Vessel Wall Contrast Enhancement Research Articles

Contrast enhancement patterns associated with acute stroke in moyamoya disease using MR vessel wall imaging.

High-resolution magnetic resonance imaging (HR-MRI) can provide valuable insights into the histopathological characteristics of moyamoya disease (MMD). However, the patterns of vessel wall contrast enhancement have not been well established. We aimed to identify the contrast enhancement patterns of the vessel walls associated with acute cerebral infarction using HR-MRI in MMD. In this retrospective study, we conducted genetic tests for Ring Finger Protein 213 (RNF213) and performed HR-MRI on patients suspected of having MMD. We analyzed wall enhancement patterns including concentric, eccentric, or mixed enhancement types, and the occurrence of acute cerebral infarction in patients who simultaneously tested positive for RNF213 and exhibited definite features of MMD on HR-MRI. Among 306 patients who underwent RNF213 tests for the evaluation of MMD, 56 showed positive RNF213, and HR-MRI was performed on 32 of them. Among the patients with acute cerebral infarction, the incidence rate was significantly higher in the group with concentric wall enhancement compared to patients without acute cerebral infarction (73.3%vs. 17.0%, p<.002). Furthermore, the incidence was notably elevated, even in patients with pure concentric wall enhancement (40.0%vs. 5.9%, p=.033). The area under the curve (AUC) for the group with any concentric wall enhancement showed a significant result of.78 (95% confidence interval [CI]:.61-.95, p=.007), whereas the predictive ability for pure concentric wall enhancement did not reach significance (AUC=.67, 95% CI:.48-.86, p=.100). Concentric wall enhancement was a significant predictor of acute cerebral infarction in patients with MMD.

Intensity Score of Vessel Wall Contrast Enhancement in MRI Allows Prediction of Disease Progression in Moyamoya Angiopathy.

The underlying pathophysiological cause of moyamoya angiopathy (MMA) is still unclear. High-resolution vessel wall imaging has become a useful tool. The aim was to study vessel wall contrast-enhancement (VW-CE) as an imaging marker to predict disease progression in MMA. Patients with MMA, who had undergone serial contrast-enhanced high-resolution MRI with concomitant and follow-up digital subtraction angiography, were analyzed retrospectively. VW-CE was semiquantified by measurement of the signal intensity of the vessel wall in in contrast-enhanced high-resolution MRI. A comparative quotient with the contrast-intensity of the pituitary stalk was calculated and graded accordingly from grade 1 to 5. VW-CE status was correlated with disease status, stroke, cerebrovascular reactivity in CO2-triggered blood-oxygen level-dependent MRI, angiographic disease progression, revascularization surgery, and follow-up imaging. Forty eight patients met the inclusion criteria. N = 56 MRI and digital subtraction angiography time-intervals were evaluated for 12 vessel sections per hemisphere each (N = 1344). N = 38 (79%) patients showed VW-CE and N = 10 (21%) did not. VW-CE was only observed in the terminal internal carotid artery and the proximal circle of Willis (N = 96/1344). Notably, patients with VW-CE significantly more often presented with acute infarction in the concomitant MRI. The incidence of angiographically proven disease progression was significantly associated with the incidence of VW-CE, and time to disease progression was earlier in higher grades of VW-CE compared with lower grades. VW-CE is a semiquantifiable marker for disease activity in patients with MMA and associated with disease progression and increased risk of stroke. VW-CE analysis can be routinely performed in patients with MMA to estimate the risk for disease progression and stroke.

Balancing Scaffold Degradation and Neo-Tissue Formation in In Situ Tissue Engineered Vascular Grafts.

