Survey of the American Society of Neuroradiology Membership on the Use and Value of Intracranial Vessel Wall MRI.

BACKGROUND AND PURPOSE: Intracranial vessel wall MR imaging is an emerging technique for intracranial vasculopathy assessment. Our aim was to investigate intracranial vessel wall MR imaging use by the American Society of Neuroradiology (ASNR) members at their home institutions, including indications and barriers to implementation. MATERIALS AND METHODS: The ASNR Vessel Wall Imaging Study Group survey on vessel wall MR imaging use, frequency, applications, MR imaging systems and field strength used, protocol development approaches, vendor engagement, reasons for not using vessel wall MR imaging, ordering-provider interest, and impact on clinical care, was distributed to the ASNR membership between April 2 and August 30, 2019. RESULTS: There were 532 responses; 79 were excluded due to nonresponse and 42 due to redundant institutional responses, leaving 411 responses. Fifty-two percent indicated that their institution performs vessel wall MR imaging, with 71.5% performed at least 1-2 times/month, most frequently on 3T MR imaging, and 87.7% using 3D sequences. Protocols most commonly included were T1-weighted pre- and postcontrast and TOF-MRA; 60.6% had limited contributions from vendors or were still in protocol development. Vasculopathy differentiation (94.4%), cryptogenic stroke (41.3%), aneurysm (38.0%), and atherosclerosis (37.6%) evaluation were the most common indications. For those not performing vessel wall MR imaging, interpretation (53.1%) or technical (46.4%) expertise, knowledge of applications (50.5%), or limitations of clinician (56.7%) or radiologist (49.0%) interest were the most common reasons. If technical/expertise obstacles were overcome, 56.4% of those not performing vessel wall MR imaging indicated that they would perform it. Ordering providers most frequently inquiring about vessel wall MR imaging were from stroke neurology (56.5%) and neurosurgery (25.1%), while 34.3% indicated that no providers had inquired. CONCLUSIONS: More than 50% of neuroradiology groups use vessel wall MR imaging for intracranial vasculopathy characterization and differentiation, emphasizing the need for additional technical and educational support, especially as clinical vessel wall MR imaging implementation continues to grow.

Decreased Subcortical T2 FLAIR Signal Associated with Seizures.

Abnormally decreased T2/T2 FLAIR signal can be seen on brain imaging of patients who are experiencing clinical or subclinical seizures and can be associated with various intracranial pathologies. We identified 29 such patients. The abnormal signal was unilateral in 75.9% of patients. It affected various lobes of the brain, but only in the anterior circulation. In 28 patients (96.6%), there was corresponding decreased signal on DWI. The ADC was normal in all cases. In 26 patients (89.7%), there was corresponding low signal on SWI/gradient recalled-echo; 44.8% of patients underwent contrast-enhanced scans, and there was no abnormal enhancement. Twenty-two (75.9%) patients had documented clinical seizures on the day of imaging. The most frequent concomitant pathology was a subdural hematoma. Electroencephalograms obtained within 24 hours of imaging were available in 65.5%. Findings of all of these electroencephalograms were abnormal, and these electroencephalogram changes were either localized to the area of the abnormal MR imaging signal (where the signal was unilateral) or were bilateral (where the MR imaging changes were bilateral). In summary, decreased white matter T2/T2 FLAIR signal changes can be seen in patients with remarkably similar clinical findings (particularly seizures). These changes are often correlated with abnormal electroencephalogram activity localized to the involved lobes.

Diagnostic Impact of Intracranial Vessel Wall MRI in 205 Patients with Ischemic Stroke or TIA.

