vivo.[58, 60] Like CMIs, cerebellar cortical infarct cavities are associated with atherosclerosis and believed to be of embolic origin.[29, 32]

2.2.3. Microbleeds

Detection of microbleeds may be of potential clinical relevance for a variety of pathologies, including include brain trauma, hypertensive microangiopathy, cerebral amyloid angiopathy (CAA) and Alzheimer's dementia (AD).[36, 61-66] A recent post-mortem study has shown a strong association between cerebral microbleeds and CMIs in CAA, suggesting a shared underlying pathophysiologic mechanism.[67] Susceptibility effects and the sensitivity of T2* and SWI for detecting microbleeds increase with field strength, and 3D dual-echo T2*-weighted imaging at 7T has been found to result in better and more reliable detection of microbleeds compared with 3D T2*-weighted imaging at 1.5T in vivo.[68] Interestingly, a recent combined in-vivo/post-mortem MRI correlation study has shown that microbleeds on in vivo MRI are specific for microhemorrhages in CAA, but that increasing the resolution of magnetic resonance images with ultra-high resolution post mortem 7T MRI (< 100^m isotropic voxels) results in the detection of more 'non-hemorrhagic' pathology.[50] Also, diagnostic confidence of rating microbleeds in vivo has not been found significantly higher at 7T compared to 3T for the diagnosis and exclusion of microbleeds and vascular malformations.[69] Visual rating of microbleeds is more challenging at 7T than at lower field strengths due to the increased susceptibility effects of adjacent structures, such as veins.[70,

71] Also, because manual detection of microbleeds may be time consuming with observer variability, automated detection systems of microbleeds have been developed.[72-74]

2.3. Aneurysms, arteriovenous malformations and cavernomas

2.3.1. Cerebral aneurysms

7T MRI has also been proven beneficial for the depiction of cerebral aneurysms, with overall image quality equaling the gold standard DSA.[75] 7T has already proven its superiority over 1.5T in the analysis of aneurysm neck and dome, as well as in the evaluation of aneurysm location at the parent vessel.[76] Using 7T TOF MRA, microaneurysms with diameters under 1 mm are now being described, e.g. ventricular microaneurysms in patients with moyamoya disease.[77] 7T MPRAGE has been found superior to 7T TOF MRA for the assessment of aneurysm features, with less artifacts and simultaneous high quality assessment of the brain with full coverage.[76] Interestingly, high-resolution vessel wall imaging has shown a strong association between ruptured aneurysms and circumferential aneurysm wall enhancement in subarachnoid hemorrhage (SAH), which may identify the site of rupture in patients with multiple intracranial aneurysms using high-resolution vessel wall imaging.[78-81] Circumferential wall enhancement has also been more frequently observed in unruptured but unstable (growing and symptomatic) aneurysms.[79, 81] Although a minority of incidentally discovered aneurysms also show wall enhancement, it still needs to be established if these are at an increased risk of rupture.[81] Apart from aneurysm vessel wall enhancement, regional differences in wall thickness of unruptured aneurysms have been demonstrated on 7T MRI, and thinner regions have been associated with regions of higher wall shear stress determined with phase-contrast MRI.[82, 83] Future studies still need to address if variations in wall thickness are associated with risk of aneurysm rupture.

2.3.2. Arteriovenous malformations and cavernomas

Although DSA is still considered the gold standard for assessment of brain arteriovenous malformations (AVMs), arterial TOF MRA has become a non-invasive alternative for detection and follow-up of AVMs.[75, 81] In a recent comparative study with 1.5T arterial TOF MRA and DSA, non-contrast-enhanced 7T MPRAGE as well as 7T arterial TOF MRA have been found superior to 1.5T arterial TOF MRA in the delineation of the nidus, feeder(s), draining vein(s), and in the relationship between AVMs and adjacent vessels (non-feeding vessels relevant for surgical treatment).[84] Compared to non-enhanced arterial TOF MRA, MPRAGE offers a very high-quality of adjacent brain structures, but is less performant in the visualization of draining veins, probably due to saturation effects of slow flowing arterialized venous blood.[84] Although overall image quality at 7T equals DSA, all described MRA techniques at 7T still miss dynamic information about the blood flow patterns within the AVM.[84] This may be overcome with phase contrast 4D flow imaging, which is a currently rapidly developing field and also possible at 7T with higher SNR than at 3T.[85] Future studies will still need to assess the diagnostic potential for treatment follow-up of brain

AVMs as hemorrhagic changes or artefacts due to embolic agents or clips could be misinterpreted as residual flow.[84] Also, the role of high-resolution vessel-wall MRI for brain AVMs still needs to be established.

