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Pathogenesis of deep white matter medullary infarcts: a diffusion weighted magnetic resonance imaging study.
J Neurol Neurosurg Psychiatry. 2005 Dec; 76(12):1659-63.JN

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.

Links

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Authors+Show Affiliations

Lee PH
Department of Neurology, School of Medicine, Ajou University, Woncheon-dong San 5, Paldal-Ku, Suwon, Kyungki-do 442-749, South Korea.
Oh SH
No affiliation info available
Bang OY
No affiliation info available
Joo IS
No affiliation info available
Huh K
No affiliation info available

MeSH

AgedCerebral InfarctionDiffusion Magnetic Resonance ImagingFemaleHumansIntracranial EmbolismMaleMedulla OblongataMiddle AgedRadiographyRisk Factors

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16291890

Citation

Lee, P H., et al. "Pathogenesis of Deep White Matter Medullary Infarcts: a Diffusion Weighted Magnetic Resonance Imaging Study." Journal of Neurology, Neurosurgery, and Psychiatry, vol. 76, no. 12, 2005, pp. 1659-63.
Lee PH, Oh SH, Bang OY, et al. Pathogenesis of deep white matter medullary infarcts: a diffusion weighted magnetic resonance imaging study. J Neurol Neurosurg Psychiatry. 2005;76(12):1659-63.
Lee, P. H., Oh, S. H., Bang, O. Y., Joo, I. S., & Huh, K. (2005). Pathogenesis of deep white matter medullary infarcts: a diffusion weighted magnetic resonance imaging study. Journal of Neurology, Neurosurgery, and Psychiatry, 76(12), 1659-63.
Lee PH, et al. Pathogenesis of Deep White Matter Medullary Infarcts: a Diffusion Weighted Magnetic Resonance Imaging Study. J Neurol Neurosurg Psychiatry. 2005;76(12):1659-63. PubMed PMID: 16291890.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathogenesis of deep white matter medullary infarcts: a diffusion weighted magnetic resonance imaging study. AU - Lee,P H, AU - Oh,S H, AU - Bang,O Y, AU - Joo,I S, AU - Huh,K, PY - 2005/11/18/pubmed PY - 2005/12/15/medline PY - 2005/11/18/entrez SP - 1659 EP - 63 JF - Journal of neurology, neurosurgery, and psychiatry JO - J Neurol Neurosurg Psychiatry VL - 76 IS - 12 N2 - 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. SN - 0022-3050 UR - https://www.unboundmedicine.com/medline/citation/16291890/Pathogenesis_of_deep_white_matter_medullary_infarcts:_a_diffusion_weighted_magnetic_resonance_imaging_study_ DB - PRIME DP - Unbound Medicine ER -