Vessel Wall Imaging of the Intracranial and Cervical Carotid Arteries

Young Jun Choi, Seung Chai Jung, Deok Hee Lee, Young Jun Choi, Seung Chai Jung, Deok Hee Lee

Abstract

Vessel wall imaging can depict the morphologies of atherosclerotic plaques, arterial walls, and surrounding structures in the intracranial and cervical carotid arteries beyond the simple luminal changes that can be observed with traditional luminal evaluation. Differentiating vulnerable from stable plaques and characterizing atherosclerotic plaques are vital parts of the early diagnosis, prevention, and treatment of stroke and the neurological adverse effects of atherosclerosis. Various techniques for vessel wall imaging have been developed and introduced to differentiate and analyze atherosclerotic plaques in the cervical carotid artery. High-resolution magnetic resonance imaging (HR-MRI) is the most important and popular vessel wall imaging technique for directly evaluating the vascular wall and intracranial artery disease. Intracranial artery atherosclerosis, dissection, moyamoya disease, vasculitis, and reversible cerebral vasoconstriction syndrome can also be diagnosed and differentiated by using HR-MRI. Here, we review the radiologic features of intracranial artery disease and cervical carotid artery atherosclerosis on HR-MRI and various other vessel wall imaging techniques (e.g., ultrasound, computed tomography, magnetic resonance, and positron emission tomography-computed tomography).

Keywords: Cervical carotid artery; High-resolution magnetic resonance; Intracranial artery; Vessel wall imaging.

Conflict of interest statement

The authors have no financial conflicts of interest.

Figures

Figure 1.
Figure 1.
Intracranial atherosclerosis. A 49-year-old female patient presented with left-side weakness and four atherosclerotic risk factors. (A) Time-of-flight magnetic resonance angiograph showing severe stenosis in the right middle cerebral artery (arrow). (B) Proton-density image showing eccentric wall thickening and atherosclerotic plaques with a remodeling index of 1.47. (C) Contrast-enhanced T1-weighted image showing strong enhancement in eccentric atherosclerotic plaques.
Figure 2.
Figure 2.
Intracranial atherosclerosis. A 58-year-old male patient presented with dizziness and three atherosclerotic risk factors. (A) Time-of-flight magnetic resonance angiograph showing severe stenosis in the left middle cerebral artery (arrow). (B) Proton-density image showing eccentric wall thickening and atherosclerotic plaques with a remodeling index of 1.04. (C) Contrast-enhanced T1-weighted image showing strong enhancement in eccentric atherosclerotic plaques.
Figure 3.
Figure 3.
Intracranial artery dissection. A 37-year-old female patient presented with dizziness. (A) Time-of-flight magnetic resonance angiograph showing severe stenosis in the right vertebral artery (arrow). (B) Intramural hematoma and aneurysmal dilatation on proton-density imaging. (C) Intramural hematoma presenting as hyperintensity and hypointensity on T2-weighted imaging, and (D) intramural hematoma presenting as hyperintensity and isointensity on T1-weighted imaging. (E) Artery distal to the dissected segment showing periarterial enhancement on contrast-enhanced T1-weighted imaging.
Figure 4.
Figure 4.
Intracranial artery dissection. A 50-year-old male patient with one atherosclerotic risk factor (smoking) presented with right-side weakness. (A) Time-of-flight magnetic resonance angiograph showing severe stenosis in the left middle cerebral artery (arrow). (C) Intramural hematoma showing hyperintensity on T1-weighted imaging (small arrows), and (E) the intimal flap seen on contrast-enhanced T1-weighted imaging (small arrows). (G) Segmental aneurysmal dilatation seen on proton-density imaging. (B) One year later, the dissecting lumen improved (arrow), and (D, F, H) the aforementioned findings disappeared. The patient was considered to have had a middle cerebral artery dissection; however, intraplaque hemorrhage underlying atherosclerosis could not be excluded completely.
Figure 5.
Figure 5.
Moyamoya disease. A 50-year-old female patient presented with dizziness. (A) Digital subtraction angiography image showing severe stenosis in the right terminal internal carotid artery and middle cerebral artery with basal collaterals. (B, C) The outer diameters of both terminal internal carotid arteries (arrows) and (D) right middle cerebral artery (arrows) decreased (remodeling index, 0.18) on proton-density imaging.
Figure 6.
Figure 6.
Moyamoya disease. A 44-year-old male patient presented with abulia. (A) Digital subtraction angiography image showing severe stenosis of the left terminal internal carotid artery and middle cerebral artery with basal collaterals. (B, C) The outer diameters of both middle cerebral arteries (arrows) decreased on proton-density imaging. (D) Left middle cerebral artery (arrow) showing a remodeling index of 0.31 on proton-density imaging with (E) concentric and mild enhancement (arrows) on contrast-enhanced T1-weighted imaging.
Figure 7.
Figure 7.
Ultrasound (US) example of an irregular plaque. The US image shows a large amount of irregular-appearing heterogeneous plaque with multifocal calcification (bright areas with shadowing) in the carotid artery.
Figure 8.
Figure 8.
Ultrasound (US) example of an echolucent plaque. The US image shows a smooth echolucent plaque (arrows) on the carotid wall.
Figure 9.
Figure 9.
Normal carotid artery showing sites for measuring intima-media thickness. The arterial wall may demonstrate two parallel echogenic lines that are separated by a relatively hypoechoic intermediate area on longitudinal ultrasound, and the distance between these lines is the intima-media thickness.
Figure 10.
Figure 10.
Computed tomography angiographic image showing ulcerated plaque (arrows) with calcification in the carotid artery.
Figure 11.
Figure 11.
Different carotid plaques on computed tomography angiography. Arrow indicates (A) calcified, (B) fatty, and (C) mixed plaque.
Figure 12.
Figure 12.
Four main components of atherosclerotic plaques. Axial magnetic resonance images obtained by using five pulse sequences. The fibrous component is isointense on T1WI, T2WI, and PDI with enhancement. Fresh hemorrhage is hyperintense on T1WI and TOF imaging and hypointense on T2WI without enhancement. The lipid core is the area that demonstrates a drop in signal intensity from PDI to T2WI. The calcification demonstrates dark signal intensity on all sequences.
Figure 13.
Figure 13.
Vulnerable plaque. Axial diffusion-weighted magnetic resonance (MR) image of the brain (top right) and MR angiographic image (bottom right) showing high-grade carotid stenosis with ipsilateral acute infarction. Axial MR images obtained by using five pulse sequences show that the plaque contains three components. A large recent hemorrhage is hyperintense on T1- and T2-weighted imaging, proton-density imaging, and TOF imaging, and multifocal calcifications are hypointense in all sequences. PDI, proton density image; T2WI, T2-weighted image; T1WI, T1-weighted image; TOF, time-of-flight image; CE-T1WI, contrast enhanced T1-weighted image.
Figure 14.
Figure 14.
Positron emission tomography-computed tomography (PET-CT): arrow indicates (A) 18F-FDG PET and (B) PET-CT showing a high uptake in left internal carotid artery, and (C) CT angiography showing severe stenosis of the left internal carotid artery with an atherosclerotic plaque.

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