Conventional and high-resolution vessel wall MRI of intracranial aneurysms: current concepts and new horizons

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  • 1 Departments of Radiology,
  • 3 Neurosurgery, and
  • 4 Neurology, Mayo Clinic College of Graduate Medical Education, Rochester, Minnesota; and
  • 2 Department of Radiology, University of Washington Medical Center, Seattle, Washington
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Intracranial aneurysms are heterogeneous in histopathology and imaging appearance. The biological behavior of different types of aneurysms is now known to depend on the structure and physiology of the aneurysm wall itself in addition to intraluminal flow and other luminal features. Aneurysm wall structure and imaging markers of physiology such as aneurysm wall enhancement have been assessed in many prior investigations using conventional-resolution MRI. Recently, high-resolution vessel wall imaging (HR-VWI) techniques with MRI have been introduced. Reports of findings on high-resolution imaging have already emerged for many types of aneurysms demonstrating detailed characterization of wall enhancement, thickness, and components, but many questions remain unexplored. This review discusses the key HR-VWI literature to date. Aneurysm wall findings on conventional-resolution MRI are also discussed as these may help one understand the potential utility and findings on HR-VWI for various aneurysm types. The authors have illustrated these points with several examples demonstrating both features already described in the literature and novel cases demonstrating the potential for future clinical and research applications.

ABBREVIATIONS ACA = anterior cerebral artery; CTA = CT angiography; DANTE = delayed alternating with nutation for tailored excitation; DIR = double inversion recovery; FOV = field of view; HIV = human immunodeficiency virus; HR-VWI = high-resolution vessel wall imaging; ICA = internal cerebral artery; IR = inversion recovery; MCA = middle cerebral artery; MPIR = magnetization-prepared inversion recovery; MRA = MR angiography; MSDE = motion-sensitive driven equilibrium; PCA = posterior cerebral artery; PD = proton density; QIR = quadruple inversion recovery; SAH = subarachnoid hemorrhage; SPACE = sampling perfection with application optimized contrast using different flip angle evolutions; VISTA = volumetric isotropic turbo spin echo acquisition; VRFA = variable refocusing flip angle; VZV = varicella zoster virus.

Intracranial aneurysms are heterogeneous in histopathology and imaging appearance. The biological behavior of different types of aneurysms is now known to depend on the structure and physiology of the aneurysm wall itself in addition to intraluminal flow and other luminal features. Aneurysm wall structure and imaging markers of physiology such as aneurysm wall enhancement have been assessed in many prior investigations using conventional-resolution MRI. Recently, high-resolution vessel wall imaging (HR-VWI) techniques with MRI have been introduced. Reports of findings on high-resolution imaging have already emerged for many types of aneurysms demonstrating detailed characterization of wall enhancement, thickness, and components, but many questions remain unexplored. This review discusses the key HR-VWI literature to date. Aneurysm wall findings on conventional-resolution MRI are also discussed as these may help one understand the potential utility and findings on HR-VWI for various aneurysm types. The authors have illustrated these points with several examples demonstrating both features already described in the literature and novel cases demonstrating the potential for future clinical and research applications.

ABBREVIATIONS ACA = anterior cerebral artery; CTA = CT angiography; DANTE = delayed alternating with nutation for tailored excitation; DIR = double inversion recovery; FOV = field of view; HIV = human immunodeficiency virus; HR-VWI = high-resolution vessel wall imaging; ICA = internal cerebral artery; IR = inversion recovery; MCA = middle cerebral artery; MPIR = magnetization-prepared inversion recovery; MRA = MR angiography; MSDE = motion-sensitive driven equilibrium; PCA = posterior cerebral artery; PD = proton density; QIR = quadruple inversion recovery; SAH = subarachnoid hemorrhage; SPACE = sampling perfection with application optimized contrast using different flip angle evolutions; VISTA = volumetric isotropic turbo spin echo acquisition; VRFA = variable refocusing flip angle; VZV = varicella zoster virus.

Intracranial aneurysms have a wide range of etiologies, pathological characteristics, imaging appearances, natural histories, and treatment options. Two recent developments have the potential to greatly advance the understanding and radiological assessment of intracranial aneurysms: 1) increased focus on aneurysm wall pathology, structure, and behavior, and 2) implementation of high-resolution vessel wall imaging (HR-VWI) techniques in clinical practice. HR-VWI complements the traditional luminal evaluation of intracranial aneurysms. However, the primary vessel wall pathology, and therefore HR-VWI appearance, varies drastically among the different types of aneurysms.

For HR-VWI, higher field strengths of at least 3T are advantageous due to the need for submillimeter spatial resolution and the resultant signal demands. Various techniques now exist in clinical practice, designed to provide optimal spatial resolution and to sharply delineate vessel walls between flowing blood and CSF; these include both 2D and 3D techniques. Two-dimensional techniques are widely available and can be readily implemented. Two-dimensional imaging in a plane perpendicular to the plane of the lumen is typically the most important imaging plane. This allows for accurate assessment of the lesion effects on the lumen and lesion morphology, better estimation of lesion and wall thickness, and the avoidance of volume averaging artifacts.41 Three-dimensional HR-VWI techniques have recently increased in utilization for vessel wall imaging. Advantages of 3D techniques include higher through-plane spatial resolution, with increased brain coverage, and the ability to perform isotropic acquisitions. Of the 3D techniques available, variable refocusing flip angle (VRFA) techniques are the most extensively studied and now predominate many clinical practices (sampling perfection with application optimized contrast using different flip angle evolutions [SPACE], Siemens Healthcare; CUBE, GE; and volumetric isotropic turbo spin echo acquisition [VISTA], Philips Healthcare)1,10,31,50 as they provide improved blood suppression in a shortened scan time relative to other 3D and 2D techniques. Three-dimensional VRFA techniques have been performed using T1, proton density (PD), and T2 contrast weightings12,42,50 for various applications, with each providing specific lesion characteristics that may help in disease differentiation and characterization. The utilization of multiple contrast weightings may be advantageous for differentiation of intracranial vasculopathies, although not yet extensively studied in aneurysms.42

A variety of blood and CSF suppression techniques can be used to enhance visualization of the vessel wall. CSF suppression techniques include antidrive and delayed alternating with nutation for tailored excitation (DANTE), while blood suppression techniques include motion-sensitive driven equilibrium (MSDE), DANTE, double inversion recovery (DIR), quadruple inversion recovery (QIR), and magnetization-prepared inversion recovery (MPIR).10,12,59,61,62,64 While some suppression techniques are used with 3D HR-VWI (MSDE, DANTE, antidrive), others can only be used with 2D techniques (DIR, QIR).34 The precise suppression techniques used may not be salient to the clinician, but it is important to recognize that some are considered research, rather than FDA-approved product methods. Additionally, HR-VWI can be performed with small field-of-view (FOV) images (on the order of 16 cm × 16 cm) to achieve exquisite detail but with limited coverage of the head or whole-head FOV images (on the order of 24 cm × 24 cm).12 Because a wide variety of techniques exist, it is important to understand those available and used at one’s institution.

