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Table of Contents    
NI FEATURE: CENTS (CONCEPTS, ERGONOMICS, NUANCES, THERBLIGS, SHORTCOMINGS) - COMMENTARY
Year : 2018  |  Volume : 66  |  Issue : 4  |  Page : 1124-1132

High-resolution magnetic resonance vessel wall imaging in cerebrovascular diseases


1 Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Neurology, Comprehensive Stroke Care Program, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India

Date of Web Publication18-Jul-2018

Correspondence Address:
Dr. P N Sylaja
Department of Neurology, Comprehensive Stroke Care Program, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.236964

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 » Abstract 


Most intracranial vascular disorders like atherosclerosis, vasculitis, and reversible cerebral vasoconstriction syndrome (RCVS) share similar lumenographic findings in traditional imaging modalities like computed tomography (CT), magnetic resonance imaging (MRI) and digital subtraction angiographic studies. Hence, there is a need for an advanced imaging modality like vessel wall imaging (VWI) to confirm the diagnosis so that appropriate clinical management could be done. Now, currently vessel wall imaging could be done in a high resolution manner with three dimensional (3D) imaging sequences. The aim of this article is to deal with the protocol as well as the current imaging applications of the high resolution VWI.


Keywords: Atherosclerosis, reversible cerebral vasoconstriction syndrome, vasculitis, vessel wall imaging
Key Message: Three dimensional high-resolution vessel wall imaging has an important role in differentiating different intracranial vasculopathies like intracranial atherosclerotic disease, vasculitis, reversible cerebral vasoconstriction syndrome, intracranial dissection, and moyamoya disease. The activity of the disease can be assessed by vessel wall contrast enhancement, and the duration of treatment can also be planned. Venous enhancement, the presence of normal vasa vasorum, and a slow vascular flow may sometimes mimic wall enhancement while interpreting contrast enhancement pattern in vessel wall imaging. In aneurysms and vascular malformations, this imaging may be used specifically to assess the site of bleeding.


How to cite this article:
Adhithyan R, Kesav P, Thomas B, Sylaja P N, Kesavadas C. High-resolution magnetic resonance vessel wall imaging in cerebrovascular diseases. Neurol India 2018;66:1124-32

How to cite this URL:
Adhithyan R, Kesav P, Thomas B, Sylaja P N, Kesavadas C. High-resolution magnetic resonance vessel wall imaging in cerebrovascular diseases. Neurol India [serial online] 2018 [cited 2018 Aug 17];66:1124-32. Available from: http://www.neurologyindia.com/text.asp?2018/66/4/1124/236964




Intracranial cerebrovascular diseases with vessel wall involvement include a range of pathologies like intracranial atherosclerotic disease (ICAD), vasculitis, reversible cerebral vasoconstriction syndrome (RCVS), dissection and moyamoya disease. Conventional imaging modalities like CT or MR angiography and even catheter angiography can assess only the vessel lumen and most pathologies show similar lumenographic findings of stenosis, luminal irregularities, or beaded appearance, which are nonspecific. As the disease pathology resides in the vessel wall, each disease shows a different pattern of vessel wall involvement. High-resolution vessel wall imaging (HRVWI) is the only method, which can assess, in vivo, the specific vessel wall pathology. Recently, HRVWI has been applied to other intracranial conditions like aneurysms and vascular malformations. VWI was traditionally done with two-dimensional (2D) black blood imaging method, which was prone to partial averaging, limited coverage, and lack of three-dimensional (3D) reconstruction. Currently, there is an increasing trend to use 3D HRVWI using high-field strength MRI. In this article, we discuss about the 3D HRVWI protocol, followed by a discussion on its applications in each of the vascular pathologies included, and the specific VWI findings by which these entities can be differentiated.

