**5.4 High-resolution MRI (HR-MRI)**

The conventional imaging such as DSA, MRA, CTA, and TCD fall short in characterizing the presence of no occlusive atherosclerotic disease, because it focuses on the vessel lumen estimate luminal stenosis by measuring blood flow velocity [2, 54].

HR-MRI can be used to assess intracranial arterial disease, both atherosclerotic and nonatherosclerotic [50].

According to Bodle, HR-MRI represents MR acquisitions using clinically available 1.5–3.0 Tesla magnetic field strength targeted to intracranial arterial pathology that are of sufficient quality to visualize the arterial wall, separate from the lumen of the proximal circle of Willis vessels. HR-MRI can be accomplished at 1.5 T by limiting the field of view to focus on a single vessel or point of interest, but higher field strength at 3 T has many advantages over conventional MRI (1.5 T). Image quality in MRI depends on several factors (e.g., slice thickness, field of view, signal-to-noise ratio, matrix size, and magnetic field strength) [50, 61]. Image acquisition is faster and there are increased signal-to-noise and contrast-to-noise ratios, with better image quality for black-blood imaging. The increased signal and contrast that 3 T provides improves the detection of complex atherosclerotic plaque and can identify plaque components in larger arteries [50, 62].

HR-MRI allows the direct assessment of intracranial atherosclerotic plaques; it is capable of characterizing plaque location, severity, and morphology, and discriminating from other nonatherosclerotic etiologies [3, 50, 51].

Bodle also suggested that an intracranial plaque with HR-MRI features of intraplaque hemorrhage and a ruptured fibrous cap in a patient with downstream ischemia is likely associated with artery-to-artery embolism, whereas a stable plaque with a large amount of fibrous tissue and small lipid core resulting in high-grade stenosis may cause hypoperfusion [50]. Thus, HR-MRI may directly determine stroke mechanism and play a role in selecting secondary prevention therapies (e.g., patients with hypoperfusion may benefit from intracranial revascularization procedures that patients with artery-to-artery embolism may not benefit) [50].

The simplest use of HR-MRI of the MCA is the calculation of the degree of MCA stenosis, which may be stated as:

%Stenosis = (1 − Lumen area/Reference lumen area) × 100, (2)

where the reference lumen area is the area of the nonoccluded lumen, preferably at a proximal segment [2].

Bodle mentioned that ICAS can be caused by diverse pathologies (e.g., atherosclerosis, inflammation, and vasospasm), with diverse treatment implications. HR-MRI may noninvasively differentiate between the etiologies of ICAS by identifying plaque components or unique enhancement patterns [50].

Patients with symptomatic (versus asymptomatic) and non-BOD type (versus BOD) ICAD had characteristic changes in: (a) the wall area (larger plaques); (b) plaque signals (eco-centric enhancement and heterogeneous signal intensity suggesting unstable plaque); and (c) remodeling patterns (positive remodeling suggesting outward expansion of the vessel wall) [63].

On the contrary, superiorly located MCA plaques (near to the orifices of penetrating arteries) are associated with BOD-type ICAD [64].

Bodle asserted that, in other vascular beds, the determination of atherosclerotic plaque constituents has helped in risk-stratify patients and select treatments. Using clinical, imaging, and pathological correlations, studies of coronary and carotid artery disease have detected characteristics that indicate plaque vulnerability: lipid core size, intraplaque hemorrhage, and fibrous cap thickness. These vulnerable plaque characteristics are also present in ICAD [50, 65] but are less well studied (**Table 3**). Bodle also noted that intraplaque hemorrhage (IPH) from rupture of plaque microvessels causing the accumulation of erythrocyte membranes, deposition of cholesterol, macrophage infiltration and enlargement of the necrotic core

**95**

persons [66].

