Correlation of hypointensities in susceptibility-weighted images to tissue histology in dementia patients with cerebral amyloid angiopathy: a postmortem MRI study.
Correlation of hypointensities in susceptibility-weighted images to tissue histology in dementia patients with cerebral amyloid angiopathy: a postmortem MRI study.
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DOI：
10.1007/s00401-009-0615-z
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发表时间：
2010-03
影响因子：
12.7
通讯作者：
Kirsch WM
中科院分区：
文献类型：
--
作者：
Schrag M;McAuley G;Pomakian J;Jiffry A;Tung S;Mueller C;Vinters HV;Haacke EM;Holshouser B;Kido D;Kirsch WM
使用铁敏感 MR 序列进行神经成像 [梯度回波 T2* 和磁化率加权成像 (SWI)] 可识别疑似脑部微出血的小信号空洞。尽管这些病变的临床意义仍不确定，但它们的分布和患病率与脑淀粉样血管病（CAA）、高血压、吸烟和认知缺陷相关。为了正确解释这些成像结果，有必要对产生信号空洞的病理进行调查。我们对患有阿尔茨海默病 (AD) 和不同程度 CAA 的死后大脑中 SWI 识别的低信号与组织病理学进行了系统关联。对 8 名 AD 患者的尸检大脑进行 3T 成像，其中 6 名患者显示出晚期 CAA；鉴定出对应于低信号的病灶并进行组织学研究。检测到多种病变；最常见的病变是急性微出血、陈旧性出血的含铁血黄素残留以及含铁血黄素环绕的小腔隙。在可以识别出血血管的病变中，β-淀粉样蛋白免疫组织化学证实血管壁中存在β-淀粉样蛋白。在最近出血的灶周区域观察到显着的细胞凋亡以及血红素加氧酶 1 活性和晚期补体激活。注意到急性外渗的血液和含铁血黄素通过扩大的 Virchow-Robin 间隙迁移，沿着局部微脉管系统传播炎症反应；一种可能导致腔隙性梗塞形成的机制。在我们的病例中，影像学结果与组织病理学的相关性表明，多种 CAA 相关病理学产生 MR 识别的信号空白，并进一步支持使用 SWI 作为该疾病的生物标志物。
Neuroimaging with iron-sensitive MR sequences [gradient echo T2* and susceptibility-weighted imaging (SWI)] identifies small signal voids that are suspected brain microbleeds. Though the clinical significance of these lesions remains uncertain, their distribution and prevalence correlates with cerebral amyloid angiopathy (CAA), hypertension, smoking, and cognitive deficits. Investigation of the pathologies that produce signal voids is necessary to properly interpret these imaging findings. We conducted a systematic correlation of SWI-identified hypointensities to tissue pathology in postmortem brains with Alzheimer’s disease (AD) and varying degrees of CAA. Autopsied brains from eight AD patients, six of which showed advanced CAA, were imaged at 3T; foci corresponding to hypointensities were identified and studied histologically. A variety of lesions was detected; the most common lesions were acute microhemorrhage, hemosiderin residua of old hemorrhages, and small lacunes ringed by hemosiderin. In lesions where the bleeding vessel could be identified, β-amyloid immunohistochemistry confirmed the presence of β-amyloid in the vessel wall. Significant cellular apoptosis was noted in the perifocal region of recent bleeds along with heme oxygenase 1 activity and late complement activation. Acutely extravasated blood and hemosiderin were noted to migrate through enlarged Virchow–Robin spaces propagating an inflammatory reaction along the local microvasculature; a mechanism that may contribute to the formation of lacunar infarcts. Correlation of imaging findings to tissue pathology in our cases indicates that a variety of CAA-related pathologies produce MR-identified signal voids and further supports the use of SWI as a biomarker for this disease.
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影响因子：
9.9
作者：
Knudsen, KA;Rosand, J;Greenberg, SM
通讯作者：
Greenberg, SM
DOI：
10.3109/13506129909007321
发表时间：
1999-09-01
期刊：
AMYLOID-INTERNATIONAL JOURNAL OF EXPERIMENTAL AND CLINICAL INVESTIGATION
影响因子：
--
作者：
Davis, J;Cribbs, DH;Van Nostrand, WE
通讯作者：
Van Nostrand, WE
影响因子：
3.3
作者：
Igase, Michiya;Tabara, Yasuharu;Miki, Tetsuro
通讯作者：
Miki, Tetsuro
影响因子：
5.1
作者：
Jellinger, K. A.;Lauda, F.;Attems, J.
通讯作者：
Attems, J.
影响因子：
3.1
作者：
Nicholl, R. M.;Balasubramaniam, V. P.;Rutherford, M. A.
通讯作者：
Rutherford, M. A.