1. Bickley S, Stalcup S, Turan T, LeMatty T, Spampinato MV
Characterization of Intracranial Atherosclerotic Stenosis Using High-Resolution MRI
Bickley S, Stalcup S, Turan T, LeMatty T, Spampinato MV
Control 2551
eEdE#: eEdE-56

2. Disclosures
This work was supported by NIH K23 NS

3. 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.

4. Vessel Wall Imaging Challenges and Solutions
Need for suppression of CSF surrounding the vessel and blood within the lumen.
Long scan times required to attain the sub-millimeter resolution required to image the arterial wall.
Low signal to noise ratio.
Acquiring slices perpendicular to the curving vessels of the Circle of Willis
Use of a combination of FLAIR and black blood imaging techniques.
Focus imaging on small segments of the portion of the vessel most likely to demonstrate pathology.
Higher field strengths, with 3T or stronger magnets.
Use of volumetric 3D sequences.

5. 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).

6. 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%):
Fibrous Cap
Lipid Core
Intraplaque Hemorrhage
Plaque Enhancement

7. 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:
Thin or Ruptured Fibrous Cap
Large Lipid Core
Intraplaque Hemorrhage

8. 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.

9. Thick Fibrous Cap Case Study
MRA
A 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).

10. Ruptured Fibrous Cap Case Study
MRA
A 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.

11. 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

12. Lipid Core Case Study Less than 25% Lipid Core
MRA
T Non contrast T1
A 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).

13. Lipid Core Case Study Greater than 25% Lipid Core
MRA
T Non contrast T1
A 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.

14. 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).

15. Intra-Plaque Hemorrhage Case Study
MRA
T T Thresholded T1
A B 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.

16. Intra-Plaque Hemorrhage Case Study
MRA
T T Thresholded T1 C
A B C
A B
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.

17. 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.

18. Plaque Enhancement Case Study No / Questionable Enhancement
Non contrast T Post-contrast T1
A B
Figure 7 : Sagittal T1 (A) and post-Gd T1 (B) images show a non enhancing plaque along the wall of the MCA (arrows).

19. Plaque Enhancement Case Study
MRA
Non contrast T Post-contrast T1
A B
Figure 8: Axial T1- weighted images before (A) and after contrast administration showing plaque enhancement (blue arrows).

20. 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.

21. 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.

22. 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.

23. 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.

24. 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.

25. 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.

26. 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).

27. Case 3: Radiology - Pathology Correlation
Turan TN et al. Atherosclerosis 2014;237: 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 T2-weighted image of the plaque (B), which demonstrate plaque components: lipid and loose matrix (yellow outline), fibrous tissue (green outline), calcium (orange stars).

28. 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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