High-resolution vessel wall imaging protocol

Presently, HRVWI is increasingly done using 3D sequences, and among these, the most commonly used sequence is variable refocusing flip angle sequences (VRFA).[1] 3D VRFA sequences have an isotropic resolution and the images can be reformatted into any plane, so that affected vessel can be studied without any partial volume artifacts. 3D VWI has a good through plane resolution, and it can cover the entire brain within a short time. [Table 1] shows the advantages of the 3D VWI method over the conventional 2D imaging method. Currently available 3D VRFA sequences by various vendors are CUBE (GE Healthcare, USA), Sampling Perfection with Application Optimized Contrast by using different flip angle evolutions (SPACE, Siemens Healthcare, Germany), and Volume Isotropic Turbo Spin Echo Acquisition (VISTA, Philips Healthcare, Netherlands). Our institute protocol consists of 3D time-of-flight magnetic resonance angiogram (TOF MRA), followed by whole brain 3D CUBE (GE healthcare, USA) sequences of T1 FS (fat saturation), T2 FS, proton density (PD), and postcontrast T1 FS. 3D TOF MRA acts as a localizer to assess the site of vessel narrowing. The entire HRVWI imaging can be done within 30–35 min, as per our protocol, with a good imaging resolution. Multiple tissue weightings like T1, T2, PD are used for better characterization of the individual lesion. VRFA sequences may be taken with good vessel flow and cerebrospinal fluid (CSF) suppression with pre-pulse delay alternating with nutation for tailored excitation (DANTE) echo train.[2] Similarly, pre-pulse sequences like double inversion recovery or motion-sensitized driven-equilibrium can be applied for better blood flow suppression.[1],[3] [Figure 1] and [Table 2] show the basic MR VWI sequences and protocol done at our institute. VWI SNR is improved with higher field strength MRI, with studies showing 7 T VWI performing significantly better than 3 T [4] with an increase in the confidence for diagnosis.[5] Susceptibility weighted imaging (SWI) sequences (SWAN [susceptibility weighted angiography-sequence] in GE, SWI in Siemens) is being added in our VWI protocol to differentiate intraluminal thrombus from plaques.
Table 1: Advantages of 3D VWI over 2D VWI method

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Figure 1: Basic sequences of VRFA HRVWI

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Table 2: High-resolution vessel wall imaging protocol followed in our institute on 3T MRI

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High-resolution vessel wall imaging in intracranial atherosclerotic disease

Intracranial atherosclerotic disease (ICAD) is one of the most common causes of ischemic stroke worldwide, especially in Asians, and it accounts for about 30–50% patients of stroke.[6],[7] Patients with ICAD have a very high, early and long-term recurrence of ischemic events even on best medical treatment, ranging from 16% to 38% during a mean follow-up of 15–24 months.[8],[9] Aggressive medical management and risk factor modification needs to be started early in patients with ICAD for reducing the risk of recurrent cerebral ischemic events,[10] implying the importance of the imaging diagnosis using VWI.

