MRI of optic neuritis in a rat model
MRI of optic neuritis in a rat model
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DOI：
10.1016/j.neuroimage.2008.02.021
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发表时间：
2008-06-01
期刊：
影响因子：
5.7
通讯作者：
Frahm, Jens
中科院分区：
文献类型：
--
作者：
Boretius, Susann;Gadjanski, Ivana;Frahm, Jens
视神经炎是多发性硬化症最常见的早期症状之一。只有很少的数据相关的磁共振成像（MRI）对比度改变与潜在的病理，即炎症，脱髓鞘，轴突损伤。在这里，我们研究了视神经炎的实验性自身免疫性脑脊髓炎的大鼠模型，通过比较体内MRI结果从多种技术（T1，T2，质子密度，磁化转移）的组织病理学。我们进一步评估了使用Gd-DTPA的血脑屏障的破坏，并间接估计作为轴突损伤的结果，通过使用锰增强MRI的细胞内钙的积累。T2加权像上的高信号和Gd-DTPA后的信号增强对视神经病变高度敏感，但不能区分轻度、中度和重度损伤。T1加权像上的信号降低不太敏感，但与组织损伤的严重程度相关。没有观察到磁化传递率的显著变化。锰离子倾向于积聚在发炎的视神经的中央部分。给药后24小时产生的信号增强与轴突丢失的严重程度呈正相关。因此，锰可能是已知与轴突损伤相关的细胞内钙积累的指标。虽然没有一种方法单独区分炎症、脱髓鞘和轴突密度降低，但它们的特异性能力应被证明对未来动物模型和人类视神经炎的体内MRI研究有用。(c)2008年爱思唯尔公司All rights reserved.
Neuritis of the optic nerve is one of the most frequent early symptoms of multiple sclerosis. There are only scarce data correlating magnetic resonance imaging (MRI) contrast alterations with the underlying pathology, that is inflammation, demyelination, and axonal damage. Here we studied optic neuritis in a rat model of experimental autoimmune encephalomyelitis by comparing in vivo MRI findings from multiple techniques (T1, T2, proton density, magnetization transfer) to histopathology. We further assessed a breakdown of the blood-brain barrier by using Gd-DTPA and indirectly estimated the intracellular accumulation of calcium as a consequence of axonal damage by using manganese-enhanced MRI. Hyperintensity on T2-weighted images and signal enhancement after Gd-DTPA were highly sensitive to lesions of the optic nerve but did not differentiate between mild, moderate, and severe damage. Signal reduction on T1-weighted images was less sensitive but correlated well with the severity of tissue damage. No significant changes in magnetization transfer ratio were observed. Manganese ions tended to accumulate in the central parts of the inflamed optic nerve. The resulting signal enhancement at 24 h after administration positively correlated with the severity of axonal loss. Thus, manganese might be an indicator of intracellular calcium accumulation that is known to be associated with axon damage. Although none of the methods alone distinguished between inflammation, demyelination, and reduced axon density, their specific capabilities should prove useful for future in vivo MRI studies of optic neuritis in both animal models and humans. (c) 2008 Elsevier Inc. All rights reserved.