Finally, 7T MRI significantly improves the visualization of cavernomas and associated developmental venous anomalies (DVA) due to a higher spatial resolution and susceptibility sensitivity.[86-88]

3. Future directions

Different experimental and functional techniques are currently being developed and tested to assess cerebrovascular function wit 7T MRI on a microvascular level.[71] Amongst others, these include 3D phase contrast (PC)-MRA and blood oxygen level dependent (BOLD) functional MRI (fMRI). 7T PC-MRA is a promising technique to visualize and measure blood flow and pulsatility, for example of the CoW and lenticulostriate arteries.[89, 90] Functional assessment with 3D PC-MRI may better discriminate between healthy and diseased arteries/arterioles compared to anatomical imaging alone, and may as such be applied to assess the relationship between white matter hyperintensities and lacunes on the one hand and blood flow in the perforating arteries on the other hand.[90, 91] BOLD fMRI, which is typically used for task-related and resting state fMRI experiments, may be adapted to measure cerebral perfusion and cerebrovascular reactivity (CVR) before and after a certain vascular challenge, such as the inhalation of carbon dioxide, breath-holding or medication administration (acetazolamide).[71] These stimuli all result in an increased blood flow to the brain and a decreased BOLD signal, and it is generally assumed that brain regions with a decreased signal change upon a certain challenge have a lower cerebrovascular reserve and are at an increased risk of future ischemia.[71] At 7T, BOLD fMRI may detect differences in cerebrovascular reactivity at a millimeter scale, and may be applied to study the association of CVR with lacunes, white matter hyperintensities and microbleeds.[92-95]

Despite all technical advancements, 7T still faces some practical challenges. First, technical improvements are needed to counter the increased magnetic field (B0) and radiofrequency field (B1) inhomogeneities (figure 7). These inhomogeneities cause signal loss and a variable flip angle, most prominently in the temporal (figure 7) and cerebellar regions, which not only hinders the evaluation of these regions in individual subjects, but also hampers group analyses of 7T datasets. The use of dielectric pads may partly overcome this problem. Upgraded head and neck coil technology with larger coverage and more homogenous magnetic fields are required for arterial spin labeling (ASL) perfusion imaging, which at present is still preferentially performed at 3T.[71] Whole brain diffusion MRI also is still challenging at 7T due to magnetic field inhomogeneities, shorter relaxation times, and increased power deposition (specific absorption rate (SAR)), although progress is currently being made to acquire high-quality and reproducible DWI and diffusion tensor imaging (DTI) datasets.[4, 96-98] Finally, promising results on implant safety - which has long been a major drawback for clinical application - have shown no increased risk of radiofrequency heating of metallic implants.[99] These safety results and the growing evidence of an additional clinical value of 7T MRI will pave the way towards certification for (regular) clinical applications in the near future.[4]

4. Conclusion

We described the added value and emerging applications of 7T MRI in the clinical evaluation of cerebrovascular disorders. 7T MRI has been proven superior to lower field-strength MRI for the evaluation of the intracranial vessel lumen and vessel walls, and allows to study the brain parenchyma for microvascular pathology on a submillimeter scale.


JH has received research support from European Research Council (ERC) grant number: ERC-2014-StG - 637024 HEARTOFSTROKE.


1. van Dalen JW, Scuric EEM, van Veluw SJ, et al. (2015) Cortical Microinfarcts Detected In Vivo on 3 Tesla MRI: Clinical and Radiological Correlates. Stroke 46:255-257. doi: 10.1161/STROKEAHA.114.007568

2. Harteveld AA, De Cocker LJ, Dieleman N, et al. (2015) High-resolution postcontrast time-of-flight MR angiography of intracranial perforators at 7.0 Tesla. PLoS One 10:e0121051. doi: 10.1371/journal.pone.0121051

3. Dieleman N, van der Kolk AG, Zwanenburg JJ, et al. (2014) Imaging intracranial vessel wall pathology with magnetic resonance imaging: current prospects and future directions. Circulation 130:192-201. doi: 10.1161/CIRCULATIONAHA.113.006919

4. Madai VI, von Samson-Himmelstjerna FC, Bauer M, et al. (2012) Ultrahigh-field mri in human ischemic stroke - a 7 Tesla study. PLoS One. doi: 10.1371/journal.pone.0037631

5. Kang C-K, Park C-A, Park C-W, et al. (2010) Lenticulostriate arteries in chronic stroke patients visualised by 7T magnetic resonance angiography. Int J Stroke 5:374-80. doi: 10.1111/j.1747-4949.2010.00464.x

6. Liebeskind DS, Cotsonis GA, Saver JL, et al. (2011) Collateral circulation in symptomatic intracranial atherosclerosis. J Cereb Blood Flow Metab 31:1293-301. doi: 10.1038/jcbfm.2010.224