The HR-VWI used at our institution and demonstrated here is a 3D PD SPACE technique. Images are acquired with a 16-cm FOV. This technique allows 0.25 mm × 0.25 mm interpolated in-plane pixel size with a slice thickness of 0.5 mm and can be acquired in any imaging plane. Such a focused technique only covers a 6-cm slab of brain unless scan time is increased, so the radiologist and clinicians must work closely with the technologists to ensure the aneurysm is fully imaged. T1- and T2-weighted images can also be obtained. In this review, conventional MRI refers broadly to more typical MRI sequences used routinely in clinical practice such as spin echo T1-weighted images at whole-brain FOV without special parameters to optimize visualization of vessel or aneurysm walls. Although the spatial resolution of these techniques varies considerably, they are typically on the order of several millimeters in slice thickness.

There are many prior studies assessing the histopathology and imaging characteristics of aneurysm walls on conventional-resolution MRI, but data assessing the utility of HR-VWI are emerging. Therefore, expected findings on HR-VWI are in part extrapolated from current knowledge of pathology and conventional-resolution MRI. Compared with conventional-resolution MRI, HR-VWI has the potential to identify smaller or more subtle areas of signal change or enhancement, more precisely delineate aneurysm wall thickness, and provide a more precise representation of the pathological composition. Some of these features could serve as imaging biomarkers to predict the biological behavior of aneurysms, identify a culprit aneurysm in the setting of subarachnoid hemorrhage (SAH), and potentially direct optimum treatment.

In this review, we highlight key studies to date addressing aneurysm vessel wall histopathology and findings on conventional-resolution MRI. This information is extrapolated to discuss potential future utility of HR-VWI. Additionally, specific literature assessing the utility of HR-VWI for some aneurysm features has emerged and is reviewed. We have illustrated these points with several examples demonstrating both features already described in the literature and novel cases demonstrating the potential for future clinical and research applications. The key vessel wall imaging findings by aneurysm type are outlined in Table 1.

TABLE 1.

Summary of typical vessel wall imaging findings and the clinical significance by aneurysm type

Aneurysm TypeKey Aneurysm Wall Imaging Findings
SaccularLack of enhancement on HR-VWI appears to be a strong indicator of an asymptomatic aneurysm w/ stable morphology.
Limited data suggest that most symptomatic or morphologically changing aneurysms demonstrate circumferential wall enhancement.
Nearly all ruptured aneurysms demonstrate circumferential enhancement or focal enhancement on HR-VWI at the rupture site.
Multiple aneurysms in the setting of SAHSeveral cases reported indicating the enhancement on HR-VWI usually identifies the culprit aneurysm.
Aneurysm after endovascular treatmentFrequent enhancement that can temporarily increase after treatment and can persist for years.
Enhancement can persist w/ or w/o a remnant.
Enhancement is typically smooth & circumferential, but can be nodular.
Most studies employ conventional-resolution MRI rather than HR-VWI.
Partially thrombosedAn onion-skin pattern w/ peripheral T1 hyperintensity is common w/in the thrombosed portion.
Absent wall enhancement on conventional-resolution MRI is associated w/ decreased growth rates.
Decreased enhancement after treatment on conventional-resolution MRI is associated w/ aneurysm shrinkage.
The intramural thrombosed component is well delineated from the lumen on HR-VWI.
Chronic fusiformEnhancement is frequent on conventional-resolution MRI & is associated w/ aneurysm growth.
Intramural thrombus & peripheral T1 hyperintensity consistent w/ repeated intramural hemorrhage is associated w/ aneurysm growth.
Current literature has employed conventional-resolution MRI.
Acute dissectingDegree of aneurysmal dilatation, intramural hematoma, & wall enhancement decrease w/ time w/ HR-VWI.
Some aneurysmal dilatation & wall enhancement can persist in the chronic phase.
Blood blisterA focal hematoma may be identified on the outer surface in the setting of rupture on HR-VWI.
Enhancement is variable but can be present in actively enlarging aneurysms based on scant data.
OncoticVariable appearance of thrombosed components and variable enhancement on HR-VWI; the significance of enhancement needs further study.
HR-VWI delineates the lumen and thrombosed components in both treated & untreated aneurysms.
MycoticCircumferential enhancement on conventional-resolution MRI is reported in several patients w/ different underlying infectious etiologies; the significance of enhancement & patterns of enhancement on HR-VWI need further study.

Saccular Aneurysms

The most common form of intracranial aneurysm is the saccular type, present in nearly 3% of the general population.51 Currently aneurysm size, location, history of prior rupture, hypertension, and ethnicity are the primary indicators used to direct treatment and predict future rupture.19 Additionally, evidence indicates that vessel wall structural and inflammatory change is associated with, and likely precedes, rupture.14

Recent studies suggest that circumferential wall enhancement on HR-VWI can identify unstable or ruptured saccular aneurysms11,22,37,43 (Fig. 1). The pathological basis for vessel wall enhancement has been presumed to represent inflammation and/or proliferation of vasa vasorum.29 Hu et al. provide limited evidence for this, demonstrating lymphocyte and phagocyte wall invasion on histological analysis of 1 ruptured and 1 unruptured saccular aneurysm that both demonstrated wall enhancement,22 but other mechanisms of enhancement remain possible. Edjlali et al. reported that circumferential wall enhancement was present on HR-VWI in 27 (87%) of 31 unstable aneurysms—including 16/17 (94%) ruptured, 5/5 (100%) changing morphology, or 6/9 (66%) symptomatic—and 28.5% of stable (any other) aneurysms.11 Overall, 27 (55%) of all aneurysms (stable or unstable) that had enhancement were unstable while 55 (93%) of all aneurysms that lacked enhancement were stable. Hu et al. studied 30 aneurysms with HR-VWI with correlation to clinical status, reporting wall enhancement in 12 (100%) of 12 potentially unstable aneurysms, including 6/6 (100%) ruptured, 1/1 (100%) changing morphology, 4/4 (100%) with symptoms due to mass effect, and 1 with symptoms in the setting of a ruptured contralateral mirror aneurysm. Overall, 12 (86%) of 14 of aneurysms with wall enhancement were ruptured, growing, or associated with symptoms and only 2 (11%) of 18 aneurysms without these associated features demonstrated wall enhancement.