Vessel wall imaging characteristics in intracranial atherosclerotic disease

  1. Wall thickening and wall enhancement pattern [Figure 2] and [Figure 3]: Most of the ICAD lesions (90%) show eccentric wall thickening and enhancement, with remaining lesions showing circumferential thickening and enhancement similar to vasculitis.[11] Eccentricity refers to a less than 360-degree vessel wall involvement or if the thickest part of the wall thickening is twice the thinnest part
  2. Wall enhancement grading and importance: Vessel wall enhancement is an indicator of ongoing inflammation, neovascularity, and instability in the plaque.[11] Enhancement [12] can be graded as 0, 1, and 2, by comparing with the signal intensity of pituitary infundibulum; with grade 0 indicating enhancement similar to the intracranial arterial walls without plaque, and grades 1 and 2 indicating less or more enhancement than the infundibulum, respectively. Grade 2 enhancement was shown to have an independent association with the culprit plaques and indicates its association with a recent ischemic event (within 4 weeks), which is independent of its thickness.[12] Also, enhancing plaques were associated with four times increased risk of stroke recurrence, with the cumulative risk of around 30%, compared to the non-enhancing plaques.[13] Recently, dynamic contrast enhancement (DCE) MRI of the plaques showed a good correlation of the K-trans (volume transfer constant) as an independent biomarker [14] with the time of onset of symptoms
  3. Plaque location: Middle cerebral artery ICAD plaques were commonly seen in inferior and ventral walls. However, superior wall plaques were more likely symptomatic and were associated with penetrating artery infarcts [15]
  4. Plaque signal intensity: T2 hyperintensity or heterogenicity is seen in ICAD lesions. Juxta-luminal T2 hyperintensity [Figure 2] represents a fibrous cap, and the subjacent T2 hypointense area indicates the fatty core. The T2 hyperintense fibrous cap helps to differentiate ICAD from vasculitis, especially when there is circumferential enhancement of the vessels. The T2 hyperintensity seen in VWI is 100% specific in differentiating ICAD from vasculitis and RCVS.[16] Cholesterol and cholesteryl esters rich fatty core in ICAD give a low signal on T2 weighted image unlike the extravascular fat that contains mainly triglycerides [17]
  5. Remodeling pattern: Pattern of remodeling can be assessed with VWI, and ICAD may be associated with either positive or negative remodeling. Plaques with positive remodeling were more vulnerable and required aggressive medical therapy than those with negative remodeling, which were usually stable.[18] VWI is more useful in posterior circulation vessels, as these vessels are associated with positive remodeling more commonly than is seen in the anterior circulation vessels and are more likely to elude angiographic detection [19]
  6. Intraplaque hemorrhage (IPH) [Figure 4]: Either T1 or magnetization-prepared rapid acquisition with gradient-echo sequence (MPRAGE) can be used to assess IPH. IPH is identified when the T1 signal intensity of the plaque in T1 FS/MPRAGE sequence is equal to or more than 150% of the adjacent extracranial muscle signal.[20] IPH was seen in less than 1/3 of the symptomatic MCA plaques. They are in fact more commonly seen (six times) in symptomatic plaques than the asymptomatic ones, indicating the vulnerability of the plaque to undergo hemorrhage.[21] The prevalence of IPH in symptomatic basilar artery plaques was higher when compared to symptomatic MCA plaques (54.5% vs 19.6%)[22]
  7. Applications of HRVWI in ICAD: According to the American Society of Neuroradiology,[23] HRVWI is used as an adjunct imaging modality to (1) differentiate ICAD from vasculitis and RCVS; (2) identify symptomatic non-stenotic plaques; (3) assess the activity of the plaques; and, (4) identify branch atheromatous disease in ICAD and predict the future risk of stroke.
Figure 2: A forty-year-old male patient with right hemiparesis and his CT angiography (a) showed left MCA wall irregularity and luminal narrowing (50%). In order to delineate the left MCA vessel abnormality, the 3D HRVWI was done. (b) MR diffusion image—left MCA territory cortical infarcts. (c) 3D T2 CUBE sagittal image and (d) 3D T2 CUBE axial reformat showing a juxta-luminal T2 hyperintense band (fibrous cap) with a hypointense area (lipid core) underneath. (e) 3D T1 FS CUBE sagittal precontrast image showing eccentric wall thickening. (f) Postcontrast T1 FS 3D CUBE better depicting the classical eccentric wall (anterior, inferior walls in this case) enhancement representative of ICAD

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Figure 3: 3D T2 CUBE (a) sagittal (b) and axial reformats of left MCA of the same patient represented in Figure 2. (c) Diagrammatic representation of the same patient showing the ICAD lesion in the MCA

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Figure 4: A sixty-nine-year-old male diabetic and hypertensive patient, with a history of left hemiparesis and slurring of speech. MRI showed acute pontine infarcts and MR angiography showed mid basilar artery luminal narrowing (50%). In order to delineate the basilar artery vessel abnormality, a 3D HRVWI was done. (a) On diffusion weighted images, restricted diffusion acute infarcts were seen in the pons. (b) On 3D TOF MR sequences, mid basilar artery luminal narrowing was seen. (c and d) 3D T1 sagittal and axial CUBE reformats showed eccentric T1 hyperintense wall thickening, with >150% of the occipital muscles T1 signal intensity

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High-resolution vessel wall imaging in reversible cerebral vasoconstriction syndrome

RCVS is characterized by thunderclap headache, with or without neurological deficits. It is due to reversible segmental vasoconstriction of the intracranial arteries. Vasoconstriction in RCVS usually resolves spontaneously within 3 months of the onset of symptoms. It may cause either intraparenchymal hemorrhages, subarachnoid hemorrhages, ischemic stroke, or transient cerebral edema.[24] Both RCVS and vasculitis may present with beading appearance, that is, segmental alternate vasodilation and constriction of intracranial arteries in luminal imaging methods (CT angiography, MR angiography, and digital subtraction angiography). There is, therefore, the need for an imaging method like VWI, to differentiate RCVS from vasculitis in the acute phase, as treatments offered for the two entitites are different. Immunosuppressants are to be administered in acute vasculitis, whereas with the false diagnosis of vasculitis in cases with RCVS, immunosuppressants may worsen the prognosis of RCVS.[25]