7. Hartkamp NS, Hendrikse J, De Cocker LJ, et al. (2016) Misinterpretation of ischaemic infarct location in relationship to the cerebrovascular territories. J Neurol Neurosurg Psychiatry jnnp-2015-312906. doi: 10.1136/jnnp-2015-312906

8. Qiao Y, Anwar Z, Intrapiromkul J, et al. (2016) Patterns and Implications of Intracranial Arterial Remodeling in Stroke Patients. Stroke 47:434-40. doi: 10.1161/STROKEAHA.115.009955

9. van der Kolk AG, Zwanenburg JJ, Brundel M, et al. (2011) Intracranial vessel wall imaging at 7.0-T MRI. Stroke 42:2478-84. doi: 10.1161/STROKEAHA.111.620443

10. Harteveld AA, van der Kolk AG, van der Worp HB, et al. (2016) High-resolution intracranial vessel wall MRI in an elderly asymptomatic population: comparison of 3T and 7T. Eur Radiol. doi: 10.1007/s00330-016-4483-3

11. Zhu C, Haraldsson H, Tian B, et al. (2016) High resolution imaging of the intracranial vessel wall at 3 and 7 T using 3D fast spin echo MRI. MAGMA 29:559-70. doi: 10.1007/s10334-016-0531-x

12. Dieleman N, van der Kolk AG, van Veluw SJ, et al. (2014) Patterns of intracranial vessel wall changes in relation to ischemic infarcts. Neurology 83:1316-20. doi: 10.1212/WNL.0000000000000868

13. Dieleman N, van der Kolk AG, Zwanenburg JJ, et al. (2016) Relations between location and type of intracranial atherosclerosis and parenchymal damage. J Cereb Blood Flow Metab 36:1271-80. doi: 10.1177/0271678X15616401

14. Dieleman N, Yang W, Abrigo JM, et al. (2016) Magnetic Resonance Imaging of Plaque Morphology, Burden, and Distribution in Patients With Symptomatic Middle Cerebral Artery Stenosis. Stroke 47:1797-802. doi: 10.1161/STROKEAHA.116.013007

Aoki S, Shirouzu I, Sasaki Y, et al. (1995) Enhancement of the intracranial arterial wall at MR imaging: relationship to cerebral atherosclerosis. Radiology 194:477-81. doi: 10.1148/radiology.194.2.7824729

Swartz RH, Bhuta SS, Farb RI, et al. (2009) Intracranial arterial wall imaging using highresolution 3-tesla contrast-enhanced MRI. Neurology 72:627-34. doi: 10.1212/01.wnl.0000342470.69739.b3

Harteveld AA, Denswil NP, Siero JC, et al. (2016) Quantitative Intracranial Atherosclerotic Plaque Characterization at 7T MRI: An Ex Vivo Study with Histologic Validation. AJNR Am J Neuroradiol 37:802-10. doi: 10.3174/ajnr.A4628

Jiang Y, Zhu C, Peng W, et al. (2016) Ex-vivo imaging and plaque type classification of intracranial atherosclerotic plaque using high resolution MRI. Atherosclerosis 249:1016. doi: 10.1016/j.atherosclerosis.2016.03.033

Majidi S, Sein J, Watanabe M, et al. (2013) Intracranial-derived atherosclerosis assessment: an in vitro comparison between virtual histology by intravascular ultrasonography, 7T MRI, and histopathologic findings. AJNR Am J Neuroradiol 34:2259-64. doi: 10.3174/ajnr.A3631

van der Kolk AG, Zwanenburg JJ, Denswil NP, et al. (2015) Imaging the intracranial atherosclerotic vessel wall using 7T MRI: initial comparison with histopathology. AJNR Am J Neuroradiol 36:694-701. doi: 10.3174/ajnr.A4178

Arai D, Satow T, Komuro T, et al. (2016) Evaluation of the Arterial Wall in Vertebrobasilar Artery Dissection Using High-Resolution Magnetic Resonance Vessel Wall Imaging. J Stroke Cerebrovasc Dis. doi: 10.1016/j.jstrokecerebrovasdis.2016.01.047

Mandell DM, Matouk CC, Farb RI, et al. (2012) Vessel Wall MRI to Differentiate Between Reversible Cerebral Vasoconstriction Syndrome and Central Nervous System Vasculitis: Preliminary Results. Stroke 43:860-862. doi: 10.1161/STROKEAHA.111.626184

