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Characterization of Intracranial Atherosclerotic
Stenosis Using High-Resolution MRI
Bickley S, Stalcup S, Turan T, LeMatty T, Spampinato MV
Control 2551
eEdE#: eEdE-56
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Disclosures
This work was supported by NIH K23 NS069668.
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Background
• Intracranial atherosclerosis is a leading cause of stroke, with a total
of 70,000 strokes caused by symptomatic intracranial arterial
stenosis (ICAS) in the US every year.
• However, there are no animal models of ICAS pathophysiology and
only a few post-mortem studies have evaluated the topic.
• Recent advances in MR imaging have allowed in vivo study of ICAS
characteristics.
• This presentation will describe intracranial arterial wall imaging
acquisition techniques and focus on the high resolution MRI (HR
MRI) appearance of ICAS.
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Vessel Wall Imaging Challenges and Solutions
Challenges
Solutions
• Need for suppression of CSF surrounding • Use of a combination of FLAIR and
black blood imaging techniques.
the vessel and blood within the lumen.
• Long scan times required to attain the • Focus imaging on small segments of
the portion of the vessel most likely
sub-millimeter resolution required to
to demonstrate pathology.
image the arterial wall.
• Higher field strengths, with 3T or
• Low signal to noise ratio.
stronger magnets.
• Acquiring slices perpendicular to the • Use of volumetric 3D sequences.
curving vessels of the Circle of Willis
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MUSC Vessel Wall Imaging Protocol
• 3T MR scanner equipped with a 32 channel head coil.
• Non-contrast 3D time of flight MR angiogram to plan the HR MRI.
• HR MRI:
– Short axis views perpendicular to the intracranial vessel of interest.
– Pre- and post-contrast T1 weighted images (TR/TE 458/16 msec, FA 180
matrix 320 x 320, 11 slices, thickness 1.2 mm, FOV 128 mm).
– T2-weighted (TR/TE 1500/66 msec, , FA 180, matrix 256 x 256, 11 slices,
thickness 1.2 mm, FOV 104 mm).
– Fluid attenuated inversion recovery (FLAIR) (TR/TE 2500/14 msec, FA 140
inversion time 1069, matrix 256 x 197, 11 slices, thickness 1.2 mm, FOV
100 mm).
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Plaque Features
Comparative studies on the correlations between high-resolution MRI
and pathological carotid endarterectomy specimens have
demonstrated that MRI can identify the following plaque
components with good sensitivity (81-90%) and specificity (74-90%):
1. Fibrous Cap
2. Lipid Core
3. Intraplaque Hemorrhage
4. Plaque Enhancement
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High-Risk Plaque Features
Several prospective studies have shown that the following
plaque features are associated with the occurrence of
stroke and TIA in extracranial carotid plaques:
1. Thin or Ruptured Fibrous Cap
2. Large Lipid Core
3. Intraplaque Hemorrhage
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Plaque Fibrous Cap
• The fibrous cap is best evaluated on T2-weighted sequences
• Fibrous cap is visually classified into thick and thin or ruptured.
• Thick fibrous cap:
Continuous hyperintense signal of the plaque adjacent to the vessel
lumen can be visualized and measured on T2.
• Thin or ruptured:
No evidence of continuous hyperintense T2 signal lining the surface of
the plaque.
– Thin fibrous cap with smooth surface
– Ruptured fibrous cap with rough surface OR clear ulceration within T2
hyperintense fibrous cap OR enhancement of plaque on post-Gd T1.
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MRA
A
Thick Fibrous Cap Case Study
B
C
Figure 1: Axial T2 (A), T1 (B), post-Gd T1-weighted images (C) demonstrate thick T2 hyperintense fibrous cap
along the wall of the basilar artery (blue arrows) without contrast enhancement (orange arrow).
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MRA
A
Ruptured Fibrous Cap Case Study
B
C
Figure 2: Coronal T2 (A), T1 (B), and post-Gd T1 (C) images of the internal carotid arteries demonstrate rough
surface (blue arrow) and contrast enhancement (orange arrow) of the right ICA plaque. The irregular surface
and avid enhancement suggest that it is a ruptured plaque.
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Lipid Core
• The lipid core is best evaluated by reviewing T1 and T2-weighted
sequences.
• T2-weighted images:
– Hypo- to isointense signal in the vessel wall Lipid Core
– Lack of T2 hypointensity in the vessel wall  No Lipid Core
• T1-weighted images:
– Iso- to hyperintense signal in the vessel wall Lipid Core
• We quantify the lipid core using a semiquantitative Lipid Core Score:
– 0: No lipid core
– 1: <25% of plaque area
– 2: >25% of plaque area
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Lipid Core Case Study
MRA
T2
A
Less than 25% Lipid Core
Non contrast T1
B
Figure 3: Axial T2 (A) and T1-weighted images (B) demonstrate T2 hypointensity of less than 25% of
the basilar artery plaque (blue arrows and arrowheads), with corresponding T1 isointense signal
(orange arrows).
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Lipid Core Case Study
MRA
T2
A
Greater than 25% Lipid Core
Non contrast T1
B
Figure 4: Coronal T2-weighted (A) and T1-weighted images (B) demonstrating T2 hypointense signal
of greater than 25% of the plaque (blue arrows), with corresponding T1 iso-hyperintense signal.
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Intraplaque Hemorrhage
• Intraplaque hemorrhage is a high-risk plaque feature best
evaluated on volumetric T1-weighted sequences.
