Branch atheromatous plaque: a major cause of lacunar infarction (high-resolution MRI study)

Abstract

Background: Lacunar infarctions account for up to 25% of all ischemic strokes and, thus, constitute a numerically important subgroup. It is important that the two pathogeneses of lacunar infarction, that is, small-vessel occlusion and branch atheromatous disease, be differentiated because prognoses and treatment strategies differ. The authors evaluated the presence of branch atheromatous plaque in parent arteries that supply lacunar infarcts by high-resolution magnetic resonance imaging (HR-MRI).

Methods: HR-MRI was performed in 15 patients with (1) a clinical presentation consistent with classical lacunar syndromes; (2) an acute lacunar infarction by diffusion-weighted imaging, measuring ≤20 mm in maximal diameter; (3) a magnetic resonance angiography showing a normal middle cerebral artery or basilar artery supplying the ischemic lesion, and (4) no other obvious etiology for small-vessel distribution ischemic stroke.

Results: The median time of vessel wall imaging after index events was 4 days (range, 2-15 days). Six of the 15 patients had a lacunar infarction in the middle cerebral artery territory, and 9 had a lesion in the basilar artery territory. HR-MRI detected underlying atheromatous plaques in 9 patients (60%) with a lacunar infarction. In these 9 patients, asymptomatic intracranial atherosclerotic stenosis was more frequent compared to patients without branch atheromatous plaque (55.6 vs. 16.7%). In pontine infarctions, ischemic lesions that extended to the pial base of the pons were more frequent in patients with branch atheromatous plaques (83.3 vs. 33.3%), and all the ischemic lesions and atheromatous plaques were on the same side (right, n = 2; left, n = 4). All plaques responsible for acute symptomatic lacunar infarction were enhanced in contrast-enhanced T1-weighted HR-MR images.

Conclusions: HR-MRI results enabled underlying symptomatic branch atheromatous disease to be detected in lacunar infarction patients. The experience gained during this study indicates that HR-MRI better delineates intracranial arterial lesions, suggesting that its use will lead to a further understanding of the mechanisms involved in stroke.

Keywords: Branch atheromatous disease; High-resolution MRI; Lacunar infarction.

Figures

Fig. 1

Imaging findings of 3 patients with branch atheromatous MCA plaques. a Patient 4: DW image with a focal high signal intensity lesion in the internal capsule, MRA without significant stenosis in the MCA, and T1, T2, PD, and T1E images demonstrating atheromatous plaque at ventral MCA with subtle enhancement. b Patient 5: DW image with a focal lesion in basal ganglia, normal MCA by MRA, and T1, T2, PD, and T1E images showing atheromatous plaque at the superior MCA with enhancement. c Patient 6: DW image with a focal corona radiata lesion, normal MCA by MRA, and T1, T2, PD, and T1E images showing atheromatous plaque at the ventrosuperior portion of the MCA with enhancement.

Fig. 2

Image findings of 6 patients with branch atheromatous plaque in the BA. a Patient 10: DW image showing a high signal intensity lesion in the right pons extending to the base surface, MRA showing no significant stenosis in the BA, and T1, T2, PD, and T1E images demonstrating atheromatous plaque at the ventrolateral portion of the BA with enhancement. b Patient 11: DW image showing a focal lesion in the right pons extending to the base surface, MRA showing a normal BA, and T1, T2, PD, and T1E images demonstrating atheromatous plaque at the lateral BA with enhancement. c Patient 12: DW image showing a focal lesion in the left pons extending to the base surface, MRA showing a normal BA, and T1, T2, PD, and T1E images demonstrating atheromatous plaque at the dorsolateral BA encroaching a perforating artery orifice with enhancement. d Patient 13: DW image showing a high signal intensity lesion in the left pons extending to the base surface, MRA showing no significant stenosis in the BA, and T1, T2, PD, and T1E images demonstrating atheromatous plaque at the ventrolateral BA with enhancement. e Patient 14: DW image showing a focal isolated lesion in the left pons, MRA showing a normal BA, and T1, T2, PD, and T1E images demonstrating small atheromatous plaque at the lateral BA with enhancement. f Patient 15: DW image showing a focal lesion in left pons extending to the base surface, MRA showing a normal BA, and T1, T2, PD, and T1E images demonstrating atheromatous plaque at the dorsolateral BA with enhancement.

Fig. 3

Imaging findings of 6 patients without branch atheromatous plaque in the MCA or BA. a–c Patients 1–3: DW images showing a focal high signal intensity lesion in the right corona radiata, left corona radiate, and left basal ganglia, and MRA showing a normal MCA. d–f Patients 7–9: DW image showing a focal isolated lesion in the right pons, left pons, and right pons extending to the basal surface, and an MRA showing no significant stenosis in the BA. All HR-MRI sequence, T1, T2, PD, and T1E images demonstrating normal vessel walls without enhancement.