In VWI, RCVS shows a concentric wall thickening but no or minimal contrast enhancement in multiple arteries.[26] An absence of contrast enhancement or a minimal contrast enhancement [Figure 5] is concordant with the histopathological finding of absence of inflammation in RCVS. The follow-up imaging shows resolution of the wall thickening and enhancement, if present, within a median interval of 3 months in all cases.[27]
Figure 5: A fifty-four-year old female patient, presented with a history of thunderclap headache. Her initial CT angiography and DSA showed left sided M1segment of MCA and left P1 branch of PCA luminal narrowing. In order to delineate the left MCA and PCA vessel abnormality, a 3D HRVWI was done. (a) On, DSA, the left MCA showed proximal M1 luminal narrowing. (b) The 3D T2 CUBE sagittal image of the MCA showed no significant intraluminal T2 hyperintensity. (c) The 3D PD CUBE coronal reformat showing the left PCA luminal narrowing and concentric wall thickening. (d) The 3D T1 postcontrast coronal reformatted image showing wall thickening, but with only minimal contrast enhancement. (e) The CT angiography axial maximum intensity projection (MIP) image after 3 months showed complete resolution of the luminal narrowing of the left M1 branch of MCA and the P1 branch of PCA, confirming the diagnosis of RCVS

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High-resolution vessel wall imaging in vasculitis

CNS vasculitis [28] may be either primary or secondary. Secondary vasculitis can be due to systemic connective tissue disorders or due to infectious agents (like varicella) [Figure 6]. In the presence of systemic vasculitis, the diagnosis of CNS vasculitis is easy. The diagnosis of definite primary angiits of the CNS (PACNS), however, requires a histopathological documentation of vasculitis on a cortico-meningeal biopsy specimen, which has only a sensitivity of 53–63%[29],[30] and the sensitivity of invasive cerebral angiography also varies between 40 and 90%.[31] The use of HRVWI that can selectively image the blood vessels can potentially assist or replace the existing invasive, less sensitive investigations, and can contribute to an early diagnosis and appropriate management of PACNS, thereby increasing the chance of improved functional outcome. CNS vasculitis, including primary CNS angiitis [Figure 7] shows concentric, smooth enhancement of the intracranial vessels.[27],[32],[33] Of the 13 patients of CNS vasculitis evaluated by Obusez et al., nine showed a concentric and three showed an eccentric pattern of enhancement, but one presented with no enhancement. Also, in their follow up after a median interval of 13.5 months, four of the six patients showed a stable persistent concentric contrast enhancement. Vessel wall T2 hyperintense signal seen in intracranial atherosclerosis is classically absent in vasculitis.[36] Contrast wall enhancement may extend beyond the lumen to the periadventitial tissues or brain parenchyma.[31] HRVWI was also found to be helpful for the assessment of the activity of varicella associated vasculitis, so that the duration of antiviral treatment can be optimized, as wall enhancement may persist even after clinical improvement.[34],[35] Terminal internal carotid arteries (ICAs), proximal M1 branch of middle cerebral artery (MCA), and A1 segment of anterior cerebral artery (ACA) are predominantly affected in varicella vasculitis and show concentric wall enhancement, which may persist for 3–24 months.[34]
Figure 6: A ten-year old girl with a history of acute left hemiparesis. The patient had varicella infection with skin lesions, 3 weeks ago. (a) On MR diffusion image, right MCA territory infarcts with diffusion restriction are seen. (b) On 3D TOF MRA, right M1 luminal narrowing is seen. (c) On 3D T2 CUBE sagittal imaging, no significant T2 hyperintensity in the affected vessel can be seen. (d) The 3D T1 FS CUBE precontrast axial reformatted image showing concentric wall thickening, with no T1 hyperintensity. (e) Postcontrast T1 FS 3D CUBE axial reformatted image depicting the classical concentric wall enhancement representative of vasculitis

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Figure 7: A case of primary CNS vasculitis. A 34-year old female patient presented with a history of severe headache, left upper-lower limb weakness, and slurring of speech. CT angiography showed a right supraclinoid ICA, along with left vertebral artery (V4) wall irregularity and luminal narrowing. No evidence of systemic vasculitis is seen in this case. In order to delineate the etiology of the intracranial vessel abnormality, vessel wall imaging was done. (a) The 3D T1 FS CUBE axial (reformat) postcontrast image shows that the left V4 segment vertebral artery had a smooth concentric vessel wall thickening and intense concentric enhancement. For comparison, the uninvolved normal right V4 vertebral artery with no wall thickening was selected. (b) The 3D T1 FS CUBE sagittal postcontrast image showing that the right supraclinoid ICA exhibits a similar concentric vessel wall thickening and enhancement

