P H Lee1, S H Oh, O Y Bang, I S Joo, K Huh. 1. Department of Neurology, School of Medicine, Ajou University, Woncheon-dong San 5, Paldal-Ku, Suwon, Kyungki-do 442-749, South Korea.
Abstract
BACKGROUND AND PURPOSE: The pathogenesis of deep white matter medullary (WMM) artery infarcts remains controversial. To address this question, we analysed the stroke patterns of WMM infarcts using diffusion weighted magnetic resonance imaging (DWI) to detect embolic signals and investigate stroke subtypes according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classifications. METHODS: We identified WMM infarcts on DWI using templates to determine the subcortical vascular territories. We classified WMM infarcts into those with small artery disease (SAD), large artery disease (LAD), cardioembolism (CE), two or more aetiologies, or undetermined aetiology. Clinical course, risk factors, and cortical spotty lesions were compared. RESULTS: Of the 1420 consecutive patients, 103 (7.3%) met the criteria for WMM infarcts. The stroke subtypes were as follows: 65 (63.1%) patients with LAD, 18 (17.5%) with SAD, 12 (11.7%) with CE, four (3.9%) with two or more aetiologies, three (2.1%) with undetermined aetiology, and one (1.0%) with other determined aetiology. LAD (87.7%) or CE (83.3%) was significantly accompanied by cortical embolic signals as compared to SAD (0%, p<0.001). The LAD infarcts were larger and tended to be chain-like in shape. Ischaemic stroke recurrence was more common in strokes with cortical embolic signals than in those without embolic signals (18.9% v 0%, p = 0.009). CONCLUSIONS: In present study, the most common pathogenesis of WMM infarcts was LAD. Our study indicates that WMM infarcts accompanying cortical embolic signals warrant evaluation of the underlying embolic sources in the large artery or the heart.
BACKGROUND AND PURPOSE: The pathogenesis of deep white matter medullary (WMM) artery infarcts remains controversial. To address this question, we analysed the stroke patterns of WMM infarcts using diffusion weighted magnetic resonance imaging (DWI) to detect embolic signals and investigate stroke subtypes according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classifications. METHODS: We identified WMM infarcts on DWI using templates to determine the subcortical vascular territories. We classified WMM infarcts into those with small artery disease (SAD), large artery disease (LAD), cardioembolism (CE), two or more aetiologies, or undetermined aetiology. Clinical course, risk factors, and cortical spotty lesions were compared. RESULTS: Of the 1420 consecutive patients, 103 (7.3%) met the criteria for WMM infarcts. The stroke subtypes were as follows: 65 (63.1%) patients with LAD, 18 (17.5%) with SAD, 12 (11.7%) with CE, four (3.9%) with two or more aetiologies, three (2.1%) with undetermined aetiology, and one (1.0%) with other determined aetiology. LAD (87.7%) or CE (83.3%) was significantly accompanied by cortical embolic signals as compared to SAD (0%, p<0.001). The LAD infarcts were larger and tended to be chain-like in shape. Ischaemic stroke recurrence was more common in strokes with cortical embolic signals than in those without embolic signals (18.9% v 0%, p = 0.009). CONCLUSIONS: In present study, the most common pathogenesis of WMM infarcts was LAD. Our study indicates that WMM infarcts accompanying cortical embolic signals warrant evaluation of the underlying embolic sources in the large artery or the heart.
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