Obusez EC, Hui F, Hajj-ali RA, et al. (2014) High-Resolution MRI Vessel Wall Imaging: Spatial and Temporal Patterns of Reversible Cerebral Vasoconstriction Syndrome and Central Nervous System Vasculitis. Am J Neuroradiol 35:1527-1532. doi: 10.3174/ajnr.A3909

Küker W, Gaertner S, Nagele T, et al. (2008) Vessel wall contrast enhancement: a diagnostic sign of cerebral vasculitis. Cerebrovasc Dis 26:23-9. doi: 10.1159/000135649

Mossa-Basha M, de Havenon A, Becker KJ, et al. (2016) Added Value of Vessel Wall Magnetic Resonance Imaging in the Differentiation of Moyamoya Vasculopathies in a Non-Asian Cohort. Stroke 47:1782-8. doi: 10.1161/STROKEAHA.116.013320

Dengler NF, Madai VI, Wuerfel J, et al. (2016) Moyamoya Vessel Pathology Imaged by Ultra-High-Field Magnetic Resonance Imaging at 7.0 T. J Stroke Cerebrovasc Dis

Saini M, Ikram K, Hilal S, et al. (2012) Silent stroke: not listened to rather than silent. Stroke 43:3102-4. doi: 10.1161/STROKEAHA.112.666461

Fanning JP, Wesley AJ, Wong AA, et al. (2014) Emerging spectra of silent brain infarction. Stroke 45:3461-71. doi: 10.1161/STROKEAHA.114.005919

De Cocker LJ, Compter A, Kappelle LJ, et al. (2016) Cerebellar Cortical Infarct Cavities and Vertebral Artery Disease. Neuroradiology

Vermeer SE, Prins ND, den Heijer T, et al. (2003) Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med 348:1215-22. doi: 10.1056/NEJMoa022066

Bernick C, Kuller L, Dulberg C, et al. (2001) Silent MRI infarcts and the risk of future stroke: the cardiovascular health study. Neurology 57:1222-9.

De Cocker LJ, Kloppenborg RP, van der Graaf Y, et al. (2015) Cerebellar Cortical Infarct Cavities: Correlation With Risk Factors and MRI Markers of Cerebrovascular Disease. Stroke 46:3154-3160.

Riba-Llena I, Koek M, Verhaaren BF, et al. (2015) Small cortical infarcts: prevalence, determinants, and cognitive correlates in the general population. Int. J. Stroke

Longstreth WT, Bernick C, Manolio TA, et al. (1998) Lacunar infarcts defined by magnetic resonance imaging of 3660 elderly people: the Cardiovascular Health Study. Arch Neurol 55:1217-25.

Del Bene A, Makin SD, Doubal FN, et al. (2013) Variations in risk factors for recent small subcortical infarcts with infarct size, shape and location. Stroke 44:3000-3006.

Wardlaw JM, Smith EE, Biessels GJ, et al. (2013) Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol 12:822-38. doi: 10.1016/S1474-4422(13)70124-8

Okuchi S, Okada T, Ihara M, et al. (2013) Visualization of lenticulostriate arteries by flow-sensitive black-blood MR angiography on a 1.5 T MRI system: a comparative study between subjects with and without stroke. AJNR Am J Neuroradiol 34:780-4. doi: 10.3174/ajnr.A3310

Zong X, Park SH, Shen D, Lin W (2016) Visualization of perivascular spaces in the human brain at 7T: sequence optimization and morphology characterization. Neuroimage 125:895-902. doi: 10.1016/j.neuroimage.2015.10.078

Park SH, Zong X, Gao Y, et al. (2016) Segmentation of perivascular spaces in 7T MR image using auto-context model with orientation-normalized features. Neuroimage 134:223-235. doi: 10.1016/j.neuroimage.2016.03.076

Potter GM, Doubal FN, Jackson CA, et al. (2010) Counting cavitating lacunes underestimates the burden of lacunar infarction. Stroke 41:267-72. doi: 10.1161/STROKEAHA.109.566307

Moreau F, Patel S, Lauzon ML, et al. (2012) Cavitation after acute symptomatic lacunar stroke depends on time, location, and MRI sequence. Stroke 43:1837-42. doi: 10.1161/STROKEAHA.111.647859

Ge Y, Zohrabian VM, Grossman RI (2008) Seven-Tesla magnetic resonance imaging: new vision of microvascular abnormalities in multiple sclerosis. Arch Neurol 65:812-6. doi: 10.1001/archneur.65.6.812

Tallantyre EC, Brookes MJ, Dixon JE, et al. (2008) Demonstrating the perivascular distribution of MS lesions in vivo with 7-Tesla MRI. Neurology 70:2076-8. doi: 10.1212/01.wnl.0000313377.49555.2e