BACKGROUND AND PURPOSE: Secondary prevention of ischemic stroke depends on determining the cause of the initial ischemic event, but standard investigations often fail to identify a cause or identify multiple potential causes. The purpose of this study was to characterize the impact of intracranial vessel wall MR imaging on the etiologic classification of ischemic stroke. MATERIALS AND METHODS: This was a single-center, retrospective study of 205 consecutive patients who were referred for vessel wall MR imaging to clarify the etiology of an ischemic stroke or TIA. An expert panel classified stroke etiology before and after incorporating vessel wall MR imaging results using a modified Trial of Org 10172 in Acute Stroke Treatment system. We measured the proportion of patients with an altered etiologic classification after vessel wall MR imaging. RESULTS: The median age was 56 years (interquartile range = 44-67 years), and 51% (106/205) of patients were men. Vessel wall MR imaging altered the etiologic classification in 55% (112/205) of patients. The proportion of patients classified as having intracranial arteriopathy not otherwise specified decreased from 31% to 4% (64/205 versus 9/205; P < .001) and the proportion classified as having intracranial atherosclerotic disease increased from 23% to 57% (48/205 versus 116/205; P < .001). Conventional work-up classification as intracranial arteriopathy not otherwise specified was an independent predictor of vessel wall MR imaging impact (OR = 8.9; 95% CI, 3.0-27.2). The time between symptom onset and vessel wall MR imaging was not a predictor of impact. CONCLUSIONS: When vessel wall MR imaging is performed to clarify the etiology of a stroke or TIA, it frequently alters the etiologic classification. This is important because the etiologic classification is the basis for therapeutic decision-making.

Improved White Matter Cerebrovascular Reactivity after Revascularization in Patients with Steno-Occlusive Disease.

BACKGROUND AND PURPOSE: One feature that patients with steno-occlusive cerebrovascular disease have in common is the presence of white matter (WM) lesions on MRI. The purpose of this study was to evaluate the effect of direct surgical revascularization on impaired WM cerebrovascular reactivity in patients with steno-occlusive disease. MATERIALS AND METHODS: We recruited 35 patients with steno-occlusive disease, Moyamoya disease (n = 24), Moyamoya syndrome (n = 3), atherosclerosis (n = 6), vasculitis (n = 1), and idiopathic stenosis (n = 1), who underwent unilateral brain revascularization using a direct superficial temporal artery-to-MCA bypass (19 women; mean age, 45.8 ± 16.5 years). WM cerebrovascular reactivity was measured preoperatively and postoperatively using blood oxygen level-dependent (BOLD) MR imaging during iso-oxic hypercapnic changes in end-tidal carbon dioxide and was expressed as %Δ BOLD MR signal intensity per millimeter end-tidal partial pressure of CO2. RESULTS: WM cerebrovascular reactivity significantly improved after direct unilateral superficial temporal artery-to-middle cerebral artery (STA-MCA) bypass in the revascularized hemisphere in the MCA territory (mean ± SD, -0.0005 ± 0.053 to 0.053 ± 0.046 %BOLD/mm Hg; P < .0001) and in the anterior cerebral artery territory (mean, 0.0015 ± 0.059 to 0.021 ± 0.052 %BOLD/mm Hg; P = .005). There was no difference in WM cerebrovascular reactivity in the ipsilateral posterior cerebral artery territory nor in the vascular territories of the nonrevascularized hemisphere (P < .05). CONCLUSIONS: Cerebral revascularization surgery is an effective treatment for reversing preoperative cerebrovascular reactivity deficits in WM. In addition, direct-STA-MCA bypass may prevent recurrence of preoperative symptoms.

High-Resolution Vessel Wall Magnetic Resonance Imaging in Angiogram-Negative Non-Perimesencephalic Subarachnoid Hemorrhage.