An essential aspect of cardiovascular in situ tissue engineering (TE) is to ensure balance between scaffold degradation and neo-tissue formation. We evaluated the rate of degradation and neo-tissue formation of three electrospun supramolecular bisurea-based biodegradable scaffolds that differ in their soft-block backbone compositions only. Scaffolds were implanted as interposition grafts in the abdominal aorta in rats, and evaluated at different time points (t = 1, 6, 12, 24, and 40 weeks) on function, tissue formation, strength, and scaffold degradation. The fully carbonate-based biomaterial showed minor degradation after 40 weeks in vivo, whereas the other two ester-containing biomaterials showed (near) complete degradation within 6-12 weeks. Local dilatation was only observed in these faster degrading scaffolds. All materials showed to some extent mineralization, at early as well as late time points. Histological evaluation showed equal and non-native-like neo-tissue formation after total degradation. The fully carbonate-based scaffolds lagged in neo-tissue formation, presumably as its degradation was (far from) complete at 40 weeks. A significant difference in vessel wall contrast enhancement was observed by magnetic resonance imaging between grafts with total compared with minimal-degraded scaffolds.

Delayed Enhancement of Intracranial Atherosclerotic Plaque Can Better Differentiate Culprit Lesions: A Multiphase Contrast-Enhanced Vessel Wall MRI Study.

Intracranial plaque enhancement (IPE) identified by contrast-enhanced vessel wall MR imaging (VW-MR imaging) is an emerging marker of plaque instability related to stroke risk, but there was no standardized timing for postcontrast acquisition. We aim to explore the optimal postcontrast timing by using multiphase contrast-enhanced VW-MR imaging and to test its performance in differentiating culprit and nonculprit lesions. Patients with acute ischemic stroke due to intracranial plaque were prospectively recruited to undergo VW-MR imaging with 1 precontrast phase and 4 consecutive postcontrast phases (9 minutes and 13 seconds for each phase). The signal intensity (SI) values of the CSF and intracranial plaque were measured on 1 precontrast and 4 postcontrast phases to determine the intracranial plaque enhancement index (PEI). The dynamic changes of the PEI were compared between culprit and nonculprit plaques on the postcontrast acquisitions. Thirty patients with acute stroke (aged 59 ± 10 years, 18 [60%] men) with 113 intracranial plaques were included. The average PEI of all intracranial plaques significantly increased (up to 14%) over the 4 phases. There was significantly increased PEI over the 4 phases for culprit plaques (an average increase of 23%), but this was not observed for nonculprit plaques. For differentiating culprit and nonculprit plaques, we observed that the performance of IPE in the second postcontrast phase (cutoff = 0.83, AUC = 0.829 [0.746-0.893]) exhibited superior accuracy when compared with PEI in the first postcontrast phase (cutoff = 0.48; AUC = 0.768 [0.680-0.843]) (P = .022). A 9-minute delay of postcontrast acquisition can maximize plaque enhancement and better differentiate between culprit and nonculprit plaques. In addition, culprit and nonculprit plaques have different enhancement temporal patterns, which should be evaluated in future studies.

A Novel Window Into Human Vascular Remodeling and Diagnosing Carotid Flow Impairment: The Petro-Occipital Venous Plexus.

Background Adaptive arterial remodeling caused by flow reduction from downstream stenosis has been demonstrated in animal studies. The authors sought to determine whether inward remodeling from downstream stenosis also occurs in humans and is detectable by ex vacuo expansion of the Rektorzik venous plexus (RVP) surrounding the petrous internal carotid artery. Methods and Results The authors analyzed 214 intracranial magnetic resonance imaging examinations that included contrast-enhanced vessel wall imaging. RVP symmetry was qualitatively assessed on vessel wall imaging. RVP thickness (RVPT) was measured on the thicker side if asymmetric or randomly assigned side if symmetric. Maximum stenosis (M1 or intracranial internal carotid artery) was measured. Posterior communicating artery and A1 diameters (>1.0 mm and 1.5 mm, respectively) defined adequate collateral outflow when proximal to the stenosis. Seventy-two patients had stenosis downstream from RVPT measurements. For those without adequate outflow (38 of 72), 95.0% with RVPT ≥1.0 mm had ≥50% stenosis compared with only 5.6% with RVPT <1.0 mm. For these 72 patients, higher RVPT (RVPT ≥1.0 mm versus <1.0 mm) and absent adequate outflow were associated with greater downstream stenosis (P<0.001) using multivariate regression. For patients with downstream stenosis without adequate outflow, asymmetric RVP thickening was associated with greater ipsilateral stenosis (P<0.001, all had ≥46% stenosis) when stenosis was unilateral and greater differences in stenosis between sides (P=0.005) when stenosis was bilateral. Conclusions Inward internal carotid artery remodeling measured by RVPT or RVP asymmetry occurs as downstream stenosis approaches 50%, unless flow is preserved through a sufficiently sized posterior communicating artery or A1, and may serve as a functional measure of substantial flow reduction from downstream stenosis.