• Hemorrhage will appear as hyperintense signal within the
plaque.
• Hemorrhage within the plaque is likely when signal intensity
within portions of the plaque is ≥150% of T1 signal of the pons
(or adjacent muscle).
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MRA
Intra-Plaque Hemorrhage Case Study
T2
T1
A
B
Thresholded T1
C
Figure 5: Sagittal T2 (A) and T1 (B) images show an eccentric T1 hyperintense plaque along the wall of the right MCA (blue
arrows). Thresholded sagittal T1-weighted image (C) demonstrates signal intensity of the MCA plaque ≥150% of T1 signal of
pons. Thresholding helps to distinguish between hemorrhage and other T1 hyperintense plaque features (i.e. lipid). Signal
intensity thresholding of T1-weighted images performed with MRIcron.
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MRA
T2
Intra-Plaque Hemorrhage Case Study
T1
Thresholded T1
C
AA
BB
C
Figure 6: Axial T2 (A) and T1 (B) images show an eccentric T2 and T1 hyperintense plaque along the wall of the basilar artery
(blue arrows). Thresholded sagittal T1-weighted image (C) demonstrates signal intensity of the MCA plaque ≥150% of T1
signal of pons. Thresholding helps to distinguish between hemorrhage and other T1 hyperintense plaque features (i.e. lipid).
Signal intensity thresholding of T1-weighted images performed with MRIcron.
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Plaque Enhancement
• Plaque enhancement can identify lesions responsible for
cerebrovascular ischemic events.
• Plaques tend to enhance within the first 4-5 weeks after an
ischemic event in the distribution of the affected vessel.
• However, plaque enhancement can be seen in vessels without
an associated ischemic event.
• When a plaque does not enhance, the affected vessel is
unlikely to cause downstream ischemia.
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Plaque Enhancement Case Study
Non contrast T1
A
No / Questionable Enhancement
Post-contrast T1
B
Figure 7 : Sagittal T1 (A) and post-Gd T1 (B) images show a non enhancing plaque along the wall of the MCA (arrows).
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Plaque Enhancement Case Study
MRA
Non contrast T1
A
Post-contrast T1
B
Figure 8: Axial T1- weighted images before (A) and after contrast administration showing plaque
enhancement (blue arrows).
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Case 1: 71 Year-Old Male
A
B
B
Figure 9: Axial FLAIR images demonstrate (A) a chronic infarction in the right cerebellar hemisphere, blue arrow;
(B) a chronic lacunar infarction in the posterior left thalamus, blue arrow.
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Case 1: 71 Year-Old Male
Figure 10
Figure 11
Figure 10: 3D TOF MRA MIPS reconstruction demonstrates focal stenosis in the mid portion of the basilar
artery, blue arrow.
Figure 11: Axial FLAIR image demonstrating eccentric plaque involving the basilar artery, blue arrow.
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Case 1: 71 Year-Old Male
A
B
B
Figure 12: (A) Axial T1-weighted pre-contrast image of the basilar artery shows an eccentric plaque.
(B) Axial T1-weighted post-contrast image of the basilar artery shows no enhancement in the plaque. This is
consistent with posterior circulation ICAS and remote infarctions.
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Case 2: 7 Year-Old Male With Recurrent Basilar Artery
Occlusion Post-Thrombectomy
Figure 13
Figures 13: Axial diffusion images demonstrate multiple areas of restricted diffusion throughout the
cerebellar hemispheres, the vermis, and in the brainstem, consistent with infarction.
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Case 2: 7 Year-Old Male With Recurrent Basilar Artery
Occlusion Post-Thrombectomy
A
B
B
Figure 14: (A) Axial T1-weighted image and (B) post-Gd T1-weighted image of the basilar artery shows
subtle thickening and enhancement of the vessel wall. The patient had multiple endovascular
procedures, and these findings most likely represent post-thrombectomy changes.
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Case 3: 81Year-Old Female With Right Sided Weakness
A
B B
Figure 15: (A) DWI image demonstrates acute watershed infarction. (B) CT angiogram of the left ICA
shows stenosis (blue arrow) along with wall calcification.
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Case 3: 81 Year-Old Female With Right Sided Weakness
MRA
A
B
Figure 16: (A) T1 and (B) T2-weighted images of a symptomatic plaque of left ICA. Lipid and loose
matrix appears isointense on T1- and hypo- isointense on T2 (yellow outline), fibrous tissue appears
hyperintense on T2 (green outline), and calcification appears dark on T1- and T2-weighted images
(orange stars).
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Case 3: Radiology - Pathology Correlation
Turan TN et al. Atherosclerosis 2014;237:460-463.
b
Figure 17: Histopathology of symptomatic left intracranial internal carotid (ICA) plaque.
Pathological specimens at the level of the stenosis stained with Hematoxylin & Eosin (A), and magnified T2weighted image of the plaque (B), which demonstrate plaque components: lipid and loose matrix (yellow
outline), fibrous tissue (green outline), calcium (orange stars).
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Conclusions
• High-resolution MRI allows the characterization of intracranial
atherosclerotic disease.
• The frequency of each plaque component in symptomatic and
asymptomatic plaques and stroke prediction in the territory of
high risk plaques are currently under investigation.
• In the future, the identification of high risk intracranial plaques
will enable the identification of vulnerable individuals who might
benefit from preventive therapeutic interventions.
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References
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