Gizewski ER, Mönninghoff C, Forsting M (2015) Perspectives of Ultra-High-Field MRI in Neuroradiology. Clin Neuroradiol 25 Suppl 2:267-73. doi: 10.1007/s00062-015-0437-4

Zwanenburg JJ, Hendrikse J, Luijten PR (2012) Generalized multiple-layer appearance of the cerebral cortex with 3D FLAIR 7.0-T MR imaging. Radiology 262:995-1001. doi: 10.1148/radiol.11110812

van Veluw SJ, Zwanenburg JJ, Engelen-Lee J, et al. (2012) In vivo detection of cerebral cortical microinfarcts with high-resolution 7T MRI. J Cereb Blood Flow Metab. doi: 10.1038/jcbfm.2012.196

van Veluw SJ, Fracasso A, Visser F, et al. (2015) FLAIR images at 7 Tesla MRI highlight the ependyma and the outer layers of the cerebral cortex. Neuroimage 104:100-109. doi: 10.1016/j.neuroimage.2014.10.011

Fracasso A, van Veluw SJ, Visser F, et al. (2016) Lines of Baillarger in vivo and ex vivo: Myelin contrast across lamina at 7T MRI and histology. Neuroimage 133:163-175. doi: 10.1016/j.neuroimage.2016.02.072

van Veluw SJ, Hilal S, Kuijf HJ, et al. (2015) Cortical microinfarcts on 3T MRI: Clinical correlates in memory-clinic patients. Alzheimers Dement. doi: 10.1016/j.jalz.2014.12.010

van Veluw SJ, Charidimou A, van der Kouwe AJ, et al. (2016) Microbleed and microinfarct detection in amyloid angiopathy: a high-resolution MRI-histopathology study. Brain. doi: 10.1093/brain/aww229

De Reuck J, Deramecourt V, Auger F, et al. (2014) Post-mortem 7.0-tesla magnetic resonance study of cortical microinfarcts in neurodegenerative diseases and vascular dementia with neuropathological correlates. J Neurol Sci 346:85-9. doi: 10.1016/j.jns.2014.07.061

van Veluw SJ, Zwanenburg JJ, Rozemuller AJ, et al. (2015) The spectrum of MR detectable cortical microinfarcts: a classification study with 7-tesla postmortem MRI and histopathology. J Cereb Blood Flow Metab 35:676-83. doi: 10.1038/jcbfm.2014.258

Zheng L, Vinters H V, Mack WJ, et al. (2013) Cerebral atherosclerosis is associated with cystic infarcts and microinfarcts but not Alzheimer pathologic changes. Stroke 44:2835-41. doi: 10.1161/STROKEAHA.113.001945

Raman MR, Preboske GM, Przybelski SA, et al. (2014) Antemortem MRI findings associated with microinfarcts at autopsy. Neurology 82:1951-8. doi: 10.1212/WNL.0000000000000471

Rotte AA de, Koning W, Hartog AG den, et al. (2014) 7.0 T MRI Detection of Cerebral Microinfarcts in Patients with a Symptomatic High-Grade Carotid artery Stenosis. J Cereb Blood Flow Metab 34:1715-1719. doi: 10.1038/jcbfm.2014.141

De Reuck JL, Auger F, Durieux N, et al. (2016) The Topography of Cortical Microinfarcts in Neurodegenerative Diseases and in Vascular Dementia: A Postmortem 7.0-Tesla Magnetic Resonance Imaging Study. Eur Neurol 76:57-61. doi: 10.1159/000447297

De Reuck JL, Deramecourt V, Auger F, et al. (2015) The significance of cortical cerebellar microbleeds and microinfarcts in neurodegenerative and cerebrovascular diseases. A post-mortem 7.0-tesla magnetic resonance study with neuropathological

correlates. Cerebrovasc Dis 39:138-43. doi: 10.1159/000371488

De Cocker LJ, van Veluw SJ, Biessels GJ, et al. (2014) Ischaemic Cavities in the Cerebellum: an ex vivo 7Tesla MRI Study with Pathologic Correlation. Cerebrovasc Dis 38:17-23. doi: 365411

De Cocker LJ, van Veluw SJ, Fowkes M, et al. (2013) Very Small Cerebellar Infarcts: Integration of Recent Insights into a Functional Topographic Classification. Cerebrovasc Dis 36:81-7. doi: 10.1159/000353668

De Cocker LJ, Geerlings MI, Hartkamp NS, et al. (2015) Cerebellar infarct patterns: The SMART-Medea study. NeuroImage Clin 8:314-321. doi: 10.1016/j.nicl.2015.02.001

Wardlaw JM, Smith C, Dichgans M (2013) Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol 12:483-97. doi: 10.1016/S1474-4422(13)70060-7

Akoudad S, Wolters FJ, Viswanathan A, et al. (2016) Association of Cerebral Microbleeds With Cognitive Decline and Dementia. JAMA Neurol. doi: 10.1001/jamaneurol.2016.1017

Knudsen KA, Rosand J, Karluk D, et al. (2001) Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria. Neurology 56:537-9.