*Diagnosis of Symptomatic Intracranial Atherosclerotic Disease*

hypointense

Hemorrhage Hyperintense Hyperintense to

Isointense Isointense/

results in atheroma growth, and plaque destabilization. A large amount of lipid within the necrotic core of a plaque is another sign of plaque vulnerability HR-MRI measurement of lipid-necrotic core area in extracranial ICA plaques correlates well

*Plaque characteristics on multiple contrast weightings based on carotid imaging literature [50, 65]*

hyperintense

hypointense (with age of hemorrhage)

Calcification Hypointense Hypointense Hypointense Hypointense

**TOF-MRA T1-weighted PD-weighted T2-weighted**

hyperintense

Hypointense to hyperintense

Hyperintense Hypointense

Hyperintense

Hypointense to hyperintense

Isointense Isointense/

HR-MRI can identify fibrous cap characteristics (thin, thick, or ruptured) in extracranial ICAs. The fibrous cap is a layer of connective tissue covering the lipid-

HR-MRI is noninvasive, but less available, still with limited clinical value, requiring extensive postprocessing. Bodle asserted that imaging characteristics in ICAD have not yet been correlated with pathological specimens because, while the HR-MRI of the extracranial ICAs can be correlated with endarterectomy specimens, intracranial vessels are not accessible to pathology sampling in live patients. Therefore, the signal characteristics of intracranial plaque components can only be

Another disadvantage is the small size (2.0–5.0 mm) and the depth of the intracranial vessels, which require relatively long acquisition times, making HR-MRI imaging difficult because of patient motion artifact and limitations in

the degree and etiology of stenoses, identify nonstenotic plaques, and identify potentially high-risk plaque components. These plaque characteristics are not visualized with conventional luminal imaging and may be important predictors of

**6. Multidetector computed tomography and multidetector computed** 

The study of the prevalence, and of the risk factors for intracranial internal carotid artery calcification (ICAC), as a marker of intracranial atherosclerosis was determined by Bos and coworkers. They assessed a white population (2495 persons) from the population-based Rotterdam Study with a no enhanced multidetector (16-slice or 64-slice) computed tomography (MDCT) of the intracranial ICAs. A calcified plaque had >130 Hounsfield units. They concluded that ICAC was highly prevalent and occurred in over 80% of older, white

**tomography angiography for the diagnosis of intracranial** 

**6.1 Nonenhanced multidetector computed tomography (MDCT)**

According to Bodle, HR-MRI can help to identify stroke mechanisms, determine

necrotic core. Thick fibrous caps are less prone to rupture [50].

extrapolated from extracranial ICAs HR-MRI [50].

**atherosclerotic disease (ICAS)**

*DOI: http://dx.doi.org/10.5772/intechopen.90250*

Fibrous cap Isointense/

with pathology [50].

**Plaque characteristic**

Lipid-rich necrotic core

**Table 3.**

resolution.

stroke [50].


#### **Table 3.**

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

and nonatherosclerotic [50].

benefit) [50].

stenosis, which may be stated as:

at a proximal segment [2].

plaque components in larger arteries [50, 62].

nating from other nonatherosclerotic etiologies [3, 50, 51].

HR-MRI can be used to assess intracranial arterial disease, both atherosclerotic

According to Bodle, HR-MRI represents MR acquisitions using clinically available 1.5–3.0 Tesla magnetic field strength targeted to intracranial arterial pathology that are of sufficient quality to visualize the arterial wall, separate from the lumen of the proximal circle of Willis vessels. HR-MRI can be accomplished at 1.5 T by limiting the field of view to focus on a single vessel or point of interest, but higher field strength at 3 T has many advantages over conventional MRI (1.5 T). Image quality in MRI depends on several factors (e.g., slice thickness, field of view, signal-to-noise ratio, matrix size, and magnetic field strength) [50, 61]. Image acquisition is faster and there are increased signal-to-noise and contrast-to-noise ratios, with better image quality for black-blood imaging. The increased signal and contrast that 3 T provides improves the detection of complex atherosclerotic plaque and can identify