Evaluation of vessel-wall contrast-enhancement on high-resolution MRI in European patients with Moyamoya disease

ObjectivesData regarding MR vessel-wall imaging (VWI) in patients with Moyamoya disease (MMD) is sparse, particularly in non-asian cohorts. We contribute data regarding the frequency of vessel wall contrast-enhancement (VW-CE) and its potential clinical significance in a European patient group. Materials and methodsPatients with a diagnosis of MMD who were examined by VWI were included in the study. VW-CE of stenoocclusive lesions of the terminal internal carotid artery and/or its proximal branches was rated qualitatively. Changes of VW-CE on available follow-up were recorded. VW-CE was correlated with diffusion-restricted lesions and magnetic resonance angiography (MRA) findings. ResultsEleven patients (eight female, three male) were included. Twenty-eight stenoocclusive lesions were analyzed, of which 16 showed VW-CE (57.1%). VW-CE was mostly concentric (n=15), rather than eccentric (n=1). In all three patients in whom follow-up VWI was available, changes of VW-CE were documented. Diffusion-restricted lesions were more frequently related to stenoocclusive lesions with VW-CE (n=9) than without VW-CE (n=2), bordering statistical significance. The affected arteries were assessed as stenotic and as occluded in 14 cases each and VW-CE was seen significantly more often in stenotic (n=12) than in occluded arteries (n=4). No correlation was found between the presence of VW-CE and moyamoya stages determined by MRA. ConclusionsOur data suggest that concentric VW-CE is a relatively frequent finding in European MMD patients. VW-CE may change over time and occur in certain stages, possibly representing “active stenosing”. Larger studies are needed to validate these findings and determine the clinical relevance of VW-CE in MMD.

Diagnostic Value of Contrast-Enhanced Vessel Wall Imaging in the Evaluation of Various Intracranial Non-Vascular Pathologies: A Single Center Experience

Diagnostic Value of Contrast-Enhanced Vessel Wall Imaging in the Evaluation of Various Intracranial Non-Vascular Pathologies: A Single Center Experience

Clinical significance of “periventricular collateral enhancement sign” in symptomatic moyamoya disease: A vessel wall imaging study

BackgroundPeriventricular collaterals are associated with high risk of hemorrhagic stroke in adult moyamoya disease (MMD). However, the clinical significance of the periventricular collateral enhancement sign (PCES), which indicates wall enhancement of periventricular collaterals on contrast-enhanced vessel wall imaging (VWI), has yet to be determined. MethodsThirty-seven patients with MMD with acute neurological symptoms were consecutively recruited. Periventricular collaterals including lenticulostriatal artery, thalamic artery, and choroidal artery collaterals were evaluated on digital subtraction angiography, and then PCES was detected on pre- and postcontrast VWI. First, the association between PCES and hemorrhagic presentation was evaluated using multivariate analyses. Second, two raters investigated the culprit vessels responsible for bleeding in hemorrhagic MMD using the Cohen kappa statistic. ResultsFifteen sites of PCES on postcontrast VWI were observed in 15 patients. Multivariate analysis revealed that hemorrhagic presentation was the only independent factor for PCES (OR = 37.3, 95%CI = 3.9–113, p =.002). In patients with hemorrhagic presentation (n = 20), the identification rate of the ruptured vessel was 80% by rater 1, with excellent agreement. (inter-rater, κ = 0.86, 95%CI = 0.59–1.00; intra-rater, κ = 0.83, 95%CI = 0.50–1.00). Choroidal (50%) and thalamic artery collaterals (15%) were the most common and the second most common types of culprit vessels. Inter-rater and intra-rater reliabilities for the classification of culprit vessels were also excellent (intra-rater, κ = 0.86, 95%CI = 0.67–1.00; inter-rater, κ = 0.93, 95%CI = 0.79–1). ConclusionAcute hemorrhagic stroke in MMD is independently associated with PCES on postcontrast VWI. PCES can help to detect the culprit vessels that are responsible for hemorrhage in patients with MMD.