Pontes-Neto OM, Auriel E, Greenberg SM (2012) Advances in our Understanding of the Pathophysiology, Detection and Management of Cerebral Amyloid Angiopathy. Eur Neurol Rev 7:134-139.

Brundel M, Reijmer YD, van Veluw SJ, et al. (2014) Cerebral microvascular lesions on high-resolution 7-Tesla MRI in patients with type 2 diabetes. Diabetes 63:3523-9. doi: 10.2337/db14-0122

Bian W, Hess CP, Chang SM, et al. (2014) Susceptibility-weighted MR imaging of radiation therapy-induced cerebral microbleeds in patients with glioma: a comparison between 3T and 7T. Neuroradiology 56:91-96. doi: 10.1007/s00234-013-1297-8

van Veluw SJ, Biessels GJ, Klijn CJ, et al. (2016) Heterogeneous histopathology of cortical microbleeds in cerebral amyloid angiopathy. Neurology 86:867-871. doi: 10.1212/WNL.0000000000002419

Conijn MM, Geerlings MI, Biessels G-J, et al. Cerebral microbleeds on MR imaging: comparison between 1.5 and 7T. AJNR Am J Neuroradiol 32:1043-9. doi: 10.3174/ajnr.A2450

Springer E, Dymerska B, Cardoso PL, et al. (2016) Comparison of Routine Brain Imaging at 3 T and 7 T. Invest Radiol 51:469-82. doi: 10.1097/RLI.0000000000000256

de Bresser J, Brundel M, Conijn MM, et al. Visual cerebral microbleed detection on 7T MR imaging: reliability and effects of image processing. AJNR Am J Neuroradiol 34:E61-4. doi: 10.3174/ajnr.A2960

Harteveld AA, van der Kolk AG, Zwanenburg JJ, et al. (2016) 7-T MRI in Cerebrovascular Diseases: Challenges to Overcome and Initial Results. Top Magn Reson Imaging 25:89-100. doi: 10.1097/RMR.0000000000000080

Kuijf HJ, de Bresser J, Geerlings MI, et al. (2012) Efficient detection of cerebral microbleeds on 7.0T MR images using the radial symmetry transform. Neuroimage

59:2266-2273. doi: 10.1016/j.neuroimage.2011.09.061

Kuijf HJ, Brundel M, de Bresser J, et al. (2013) Semi-Automated Detection of Cerebral Microbleeds on 3.0 T MR Images. PLoS One 8:e66610. doi: 10.1371/journal.pone.0066610

van den Heuvel TLA, van der Eerden AW, et al. (2016) Automated detection of cerebral microbleeds in patients with Traumatic Brain Injury. NeuroImage Clin. doi: 10.1016/j.nicl.2016.07.002

Wrede KH, Matsushige T, Goericke SL, et al. (2016) Non-enhanced magnetic resonance imaging of unruptured intracranial aneurysms at 7 Tesla: Comparison with digital subtraction angiography. Eur Radiol. doi: 10.1007/s00330-016-4323-5

Wrede KH, Dammann P, Monninghoff C, et al. (2014) Non-Enhanced MR Imaging of Cerebral Aneurysms: 7 Tesla versus 1.5 Tesla. PLoS One 9:e84562. doi: 10.1371/journal.pone.0084562

Matsushige T, Kraemer M, Schlamann M, et al. (2016) Ventricular Microaneurysms in Moyamoya Angiopathy Visualized with 7T MR Angiography. Am J Neuroradiol. doi: 10.3174/ajnr.A4786

Matouk CC, Mandell DM, Gunel M, et al. (2013) Vessel wall magnetic resonance imaging identifies the site of rupture in patients with multiple intracranial aneurysms: proof of principle. Neurosurgery 72:492-6; discussion 496. doi: 10.1227/NEU.0b013e31827d1012

Edjlali M, Gentric J-C, Regent-Rodriguez C, et al. (2014) Does aneurysmal wall enhancement on vessel wall MRI help to distinguish stable from unstable intracranial aneurysms? Stroke 45:3704-6. doi: 10.1161/STR0KEAHA.114.006626

Nagahata S, Nagahata M, Obara M, et al. (2014) Wall Enhancement of the Intracranial Aneurysms Revealed by Magnetic Resonance Vessel Wall Imaging Using Three-Dimensional Turbo Spin-Echo Sequence with Motion-Sensitized Driven-Equilibrium: A Sign of Ruptured Aneurysm? Clin Neuroradiol. doi: 10.1007/s00062-014-0353-z

