The identification of cerebral microinfarctions with magnetic resonance imaging (MRI) and histological methods remains challenging in aging and dementia. Here, we matched pathological changes in the microvasculature of cortical cerebral microinfarcts to MRI signals using single 100 μm-thick histological sections scanned with ultra-high-resolution 11.7 T MRI. Histologically, microinfarcts were located in superficial or deep cortical layers or transcortically, compatible with the pattern of layer-specific arteriolar blood supply of the cerebral cortex. Contrary to acute microinfarcts, at chronic stages the core region of microinfarcts showed pallor with extracellular accumulation of lipofuscin and depletion of neurons, a dense meshwork of collagen 4-positive microvessels with numerous string vessels, CD68-positive macrophages and glial fibrillary acidic protein (GFAP)-positive astrocytes. In MRI scans, cortical microinfarcts at chronic stages, called chronic cortical microinfarcts here, gave hypointense signals in T1-weighted and hyperintense signals in T2-weighted images when thinning of the tissue and cavitation and/or prominent iron accumulation were present. Iron accumulation in chronic microinfarcts, histologically verified with Prussian blue staining, also produced strong hypointense T2*-weighted signals. In summary, the microinfarct core was occupied by a dense microvascular meshwork with string vessels, which was invaded by macrophages and astroglia and contained various degrees of iron accumulation. While postmortem ultra-high-resolution single-section imaging improved MRI-histological matching and the structural characterization of chronic cortical cerebral microinfarcts, miniscule microinfarcts without thinning or iron accumulation could not be detected with certainty in the MRI scans. Moreover, string vessels at the infarct margin indicate disturbances in the microcirculation in and around microinfarcts, which might be exploitable in the diagnostics of cortical cerebral microinfarcts with MRI in vivo.

中文翻译：

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皮层脑微梗死后超高分辨率单节MRI的组织学相关性。

在衰老和痴呆症中，通过磁共振成像（MRI）和组织学方法鉴定脑微梗塞仍然具有挑战性。在这里，我们使用单个超薄的11.7 T MRI扫描的100μm厚的组织切片，将皮质大脑微梗塞微血管的病理变化与MRI信号相匹配。从组织学上讲，微梗塞位于浅层或深层皮质或经皮层，与大脑皮质的特定层小动脉血供的模式兼容。与急性微梗塞相反，在慢性阶段，微梗塞的核心区域表现为苍白，脂质体中有胞外积聚和神经元耗竭，胶原4阳性的微血管密集网状结构，并有许多细血管，CD68阳性巨噬细胞和胶质原纤维酸性蛋白（GFAP）阳性星形胶质细胞。在MRI扫描中，当存在组织变薄和空化现象和/或明显的铁蓄积时，处于慢性阶段的皮质微梗塞（在此称为慢性皮质微梗塞）会在T1加权图像中产生低信号，在T2加权图像中产生高强度信号。经普鲁士蓝染色在组织学上证实的慢性微梗塞中的铁蓄积也产生了强烈的低T2 *加权信号。综上所述，微梗塞核心被密集的微血管网状结构所占据，该网状血管具有线状血管，并被巨噬细胞和星形胶质细胞侵入，并含有不同程度的铁蓄积。事后超高分辨率单节成像改善了MRI的组织学匹配和慢性皮质脑微梗死的结构特征，但在MRI扫描中不能确定地检测到没有变薄或铁积累的微小微梗死。此外，在梗塞边缘的弦状血管表明微梗塞内部和周围的微循环受到干扰，这在体内MRI诊断皮质脑微梗塞中可能是可利用的。