PURPOSE: Standard magnetic resonance imaging (MRI) rarely identifies the cause of hemorrhage in patients with an angiogram-negative, non-perimesencephalic subarachnoid hemorrhage (SAH). Yet up to 10 % of these patients have recurrent hemorrhage. The aim of the study was to explore the potential role of high-resolution contrast-enhanced 3-Tesla vessel wall-MRI in patients with angiogram-negative SAH. METHODS: We performed intracranial vessel wall-MRI of the circle of Willis using a 3-Tesla scanner in consecutive patients presenting with a spontaneous, angiogram-negative, non-perimesencephalic SAH. Vessel wall-MRI included T1-, T2-, and gadolinium-enhanced T1-weighted two-dimensional black-blood sequences in multiple planes (voxel size 0.4 × 0.4 × 2.0 mm). Two neuroradiologists independently scored abnormalities of the arterial wall. RESULTS: In all, 11 patients (mean age 59 years) underwent vessel wall-MRI. A total of seven patients had vessel wall abnormalities despite normal catheter angiography. Two patients had focal abnormalities contiguous with the outer margin of the basilar artery wall for which we considered a differential of ruptured blood blister aneurysm, thrombosed aneurysm, and loculated extramural blood from elsewhere. Two patients had arterial wall enhancement involving multiple arteries, possibly secondary to SAH. Three patients had arterial wall enhancement at sites of dural penetration, remote from the SAH, likely related to age and atherosclerotic risk factors. Vessel wall-MRI did not alter patient management in this cohort. CONCLUSION: Vessel wall-MRI showed abnormalities in seven patients with angiogram-negative SAH. These findings did not alter patient management, but the findings may be useful for other physicians who choose to perform vessel wall-MRI in this patient population.

Intracranial Vessel Wall MRI: Principles and Expert Consensus Recommendations of the American Society of Neuroradiology.

Intracranial vessel wall MR imaging is an adjunct to conventional angiographic imaging with CTA, MRA, or DSA. The technique has multiple potential uses in the context of ischemic stroke and intracranial hemorrhage. There remain gaps in our understanding of intracranial vessel wall MR imaging findings and research is ongoing, but the technique is already used on a clinical basis at many centers. This article, on behalf of the Vessel Wall Imaging Study Group of the American Society of Neuroradiology, provides expert consensus recommendations for current clinical practice.

Vascular Dysfunction in Leukoaraiosis.

BACKGROUND AND PURPOSE: The pathogenesis of leukoaraiosis has long been debated. This work addresses a less well-studied mechanism, cerebrovascular reactivity, which could play a leading role in the pathogenesis of this disease. Our aim was to evaluate blood flow dysregulation and its relation to leukoaraiosis. MATERIALS AND METHODS: Cerebrovascular reactivity, the change in the blood oxygen level-dependent 3T MR imaging signal in response to a consistently applied step change in the arterial partial pressure of carbon dioxide, was measured in white matter hyperintensities and their contralateral spatially homologous normal-appearing white matter in 75 older subjects (age range, 50-91 years; 40 men) with leukoaraiosis. Additional quantitative evaluation of regions of leukoaraiosis was performed by using diffusion (n = 75), quantitative T2 (n = 54), and DSC perfusion MRI metrics (n = 25). RESULTS: When we compared white matter hyperintensities with contralateral normal-appearing white matter, cerebrovascular reactivity was lower by a mean of 61.2% ± 22.6%, fractional anisotropy was lower by 44.9 % ± 6.9%, and CBF was lower by 10.9% ± 11.9%. T2 was higher by 61.7% ± 13.5%, mean diffusivity was higher by 59.0% ± 11.7%, time-to-maximum was higher by 44.4% ± 30.4%, and TTP was higher by 6.8% ± 5.8% (all P < .01). Cerebral blood volume was lower in white matter hyperintensities compared with contralateral normal-appearing white matter by 10.2% ± 15.0% (P = .03). CONCLUSIONS: Not only were resting blood flow metrics abnormal in leukoaraiosis but there is also evidence of reduced cerebrovascular reactivity in these areas. Studies have shown that reduced cerebrovascular reactivity is more sensitive than resting blood flow parameters for assessing vascular insufficiency. Future work is needed to examine the sensitivity of resting-versus-dynamic blood flow measures for investigating the pathogenesis of leukoaraiosis.