Characterization of Restenosis following Carotid Endarterectomy Using Contrast-Enhanced Vessel Wall MR Imaging.

Restenosis is an important determinant of the long-term efficacy of carotid endarterectomy. Our aim was to assess the role of high-resolution vessel wall MR imaging for characterizing restenosis after carotid endarterectomy. Patients who underwent vessel wall MR imaging after carotid endarterectomy were included in this study. Restenotic lesions were classified as myointimal hyperplasia or recurrent atherosclerotic plaques based on MR imaging features of lesion compositions. Imaging characteristics of myointimal hyperplasia were compared with those of normal post-carotid endarterectomy and recurrent plaque groups. Recurrent plaques were matched with primary plaques by categories of stenosis, and differences in plaque features were compared between the 2 groups. Twenty-two recurrent lesions from 18 patients (14 unilateral and 4 bilateral) were classified as myointimal hyperplasia or recurrent plaque. Myointimal hyperplasia showed no difference in enhancement compared with normal post-carotid endarterectomy vessels (5 unilateral) but showed stronger enhancement than recurrent plaques (80.10% [SD, 42.42%] versus 56.74% [SD, 46.54%], P = .042). A multivariate logistic regression model of plaque-feature detection in recurrent plaques compared with primary plaques adjusted for maximum wall thickness revealed that recurrent plaques were longer (OR, 4.27; 95% CI, 1.32-13.85; P = .015) and more likely to involve a flow divider and side walls (OR, 6.96; 95% CI, 1.37-35.28; P = .019). Recurrent plaques had a higher prevalence of intraplaque hemorrhage (61.5% versus 30.8%, P = .048) by a χ2 test, but compositional differences were not significant in the multivariate model. Vessel wall MR imaging can distinguish recurrent plaques from myointimal hyperplasia and reveal features that may differ between primary and recurrent plaques, highlighting its value for evaluating patients with carotid restenosis.

Diagnosis and follow-up evaluation of central nervous system vasculitis: an evaluation of vessel-wall MRI findings

ObjectiveTo approach the clinical value of MRI with vessel wall imaging (VWI) in patients with central nervous system vasculitis (CNSV), we analyzed patterns of VWI findings both at the time of initial presentation and during follow-up.MethodsStenoocclusive lesions, vessel-wall contrast enhancement (VW-CE) and diffusion-restricted lesions were analyzed in patients with a diagnosis of CNSV. On available VWI follow-up, progression, regression or stability of VW-CE were evaluated and correlated with the clinical status.ResultsOf the 45 patients included, 28 exhibited stenoses visible on MR angiography (MRA-positive) while 17 had no stenosis (MRA-negative). VW-CE was found in 2/17 MRA-negative and all MRA-positive patients (p < 0.05). 79.1% (53/67) of stenoses showed VW-CE. VW-CE was concentric in 88.3% and eccentric in 11.7% of cases. Diffusion-restricted lesions were found more frequently in relation to stenoses with VW-CE than without VW-CE (p < 0.05). 48 VW-CE lesions in 23 patients were followed over a median time of 239.5 days. 13 VW-CE lesions (27.1%) resolved completely, 14 (29.2%) showed partial regression, 17 (35.4%) remained stable and 4 (8.3%) progressed. 22/23 patients received immunosuppressive therapy for the duration of follow-up. Patients with stable or progressive VW-CE were more likely (p < 0.05) to have a relapse (14/30 cases) than patients with partial or complete regression of VW-CE (5/25 cases).ConclusionConcentric VW-CE is a common finding in medium/large-sized vessel CNSV. VW-CE might represent active inflammation in certain situations. However, follow-up VWI findings proved ambiguous as persisting VW-CE despite immunosuppressive therapy and clinical remission was a frequent finding.

