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Nonstenotic Culprit Plaque: The Utility of High-Resolution Vessel Wall MRI of Intracranial Vessels after Ischemic Stroke.

de Havenon A, Yuan C, Tirschwell D, Hatsukami T, Anzai Y, Becker K, Sultan-Qurraie A, Mossa-Basha M - Case Rep Radiol (2015)

Bottom Line: Intracranial atherosclerotic disease (ICAD) accounts for 9-15% of ischemic stroke in the United States.As a result, they were referred for high-resolution magnetic resonance imaging (HR-MRI) of the arterial vessel wall, which identified a nonstenotic plaque with multiple high-risk features, identifying it as the etiology of the patient's thromboembolic events.The diagnosis resulted in a transition from anticoagulation to antiplatelet therapy, after which the patient's clinical events resolved.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University of Utah, 175 North Medical Drive, Salt Lake City, UT 84132, USA.

ABSTRACT
Intracranial atherosclerotic disease (ICAD) accounts for 9-15% of ischemic stroke in the United States. Although highly stenotic ICAD accounts for most of the strokes, it is assumed that nonstenotic ICAD (nICAD) can result in stroke, despite being missed on standard luminal imaging modalities. We describe a patient with nICAD who suffered recurrent thromboembolic stroke and TIA but had a negative conventional stroke workup. As a result, they were referred for high-resolution magnetic resonance imaging (HR-MRI) of the arterial vessel wall, which identified a nonstenotic plaque with multiple high-risk features, identifying it as the etiology of the patient's thromboembolic events. The diagnosis resulted in a transition from anticoagulation to antiplatelet therapy, after which the patient's clinical events resolved. HR-MRI is an imaging technique that has the potential to guide medical management for patients with ischemic stroke, particularly in cryptogenic stroke.

No MeSH data available.


Related in: MedlinePlus

(a) Axial diffusion-weighted MRI showed punctate cortical areas of diffusion restriction (white arrow), consistent with an embolic source of ischemia. (b) Sagittal CT angiogram shows high-grade narrowing (white arrow) of the right supraclinoid ICA, presumed secondary to thrombus which was in close proximity to focal ICA calcification (not seen). (c) Lateral DSA performed two weeks after the prior CTA shows no significant stenosis or other vascular abnormality of the right anterior circulation. (d) Lateral DSA shows a patent right cervical internal carotid artery. (e) Sagittal T2-weighted HR-MRI of the supraclinoid ICA shows atherosclerotic plaque along the anterior wall of the supraclinoid ICA, with discontinuous juxtaluminal T2 hyperintense band (white arrows), and deeper T2 hypointensity representing the lipid necrotic core (red arrows). (f) Sagittal T1 postcontrast HR-MRI at the same level shows T1 hypointense plaque with focal enhancement along the juxtaluminal surface, which was not present on the precontrast T1 image, and a normal to eccentrically enlarged vessel lumen (white arrow).
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fig1: (a) Axial diffusion-weighted MRI showed punctate cortical areas of diffusion restriction (white arrow), consistent with an embolic source of ischemia. (b) Sagittal CT angiogram shows high-grade narrowing (white arrow) of the right supraclinoid ICA, presumed secondary to thrombus which was in close proximity to focal ICA calcification (not seen). (c) Lateral DSA performed two weeks after the prior CTA shows no significant stenosis or other vascular abnormality of the right anterior circulation. (d) Lateral DSA shows a patent right cervical internal carotid artery. (e) Sagittal T2-weighted HR-MRI of the supraclinoid ICA shows atherosclerotic plaque along the anterior wall of the supraclinoid ICA, with discontinuous juxtaluminal T2 hyperintense band (white arrows), and deeper T2 hypointensity representing the lipid necrotic core (red arrows). (f) Sagittal T1 postcontrast HR-MRI at the same level shows T1 hypointense plaque with focal enhancement along the juxtaluminal surface, which was not present on the precontrast T1 image, and a normal to eccentrically enlarged vessel lumen (white arrow).

Mentions: We describe a middle-aged patient with no relevant past medical history who presented to an outside hospital with a two-day history of left upper extremity paresthesias and weakness. MRI of the brain showed several punctate areas of cortical diffusion restriction around the central sulcus (in the right middle cerebral artery territory) consistent with embolic infarcts (Figure 1(a)). MRA of the head and neck, including the aortic arch, carotid ultrasound, and transesophageal echocardiogram were unremarkable. The patient was started on low-dose aspirin and a statin. After discharge the symptoms improved, but two weeks later the patient had recurrence of left upper extremity paresthesias and weakness with extension of the sensory change into the left leg. The symptoms quickly resolved and repeat MRI showed no new infarcts. Noncontrast head CT showed a focal calcification involving the right supraclinoid ICA. Luminal imaging with CT angiogram showed marked stenosis of the right supraclinoid ICA adjacent to the calcification seen on noncontrast CT (Figure 1(b)), which had resolved on follow-up noncontrast 3D time of flight MR angiogram done later that day. This transient stenosis was thought to be related to a thrombus that resolved. The patient was anticoagulated with intravenous heparin and transitioned to warfarin. They had no identifiable thrombophilia and extended ambulatory cardiac monitoring was unremarkable.