Identifying Significant Changes in Cerebrovascular Reactivity to Carbon Dioxide.

BACKGROUND AND PURPOSE: Changes in cerebrovascular reactivity can be used to assess disease progression and response to therapy but require discrimination of pathology from normal test-to-test variability. Such variability is due to variations in methodology, technology, and physiology with time. With uniform test conditions, our aim was to determine the test-to-test variability of cerebrovascular reactivity in healthy subjects and in patients with known cerebrovascular disease. MATERIALS AND METHODS: Cerebrovascular reactivity was the ratio of the blood oxygen level-dependent MR imaging response divided by the change in carbon dioxide stimulus. Two standardized cerebrovascular reactivity tests were conducted at 3T in 15 healthy men (36.7 ± 16.1 years of age) within a 4-month period and were coregistered into standard space to yield voxelwise mean cerebrovascular reactivity interval difference measures, composing a reference interval difference atlas. Cerebrovascular reactivity interval difference maps were prepared for 11 male patients. For each patient, the test-retest difference of each voxel was scored statistically as z-values of the corresponding voxel mean difference in the reference atlas and then color-coded and superimposed on the anatomic images to create cerebrovascular reactivity interval difference z-maps. RESULTS: There were no significant test-to-test differences in cerebrovascular reactivity in either gray or white matter (mean gray matter, P = .431; mean white matter, P = .857; paired t test) in the healthy cohort. The patient cerebrovascular reactivity interval difference z-maps indicated regions where cerebrovascular reactivity increased or decreased and the probability that the changes were significant. CONCLUSIONS: Accounting for normal test-to-test differences in cerebrovascular reactivity enables the assessment of significant changes in disease status (stability, progression, or regression) in patients with time.

Intracranial vessel wall MRI.

There are many different methods of imaging the intracranial arteries; however, the vast majority of currently used techniques are based on luminal imaging. Although this is useful, it does have limitations as many different pathological processes can produce the same appearance. Therefore, directly imaging the site of the pathology - the vessel wall itself - offers the hope of discriminating between different disease processes. In this review, we will discuss the current status of vessel wall magnetic resonance imaging alongside its potential usefulness in differentiating between various disease entities.

A conceptual model for CO2-induced redistribution of cerebral blood flow with experimental confirmation using BOLD MRI.

Cerebrovascular reactivity (CVR) is the change in cerebral blood flow (CBF) in response to a change in a vasoactive stimulus. Paradoxical reductions in CBF in response to vasodilatory stimulation ('steal') are associated with vascular pathology. However, a pathophysiological interpretation of 'steal' requires a comprehensive conceptual model linking pathology and changes in blood flow. Herein, we extend a simple model explaining steal published in the late 1960s by incorporating concepts of CBF regulation from more recent studies to generate a comprehensive dynamic model. The main elements of the model are: (a) the relationship between changes in CBF and the arterial partial pressure of carbon dioxide (PaCO2) in healthy vascular regions is sigmoidal; (b) vascular regions vasodilate to compensate for decreased perfusion pressure, leading to (c) an encroachment on vasodilatory reserve and, reduced CVR; (d) a vasodilatory stimulus may increase CBF capacity above the flow capacity of major cerebral blood vessels; and (e) this limitation induces competitive intra-cerebral redistribution of flow from territories with low vasodilatory reserve to those with high reserve. We used CVR measurements generated by applying precise, computer-controlled changes in PaCO2 as the vasoactive stimulus, and measured blood oxygen level dependent (BOLD) MRI signals as high resolution surrogates of CBF to test predictions derived from this model. Subjects were 16 healthy adults and 16 patients with known cerebral steno-occlusive diseases. We observed regional sigmoidal PaCO2-BOLD response curves with a range of slopes; graded changes in PaCO2 resulted in redistributions of BOLD signal consistent with the known underlying vascular pathology and predictions of the model. We conclude that this model can be applied to provide a hemodynamic interpretation to BOLD signal changes in response to hypercapnia, and thereby aid in relating CVR maps to pathophysiological conditions.