Primary vasculitis of internal carotid and vertebral arteries: a role of cytokines, transforming growth factor beta 1 and basic fibroblast growth factor

To study clinical/laboratory signs of primary vasculitis (PV) of the internal carotid artery (ICA) and vertebral artery (VA). We examined 31 patients (23 men, 74%, mean age - 36.2±5.7 years) with ICA/VA PV verified by vessel wall contrast enhancement on black blood MRI (T1-weighted fat and blood suppressed sequences with- and without contrast injection) at the Research Center of Neurology (Moscow) from January 2012 to September 2019. Systemic vasculitis was excluded in all cases. Interleukins (IL-1β, IL-2, IL-6, IL-17), TNF-a, transforming growth factor beta 1 (TGF-β1) and basic fibroblast growth factor (bFGF) were analyzed by ELISA in 25 patients. Control group consisted of 21 healthy volunteers (12 men, 57%; mean age - 35.3±10.2 years). Clinical manifestations of ICA/VA PV included: ischemic stroke (IS) (94%), which combined with transient ischemic attacks (TIA) in 35%; isolated TIA (3%); Tolosa-Hunt syndrome (3%). Recurrent strokes were observed in 41% of patients on average in 5.3±2.1 months. Carotid artery was involved in 77%, VA - in 16%, both arteries - in 7%. Concomitant involvement of ICA/VA branches was in 19% patients. The level of arterial damage was follows: Intracranial part of arteries involved in 55%, intra-extracranial - in 35%, extracranial - in 10%. Bilateral involvement was found in 26%. Headache/neck pain in the acute IS period was observed in 21%. IS severity (NIHSS) was as follows: moderate (59%), mild (34%), moderately severe (7%). Disability after 3 months according to mRankin scale was as follows: mild (72%) moderate (21%), none (7%). The laboratory study revealed an increased levels of IL-6 (8.19±3.89 pg/ml vs 4.7±1.48 in control, p=0.000), IL-2 (5.64±1.82 pg/ml vs 4.30±1.65, p=0.013), TNF-a (36.9±33.66 pg/ml vs 12.68±5.93, p=0.000), TGF β1 (2.77±1.60 pg/ml vs 1.63±0.64, p=0.006) and bFGF (417.67±132.68 pg/ml vs 335.71±105.08, p=0.018). The levels of IL-1β and IL-17 did not differ significantly from the control. ICA/VA PV has a number of clinical peculiarities. Proinflammatory cytokines produced by Th17 and Th1 CD4+ lymphocytes as well as bFGF and TGR-β1 play a role in its pathogenesis. Normal levels of IL-1β and IL-17 suggest that they are not significant in the development of isolated inflammation in ICA/PA, in contrast to systemic inflammation in giant cell arteritis, in which, according to literature data, their level increases. Isolated ICA/PA inflammation seems to be caused by transaxonal (trigeminal nerve, upper-cervical roots, autonomic nerves) spread of pathogens that initiate immune inflammation in the ICA/PA wall.

Quantification of vessel wall contrast enhancement to monitor disease progression in Moyamoya disease

Quantification of vessel wall contrast enhancement to monitor disease progression in Moyamoya disease

Large and Small Cerebral Vessel Involvement in Severe COVID-19: Detailed Clinical Workup of a Case Series.