Fig. 1.
Fig. 1.

Basilar trunk aneurysm in a 59-year-old woman who initially presented for evaluation of a cribriform plate meningioma (not shown). A: Axial T1-weighted contrast-enhanced MRI at the time of initial presentation demonstrated an incidental focal dilation and the vertebrobasilar junction measuring about 6 mm (arrow) in addition to vertebrobasilar dolichoectasia. B: Follow-up head MRI performed approximately 5 years later was conducted for follow-up of a cribriform plate meningioma (not shown). The focal aneurysmal dilation at the vertebrobasilar junction appeared to have enlarged (arrow), now measuring about 9 mm in transverse dimension. C: The patient presented approximately 4 years later with sudden onset dysarthria. MRI showed a perforator infarct in the right pons. D and E: After CTA demonstrated a large basilar trunk aneurysm, precontrast (D) and postcontrast (E) PD-weighted HR-VWI was performed. This demonstrated marked smooth eccentric enhancement of the aneurysm wall. The aneurysm measured 23 mm in maximum dimension. F: In anticipation of flow diversion therapy, a diagnostic cerebral angiogram was performed. The patient was then placed on aspirin and clopidogrel and scheduled to undergo flow diversion treatment of the aneurysm a week later. However, she died in her sleep days before the scheduled procedure, presumably due to aneurysmal rupture.

There is conflicting evidence on the relationship of aneurysm wall enhancement and aneurysm size. Edjlali et al. found no relationship between enhancement and size in aneurysms ranging from 4 to 8 mm,11 and Hu et al. found no relationship between aneurysms ranging in size from 3.4 to 55.4 mm.22 In contrast, Liu et al. found that the frequency of wall enhancement is positively correlated with aneurysm size in 61 unruptured aneurysms ranging in size from 2.9 to 30.5 mm (odds ratio 2.46 per mm increase in size).33 The reasons for this lack of agreement are not entirely clear, although it could be explained by the inclusion of ruptured aneurysms that may demonstrate enhancement regardless of size in the studies by Edjlali et al. and Hu et al.11,22 compared with inclusion of only unruptured aneurysms in the study by Liu et al.33

There are only limited data assessing the significance of the magnitude of aneurysm wall enhancement. Nagahata et al. found that only 4.8% of unruptured saccular aneurysms demonstrate strong enhancement and 82% demonstrated no enhancement.43 Two of 4 of these unruptured aneurysms with strong enhancement were considered unstable, 1 symptomatic, and 1 growing.43 Omakada et al. reported a higher degree of enhancement on HR-VWI measured quantitatively, but compared ruptured aneurysms to unruptured aneurysms in two pooled groups.48 By this method, the degree of enhancement is expected to be higher in the ruptured group partly due to a presumed higher percentage of aneurysms with wall enhancement and does not directly demonstrate that the degree of enhancement in ruptured aneurysms is greater than that in unruptured enhancing aneurysms. Additionally, peri-aneurysmal inflammatory change is expected to increase in the setting of rupture, which likely increased the magnitude of enhancement in these 2 studies compared with nonruptured aneurysms.

Beyond vessel wall enhancement, HR-VWI can characterize architectural details of aneurysms such as aneurysm wall thickness. Correlation of HR-VWI estimation and microscopic evaluation has shown that aneurysm wall thickness can be estimated on imaging when it exceeds imaging spatial resolution.54 However, aneurysm wall thickness is often below the spatial resolution of current vessel wall imaging techniques (0.02–0.5 mm).27 Kleinloog et al. conclude that the thickness of such thin-walled aneurysms can be estimated by the signal intensity on nonenhanced T1-weighted vessel wall images at 7 T, but only 2 aneurysms included in this study had histopathological confirmation of wall thickness.27 Such reliance of signal intensity on wall thickness would raise the possibility that the visually perceived degree of enhancement of the aneurysm wall varies with wall thickness, but this possibility has not been specifically assessed to our knowledge.

In summary, the current literature suggest that saccular aneurysms with wall enhancement on HR-VWI are frequently unstable (changing morphology, symptomatic, or ruptured) and that more urgent treatment may be reasonable whereas the preponderance of saccular aneurysms without wall enhancement appears to be stable and that less urgent treatment or observation may be reasonable. However, these assertions are based on retrospective data that include relatively large percentages of ruptured aneurysms,11,43 which selects for aneurysms with wall enhancement, with relatively fewer data on unstable unruptured aneurysms. HR-VWI features of unstable aneurysms may prove to be variable, because several histopathological forms of aneurysm walls associated with rupture are described with varying patterns of smooth muscle cell infiltration, wall thickness, presence of associated organizing luminal thrombus, and wall cellularity.14

Aneurysms in the Setting of SAH

In addition to predicting natural history, HR-VWI can provide useful information in the setting of acute SAH. In a study of 61 patients with aneurysmal SAH, Nagahata et al. demonstrated that strong wall enhancement is 95.2% specific for rupture but with a sensitivity of only 73.8% and that any (strong or faint) wall enhancement was 98.6% sensitive, but had limited specificity of 81.9%.43 Interestingly, the authors found that focal strong enhancement at the aneurysm apex was associated with the point of rupture as noted during surgery in nearly 50% of such cases.43 This finding suggests that the mechanism of focal enhancement in ruptured aneurysms may involve physical disruption or a robust local inflammatory reaction at the rupture site.

The findings by Nagahata et al. raise the possibility that enhancement could help identify the ruptured aneurysm when multiple aneurysms are present. A case series including 3 patients with multiple aneurysms provides initial evidence that HR-VWI can identify the culprit aneurysm in the setting of acute SAH.37 This observation is important because the distribution of SAH is not highly predictive of aneurysm location.55 This information could also triage acute treatment toward the culprit aneurysm. Overall, it is not surprising that ruptured aneurysms demonstrate frequent enhancement, because inflammatory cells are isolated from ruptured aneurysms.14

HR-VWI could potentially provide insight into the source of nonaneurysmal SAH as well. In a study of 11 patients with angiogram-negative nonperimesencephalic SAH, Coutinho et al. reported focal abnormalities on HR-VWI in the basilar artery wall in 2 patients (19%).8 This was postulated to represent a tiny thrombosed aneurysm, loculated extramural blood, or a ruptured blood-blister aneurysm.