Measuring cerebrovascular reactivity: what stimulus to use?

Cerebrovascular reactivity is the change in cerebral blood flow in response to a vasodilatory or vasoconstrictive stimulus. Measuring variations of cerebrovascular reactivity between different regions of the brain has the potential to not only advance understanding of how the cerebral vasculature controls the distribution of blood flow but also to detect cerebrovascular pathophysiology. While there are standardized and repeatable methods for estimating the changes in cerebral blood flow in response to a vasoactive stimulus, the same cannot be said for the stimulus itself. Indeed, the wide variety of vasoactive challenges currently employed in these studies impedes comparisons between them. This review therefore critically examines the vasoactive stimuli in current use for their ability to provide a standard repeatable challenge and for the practicality of their implementation. Such challenges include induced reductions in systemic blood pressure, and the administration of vasoactive substances such as acetazolamide and carbon dioxide. We conclude that many of the stimuli in current use do not provide a standard stimulus comparable between individuals and in the same individual over time. We suggest that carbon dioxide is the most suitable vasoactive stimulus. We describe recently developed computer-controlled MRI compatible gas delivery systems which are capable of administering reliable and repeatable vasoactive CO2 stimuli.

Intracranial atherosclerotic plaque enhancement in patients with ischemic stroke.

BACKGROUND AND PURPOSE: Inflammation of an atherosclerotic plaque is a well-known risk factor in the development of ischemic stroke and myocardial infarction. MR imaging is capable of characterizing inflammation by assessing plaque enhancement in both extracranial carotid arteries and coronary arteries. Our goal was to determine whether enhancing intracranial atherosclerotic plaque was present in the vessel supplying the territory of infarction by using high-resolution vessel wall MR imaging. MATERIALS AND METHODS: High-resolution vessel wall 3T MR imaging studies performed in 29 patients with ischemic stroke and intracranial vascular stenoses were reviewed for presence and strength of plaque enhancement. RESULTS: Sixteen patients were studied during the acute phase (<4 weeks from acute stroke), 5 patients in the subacute phase (4-12 weeks), and 8 patients in the chronic phase (>12 weeks) of the ischemic injury. In all of the acute phase patients, atherosclerotic plaque in the vessel supplying the stroke territory demonstrated strong enhancement. There was a trend of decreasing enhancement as the time of imaging relative to the ischemic event increased. CONCLUSIONS: Strong pathologic enhancement of intracranial atherosclerotic plaque was seen in all patients imaged within 4 weeks of ischemic stroke in the vessel supplying the stroke territory. The strength and presence of enhancement of the atherosclerotic plaque decreased with increasing time after the ischemic event. These findings suggest a relationship between enhancing intracranial atherosclerotic plaque and acute ischemic stroke.

Osteogenesis imperfecta, multiple intra-abdominal arterial dissections and a ruptured dissecting-type intracranial aneurysm.

We describe an adult patient with a ruptured dissecting-type superior cerebellar artery aneurysm and known osteogenesis imperfecta. He was successfully treated with coil embolization and intentional parent vessel sacrifice. During his hospital admission, he also suffered from abdominal distension. An incidental note was made of multiple intra-abdominal arterial dissections. These were managed conservatively. We review the rare association of osteogenesis imperfecta and intracranial aneurysms, as well as discuss management implications.

Mapping white matter diffusion and cerebrovascular reactivity in carotid occlusive disease.