Case series indicating cerebrovascular disorders in coronavirus disease 2019 (COVID-19) have been published. Comprehensive workups, including clinical characteristics, laboratory, electroencephalography, neuroimaging, and cerebrospinal fluid findings, are needed to understand the mechanisms. We evaluated 32 consecutive critically ill patients with COVID-19 treated at a tertiary care center from March 9 to April 3, 2020, for concomitant severe central nervous system involvement. Patients identified underwent computed tomography, magnetic resonance imaging, electroencephalography, cerebrospinal fluid analysis, and autopsy in case of death. Of 32 critically ill patients with COVID-19, 8 (25%) had severe central nervous system involvement. Two presented with lacunar ischemic stroke in the early phase and 6 with prolonged impaired consciousness after termination of analgosedation. In all but one with delayed wake-up, neuroimaging or autopsy showed multiple cerebral microbleeds, in 3 with additional subarachnoid hemorrhage and in 2 with additional small ischemic lesions. In 3 patients, intracranial vessel wall sequence magnetic resonance imaging was performed for the first time to our knowledge. All showed contrast enhancement of vessel walls in large cerebral arteries, suggesting vascular wall pathologies with an inflammatory component. Reverse transcription-polymerase chain reactions for SARS-CoV-2 in cerebrospinal fluid were all negative. No intrathecal SARS-CoV-2-specific IgG synthesis was detectable. Different mechanisms of cerebrovascular disorders might be involved in COVID-19. Acute ischemic stroke might occur early. In a later phase, microinfarctions and vessel wall contrast enhancement occur, indicating small and large cerebral vessels involvement. Central nervous system disorders associated with COVID-19 may lead to long-term disabilities. Mechanisms should be urgently investigated to develop neuroprotective strategies.

Increased diagnostic accuracy of giant cell arteritis using three-dimensional fat-saturated contrast-enhanced vessel-wall magnetic resonance imaging at 3 T.

To compare the diagnostic accuracy of 3D versus 2D contrast-enhanced vessel-wall (CE-VW) MRI of extracranial and intracranial arteries in the diagnosis of GCA. This prospective two-center study was approved by a national research ethics board and enrolled participants from December 2014 to October 2017. A protocol including both a 2D and a 3D CE-VW MRI at 3 T was performed in all patients. Two neuroradiologists, blinded to clinical data, individually analyzed separately and in random order 2D and 3D sequences in the axial plane only or with reformatting. The primary judgment criterion was the presence of GCA-related inflammatory changes of extracranial arteries. Secondary judgment criteria included inflammatory changes of intracranial arteries and the presence of artifacts. A McNemar's test was used to compare 2D to 3D CE-VW MRIs. Seventy-nine participants were included in the study (42 men and 37 women, mean age 75 (± 9.5 years)). Fifty-one had a final diagnosis of GCA. Reformatted 3D CE-VW was significantly more sensitive than axial-only 3D CE-VW or 2D CE-VW when showing inflammatory change of extracranial arteries: 41/51(80%) versus 37/51 (73%) (p = 0.046) and 35/50 (70%) (p = 0.03). Reformatted 3D CE-VW was significantly more specific than 2D CE-VW: 27/27 (100%) versus 22/26 (85%) (p = 0.04). 3D CE-VW showed higher sensitivity than 2D CE-VW when detecting inflammatory changes of intracranial arteries: 10/51(20%) versus 4/50(8%), p = 0.01. Interobserver agreement was excellent for both 2D and 3D CE-VW MRI: κ = 0.84 and 0.82 respectively. 3D CE-VW MRI supported more accurate diagnoses of GCA than 2D CE-VW. • 3D contrast-enhanced vessel-wall magnetic resonance imaging is a high accuracy, non-invasive diagnostic tool used to diagnose giant cell arteritis. • 3D contrast-enhanced vessel-wall imaging is feasible for clinicians to complete within a relatively short time, allowing immediate assessment of extra and intracranial arteries. • 3D contrast-enhanced vessel-wall magnetic resonance imaging might be considered a diagnostic tool when intracranial manifestation of GCA is suspected.