HR-MRI allows the direct assessment of intracranial atherosclerotic plaques; it is capable of characterizing plaque location, severity, and morphology, and discrimi-

The simplest use of HR-MRI of the MCA is the calculation of the degree of MCA

%Stenosis = (1 − Lumen area/Reference lumen area) × 100, (2)

Bodle mentioned that ICAS can be caused by diverse pathologies (e.g., atherosclerosis, inflammation, and vasospasm), with diverse treatment implications. HR-MRI may noninvasively differentiate between the etiologies of ICAS by identi-

Patients with symptomatic (versus asymptomatic) and non-BOD type (versus BOD) ICAD had characteristic changes in: (a) the wall area (larger plaques); (b) plaque signals (eco-centric enhancement and heterogeneous signal intensity suggesting unstable plaque); and (c) remodeling patterns (positive remodeling sug-

On the contrary, superiorly located MCA plaques (near to the orifices of pen-

Bodle asserted that, in other vascular beds, the determination of atherosclerotic plaque constituents has helped in risk-stratify patients and select treatments. Using clinical, imaging, and pathological correlations, studies of coronary and carotid artery disease have detected characteristics that indicate plaque vulnerability: lipid core size, intraplaque hemorrhage, and fibrous cap thickness. These vulnerable plaque characteristics are also present in ICAD [50, 65] but are less well studied (**Table 3**). Bodle also noted that intraplaque hemorrhage (IPH) from rupture of plaque microvessels causing the accumulation of erythrocyte membranes, deposition of cholesterol, macrophage infiltration and enlargement of the necrotic core

fying plaque components or unique enhancement patterns [50].

gesting outward expansion of the vessel wall) [63].

etrating arteries) are associated with BOD-type ICAD [64].

where the reference lumen area is the area of the nonoccluded lumen, preferably

Bodle also suggested that an intracranial plaque with HR-MRI features of intraplaque hemorrhage and a ruptured fibrous cap in a patient with downstream ischemia is likely associated with artery-to-artery embolism, whereas a stable plaque with a large amount of fibrous tissue and small lipid core resulting in high-grade stenosis may cause hypoperfusion [50]. Thus, HR-MRI may directly determine stroke mechanism and play a role in selecting secondary prevention therapies (e.g., patients with hypoperfusion may benefit from intracranial revascularization procedures that patients with artery-to-artery embolism may not

**94**

*Plaque characteristics on multiple contrast weightings based on carotid imaging literature [50, 65]*

results in atheroma growth, and plaque destabilization. A large amount of lipid within the necrotic core of a plaque is another sign of plaque vulnerability HR-MRI measurement of lipid-necrotic core area in extracranial ICA plaques correlates well with pathology [50].

HR-MRI can identify fibrous cap characteristics (thin, thick, or ruptured) in extracranial ICAs. The fibrous cap is a layer of connective tissue covering the lipidnecrotic core. Thick fibrous caps are less prone to rupture [50].

HR-MRI is noninvasive, but less available, still with limited clinical value, requiring extensive postprocessing. Bodle asserted that imaging characteristics in ICAD have not yet been correlated with pathological specimens because, while the HR-MRI of the extracranial ICAs can be correlated with endarterectomy specimens, intracranial vessels are not accessible to pathology sampling in live patients. Therefore, the signal characteristics of intracranial plaque components can only be extrapolated from extracranial ICAs HR-MRI [50].

Another disadvantage is the small size (2.0–5.0 mm) and the depth of the intracranial vessels, which require relatively long acquisition times, making HR-MRI imaging difficult because of patient motion artifact and limitations in resolution.

According to Bodle, HR-MRI can help to identify stroke mechanisms, determine the degree and etiology of stenoses, identify nonstenotic plaques, and identify potentially high-risk plaque components. These plaque characteristics are not visualized with conventional luminal imaging and may be important predictors of stroke [50].
