No abstract

Although most therapeutic efforts and experimental stroke models focus on the concept of complete occlusion of the middle cerebral artery as a result of embolism from the carotid artery or cardiac chamber, relatively little is known about the stroke mechanism of intrinsic middle cerebral artery stenosis. Differences in stroke pathophysiology may require different strategies for prevention and treatment. We prospectively studied 30 consecutive acute ischemic stroke patients with middle cerebral artery stenosis detected by transcranial Doppler and magnetic resonance angiography. Patients underwent microembolic signal monitoring by transcranial Doppler and diffusion-weighted magnetic resonance imaging. Characteristics of acute infarct on diffusion-weighted magnetic resonance imaging were categorized according to the number (single or multiple infarcts) and the pattern of cerebral infarcts (cortical, border zone, or perforating artery territory infarcts). The data of microembolic signals and diffusion-weighted magnetic resonance imaging were assessed blindly and independently by separate observers. Diffusion-weighted magnetic resonance imaging showed that 15 patients (50%) had single acute cerebral infarcts and 15 patients had multiple acute cerebral infarcts. Among patients with multiple acute infarcts, unilateral, deep, chainlike border zone infarcts were the most common pattern (11 patients, 73%), and for single infarcts, penetrating artery infarcts were the most common (10 patients, 67%). Microembolic signals were detected in 10 patients (33%). The median number of microembolic signals per 30 minutes was 15 (range, 3-102). Microembolic signals were found in 9 patients with multiple infarcts and in 1 patient with a single infarct (p = 0.002, chi(2)). The number of microembolic signals predicted the number of acute infarcts on diffusion-weighted magnetic resonance imaging (linear regression, adjusted R(2) =0.475, p < 0.001). Common stroke mechanisms in patients with middle cerebral artery stenosis are the occlusion of a single penetrating artery to produce a small subcortical lacuna-like infarct and an artery-to-artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, especially along the border zone region.

HST1 within MCA plaque on HR-MRI is associated with ipsilateral stroke. Our results provide new insight into the vascular biology of MCA atherosclerosis.

Background and Purpose-Microanatomy studies reveal that most penetrating branches of middle cerebral artery (MCA) arise from the dorsal-superior surface of the trunk. Using high-resolution MRI, we sought to explore the plaque distribution of MCA atherosclerosis and its clinical relevance in relation to the orifices of penetrating arteries. Methods-We retrospectively analyzed the imaging and clinical data of 86 patients with atherosclerotic MCA stenosis. On high-resolution MRI, plaques were categorized based on the involvement of the superior, inferior, ventral, or dorsal MCA wall. The relationship of plaque distribution and clinical presentation was analyzed. Results-A total of 92 stenotic MCAs (40 symptomatic and 52 asymptomatic) on 828 image slices were studied.Overall, of the 251 slices with identified plaques, plaques were more frequently located at the ventral (44.8%) and inferior (31.7%) wall as compared with the superior (14.3%) and dorsal wall (9.0%; PϽ0.001). Symptomatic MCA stenosis had more superior (Pϭ0.016) and less inferior (Pϭ0.023) wall plaques than asymptomatic stenosis. Within the group of symptomatic MCA stenosis, vessels with penetrating artery infarctions had more superior (Pϭ0.001) but less ventral (Pϭ0.038) and inferior (Pϭ0.024) plaques than without penetrating artery infarctions. Conclusions-MCA plaques tend to locate opposite to the orifices of penetrating arterial branches. Further studies are required to investigate whether MCA plaque distribution is an independent determinant of stroke occurrence and its subtypes. (Stroke. 2011;42:2957-2959.)