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Differentiating intracranial atherosclerotic disease from vasculitis and reversible cerebral vasoconstriction syndrome

The main differential diagnosis for ICAD lesions are vasculitis and RCVS. To differentiate these entities [Figure 8], the first step in VWI is to look for the juxta-luminal T2 hyperintensity (fibrous cap) at the site of lesion. In a study by Mossa-Basha et al., T2 hyperintensity was shown to have a 79% sensitivity and a 100% specificity in differentiating ICAD from vasculitis and RCVS.[36] As some ICAD lesions do not have T2 hyperintensity, the second step is the evaluation of the 3D T1sequence. Eccentric wall thickening and enhancement helps in diagnosing ICAD. The final sequence to evaluate is the postcontrast 3D T1 sequence, in which grade 2 concentric enhancement favors vasculitis whereas no enhancement or a minimal enhancement favors RCVS.
Figure 8: Algorithm for differentiating ICAD from vasculitis and RCVS

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High-resolution vessel wall imaging in Moyamoya disease

Moyamoya disease (MMD) is an idiopathic condition, with progressive narrowing of bilateral supraclinoid ICA segments and it has a bimodal age distribution at first and fourth decades.[37] In middle-aged patients with atherosclerotic risk factors, it is difficult to differentiate MMD from moyamoya syndrome due to ICAD, by luminal angiographic methods, as both may show luminal narrowing. There is a need to differentiate these two conditions, as MMD is treated with surgical methods like EDAMS (encephalo-duro-arterio-myo-synangiosis) or superficial temporal artery-middle cerebral artery (STA-MCA) bypass, whereas ICAD is treated with antiplatelets and statins.

It is important to understand vessel remodeling for diagnosing MMD [Figure 9]. The vessel boundary could be traced better on T2 or PD images and the remodeling ratio is calculated by estimating the ratio of outer wall area at the lesion site to the reference vessel. If it is less than 0.95, it indicates a negative remodelling; and, if it is more than 1.05, it indicates a positive remodeling. Recent studies have shown that in majority of the patients with MMD, the vessel shows a negative remodeling, unlike in ICAD. The outer wall diameter of the terminal ICA and proximal MCA are smaller in MMD patients, in affected as well as unaffected vessels in comparison to vessels in ICAD. Most of the MMD vessels showed concentric wall thickening [Figure 9] and concentric wall enhancement (90% cases), unlike the ICAD vessels, which show eccentric wall thickening and enhancement.[38] In a study by Ryoo et al.,[38] the middle cerebral artery remodeling index in MMD versus ICAD was 0.19 ± 0.11 versus 1.00 ± 0.43, and the outer wall area in MMD versus ICAD was 0.32 ± 0.22 versus 6.00 ± 2.72. Patients with MMD show wall enhancement regardless of the symptoms unlike those with ICAD in whom enhancement occurs mostly in symptomatic vessels.[39] The thickened vessel wall shows a more homogenous signal intensity on T2 weighted images when compared to ICAD. Involvement of the posterior circulation is less common in MMD in comparison to ICAD.
Figure 9: A thirty-one year old female patient presented with recurrent episodes of right hemispheric transient ischemic attacks and seizures. The initial CT angiography and DSA showed bilateral ICA and M1 segment of MCA luminal narrowing. In order to delineate the etiology of ICA vessel abnormality and to differentiate moya moya disease from vasculitis and ICAD, a 3D HRVWI was done. (a) The DSA showed right supraclinoid ICA severe luminal narrowing. (b) The 3D T2 CUBE axial image showed that bilateral ICA supraclinoid segment exhibited no significant intraluminal T2 hyperintensity. (c) The 3D precontrast 3D T1 axial reformatted image showed concentric wall thickening. (d-f) 3D postcontrast coronal, sagittal (right ICA), axial reformatted images showed bilateral ICA mild concentric wall enhancement with negative remodeling

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High-resolution vessel wall imaging in dissection