Subacute vessel wall imaging at 7-T MRI in post-thrombectomy stroke patients

PurposeReports from 3-T vessel wall MRI imaging have shown contrast enhancement following thrombectomy for acute stroke, suggesting potential intimal damage. Comparisons have shown higher SNR and more lesions detected by vessel wall imaging when using 7 T compared with 3 T. The aim of this study was to investigate the vessel walls after stent retriever thrombectomy using high-resolution vessel wall imaging at 7 T.MethodsSeven patients with acute stroke caused by occlusion of the distal internal carotid artery (T-occlusion), or proximal medial cerebral artery, and treated by stent retriever thrombectomy with complete recanalization were included and examined by 7-T MRI within 2 days. The MRI protocol included a high-resolution black blood sequence with prospective motion correction (iMOCO), acquired before and after contrast injection. Flow measurements were performed in the treated and untreated M1 segments.ResultsAll subjects completed the MRI examination. Image quality was independently rated as excellent by two neuroradiologists for all cases, and the level of motion artifacts did not impair diagnostic quality, despite severe motion in some cases. Contrast enhancement correlated with the deployment location of the stent retrievers. Flow data showed complete restoration of flow after treatment.ConclusionVessel wall imaging with prospective motion correction can be performed in patients following thrombectomy with excellent imaging quality at 7 T. We show that vessel wall contrast enhancement is the normal post-operative state and corresponds to the deployment location of the stent retriever.

Decreased Antiatherogenic Protein Levels are Associated with Aneurysm Structure Alterations in MR Vessel Wall Imaging

Objective: Thickened intracranial aneurysm wall with atherosclerotic remodeling is a part of its degenerative scenario. Current magnetic resonance (MR)-vessel wall imaging enables the detection of atherosclerotic wall thickening as aneurysm wall enhancement. The purpose of this study was to examine the correlation between identified atherosclerotic remodeling in vessel wall imaging, and systemic atherosclerosis-related risk factors. Methods: A total of 39 aneurysms in 38 consecutive patients scheduled to undergo microsurgical clipping or endovascular coiling of intracranial aneurysms were prospectively evaluated. All patients underwent aneurysm MR-vessel wall imaging and the presence of aneurysm wall enhancement on contrast-enhanced vessel wall imaging was evaluated. The relationship between aneurysm wall enhancement and patient demographic data, aneurysm morphology and atherosclerosis-related risk factors including blood laboratory data were assessed. Results: Aneurysm wall enhancement was detected in 19 of 39 intracranial aneurysms (48.7%). The maximum diameter of the intracranial aneurysm (P < .01), apolipoprotein A2 (P < .01) and apolipoprotein C2 (P = .01) was significantly associated with the presence of aneurysm wall enhancement. In multivariate logistic regression analyses, the maximum diameter of the intracranial aneurysm (odds ratio: 1.67, 95% confidence interval: 1.17-3.05) and decreased apolipoprotein A2 (odds ratio: 0.62, 95% confidence interval: 0.34-0.97) was significantly correlated with aneurysm wall enhancement. Conclusions: Rather than atherosclerotic factors, antiatherogenic proteins reduction was associated with aneurysm wall enhancement in vessel wall imaging. To elucidate antiatherogenic factors might to help find out promoting factor of unruptured intracranial aneurysms instability.

Temporal course and implications of intracranial atherosclerotic plaque enhancement on high-resolution vessel wall MRI.

Little is known about the natural history of intracranial atherosclerotic plaque enhancement and its clinical implications. Our objective was to investigate the value of follow-up high-resolution contrast-enhanced vessel wall MRI (VWMRI) for classifying culprit plaques in patients with intracranial atherosclerotic disease (ICAD). Fourteen patients with symptomatic ICAD (50% females; median age 48years) underwent serial 3T VWMRI. Fifty-five plaques were identified and graded based on the likelihood of having caused the ischemic event (non-culprit, indeterminate, culprit) and degree of enhancement (0, 1, 2) at baseline and follow-up (median follow-up, 140days). For accuracy analysis, plaque enhancement at baseline and stable or increasing plaque enhancement at follow-up was tested to identify a culprit plaque, and areas under the receiver operating characteristic curves (AUCs) were compared. In 37/55 (67.3%) plaques, enhancement grade remained unchanged. Lack of enhancement was only seen in non-culprit plaques at baseline, and none developed enhancement over time. Enhancement never changed more than one grade. Thirty-seven percent (10/27) of non-culprit plaques that enhanced decreased in enhancement grade at follow-up, but no culprit plaques decreased in enhancement. AUC of baseline and follow-up plaque enhancement combined was significantly larger than AUC of baseline plaque enhancement alone to identify culprit plaques (0.733 vs. 0.567, p = 0.0001). Contrast enhancement of ICAD can persist months after the ischemic event. Lack of enhancement at baseline or a decrease in enhancement at follow-up suggests that the plaque is not culprit. Persistent enhancement from baseline to follow-up improves accuracy in identifying culprit plaques.