The utility in patients with a perimesencephalic pattern is less certain. The origin of perimesencephalic subarachnoid blood remains unknown, although it has been suggested it may result from a small thrombosed and obliterated aneurysm, basilar artery dissections, or venous variants.53 It is possible that HR-VWI could identify the site of a small aneurysm or subtle basilar artery dissection, and shed light on the mechanisms of perimesencephalic hemorrhages, but this remains undemonstrated. In fact, a series of 7 patients with perimesencephalic patterns had basilar arteries assessed at 7T, but the artery was normal in all cases without evidence of dissection or intramural hematoma.57

The cumulative literature assessing HR-VWI in the setting of SAH shows that it can help identify a culprit aneurysm when multiple aneurysms are present, but there is not strong evidence to direct use in the setting of nonaneurysmal SAH.

Aneurysm Follow-Up After Endovascular Treatment

A few studies have evaluated the incidence of vessel wall enhancement on conventional-resolution MRI after endovascular treatment.13,38,56 Su et al. retrospectively studied the rate of wall enhancement and surrounding brain edema in 132 aneurysms after endovascular treatment.56 Eighty-five aneurysms (64.4%) had wall enhancement, which was significantly more likely with larger aneurysms or those that were embedded in the brain with surrounding edema.56 Interestingly, steroid use was not associated with a decreased rate of enhancement.56 While the association with coil packing density with vessel wall enhancement did not reach statistical significance in this study, an earlier study by this group reported that coil packing density was associated with a greater likelihood of vessel wall enhancement.13 This aneurysmal enhancement can either temporarily increase following treatment, presumably due to an inflammatory response to heal the aneurysm or to isolate the coils, or can be steady and consistent over time.56 After flow-diverter treatment, vessel wall enhancement may be observed with or without an aneurysm remnant and with or without prior rupture with prior coil embolization.38 We have observed that a nonthrombosed aneurysm after flow-diverter treatment with wall enhancement may progress to complete aneurysm occlusion (Fig. 2). McGuinness et al. reported that vessel wall enhancement was smooth and circumferential in 8 (36%) of 22 patients and focal and nodular in 3 (14%) of 22 patients with flow-diverter–treated aneurysms imaged 2–10 days after the procedure.38

Fig. 2.
Fig. 2.

Evaluation of a treated aneurysm in a 42-year-old woman with increasing headaches. A: Imaging and CSF evaluation was negative for SAH, but a CT angiogram did reveal a partially thrombosed 1.9-cm right ophthalmic aneurysm and a 1.4-cm left ophthalmic aneurysm. The right ophthalmic aneurysm was treated with balloon-assisted coil embolization, and 5 days later the left ophthalmic aneurysm was treated with Pipeline embolization. B–D: A follow-up Gd bolus MR angiogram demonstrated complete occlusion of the right aneurysm and persistent flow in the left aneurysm. C and D: Concurrent axial PD HR-VWI before and after Gd administration demonstrated absent wall enhancement on the right, but a smooth rim of enhancement on the left. E: The visualization of the enhancement on the left is enhanced with a subtraction image. F: The treated left ophthalmic aneurysm became occluded at the 2-month follow-up evaluation as demonstrated on a Gd bolus MR angiogram.

These studies conclude that conventional-resolution MRI vessel wall enhancement is a common posttreatment finding, can persist for years, and should be considered an expected posttreatment finding.13,38,56 However, these studies did not include routine pretreatment MRI examinations, and the rate and significance of pretreatment vessel wall enhancement remains undefined. Histopathological studies of coiled aneurysms reveal increasing inflammatory cell infiltration during the 1st month following coil embolization followed by aneurysm dome neovascularization, which could account for early and persistent enhancement, respectively.5 Although reports of HR-VWI findings in treated aneurysms are currently lacking, different aneurysms with near-contemporaneous treatment in the same patient may demonstrate different levels of wall enhancement on HR-VWI (Fig. 2).

Partially Thrombosed Aneurysms

Partially thrombosed aneurysms constitute a unique aneurysm class. The thrombosed component consists histopathologically of repeated subadventitial hemorrhages within the wall itself rather than the lumen and therefore demonstrates unique vessel wall findings on MRI.28 In contradistinction to saccular aneurysms, this class most commonly presents with symptoms due to mass effect.28,29

On conventional-resolution MRI, the mural thrombus has been described as either homogeneous or heterogenous,36 often demonstrating an “onion skin” pattern of thrombus of varying ages.28,58 Several reports described T1 hyperintensity in the peripheral thrombus, distant from the lumen,25,28,36,58 consistent with the mechanism that acute hemorrhage preferentially occurs in the subadventitia from the vasa vasorum. Martin et al. reported that thrombosed components consistently had stable signal intensities in 9 aneurysms followed over time, including peripheral T1 hyperintensity, which suggests a constant remodeling process with ongoing intramural hemorrhage.36

Over time, the thrombosed portion may enlarge independently from the lumen, including with stable25 or decreased36 lumen size. The thrombosed component can also enlarge after complete luminal occlusion.20,26 Therefore, it is important to assess the size and characteristics of both the thrombosed portion and lumen during image interpretation. HR-VWI nicely depicts both the thrombosed and luminal components (Fig. 3). We have observed that aneurysm walls may demonstrate asymmetrical enhancement isolated to noncalcified regions, but the significance of this pattern is undetermined (Fig. 4).

Fig. 3.
Fig. 3.

Nonenhancing partially thrombosed basilar tip aneurysm in a 45-year-old woman under evaluation for chronic neck pain. A: Coronal T2-weighted cervical spine MRI demonstrates an incidental 15-mm partially thrombosed basilar tip aneurysm (arrows). Following discovery of the aneurysm it was found that she had a several-month history of headaches. B and C: Axial pre- (B) and postcontrast (C) PD HR-VWI images demonstrated a laminated thrombus in the aneurysmal sac without any appreciable aneurysm wall enhancement. The lumen and the thrombus are readily distinguishable; the thrombus is observed within the wall itself rather than the lumen. D: Susceptibility-weighted images again demonstrated the laminated thrombus. Based on the lack of enhancement the patient was instructed not to rush to treatment and that she could be treated at a time that would be convenient for her. E: A preembolization cerebral angiogram demonstrates the luminal component of the partially thrombosed aneurysm. F: The aneurysm was successfully treated with endovascular coiling.

Fig. 4.
Fig. 4.

