Vessel wall imaging for intracranial vascular disease evaluation

Abstract

Accurate and timely diagnosis of intracranial vasculopathies is important owing to the significant risk of morbidity with delayed and/or incorrect diagnosis both from the disease process and inappropriate therapies. Conventional luminal imaging techniques for analysis of intracranial vasculopathies are limited to evaluation of changes in the vessel lumen. Vessel wall MRI techniques can allow direct characterization of pathologic changes of the vessel wall. These techniques may improve diagnostic accuracy and improve patient outcomes. Extracranial carotid vessel wall imaging has been extensively investigated in patients with atherosclerotic disease and has been shown to accurately assess plaque composition and identify vulnerable plaque characteristics that may predict stroke risk beyond luminal stenosis alone. This review provides a brief history of vessel wall MRI, an overview of the intracranial vessel wall MRI techniques, its applications, and imaging findings of various intracranial vasculopathies pertinent to the neurointerventionalist, neurologist, and neuroradiologist. We searched MEDLINE, PubMed, and Google for English publications containing any of the following terms: 'intracranial vessel wall imaging', 'intracranial vessel wall', and 'intracranial vessel wall MRI'.

Keywords: Artery; Atherosclerosis; MRI; Vasculitis; Vessel Wall.

Figure 1

Atherosclerosis (A–D) and moyamoya disease (E–H). (A–D) A middle-aged homeless patient with 30 pack-year smoking history and IV drug abuse presented with a 4-day history of left middle cerebral artery (MCA) territory stroke. Axial diffusion-weighted imaging (A) shows multiple left MCA territory infarcts. Axial MR angiography (MRA) maximum intensity projection (MIP) (B) shows high-grade left MCA narrowing (arrowhead). Sagittal oblique T1 pre-contrast (C) and post-contrast (D) vessel wall sequences of the left MCA show an eccentric enhancing lesion with wall thickening and outward remodeling (short arrow), compatible with intracranial atherosclerotic disease. (E–H) A middle-aged patient without vascular risk factors, history of genetic syndromes, prior radiation, or evidence of central nervous system vasculitis presented with intermittent headaches and otherwise unremarkable clinical results. On axial MRA MIP (E) there is occlusion of the left carotid terminus (arrowhead) with attenuation of the right carotid terminus and proximal MCA. On axial T1 pre-contrast (F) and post-contrast (G) MRI of the carotid terminus and sagittal T1 post-contrast (H) MRI of the proximal MCA vessel wall there is no evidence of vessel wall enhancement, wall thickening, or outward remodeling (long arrows), most compatible with moyamoya disease.

Figure 2

Vasculitis and reversible cerebral vasoconstriction syndrome. (A–F) Young patient who presented with aphasia and bilateral middle cerebral artery (MCA) territory infarcts. Cerebrospinal fluid analysis indicated the presence of anti-varicella zoster virus (anti-VZV) antibodies, confirming a diagnosis of VZV vasculitis. Three-dimensional reconstruction of the posterior circulation from time-of-flight (TOF) MR angiography (MRA) (A) shows high-grade stenosis of the right P2 posterior cerebral artery (short arrow). There were additional stenoses involving the inferior division of the bilateral M1 MCA and bilateral A2 anterior cerebral artery (not shown). On T1 post-contrast intracranial vessel wall imaging (IVWI) (B), there is a circumferential enhancing lesion involving the stenotic segment (long arrow), compatible with inflammatory vasculopathy. On follow-up IVWI and TOF MRA performed 2 months (C and D) and 4 months (E and F) later, there is progressive improved luminal patency (short arrow, C and E) and diminished wall enhancement (long arrow, D and F), which corresponded with clinical improvement. (G–J) A middle-aged patient with a history of depression and selective serotonin reuptake inhibitor use, who presented with severe headache and stroke symptoms, was found to have bilateral watershed distribution infarcts on diffusion-weighted imaging (not included). Coronal MRA maximum intensity projection of the intracranial arteries (G) shows diffuse intradural arterial stenosis (arrowheads). Axial T1-weighted black-blood pre-contrast (H) and post-contrast (I) sequences show no evidence of appreciable wall enhancement. Follow-up MRA (J) performed 1 month later shows significant improvement in the degree of diffuse luminal narrowing.

Figure 3

Ruptured intracranial aneurysm. A middle-aged patient presented with sudden-onset severe headache. Axial non-contrast CT of the head (A) demonstrates prominent left frontal intraparenchymal hemorrhage, subarachnoid and intraventricular hemorrhage. Sagittal multiplanar reformat of CT angiography (CTA) (B) shows a left A2 anterior cerebral artery (ACA) aneurysm (arrowhead), which was in close proximity to the intraparenchymal hematoma. Intracranial vessel wall imaging was performed 2 days after aneurysm rupture. Sagittal T1 pre-contrast vessel wall sequence (C) shows the left A2 ACA aneurysm (arrowhead) adjacent to the medial aspect of the parenchymal hematoma. A sagittal T1 post-contrast vessel wall image (D) shows both vessel wall (long arrow) and intraluminal (curved arrow) enhancement. Intraluminal enhancement might have been secondary to stagnant or turbulent flow, or thrombus.