Incidental Cerebral Microbleeds and Cerebral Blood Flow in Elderly Individuals.
Incidental Cerebral Microbleeds and Cerebral Blood Flow in Elderly Individuals.
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DOI：
10.1001/jamaneurol.2015.1359
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发表时间：
2015-09
期刊：
影响因子：
29
通讯作者：
Klunk WE
中科院分区：
文献类型：
--
作者：
Gregg NM;Kim AE;Gurol ME;Lopez OL;Aizenstein HJ;Price JC;Mathis CA;James JA;Snitz BE;Cohen AD;Kamboh MI;Minhas D;Weissfeld LA;Tamburo EL;Klunk WE
脑微出血（CMB）是血液分解产物的集合，是老年人磁共振成像中常见的偶然发现。脑微出血与认知缺陷有关，但机制尚不清楚。研究表明，与症状性脑淀粉样血管病相关的CMB患者具有异常的血管反应性和脑血流量（CBF），但据我们所知，尚未报道患有偶发性CMB的健康个体的脑血流量异常。评价偶发性CMB与静息态CBF、脑代谢、脑血管疾病、β-淀粉样蛋白（Aβ）和认知的相关性。2010年5月1日至2013年5月1日，在匹兹堡的一家学术医学中心对55名平均（SD）年龄为86.8（2.7）岁的认知正常个体进行了一项横断面研究;数据分析于2013年6月10日至2015年4月9日进行。3-使用磁共振成像或梯度回波进行Tesla磁共振成像，以评估CMB，CBF的动脉自旋标记，以及萎缩、白色高信号和梗死的T1和T2加权成像。使用氟脱氧葡萄糖进行正电子发射断层扫描以测量脑代谢，并使用匹兹堡化合物B测量纤维状Aβ。进行神经心理学评估，包括临床痴呆评定量表。磁共振图像的存在和CMB的位置进行了评级。肺叶CMB被细分为皮质或皮质下。通过体素分析和感兴趣区域分析，将CBF、代谢和Aβ的测量结果与CMB的存在和数量进行比较。在体素分析和感兴趣区域分析中，皮质CMB的存在与多个区域的CBF显著降低相关（整体CBF的百分比差异为-25.3%; P = .0003），顶叶皮质（-37.6%; P < .0001）和楔前叶（-31.8%; P = .0006）的降低幅度最大。有任何CMB的参与者表现出CBF减少的非显著趋势。患有皮质CMB的参与者与更高的梗死患病率显著相关（24% vs 6%; P = 0.047），并且在临床痴呆评定量表上表现出更高的缺陷患病率趋势（45% vs 19%; P = 0.12）。皮质淀粉样蛋白（通过匹兹堡化合物B正电子发射断层扫描测量）在有和没有CMB的参与者之间没有差异（P = 0.60）。在认知功能正常的老年人中，皮质位置的偶发性CMB与静息态CBF的广泛减少相关。慢性低灌注可能使这些人处于神经元损伤和神经变性的风险中。我们的研究结果表明，静息态CBF是CMB相关小血管疾病的标志物。
Cerebral microbleeds (CMBs) are collections of blood breakdown products that are a common incidental finding in magnetic resonance imaging of elderly individuals. Cerebral microbleeds are associated with cognitive deficits, but the mechanism is unclear. Studies show that individuals with CMBs related to symptomatic cerebral amyloid angiopathy have abnormal vascular reactivity and cerebral blood flow (CBF), but, to our knowledge, abnormalities in cerebral blood flow have not been reported for healthy individuals with incidental CMBs. To evaluate the association of incidental CMBs with resting-state CBF, cerebral metabolism, cerebrovascular disease, β-amyloid (Aβ), and cognition. A cross-sectional study of 55 cognitively normal individuals with a mean (SD) age of 86.8 (2.7) years was conducted from May 1, 2010, to May 1, 2013, in an academic medical center in Pittsburgh; data analysis was performed between June 10, 2013, and April 9, 2015. 3-Tesla magnetic resonance imaging was performed with susceptibility-weighted imaging or gradient-recalled echo to assess CMBs, arterial spin labeling for CBF, and T1- and T2-weighted imaging for atrophy, white matter hyperintensities, and infarcts. Positron emission tomography was conducted with fluorodeoxyglucose to measure cerebral metabolism and Pittsburgh compound B for fibrillar Aβ. Neuropsychological evaluation, including the Clinical Dementia Rating scale, was performed. Magnetic resonance images were rated for the presence and location of CMBs. Lobar CMBs were subclassified as cortical or subcortical. Measurements of CBF, metabolism, and Aβ were compared with the presence and number of CMBs with voxelwise and region-of-interest analyses. The presence of cortical CMBs was associated with significantly reduced CBF in multiple regions on voxelwise and region-of-interest analyses (percentage difference in global CBF, −25.3%; P = .0003), with the largest reductions in the parietal cortex (−37.6%; P < .0001) and precuneus (−31.8%; P = .0006). Participants with any CMBs showed a nonsignificant trend toward reduced CBF. Participants with cortical CMBs had a significant association with greater prevalence of infarcts (24% vs 6%; P = .047) and demonstrated a trend to greater prevalence of deficits demonstrated on the Clinical Dementia Rating scale (45% vs 19%; P = .12). There was no difference in cortical amyloid (measured by Pittsburgh compound B positron emission tomography) between participants with and without CMBs (P = .60). In cognitively normal elderly individuals, incidental CMBs in cortical locations are associated with widespread reductions in resting-state CBF. Chronic hypoperfusion may put these people at risk for neuronal injury and neurodegeneration. Our results suggest that resting-state CBF is a marker of CMB-related small-vessel disease.