Partially thrombosed aneurysm with mural calcification and eccentric wall enhancement in a 49-year-old woman with an incidentally discovered left posterior inferior cerebellar artery aneurysm. A: Coronal CTA maximum intensity projection image demonstrates a small lumen and a larger predominantly calcified (arrowhead) peripheral thrombosed component. B: Coronal PD HR-VWI with Gd delineates the inner lumen (arrowhead) and thrombosed wall as a peripheral dark cap. There is eccentric wall enhancement of the aneurysm wall only along the medial margin at the margin with the vertebral artery (arrow) corresponding to a noncalcified portion of the aneurysm wall. The remainder of the aneurysm wall, which was largely calcified, does not demonstrate enhancement.

Peripheral vessel wall enhancement has also been reported in the majority of partially thrombosed aneurysms using conventional-resolution MRI or CT.23,28,36,52,58 Roccatagliata et al. reported aneurysm wall enhancement in 63.2% of 22 aneurysms on conventional-resolution MRI and considered this to be a surrogate of inflammation.52 In 1 small series, Iihara et al. found that among 10 partially thrombosed aneurysms with wall enhancement, decreased enhancement in the postoperative setting in 5 cases (50%) was significantly associated with a reduction in aneurysm size. At the same time, 3 aneurysms with both absent wall enhancement and absent surrounding T2 FLAIR hyperintensity had decreased growth potential prior to treatment and less aneurysm shrinkage after treatment compared with 14 aneurysms with wall enhancement and/or surrounding T2 FLAIR hyperintensity.23 These findings suggest that more aggressive treatment in partially thrombosed aneurysms with wall enhancement may be warranted. Although direct radiological-pathological correlation is lacking, peripheral enhancement may be due to inflammation and/or underlying neoangiogenesis. Indeed, inflammatory change has been identified on histopathological analysis of the thrombosed component.3 Additionally, Nagahiro et al. reported intrathrombotic blood vessels in 2 such aneurysms on histopathological analysis, and assessment for correlate findings within the central thrombus on HR-VWI in the future could be useful.44

Overall, the vast majority of the literature assessing vessel wall characteristics of partially thrombosed aneurysms is derived from conventional-resolution MRI. However, it is clear that HR-VWI more precisely delineates the thrombosed component and the lumen.

Chronic Fusiform Aneurysms

Intracranial fusiform aneurysms may be subclassified in several ways. Broadly, these may be categorized as atherosclerotic or nonatherosclerotic. While advanced atherosclerosis can result in a fusiform-shaped artery, nonatherosclerotic fusiform aneurysms are more common.40 Nonatherosclerotic fusiform aneurysms can be categorized as chronic or acute dissecting, which are discussed separately. The classification scheme is important because the findings on HR-VWI should differ by category.

The common histopathological feature of chronic fusiform aneurysms is damaged or frankly disrupted internal elastic lamina, which could be observed with or without intimal thickening or associated atherosclerotic plaque.39,45 Mizutani et al. identified distinct subtypes including segmental ectasia and chronic dolichoectatic dissecting aneurysms. Segmental ectasias are asymptomatic fusiform enlargements with stretched or fragmented internal elastic lamina without associated thrombus; these are believed to have a benign clinical course. Chronic dolichoectatic dissecting aneurysms demonstrate fragmented internal elastic lamina with intimal thickening and an organized thrombus; these frequently enlarge with time and are symptomatic.

Nakatomi et al. reported conventional-resolution imaging findings of 16 fusiform aneurysms, 8 with histopathological correlation.45 In this study, vessel wall enhancement was present in 5 (100%) of 5 aneurysms within histopathologically confirmed neoangiogenesis within the intima and was noted in 9 (56%) of 16 symptomatic aneurysms.45 All 8 aneurysms (100%) with intramural hemorrhage increased in size on serial examinations while all 8 aneurysms (100%) without intramural hemorrhage did not change in size.45 In vertebrobasilar aneurysms, T1 hyperintensity consistent with recent hemorrhage is associated with an increased likelihood of growth.35,46 Many other aneurysm features associated with growth have been identified, including intramural thrombus, the presence of daughter sacs, and overall size.46

These vessel wall features associated with fusiform aneurysm enlargement are important because they demonstrate variable growth over time, generally have a poor prognosis, and are difficult to treat.46 Cumulatively, the literature has identified many vessel wall features on conventional imaging that can predict such growth, including important aneurysm wall features such as intramural thrombus and peripheral intramural T1 hyperintensity. Improved identification of these features could potentially prompt closer surveillance or treatment.

Acute Dissecting Aneurysms

Acute dissecting fusiform aneurysms result from acute disruption of the internal elastic lamina with subadventitial dissection. These may occur concurrently with subintimal dissection planes and areas of luminal narrowing. This most often affects the vertebrobasilar arteries, but can also occur at other locations including the internal carotid artery (ICA) and middle cerebral artery (MCA).39 These typically demonstrate an entry-point communication between the pseudolumen and parent vessel lumen.39 The dissection may end blindly within the pseudolumen or less commonly demonstrate a second exit-point back to the lumen.39 This distinction is important because dissecting aneurysms that have a second exit point to the lumen have a more stable clinical course.39

Initial studies of HR-VWI of intracranial dissection have shown that features of dissection including an intimal flap, double lumen, and intramural hematoma can be identified, including cases with dissecting aneurysms.49,60 Both the wall of the lumen and outer margin of the artery can enhance; a small portion of intramural hematomas also reportedly enhance.49,60 Wang et al. identified areas suggestive of disruption of the outer margin of the affected artery in 2 (33%) of 6 patients studied with SAH.60 Park et al. retrospectively studied 41 intracranial vertebral artery dissections with serial HR-VWI to characterize the imaging features over time.49 This study found a decrease in aneurysmal dilation, intramural hematoma signal intensity, and degree of wall enhancement over time.49 However, aneurysmal dilation and mild wall enhancement persisted in 4 (44%) and 7 (78%) of 9 patients studied in the chronic phase, respectively.49 Overall, these studies indicate that HR-VWI can identify and help distinguish recent from chronic dissecting aneurysms.

