Mechanism of medullary infarction based on arterial territory involvement.
OBJECTIVE
The blood supply to the medulla oblongata is distinct from that of other areas of the brainstem, and thus the mechanism underlying medullary infarctions may be distinct. However, few studies have investigated this.


METHODS
Of 3833 stroke patients who were on the stroke registry between February 1999 and April 2008, those with medullary infarctions demonstrated on diffusion-weighted magnetic resonance imaging were enrolled. We analyzed the topography, the involved arterial territories, and the etiologic mechanisms of the lesions.


RESULTS
In total, 142 patients were enrolled in the study. Bilateral medullary infarctions were rare (2.2%). Lesions involving the anteromedial or lateral territories were common in the upper medulla oblongata, whereas lateral territorial involvements were common in the middle and lower regions of the medulla oblongata. Significant stenosis (>50%) or occlusion of the vertebral artery was common (52.2%). Among stroke subtypes, large-artery atherosclerosis was most common (34.5%), while lacunae and cardioembolism were rare (3.5% and 4.2%, respectively). Vertebral artery dissection was frequent. The stroke mechanisms differed with the involved vascular territories. Large-artery atherosclerosis produced lesions in the lateral, anteromedial, and posterior territories. None of the cardioembolisms or other etiologies involved anteromedial or anterolateral territories, but all involved the lateral and/or posterior territories. Lacunar infarction was found only in the anteromedial and anterolateral territories.


CONCLUSIONS
The topography and mechanisms of infarctions involving the medulla oblongata are different with the involved arterial territories. These findings may be associated with the distinct pattern of arterial supply to the medulla oblongata.
Department of Neurology, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Kyoungsub
K
Kim
Hye Sun
HS
Lee
Yo Han
YH
Jung
Young Dae
YD
Kim
Hyo Suk
HS
Nam
Chung Mo
CM
Nam
Seung Min
SM
Kim
Ji Hoe
JH
Heo