The Relationship between Hematoma Iron Content and Perihematoma Edema: An MRI Study

被引:49
作者
Lou, Min [2 ]
Lieb, Kathrin [1 ]
Selim, Magdy [1 ]
机构
[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Neurol,Stroke Div, Boston, MA 02215 USA
[2] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Hangzhou 310003, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
Iron; Edema; Hematoma; Intracerebral hemorrhage; Magnetic resonance imaging; OXIDATIVE BRAIN-INJURY; INTRACEREBRAL HEMORRHAGE; FERRITIN; AGE; DISEASE; ERYTHROCYTES; APPEARANCE; T2;
D O I
10.1159/000199464
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Iron neurotoxicity has been linked to delayed neuronal injury and edema formation after intracerebral hemorrhage (ICH). We have previously shown that serum ferritin, an indicator of body iron load, correlates with the relative perihematoma edema volume (RPHEV) on days 3-4 after ICH. We undertook this study to directly examine the relationship between in vivo brain and hematoma iron content, measured by MRI, and RPHEV. Methods: We retrospectively reviewed prospectively collected clinical and laboratory data from 36 consecutive patients with acute spontaneous lobar ICH who had MRI performed within 2-4 days of ICH onset. We measured hematoma and edema volumes, and the signal intensity on T-2-weighted images (T2SI), as an estimate of iron content, in the hematoma and contralateral globus pallidus (GP). We calculated the RPHEV and T2SI in the hematoma and GP, relative to T2SI in the frontal deep white matter which contains negligible iron, to estimate the hematoma and brain iron load. We used Spearman correlation coefficient to determine the association of relative T2SI of the hematoma and GP with RPHEV. Results: We found a significant inverse correlation between the relative T2SI in the hematoma ( r = -0.75, p < 0.001) and to a lesser extent in the GP ( r = -0.34, p = 0.04) and the RPHEV. Conclusions: Our findings suggest that in vivo brain and hematoma iron content, as measured by MRI, is linked to perihematoma edema after ICH, and provide further support to existing preclinical evidence linking iron-mediated toxicity to delayed neuronal injury after ICH. Copyright (C) 2009 S. Karger AG, Basel
引用
收藏
页码:266 / 271
页数:6
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