From the Department of Radiology (I.M.N., R.N.B.)
Center for Biomedical Image Computing and Analytics (I.M.N., M.-K.H., G.E., H.B., C.D.).
AJNR Am J Neuroradiol. 2019 Aug;40(8):1291-1298. doi: 10.3174/ajnr.A6119. Epub 2019 Jul 25.
White matter lesions are 1 age-related manifestation of cerebrovascular disease, but subthreshold abnormalities have been identified in nonlesional WM. We hypothesized that structural and physiologic MR imaging findings of early cerebrovascular disease can be measured in middle-aged subjects in tissue adjacent to WM lesions, termed "penumbra."
WM lesions were defined using automated segmentation in 463 subjects, 43-56 years of age, from the Coronary Artery Risk Development in Young Adults (CARDIA) longitudinal observational cohort study. We described 0- to 2-mm and 2- to 4-mm-thick spatially defined penumbral WM tissue ROIs as rings surrounding WM lesions. The remaining WM was defined as distant normal-appearing WM. Mean signal intensities were measured for FLAIR, T1-, and T2-weighted images, and from fractional anisotropy, mean diffusivity, CBF, and vascular reactivity maps. Group comparisons were made using Kruskal-Wallis and pair-wise tests.
Lesion volumes averaged 0.738 ± 0.842 cm (range, 0.005-7.27 cm). Mean signal intensity for FLAIR, T2, and mean diffusivity was increased, while T1, fractional anisotropy, and CBF were decreased in white matter lesions versus distant normal-appearing WM, with penumbral tissues showing graded intermediate values (corrected < .001 for all group/parameter comparisons). Vascular reactivity was significantly elevated in white matter lesions and penumbral tissue compared with distant normal-appearing white matter (corrected ≤ .001).
Even in relatively healthy 43- to 56-year-old subjects with small white matter lesion burden, structural and functional MR imaging in penumbral tissue reveals significant signal abnormalities versus white matter lesions and other normal WM. Findings suggest that the onset of WM injury starts by middle age and involves substantially more tissue than evident from focal white matter lesions visualized on structural imaging.
脑白质病变是年龄相关性脑血管病的一种表现，但在非病变脑白质中已发现亚临床异常。我们假设，在中年受试者的脑白质病变周围组织（称为“半影区”）中，可以测量早期脑血管病的结构和生理磁共振成像（MR）表现。
在来自冠状动脉风险发展在年轻人（CARDIA）纵向观察队列研究的 463 名 43-56 岁的受试者中，使用自动分割法定义脑白质病变。我们描述了厚度为 0-2mm 和 2-4mm 的空间限定的半影区脑白质组织 ROI，这些 ROI 为围绕脑白质病变的环状。其余脑白质被定义为距离正常的脑白质。对 FLAIR、T1-和 T2-加权图像以及各向异性分数、平均弥散系数、脑血流（CBF）和血管反应性图的平均信号强度进行了测量。使用 Kruskal-Wallis 和两两 检验进行组间比较。
病变体积平均为 0.738±0.842cm（范围，0.005-7.27cm）。与距离正常的脑白质相比，FLAIR、T2 和平均弥散系数的平均信号强度增加，而 T1、各向异性分数和 CBF 降低，半影区组织显示出逐渐增加的中间值（所有组/参数比较均校正 <.001）。与距离正常的脑白质相比，脑白质病变和半影区组织的血管反应性显著升高（校正 ≤.001）。
即使在 43-56 岁相对健康的、仅有少量脑白质病变负荷的受试者中，半影区组织的结构和功能 MR 成像与脑白质病变和其他正常脑白质相比，也显示出明显的信号异常。这些发现表明，脑白质损伤的起始发生在中年，并涉及比结构成像上可见的局灶性脑白质病变更多的组织。