Blood-Blister Aneurysms

Blood-blister aneurysms are small, broad-based, hemispherically shaped aneurysms that occur along the dorsal surface of the supraclinoid ICA opposite the origin of the posterior communicating artery. These are very fragile aneurysms and the majority present with SAH.18 Ishikawa et al. reported such an aneurysm on autopsy at the site of a disrupted internal elastic lamina and tunica media with a thin covering consisting of only fibrous tissue and adventitia.24 Ishikawa et al. did not identify a dissection, although other authors have postulated that a dissection is the initiating event.18 Blood-blister aneurysms are sometimes initially angiographically occult and require second-look angiograms for identification.18

Horie et al. report a case of HR-VWI used to detect an angiographically occult blood-blister aneurysm.21 While an abnormality was not identified in the vessel wall itself, a focal T1 hyperintense thrombus was found on the immediate outer surface of the aneurysm. In our experience, vessel wall enhancement can be absent in blood-blister aneurysms on HR-VWI (Fig. 5). Lack of vessel wall enhancement is not surprising with this type of aneurysm given the very thin wall. However, we have also observed wall enhancement in an actively enlarging blood-blister aneurysm (Fig. 6). Because such information is currently based on personal observation and scant data, future HR-VWI investigations assessing the relationship between enhancement and stability are needed to direct use and interpretation in clinical practice.

Fig. 5.
Fig. 5.

Blister-type aneurysm in a 42-year-old woman who had a 14-day history of severe headaches. None of the headaches were characterized as thunderclap headaches, however. Initial noncontrast CT was negative for SAH, but a lumbar puncture was not performed. A: CTA at initial imaging evaluation demonstrated a 2-mm tubular-shaped aneurysm arising off of the dorsal wall of the right supraclinoid ICA (arrow). B and C: Three-dimensional (B) and 2D (C) right ICA cerebral angiograms again demonstrate the 2-mm tubular-shaped aneurysm (arrows). However, just distal to the focal aneurysmal outpouching there was undulation in the contour of the dorsal wall of the supraclinoid ICA (arrowhead), which suggests that this aneurysm could represent a blister aneurysm. D and E: Pre- (D) and postcontrast (E) PD-weighted HR-VWI sequences demonstrate no appreciable enhancement of the aneurysm wall (arrows) to suggest active inflammation. The patient was taken to surgery, and the aneurysm was treated with a Sundt clip. The wall of the aneurysm and vessel was quite friable during surgery, and the wall was reinforced with fibrin glue and cottonoid.

Fig. 6.
Fig. 6.

Depiction of a growing blood-blister aneurysm with wall enhancement. The initial clinical presentation included SAH in the left sylvian fissure (not shown). A–C: Three-dimensional volume-rendered CTA image on presentation demonstrates a very subtle contour abnormality along the superior surface of the left ICA (A); 3D volume-rendered CTA image 4 days after presentation demonstrates a small subtle blood-blister aneurysm (B); and a 3D volume-rendered CTA image 8 days after presentations demonstrates an enlarging blood-blister aneurysm (C). D and E: Coronal PD-weighted HR-VWI before (D) and after (E) Gd, obtained 5 days after presentation, demonstrates thin smooth-wall enhancement of the aneurysm (arrows). This aneurysm was treated with a Pipeline stent.

Myxomatous and Other Oncotic Aneurysms

The imaging and clinical features of oncotic aneurysms vary by underlying neoplasm. While the exact etiology is still debated, there is strong evidence that direct implantation of tumor emboli into the vessel wall itself is the initial event.6

Myxomatous aneurysms resulting from embolic tumor particles in patients with cardiac myxoma are the most common subtype of oncotic aneurysm.63 Histological examination has revealed subintimal growth of tumor and vessel wall disruption.15,63 These are typically multiple, fusiform, and involve distal cerebral artery branches6,63 and can present concurrently with an atrial myxoma years after resection.63 These aneurysms are typically slow-growing and difficult to treat, requiring long-term imaging follow-up.

Prior studies on the imaging appearance of myxomatous aneurysms have evaluated the luminal characteristics,6,63 but there is little information on the imaging characteristics of the aneurysm walls that harbor the primary pathology. In our experience with HR-VWI, the aneurysm wall appearance demonstrates considerable variation in enhancement patterns and in the presence and appearance of the thrombosed component (Fig. 7). The precise size and morphology of both the lumen and thrombosed components are better depicted on HR-VWI than on conventional-resolution MRI. HR-VWI can also precisely delineate size and mass-effect of thrombosed portions of the aneurysm after treatment.

Fig. 7.
Fig. 7.

Depiction of the lumen and thrombosed components of treated and untreated myxomatous aneurysms in a 59-year-old man with a history of resected atrial myxoma. Five years after resection, multiple fusiform cerebral aneurysms were discovered, including a partially thrombosed left MCA aneurysm. The left MCA aneurysm continued to enlarge over 4 years of observation and was treated with coil embolization. A: Two years after embolization, a 3D time-of-flight MR angiogram demonstrated a T1 signal within the thrombosed component of the left aneurysm and 2 untreated right insular MCA aneurysms. On 3D time-of-flight images, evaluation of the lumens was limited due to potential signal loss and evaluation for a remnant was limited due to intrinsic T1 signal of the thrombus. B: A Gd bolus MR angiogram demonstrates the true size of the lumens on the right and confirms that the giant left aneurysm remains thrombosed (not shown in entirety due to size). C–F: Axial PD HR-VWI before (C, and more inferiorly E) and after (D, and more inferiorly F) Gd delineates the lumen and thrombosed components in detail. The very large thrombosed aneurysm on the left did not demonstrate enhancement; this thrombosed component had decreased in size over serial examinations. Mild wall enhancement circumscribes the lumen of the partially thrombosed right insular MCA aneurysm (arrow). In contradistinction, the adjacent fusiform right MCA aneurysm did not demonstrate wall enhancement (arrowhead).

Mycotic Aneurysms

Cerebral mycotic aneurysms may result from various microorganisms including viruses, bacteria, mycobacteria, parasites, and fungi. Immunocompromised status is a risk factor, but these may also develop in immunocompetent patients. In general, these aneurysms have a tendency to be peripheral, multiple, and fusiform, but irregular, dissecting, or saccular aneurysms are reported.4,30 The primary pathology includes fibroinflammatory tissue and arterial wall destruction, which can lead to contained pseudoaneurysm or rupture.30

CNS varicella zoster virus (VZV) vasculopathy can accompany either primary or reactivation zoster infection.2,16 VZV vasculopathy may be observed in immunocompromised patients with or without a skin eruption, including those with human immunodeficiency virus (HIV) or those undergoing high-dose steroid treatment. VZV aneurysms are uncommon, but are important to characterize because they have the potential to rupture. HR-VWI has been evaluated in a small number of patients with CNS VZV vasculopathy,7 but not specifically in patients with VZV aneurysms.