Nonstenotic Culprit Plaque: The Utility of High-Resolution Vessel Wall MRI of Intracranial Vessels after Ischemic Stroke.

de Havenon A, Yuan C, Tirschwell D, Hatsukami T, Anzai Y, Becker K, Sultan-Qurraie A, Mossa-Basha M - Case Rep Radiol (2015)

(a) Axial diffusion-weighted MRI showed punctate cortical areas of diffusion restriction (white arrow), consistent with an embolic source of ischemia. (b) Sagittal CT angiogram shows high-grade narrowing (white arrow) of the right supraclinoid ICA, presumed secondary to thrombus which was in close proximity to focal ICA calcification (not seen). (c) Lateral DSA performed two weeks after the prior CTA shows no significant stenosis or other vascular abnormality of the right anterior circulation. (d) Lateral DSA shows a patent right cervical internal carotid artery. (e) Sagittal T2-weighted HR-MRI of the supraclinoid ICA shows atherosclerotic plaque along the anterior wall of the supraclinoid ICA, with discontinuous juxtaluminal T2 hyperintense band (white arrows), and deeper T2 hypointensity representing the lipid necrotic core (red arrows). (f) Sagittal T1 postcontrast HR-MRI at the same level shows T1 hypointense plaque with focal enhancement along the juxtaluminal surface, which was not present on the precontrast T1 image, and a normal to eccentrically enlarged vessel lumen (white arrow).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4543789&req=5

fig1: (a) Axial diffusion-weighted MRI showed punctate cortical areas of diffusion restriction (white arrow), consistent with an embolic source of ischemia. (b) Sagittal CT angiogram shows high-grade narrowing (white arrow) of the right supraclinoid ICA, presumed secondary to thrombus which was in close proximity to focal ICA calcification (not seen). (c) Lateral DSA performed two weeks after the prior CTA shows no significant stenosis or other vascular abnormality of the right anterior circulation. (d) Lateral DSA shows a patent right cervical internal carotid artery. (e) Sagittal T2-weighted HR-MRI of the supraclinoid ICA shows atherosclerotic plaque along the anterior wall of the supraclinoid ICA, with discontinuous juxtaluminal T2 hyperintense band (white arrows), and deeper T2 hypointensity representing the lipid necrotic core (red arrows). (f) Sagittal T1 postcontrast HR-MRI at the same level shows T1 hypointense plaque with focal enhancement along the juxtaluminal surface, which was not present on the precontrast T1 image, and a normal to eccentrically enlarged vessel lumen (white arrow).
Mentions: We describe a middle-aged patient with no relevant past medical history who presented to an outside hospital with a two-day history of left upper extremity paresthesias and weakness. MRI of the brain showed several punctate areas of cortical diffusion restriction around the central sulcus (in the right middle cerebral artery territory) consistent with embolic infarcts (Figure 1(a)). MRA of the head and neck, including the aortic arch, carotid ultrasound, and transesophageal echocardiogram were unremarkable. The patient was started on low-dose aspirin and a statin. After discharge the symptoms improved, but two weeks later the patient had recurrence of left upper extremity paresthesias and weakness with extension of the sensory change into the left leg. The symptoms quickly resolved and repeat MRI showed no new infarcts. Noncontrast head CT showed a focal calcification involving the right supraclinoid ICA. Luminal imaging with CT angiogram showed marked stenosis of the right supraclinoid ICA adjacent to the calcification seen on noncontrast CT (Figure 1(b)), which had resolved on follow-up noncontrast 3D time of flight MR angiogram done later that day. This transient stenosis was thought to be related to a thrombus that resolved. The patient was anticoagulated with intravenous heparin and transitioned to warfarin. They had no identifiable thrombophilia and extended ambulatory cardiac monitoring was unremarkable.

Bottom Line: Intracranial atherosclerotic disease (ICAD) accounts for 9-15% of ischemic stroke in the United States.As a result, they were referred for high-resolution magnetic resonance imaging (HR-MRI) of the arterial vessel wall, which identified a nonstenotic plaque with multiple high-risk features, identifying it as the etiology of the patient's thromboembolic events.The diagnosis resulted in a transition from anticoagulation to antiplatelet therapy, after which the patient's clinical events resolved.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University of Utah, 175 North Medical Drive, Salt Lake City, UT 84132, USA.

ABSTRACT
Intracranial atherosclerotic disease (ICAD) accounts for 9-15% of ischemic stroke in the United States. Although highly stenotic ICAD accounts for most of the strokes, it is assumed that nonstenotic ICAD (nICAD) can result in stroke, despite being missed on standard luminal imaging modalities. We describe a patient with nICAD who suffered recurrent thromboembolic stroke and TIA but had a negative conventional stroke workup. As a result, they were referred for high-resolution magnetic resonance imaging (HR-MRI) of the arterial vessel wall, which identified a nonstenotic plaque with multiple high-risk features, identifying it as the etiology of the patient's thromboembolic events. The diagnosis resulted in a transition from anticoagulation to antiplatelet therapy, after which the patient's clinical events resolved. HR-MRI is an imaging technique that has the potential to guide medical management for patients with ischemic stroke, particularly in cryptogenic stroke.

No MeSH data available.


Related in: MedlinePlus