Evaluating regional blood spinal cord barrier dysfunction following spinal cord injury using longitudinal dynamic contrast-enhanced MRI.

Evaluating regional blood spinal cord barrier dysfunction following spinal cord injury using longitudinal dynamic contrast-enhanced MRI.
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DOI:
10.1186/1471-2342-9-10
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发表时间:
2009-06-11
影响因子:
2.7
通讯作者:
Bilgen M
Bilgen M
中科院分区:
医学4区
文献类型:
--
作者:
Tatar I;Chou PC;Desouki MM;El Sayed H;Bilgen M

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啮齿动物模型中脊髓损伤 (SCI) 的体内临床前成像为转化研究提供了临床相关信息。本文使用多模态磁共振成像 (MRI) 来研究 SCI 小鼠模型中 SCI 后神经血管病理学和血脊髓屏障 (BSCB) 通透性的变化。 C57BL/6 雌性小鼠 (n = 5) 在胸部 T11 水平遭受挫伤,并在受伤后第 1 天和第 3 天使用解剖、动态对比增强 (DCE-MRI) 和扩散张量成像 (DTI) 进行扫描。死后用针对神经血管变化的组织病理学染色对受伤的脊髓进行评估。实施计算模型来映射对比度增强引起的屏障功能的局部变化。使用半自动分割确定屏障功能障碍的脊髓组织的面积和体积。从获得的 DCE-MRI 数据得出的定量图描绘了受损脊髓中 BSCB 渗透性变化的程度。在损伤部位,受损屏障在第 1 天占据了总横截面的约 70% 和总体积的 48%,但在第 3 天相应的测量值分别减少至 55% 和 25%。这些变化意味着受伤 SC 中微脉管系统及其结构的时空重塑。扩散计算包括纵向和横向扩散率以及分数各向异性指数。渗透性和扩散测量的比较表明,屏障功能障碍的受损脊髓区域发生了以更大的轴突损失和脱髓鞘形式出现的结构变化,这得到了组织病理学评估的支持。这项研究的结果共同证明了定量绘制小鼠受损脊髓的区域 BSCB 功能障碍并使用体内 DCE-MRI 和 DTI 协议获得有关其结构完整性的补充信息的可行性。这种能力预计将在纵向临床前实验中表征 SCI 后的神经血管变化和重组方面发挥重要作用,但具有潜在的临床意义。
In vivo preclinical imaging of spinal cord injury (SCI) in rodent models provides clinically relevant information in translational research. This paper uses multimodal magnetic resonance imaging (MRI) to investigate neurovascular pathology and changes in blood spinal cord barrier (BSCB) permeability following SCI in a mouse model of SCI. C57BL/6 female mice (n = 5) were subjected to contusive injury at the thoracic T11 level and scanned on post injury days 1 and 3 using anatomical, dynamic contrast-enhanced (DCE-MRI) and diffusion tensor imaging (DTI). The injured cords were evaluated postmortem with histopathological stains specific to neurovascular changes. A computational model was implemented to map local changes in barrier function from the contrast enhancement. The area and volume of spinal cord tissue with dysfunctional barrier were determined using semi-automatic segmentation. Quantitative maps derived from the acquired DCE-MRI data depicted the degree of BSCB permeability variations in injured spinal cords. At the injury sites, the damaged barriers occupied about 70% of the total cross section and 48% of the total volume on day 1, but the corresponding measurements were reduced to 55% and 25%, respectively on day 3. These changes implied spatio-temporal remodeling of microvasculature and its architecture in injured SC. Diffusion computations included longitudinal and transverse diffusivities and fractional anisotropy index. Comparison of permeability and diffusion measurements indicated regions of injured cords with dysfunctional barriers had structural changes in the form of greater axonal loss and demyelination, as supported by histopathologic assessments. The results from this study collectively demonstrated the feasibility of quantitatively mapping regional BSCB dysfunction in injured cord in mouse and obtaining complementary information about its structural integrity using in vivo DCE-MRI and DTI protocols. This capability is expected to play an important role in characterizing the neurovascular changes and reorganization following SCI in longitudinal preclinical experiments, but with potential clinical implications.