VZV aneurysms may demonstrate complex shapes, develop rapidly, and variably resolve with antiviral and antiinflammatory medications.32 In our clinical experience, we have observed peripheral enhancement in multiple aneurysms in an immunocompromised patient with presumed VZV vasculopathy on conventional-resolution MRI (luminal imaging findings reported previously Daugherty et al.;9 Fig. 8).

Fig. 8.
Fig. 8.

VZV aneurysm with an enhancing wall on conventional-resolution MRI in a 14-year-old girl with a history of combined immune deficiency. Intravenous immunoglobulin therapy was administered monthly. This patient presented with sudden-onset right-arm tingling and weakness and subsequently developed right-face and -neck tingling and right-arm weakness. Following an extensive infectious disease workup including serology, sputum samples, and a lumbar puncture, the CSF polymerase chain reaction for VZV was positive. There was no known history of dermatological manifestations of VZV. The patient was put on a prolonged course of acyclovir followed by lifelong valacyclovir. After more than 7 years of follow-up the patient has not experienced any recurrent symptoms related to her VZV vasculopathy. A: Axial diffusion-weighted MRI shows a left thalamic infarct. B: Conventional cerebral angiogram shows diffuse dilation of the basilar artery and both P1 segments. There is a more focal dilation in the left P1 segment. C and D: Pre- (C) and postcontrast (D) conventional-resolution T1-weighted images show circumferential wall enhancement of the dilated basilar artery. E and F: Pre- (E) and postcontrast (F) conventional-resolution T1-weighted images also demonstrate circumferential enhancement of the basilar tip and right P1 segment.

Aneurysm formation in the HIV setting is incompletely understood, but may be due to a variety of infections such as VZV or may be attributed to HIV itself.17 These are more common with low CD4 counts and high viral loads. O’Charoen et al. report peripheral enhancement on conventional-resolution MRI in a cerebral aneurysm attributed directly to HIV vasculopathy.47 Inflammation may depend on immune status as histopathological evaluation of aneurysms from pediatric patients with HIV have revealed little to no inflammation.17

The most common culprits of bacterial mycotic aneurysms are Staphylococcus or Streptococcus species;30 response to antibiotics is variable and currently unpredictable.2,30 Cerebral bacterial mycotic aneurysms may occasionally mimic a berry aneurysm on conventional imaging methods, and blood cultures are sterile in 18%–50% of patients.30 By analogy, periaortic enhancement is variably reported in mycotic aortic aneurysms.30

Overall, the frequency and clinical significance of aneurysm wall enhancement in the various types of mycotic cerebral aneurysms in either immunocompromised or immunocompetent patients is not fully defined on conventional-resolution MRI and is essentially unexplored on HR-VWI.

Future Directions and Conclusions

The biological behavior of the many types of intracranial aneurysms varies widely and is largely dependent on differences in vessel wall pathology including inflammation, neoangiogenesis, intramural hemorrhage, tumor implantation, and physical disruption. HR-VWI offers the potential to identify imaging surrogates of these vessel wall features and to therefore identify imaging biomarkers of aneurysm behavior.

HR-VWI will characterize aneurysm walls in greater in-vivo detail than previously possible and may complement forms of luminal imaging. Although some data on HR-VWI of aneurysms exist, such data are far less abundant than current data grossly characterizing aneurysm walls with conventional MRI or histopathology for many types of aneurysms. The potential exists to build upon this current knowledge with HR-VWI, and future studies of the utility of aneurysm wall findings to direct medical or interventional treatments are needed. It is important to recognize that, while retrospective data evaluating intracranial aneurysms with HR-VWI are emerging, future prospective studies are needed to establish the histopathological basis for imaging findings, assess the ability to predict biological behavior, compare the diagnostic utility with conventional imaging, and determine the impact on patient outcome for the various types of aneurysms discussed herein.

The current understanding of aneurysm wall findings on HR-VWI is evolving; we hope this review of the current knowledge of HR-VWI, conventional-resolution imaging, and key histopathology of aneurysm walls can help guide current clinical practice and future research.

Acknowledgments

We would like to thank Sonia Watson and Andrea Moran for their help in editing this manuscript.

Disclosures

Dr. Lanzino has served as a consultant to Medtronic.

Author Contributions

Conception and design: Lehman, Brinjikji, Kallmes, Huston. Acquisition of data: Lehman. Drafting the article: Lehman, Huston. Critically revising the article: all authors. Reviewed submitted version of manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: Lehman.

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Contributor Notes

Correspondence Vance T. Lehman, Department of Radiology, Mayo Clinic College of Graduate Medical Education, 200 First St. SW, Rochester, MN 55905. email: lehman.vance@mayo.edu.

INCLUDE WHEN CITING Published online June 9, 2017; DOI: 10.3171/2016.12.JNS162262.

Disclosures Dr. Lanzino has served as a consultant to Medtronic.

  • View in gallery

    Basilar trunk aneurysm in a 59-year-old woman who initially presented for evaluation of a cribriform plate meningioma (not shown). A: Axial T1-weighted contrast-enhanced MRI at the time of initial presentation demonstrated an incidental focal dilation and the vertebrobasilar junction measuring about 6 mm (arrow) in addition to vertebrobasilar dolichoectasia. B: Follow-up head MRI performed approximately 5 years later was conducted for follow-up of a cribriform plate meningioma (not shown). The focal aneurysmal dilation at the vertebrobasilar junction appeared to have enlarged (arrow), now measuring about 9 mm in transverse dimension. C: The patient presented approximately 4 years later with sudden onset dysarthria. MRI showed a perforator infarct in the right pons. D and E: After CTA demonstrated a large basilar trunk aneurysm, precontrast (D) and postcontrast (E) PD-weighted HR-VWI was performed. This demonstrated marked smooth eccentric enhancement of the aneurysm wall. The aneurysm measured 23 mm in maximum dimension. F: In anticipation of flow diversion therapy, a diagnostic cerebral angiogram was performed. The patient was then placed on aspirin and clopidogrel and scheduled to undergo flow diversion treatment of the aneurysm a week later. However, she died in her sleep days before the scheduled procedure, presumably due to aneurysmal rupture.

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    Evaluation of a treated aneurysm in a 42-year-old woman with increasing headaches. A: Imaging and CSF evaluation was negative for SAH, but a CT angiogram did reveal a partially thrombosed 1.9-cm right ophthalmic aneurysm and a 1.4-cm left ophthalmic aneurysm. The right ophthalmic aneurysm was treated with balloon-assisted coil embolization, and 5 days later the left ophthalmic aneurysm was treated with Pipeline embolization. B–D: A follow-up Gd bolus MR angiogram demonstrated complete occlusion of the right aneurysm and persistent flow in the left aneurysm. C and D: Concurrent axial PD HR-VWI before and after Gd administration demonstrated absent wall enhancement on the right, but a smooth rim of enhancement on the left. E: The visualization of the enhancement on the left is enhanced with a subtraction image. F: The treated left ophthalmic aneurysm became occluded at the 2-month follow-up evaluation as demonstrated on a Gd bolus MR angiogram.