Primary central nervous system vasculitis

Primary vasculitis (angiitis) of the central nervous system (PACNS) is a rare disease targeting the vessels of the brain, spinal cord and leptomeninges without systemic involvement. The etiology is not clear enough. The authors review clinical, laboratory and radiological features of PACNS. Clinical manifestations are variable and depend on the caliber of affected vessels. The main clinical manifestations of small sized vessel vasculitis include encephalopathy (cognitive disorders, epileptic seizures), headache and transient cerebral ischemia. The main clinical presentation of vasculitis of medium/large cerebral arteries is ischemic strokes, which usually develop in different vascular territories. CSF findings in the majority of patients show modest lymphocytic pleocytosis, elevated protein level and occasionally the presence of oligoclonal bands. MRI data are not specific and include infarcts, hyperintensity (FLAIR) and sometimes tumor-like lesions. The gold standard for the verification of PACNS affected small-sized arteries is brain and leptomeningeal biopsy. Cerebral angiography allows the verification of vasculitis of medium and large cerebral arteries revealing segmental narrowings (beading). High resolution black blood MRI before and after contrast injection may visualize intracranial vessel wall contrast enhancement - the sign of inflammation in intracranial arteries. Treatment of PACNS includes corticosteroids and cyclophosphamide. In the case of patient intolerance, rituximab and blockers of tumor necrosis factor may be used.

Cavernous brain malformations and their relation to black blood MRI in respect to vessel wall contrast enhancement

BackgroundInflammatory responses are implicated as crucial patho-mechanisms of vascular brain malformations. Inflammation is suggested to be a key contributor to aneurysm rupture; however it is unclear whether inflammation contributes similarly to bleeding of cerebral cavernous malformations (CCMs). Black blood MRI is a sequence which identifies inflammation in blood vessel walls and in the present study is used to detect inflammatory response in CCMs.MethodsFifteen patients with 17 CCMs treated in our department in 2017 were retrospectively analysed. All patients received black blood MRIs and the results were analysed in correlation with, size and bleeding of CCMs.ResultsSize and bleeding status of CCMs did not correlate with contrast enhancement in the CCM wall. One of 3 patients with bleeding displayed contrast enhancement in black blood MRI, whereas the others had non enhancing lesions. Because of the small number of cases a statistical analysis was not performed.ConclusionIn this limited cohort, inflammatory reactions in CCMs could not be detected by black blood MRI suggesting that the level of inflammation is minimal in these lesions and those different patho-mechanisms play a more important role in the rupture of CCMs.

High-resolution MRI vessel wall imaging in varicella zoster virus vasculopathy

Contrast-enhanced vessel wall imaging high-resolution MRI (HRMR) has revealed vessel wall thickening and enhancement in multiple intracranial vasculopathies, including varicella zoster virus (VZV) vasculopathy. We retrospectively reviewed a database of patients with virologically-verified VZV vasculopathy, who underwent initial and follow-up HRMR between April 2011 and May 2014. Six patients were identified. Baseline demographic and clinical characteristics were collected, including stroke risk factors, history of VZV-related disorders, neurological presentation, course and antiviral treatment. Initial HRMR in patients with VZV vasculopathy demonstrated various patterns of stenosis, vessel wall thickening and enhancement, predominantly in terminal internal carotid artery segments and the M1 segment of the middle cerebral arteries. Follow-up HRMR showed improvement of stenosis, with reduced vessel wall thickening and enhancement at multiple times after treatment. HRMR has the potential to assist in diagnosis and treatment of VZV vasculopathy.