Matouk CC, Cord BJ, Yeung J, et al. (2016) High-resolution Vessel Wall Magnetic Resonance Imaging in Intracranial Aneurysms and Brain Arteriovenous Malformations. Top Magn Reson Imaging 25:49-55. doi: 10.1097/RMR.0000000000000084

Kleinloog R, Korkmaz E, Zwanenburg JJM, et al. (2014) Visualization of the aneurysm wall: a 7.0-tesla magnetic resonance imaging study. Neurosurgery 75:614-22; discussion 622. doi: 10.1227/NEU.0000000000000559

Blankena R, Kleinloog R, Verweij BH, et al. (2016) Thinner Regions of Intracranial Aneurysm Wall Correlate with Regions of Higher Wall Shear Stress: A 7T MRI Study. AJNR Am J Neuroradiol. doi: 10.3174/ajnr.A4734

Wrede KH, Dammann P, Johst S, et al. (2016) Non-Enhanced MR Imaging of Cerebral Arteriovenous Malformations at 7 Tesla. Eur Radiol 26:829-39. doi: 10.1007/s00330-015-3875-0

Markl M, Schnell S, Wu C, et al. (2016) Advanced flow MRI: emerging techniques and applications. Clin Radiol 71:779-795. doi: 10.1016/j.crad.2016.01.011

Schlamann M, Maderwald S, Becker W, et al. (2010) Cerebral cavernous hemangiomas at 7 Tesla: initial experience. Acad Radiol 17:3-6. doi: 10.1016/j.acra.2009.10.001

Dammann P, Barth M, Zhu Y, et al. (2010) Susceptibility weighted magnetic resonance imaging of cerebral cavernous malformations: prospects, drawbacks, and first experience at ultra-high field strength (7-Tesla) magnetic resonance imaging. Neurosurg Focus 29:E5. doi: 10.3171/2010.6.FOCUS10130

Dammann P, Wrede KH, Maderwald S, et al. (2013) The venous angioarchitecture of sporadic cerebral cavernous malformations: a susceptibility weighted imaging study at 7 T MRI. J Neurol Neurosurg Psychiatry 84:194-200. doi: 10.1136/jnnp-2012-302599

van Ooij P, Zwanenburg JJ, Visser F, et al. (2013) Quantification and visualization of flow in the Circle of Willis: time-resolved three-dimensional phase contrast MRI at 7 T compared with 3 T. Magn Reson Med 69:868-76. doi: 10.1002/mrm.24317

Kang C-K, Park C-A, Lee DS, et al. (2016) Velocity measurement of microvessels using phase-contrast magnetic resonance angiography at 7 Tesla MRI. Magn Reson Med 75:1640-6. doi: 10.1002/mrm.25600

Bouvy WH, Geurts LJ, Kuijf HJ, et al. (2015) Assessment of blood flow velocity and pulsatility in cerebral perforating arteries with 7-T quantitative flow MRI. NMR Biomed. doi: 10.1002/nbm.3306

Conijn MMA, Hoogduin JM, van der Graaf Y, et al. (2012) Microbleeds, lacunar infarcts, white matter lesions and cerebrovascular reactivity — A 7T study. Neuroimage 59:950-956. doi: 10.1016/j.neuroimage.2011.08.059

Siero JCW, Hermes D, Hoogduin H, et al. (2014) BOLD matches neuronal activity at the mm scale: A combined 7T fMRI and ECoG study in human sensorimotor cortex. Neuroimage 101:177-184. doi: 10.1016/j.neuroimage.2014.07.002

Bhogal AA, Siero JCW, Fisher JA, et al. (2014) Investigating the non-linearity of the BOLD cerebrovascular reactivity response to targeted hypo/hypercapnia at 7T. Neuroimage 98:296-305. doi: 10.1016/j.neuroimage.2014.05.006

Bhogal AA, Philippens MEP, Siero JCW, et al. (2015) Examining the regional and cerebral depth-dependent BOLD cerebrovascular reactivity response at 7T. Neuroimage 114:239-248. doi: 10.1016/j.neuroimage.2015.04.014

Vu AT, Auerbach E, Lenglet C, et al. (2015) High resolution whole brain diffusion imaging at 7T for the Human Connectome Project. Neuroimage 122:318-331. doi: 10.1016/j.neuroimage.2015.08.004

Andersson JLR, Sotiropoulos SN (2016) An integrated approach to correction for off-resonance effects and subject movement in diffusion MR imaging. Neuroimage 125:1063-78. doi: 10.1016/j.neuroimage.2015.10.019

