Niwa Atsushi, Ii Yuichiro, Shindo Akihiro, Matsuo Ko, Ishikawa Hidehiro, Taniguchi Akira, Takase Shinichi, Maeda Masayuki, Sakuma Hajime, Akatsu Hiroyasu, Hashizume Yoshio, Tomimoto Hidekazu
Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan.
Department of Radiology, Mie University Hospital, Mie, Japan.
J Alzheimers Dis. 2017;59(3):951-959. doi: 10.3233/JAD-161242.
Microvascular lesions including cortical microinfarctions (CMIs) and cerebral lobar microbleeds (CMBs) are usually caused by cerebral amyloid angiopathy (CAA) in the elderly and are correlated with cognitive decline. However, their radiological-histopathological coincidence has not been revealed systematically with widely used 3-Tesla (3T) magnetic resonance imaging (MRI). The purpose of the present study is to delineate the histopathological background corresponding to MR images of these lesions. We examined formalin-fixed 10-mm thick coronal brain blocks from 10 CAA patients (five were also diagnosed with Alzheimer's disease, three with dementia with Lewy bodies, and two with CAA only) with dementia and six non CAA patients with neurodegenerative disease. Using 3T MRI, both 3D-fluid attenuated inversion recovery (FLAIR) and 3D-double inversion recovery (DIR) were examined to identify CMIs, and T2* and susceptibility-weighted images (SWI) were examined to identify CMBs. These blocks were subsequently examined histologically and immunohistochemically. In CAA patients, 48 CMIs and 6 lobar CMBs were invariably observed in close proximity to degenerated Aβ-positive blood vessels. Moreover, 16 CMIs (33%) of 48 were detected with postmortem MRI, but none were seen when the lesion size was smaller than 1 mm. In contrast, only 1 undeniable CMI was founded with MRI and histopathology in 6 non CAA patients. Small, cortical high-intensity lesions seen on 3D-FLAIR and 3D-DIR images likely represent CMIs, and low-intensity lesions in T2* and SWI correspond to CMBs with in vivo MRI. Furthermore, a close association between amyloid-laden vessels and these microvascular lesions indicated the contribution of CAA to their pathogenesis.
微血管病变,包括皮质微梗死(CMIs)和脑叶微出血(CMBs),在老年人中通常由脑淀粉样血管病(CAA)引起,并且与认知功能下降相关。然而,使用广泛应用的3特斯拉(3T)磁共振成像(MRI)尚未系统地揭示它们的放射学-组织病理学一致性。本研究的目的是描绘这些病变的磁共振图像对应的组织病理学背景。我们检查了10例患有痴呆的CAA患者(5例也被诊断为阿尔茨海默病,3例患有路易体痴呆,2例仅患有CAA)和6例患有神经退行性疾病的非CAA患者的福尔马林固定的10毫米厚冠状脑块。使用3T MRI,检查三维液体衰减反转恢复(FLAIR)和三维双反转恢复(DIR)以识别CMIs,并检查T2和磁敏感加权成像(SWI)以识别CMBs。随后对这些脑块进行组织学和免疫组织化学检查。在CAA患者中,在退化的Aβ阳性血管附近总是观察到48个CMIs和6个脑叶CMBs。此外,48个CMIs中有16个(33%)在死后MRI中被检测到,但当病变大小小于1毫米时未观察到任何CMIs。相比之下,在6例非CAA患者中,MRI和组织病理学仅发现1个不可否认的CMI。在三维FLAIR和三维DIR图像上看到的小的皮质高强度病变可能代表CMIs,而T2和SWI中的低强度病变在活体MRI中对应于CMBs。此外,富含淀粉样蛋白的血管与这些微血管病变之间的密切关联表明CAA在其发病机制中的作用。