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    Nonenhancing partially thrombosed basilar tip aneurysm in a 45-year-old woman under evaluation for chronic neck pain. A: Coronal T2-weighted cervical spine MRI demonstrates an incidental 15-mm partially thrombosed basilar tip aneurysm (arrows). Following discovery of the aneurysm it was found that she had a several-month history of headaches. B and C: Axial pre- (B) and postcontrast (C) PD HR-VWI images demonstrated a laminated thrombus in the aneurysmal sac without any appreciable aneurysm wall enhancement. The lumen and the thrombus are readily distinguishable; the thrombus is observed within the wall itself rather than the lumen. D: Susceptibility-weighted images again demonstrated the laminated thrombus. Based on the lack of enhancement the patient was instructed not to rush to treatment and that she could be treated at a time that would be convenient for her. E: A preembolization cerebral angiogram demonstrates the luminal component of the partially thrombosed aneurysm. F: The aneurysm was successfully treated with endovascular coiling.

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    Partially thrombosed aneurysm with mural calcification and eccentric wall enhancement in a 49-year-old woman with an incidentally discovered left posterior inferior cerebellar artery aneurysm. A: Coronal CTA maximum intensity projection image demonstrates a small lumen and a larger predominantly calcified (arrowhead) peripheral thrombosed component. B: Coronal PD HR-VWI with Gd delineates the inner lumen (arrowhead) and thrombosed wall as a peripheral dark cap. There is eccentric wall enhancement of the aneurysm wall only along the medial margin at the margin with the vertebral artery (arrow) corresponding to a noncalcified portion of the aneurysm wall. The remainder of the aneurysm wall, which was largely calcified, does not demonstrate enhancement.

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    Blister-type aneurysm in a 42-year-old woman who had a 14-day history of severe headaches. None of the headaches were characterized as thunderclap headaches, however. Initial noncontrast CT was negative for SAH, but a lumbar puncture was not performed. A: CTA at initial imaging evaluation demonstrated a 2-mm tubular-shaped aneurysm arising off of the dorsal wall of the right supraclinoid ICA (arrow). B and C: Three-dimensional (B) and 2D (C) right ICA cerebral angiograms again demonstrate the 2-mm tubular-shaped aneurysm (arrows). However, just distal to the focal aneurysmal outpouching there was undulation in the contour of the dorsal wall of the supraclinoid ICA (arrowhead), which suggests that this aneurysm could represent a blister aneurysm. D and E: Pre- (D) and postcontrast (E) PD-weighted HR-VWI sequences demonstrate no appreciable enhancement of the aneurysm wall (arrows) to suggest active inflammation. The patient was taken to surgery, and the aneurysm was treated with a Sundt clip. The wall of the aneurysm and vessel was quite friable during surgery, and the wall was reinforced with fibrin glue and cottonoid.

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    Depiction of a growing blood-blister aneurysm with wall enhancement. The initial clinical presentation included SAH in the left sylvian fissure (not shown). A–C: Three-dimensional volume-rendered CTA image on presentation demonstrates a very subtle contour abnormality along the superior surface of the left ICA (A); 3D volume-rendered CTA image 4 days after presentation demonstrates a small subtle blood-blister aneurysm (B); and a 3D volume-rendered CTA image 8 days after presentations demonstrates an enlarging blood-blister aneurysm (C). D and E: Coronal PD-weighted HR-VWI before (D) and after (E) Gd, obtained 5 days after presentation, demonstrates thin smooth-wall enhancement of the aneurysm (arrows). This aneurysm was treated with a Pipeline stent.

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    Depiction of the lumen and thrombosed components of treated and untreated myxomatous aneurysms in a 59-year-old man with a history of resected atrial myxoma. Five years after resection, multiple fusiform cerebral aneurysms were discovered, including a partially thrombosed left MCA aneurysm. The left MCA aneurysm continued to enlarge over 4 years of observation and was treated with coil embolization. A: Two years after embolization, a 3D time-of-flight MR angiogram demonstrated a T1 signal within the thrombosed component of the left aneurysm and 2 untreated right insular MCA aneurysms. On 3D time-of-flight images, evaluation of the lumens was limited due to potential signal loss and evaluation for a remnant was limited due to intrinsic T1 signal of the thrombus. B: A Gd bolus MR angiogram demonstrates the true size of the lumens on the right and confirms that the giant left aneurysm remains thrombosed (not shown in entirety due to size). C–F: Axial PD HR-VWI before (C, and more inferiorly E) and after (D, and more inferiorly F) Gd delineates the lumen and thrombosed components in detail. The very large thrombosed aneurysm on the left did not demonstrate enhancement; this thrombosed component had decreased in size over serial examinations. Mild wall enhancement circumscribes the lumen of the partially thrombosed right insular MCA aneurysm (arrow). In contradistinction, the adjacent fusiform right MCA aneurysm did not demonstrate wall enhancement (arrowhead).

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    VZV aneurysm with an enhancing wall on conventional-resolution MRI in a 14-year-old girl with a history of combined immune deficiency. Intravenous immunoglobulin therapy was administered monthly. This patient presented with sudden-onset right-arm tingling and weakness and subsequently developed right-face and -neck tingling and right-arm weakness. Following an extensive infectious disease workup including serology, sputum samples, and a lumbar puncture, the CSF polymerase chain reaction for VZV was positive. There was no known history of dermatological manifestations of VZV. The patient was put on a prolonged course of acyclovir followed by lifelong valacyclovir. After more than 7 years of follow-up the patient has not experienced any recurrent symptoms related to her VZV vasculopathy. A: Axial diffusion-weighted MRI shows a left thalamic infarct. B: Conventional cerebral angiogram shows diffuse dilation of the basilar artery and both P1 segments. There is a more focal dilation in the left P1 segment. C and D: Pre- (C) and postcontrast (D) conventional-resolution T1-weighted images show circumferential wall enhancement of the dilated basilar artery. E and F: Pre- (E) and postcontrast (F) conventional-resolution T1-weighted images also demonstrate circumferential enhancement of the basilar tip and right P1 segment.

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