Sotiropoulos SN, Hernández-Fernández M, Vu AT, et al. (2016) Fusion in diffusion MRI for improved fibre orientation estimation: An application to the 3T and 7T data of the Human Connectome Project. Neuroimage 134:396-409. doi: 10.1016/j.neuroimage.2016.04.014

Kraff O, Wrede KH, Schoemberg T, et al. (2013) MR safety assessment of potential RF heating from cranial fixation plates at 7 T. Med Phys 40:042302. doi: 10.1118/1.4795347

van der Kolk AG, Hendrikse J, Brundel M, et al. (2013) Multi-sequence whole-brain intracranial vessel wall imaging at 7.0 tesla. Eur Radiol 23:2996-3004. doi:


Figures and figure legends

Figure 1. Ultra-high resolution imaging of ischemic stroke. Axial 7T 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

2200ms, acquired voxel size 0.8x0.8x0.8mm3, reconstructed voxel size 0.5x0.5x0.5mm3, field-of-view 250x250x190mm3, scan duration 10:48min. 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.

Figure 2. MR Angiography of the intracranial perforating arteries. MR Angiography of the intracranial perforating arteries. Coronal Maximum Intensity Projection (MIP) of a 7T Time-of-Flight (TOF) MRA, repetition time 16ms, echo time 3.3ms, acquired voxel size 0.25x0.3x0.4mm3, reconstructed voxel size 0.2x0.2x0.2mm3, field-of-view 200x190x50mm3, scan duration 9:54min, 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.

Figure 3. Intracranial vessel wall imaging at 3T and 7T. Intracranial vessel wall imaging at 3T and 7T. 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 3T contrast-enhanced T1 Volume Isotropically Reconstructed Turbo Spin Echo Acquisition (VIRTA), repetition time 1500ms, echo time 36ms, acquired voxel size 0.6x0.6x1.0mm3, reconstructed voxel size 0.5x0.5x0.5mm3, field-of-view 200x167x45mm3, scan duration 6:42min.[14] 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 7T post-contrast T1 Magnetization Preparation Inversion Recovery (MPIR) TSE acquisition, repetition time 3952ms, echo time 37ms, inversion time 1375, acquired voxel size 0.8x0.8x0.8mm3, reconstructed voxel size 0.5x0.5x0.5mm3, field-of-view 250x250x190mm3, scan time 10:40min.[9, 100] The arterial vessel walls (arrowheads) are better seen due to an improved contrast with blood and cerebrospinal fluid, which is almost completely suppressed.

Figure 4. Cortical microinfarcts. 7T 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 2200ms, acquired voxel size 0.8x0.8x0.8mm3, reconstructed voxel size 0.5x0.5x0.5mm3, field-of-view 250x250x190mm3, scan duration 10:48min. (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.[51]

Figure 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 3500ms, echo time 164ms, acquired voxel size 0.4x0.4x0.4mm3, no SENSE acceleration, scan duration 112min) 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)

Figure 6. Cerebellar cortical infarct cavity on 7T post-mortem MRI. Cerebellar cortical infarct cavity (white arrow) in the left cerebellar hemisphere on T2-weighted 7T postmortem MRI; 3D TSE; TR 3000 ms; TE 207 ms; reduced focusing angle of 40°; acquired voxel size 0.70 x 0.70 x 0.70 mm3; matrix size 284x169;FOV 200 x 119 x 120 mm3; SENSE: 2x2; scan duration 8:39min. 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 1.5T MRI scans.[58, 60]

X ^ - -

Figure 7. B1-inhomogeneity artifacts on a 7T MR FLAIR images of a 42-year-old female with a recent left-sided ischemic stroke. (A) A transverse 3T FLAIR image, repetition time 10000ms, echo time 120ms, inversion time 2800ms, acquired voxel size 0.75x1.27x4.00mm3, reconstructed voxel size 0.4x0.4x4.0mm3, field-of-view 230x182x129mm3, scan duration 2:00min. 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 7T FLAIR image, repetition time 8000ms, echo time 300ms, inversion time 2200ms, acquired voxel size 0.8x0.8x0.8mm3, reconstructed voxel size 0.5x0.5x0.5mm3, field-of-view 250x250x190mm3, scan time 10:48min. 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 3T MR image in (A) (white arrowheads).


• Clinically feasible stroke imaging protocols at 7T have been developed

• DWI still limits the use of 7T MRI in acute stroke patients

• Submillimeter cerebrovascular lesions have come within the detection limit of 7T

• 7T allows to study the healthy and diseased intracranial arterial vessel walls

• Evaluation of cerebral aneurysms and AVMs may benefit from 7T MRI