5 mm 기준으로하여열공경색증을진단하는것이아직도유효한가?: 확산강조자기공영형상과자기공영혈관촬영술을이용한연구
Is 15 mm Criteria for Lacunar Infarction Still Valid?:Analysis of Mechanism of Deep Subcortical Infarctionusing Diffusion-Weighted MRI and MR Angiography
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Background: The ‘lacunar hypothesis’has been challenged since small (diameter <15 mm) subcortical infarctscan be produced by middle cerebral artery disease (MCAD) or cardioembolism (CE) while a larger infarct canoccur without evidence of MCAD or CE. We sought to assess whether lacunar hypothesis based on size criteriaonly is still valid. Methods: We studied 103 patients who 1) had acute (≤72 hours after onset), deep subcorticalMCA territory infarcts detected by diffusion-weighted MRI 2) underwent MR angiography. Stroke mechanismswere categorized as 1) MCAD when there was a corresponding MCA lesion, 2) CE when there was emboligenicheart disease without MCAD, and 3) small vessel disease (SVD) when there was neither CE nor MCAD. SVDwas further divided into definite SVD (dSVD, diameter <15 mm) or probable SVD (pSVD, diameter ≥15 mm).Results: Sixty-five patients (63%) had SVD (35 pSVD and 30 dSVD), 29 (28%) had MCAD, and nine (8.7 %)had CE. The diameter of infarcts was greater in CE than that of either MCAD (p<0.05) or SVD (p<0.01).Although it was greater in MCAD than in dSVD (p<0.01), but there was no difference in size between MCAD andpSVD (p=0.33) or MCAD and SVD (p=0.25). While patients with CE more often had cortical symptoms thanSVD (p<0.05) or MCAD+SVD (p<0.01), there was no difference in clinical features or risk factors betweenMCAD and SVD, and pSVD and dSVD. Conclusions: The deep subcortical infarcts associated with CE are dif-ferentiated from MCAD or SVD by the size and clinical features. However, there are no clinical diff e r e n c e sbetween MCAD and SVD, and pSVD and dSVD. There seems to be no rationale for 15 mm criteria for ‘lacunarinfarction’.
Abstract
Background: The ‘lacunar hypothesis’has been challenged since small (diameter <15 mm) subcortical infarctscan be produced by middle cerebral artery disease (MCAD) or cardioembolism (CE) while a larger infarct canoccur without evidence of MCAD or CE. We sought to assess whether lacunar hypothesis based on size criteriaonly is still valid. Methods: We studied 103 patients who 1) had acute (≤72 hours after onset), deep subcorticalMCA territory infarcts detected by diffusion-weighted MRI 2) underwent MR angiography. Stroke mechanismswere categorized as 1) MCAD when there was a corresponding MCA lesion, 2) CE when there was emboligenicheart disease without MCAD, and 3) small vessel disease (SVD) when there was neither CE nor MCAD. SVDwas further divided into definite SVD (dSVD, diameter <15 mm) or probable SVD (pSVD, diameter ≥15 mm).Results: Sixty-five patients (63%) had SVD (35 pSVD and 30 dSVD), 29 (28%) had MCAD, and nine (8.7 %)had CE. The diameter of infarcts was greater in CE than that of either MCAD (p<0.05) or SVD (p<0.01).Although it was greater in MCAD than in dSVD (p<0.01), but there was no difference in size between MCAD andpSVD (p=0.33) or MCAD and SVD (p=0.25). While patients with CE more often had cortical symptoms thanSVD (p<0.05) or MCAD+SVD (p<0.01), there was no difference in clinical features or risk factors betweenMCAD and SVD, and pSVD and dSVD. Conclusions: The deep subcortical infarcts associated with CE are dif-ferentiated from MCAD or SVD by the size and clinical features. However, there are no clinical diff e r e n c e sbetween MCAD and SVD, and pSVD and dSVD. There seems to be no rationale for 15 mm criteria for ‘lacunarinfarction’.