The most common locations for intracranial dissections are supraclinoid ICA, M1 segment of MCA, and intracranial vertebral arteries. Intracranial dissection is associated with either an ischemic stroke or subarachnoid hemorrhage. Dissection may be associated with either an aneurysm formation or luminal narrowing. Hence, an early detection is necessary as an early medical or interventional treatment can avoid potentially serious complications. The pathognomonic signs [Figure 10] in VWI seen in intracranial vessel dissection are the formation of an intimal flap, and intramural hematoma, and a double lumen.[40] Jin Woo Kim et al., showed that the 3D PD sequence was much better in detecting the presence of the intimal flap compared to the 3D T1 pre- and postcontrast sequences; however, there was no significant difference between the sequences in detecting an intramural hematoma and vessel dilatation.[41] An intramural hematoma appears T1 hyperintense and it could be difficult to differentiate this hematoma from an ICAD associated intraplaque hemorrhage. The T1 signal intensity may become isointense in acute and chronic conditions. In a study by Arai et al.,[42] postcontrast T1 sequences showed an eccentric contrast enhancement at the site of dissection in four of the five cases of vertebral or basilar artery dissection. Eccentric enhancement can also be seen in the vessel just proximal or distal to the site of dissection.
Figure 10: A forty-year old male patient presented with sudden onset symptoms and signs of Wallenberg syndrome. MR diffusion confirmed the left PICA territory infarct with MR TOF showing focal dilatation of the left distal V4 vertebral artery. In this patient, VWI was done to look into the vessel wall pathology. (a) The MR diffusion image showed left posterolateral medullary acute infarct with diffusion restriction. (b) The 3D TOF MRA showed focal aneurysmal dilatation of the left distal V4 segment of the vertebral artery. (c) The 3D T2 VWI axial image showed the classical double lumen with the intimal flap and T2 hyperintense intramural hematoma. (d) The left vertebral artery angiogram on DSA showed focal aneurysmal dilatation of the left V4 vertebral artery

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High-resolution vessel wall imaging in aneurysms and intracranial vascular malformations

More recently, the utility of VWI in the management of cerebral aneurysms [43],[44] and intracranial vascular malformations has been reported. Silent saccular aneurysms are seen in 4% of the normal population and an imaging modality is needed to differentiate a stable versus an unstable aneurysm to determine the need for an intervention. Edjlali et al.,[44] found that circumferential aneurysmal wall enhancement (CAWE) was seen more frequently in an unstable aneurysm (ruptured, changing morphology, or symptomatic) than a stable aneurysm (87% vs 28.5%) and CAWE is the only independent predictor of instability of an aneurysm. The proposed mechanism of aneurysm wall enhancement is an increased density of vasa vasorum or inflammatory cell infiltration. VWI can also be used to identify the culprit aneurysm when subarachnoid hemorrhage and multiple aneurysms are seen.[45] The utility of VWI in nonaneurysmal SAH has still not been well-defined. In our experience, myxomatous aneurysms [46],[47] that occur in distal cerebral arteries, years after the atrial myxoma excision, showed a circumferential thick enhancement. VWI may also be useful to locate the site of the rupture in the case of bled intracranial arteriovenous malformations, especially when multiple high-risk angiographic features are seen.[48]

Limitations

An experienced neuroradiologist is required to perform and interpret the images of VWI. As high-resolution imaging is being performed, additional imaging time and cost is involved. It may also be noted that there are only limited histopathological correlated studies of VWI and hence a comparison with the gold standard histopathological evaluation has not been done in the majority of studies. The major pitfalls while performing and interpreting VWI include (1) misinterpreting the normal enhancement of veins running along the intracranial arteries as an abnormal arterial enhancement, (2) artefacts can arise due to the slow flow and patient motion, (3) normal enhancement of vasa vasorum in large intracranial arteries near the skull base can be mistaken as vessel wall enhancement, and (4) enhancing cavernous venous plexus can be misinterpreted as abnormal arterial wall enhancement.


 » Conclusion Top


3D HRVWI has an important role in differentiating different intracranial vasculopathies like ICAD, vasculitis, RCVS, intracranial dissection, and MMD [Table 3]. The differentiation of ICAD, vasculitis, and RCVS has implications in patient management and this can be done more specifically by using HRVWI. The activity of the disease can be assessed by vessel wall contrast enhancement and the duration of treatment can also be planned. Venous enhancement, the presence of normal vasa vasorum, and a slow flow may sometimes mimic wall enhancement and should be kept in mind while interpreting contrast enhancement pattern in VWI. More recently, HRVWI has been applied in aneurysms and vascular malformations specifically to know the site of bleeding. There is a need for studies that correlate histopathology with the VWI findings.
Table 3: Summary of HRVWI findings of cerebrovascular disorders

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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