OBJECTIVE: To characterize the relationship between cerebrovascular reactivity (CVR) and white matter (WM) diffusion in patients with internal carotid artery (ICA) occlusive disease. METHODS: In this exploratory observational study, 41 patients with severe stenosis or occlusion of the extracranial ICA and 12 healthy control subjects underwent CVR mapping using the fMRI response to hypercapnia. Conventional anatomic and diffusion-weighted MRI sequences were used to calculate maps of the apparent diffusion coefficient (ADC) and to exclude areas of previous ischemic injury. In all subjects, ADC was compared between WM with positive and negative CVR. In 27 patients with unilateral ICA involvement, ADC and CVR were compared between ipsilateral and contralateral WM while covarying for relevant clinical risk factors. RESULTS: In patients with bilateral disease and in the ipsilateral hemisphere of patients with unilateral disease, negative CVR was associated with increased WM ADC (p < 0.01 and p < 0.005, respectively). In patients with unilateral disease, the ipsilateral CVR deficit was correlated with the degree of hemispheric WM ADC elevation (p < 0.005). ADC elevation remained significant after correction for potential confounding risk factors. CONCLUSIONS: CVR impairment is associated with ADC elevation in normal-appearing WM of patients with severe stenosis or occlusion of the extracranial ICA. This finding is consistent with the presence of early, low-grade ischemic injury.

Quantitative measurement of cerebrovascular reactivity by blood oxygen level-dependent MR imaging in patients with intracranial stenosis: preoperative cerebrovascular reactivity predicts the effect of extracranial-intracranial bypass surgery.

BACKGROUND AND PURPOSE: CVR is a measure of cerebral hemodynamic impairment. A recently validated technique quantifies CVR by using a precise CO(2) vasodilatory stimulus and BOLD MR imaging. Our aim was to determine whether preoperative CO(2) BOLD CVR predicts the hemodynamic effect of ECIC bypass surgery in patients with intracranial steno-occlusive disease. MATERIALS AND METHODS: Twenty-five patients undergoing ECIC bypass surgery for treatment of intracranial stenosis or occlusion were recruited. CVR was measured preoperatively and postoperatively and expressed as %ΔBOLD MR signal intensity per mm Hg ΔPetCO(2). Using normative data from healthy subjects, we stratified patients on the basis of preoperative CVR into 3 groups: normal CVR, reduced CVR, and negative (paradoxical) CVR. Wilcoxon 2-sample tests (2-sided, α = 0.05) were used to determine whether the 3 groups differed with respect to change in CVR following bypass surgery. RESULTS: The group with normal preoperative CVR demonstrated no significant change in CVR following bypass surgery (mean, 0.22% ± 0.05% to 0.22% ± 0.01%; P = .881). The group with reduced preoperative CVR demonstrated a significant improvement following bypass surgery (mean, 0.08% ± 0.05% to 0.21 ± 0.08%; P < .001), and the group with paradoxical preoperative CVR demonstrated the greatest improvement (mean change, -0.04% ± 0.03% to 0.27% ± 0.03%; P = .028). CONCLUSIONS: Preoperative measurement of CVR by using CO(2) BOLD MR imaging predicts the hemodynamic effect of ECIC bypass in patients with intracranial steno-occlusive disease. The technique is potentially useful for selecting patients for surgical revascularization.

Labyrinthine ossification: etiologies and CT findings.

Ossification of the membranous labyrinth (labyrinthitis ossificans) develops as the final result of many inflammatory processes, for example, meningitis, blood-borne septic emboli, middle ear infection, and cholesteatoma. Labyrinthine ossification may also occur as a result of previous labyrinthectomy or secondary to trauma. Seven cases of labyrinthine ossification accompanied by severe vertigo and total hearing loss in the affected ear are discussed. The computed tomographic appearance of varying degrees of ossification, the clinical and surgical circumstances from which this disorder may develop, and the various approaches to labyrinthectomy are described.

GLC-mass spectral analysis of psilocin and psilocybin.

With the combined technique of GLC-mass spectrometry, psilocin and psilocybin, two hallucinogenic indoles, were analyzed as their trimethylsilyl derivatives. The method was applied to these two components in an extract of Psilocybe cubensis (Earle) Sing.