首页> 外文OA文献 >Does signal-attenuation on high-field T2-weighted MRI of the brain reflect regional cerebral iron deposition? Observations on the relationship between regional cerebral water proton T2 values and iron levels.
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Does signal-attenuation on high-field T2-weighted MRI of the brain reflect regional cerebral iron deposition? Observations on the relationship between regional cerebral water proton T2 values and iron levels.

机译:脑高场T2加权MRI上的信号衰减是否反映了局部脑铁沉积?关于区域脑水质子T2值与铁水平之间关系的观察。

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摘要

T2-weighted MRI shows attenuated signals from the basal ganglia, such signal attenuation being more evident at high magnetic field strengths of 1.5 tesla (T). The basal ganglia contain high levels of iron, and it has been suggested that these iron deposits lead to shortening of bulk water T2 protons via a mechanism involving diffusion of water through local magnetic field gradients generated by the iron. This mechanism generates a relaxation contribution that is proportional to the square of the applied static field B0, and if it is significant the relaxation rate 1/T2 should be strongly dependent on Bo. T2-weighted MRI would then provide a potential means of imaging regional cerebral iron levels at field strengths that are high enough for this mechanism to be important. The bulk water proton spin-spin relaxation times (T2) of samples from caudate nucleus, frontal cortex, and white matter, taken from fresh cerebral necropsy material of four subjects dying of non-neurological conditions, and one subject with Parkinson's disease have been measured. T2 values were compared with regional cerebral iron content. At high field strengths (2.35 T and 8.5 T) no significant variation in regional cerebral water proton T2 values was found; caudate, cortex and white matter had similar water proton spin-spin relaxation times in spite of the variation in their iron content. Increasing the field strength from 2.35 T to 8.5 T resulted in a generalised 50% decrease in mean regional cerebral T2 values, as opposed to the 13-fold decrease expected if T2 relaxation was dominated by a mechanism that is dependent on B02. It was thus not possible to provide evidence that iron deposition per se is responsible for the attenuated signal obtained from the basal ganglia in T2-weighted MRI.
机译:T2加权MRI显示来自基底神经节的衰减信号,这种信号衰减在1.5特斯拉(T)的高磁场强度下更为明显。基底神经节含有高水平的铁,并且已经表明这些铁沉积物通过涉及通过铁产生的局部磁场梯度使水扩散的机制导致大量水T2质子的缩短。该机制产生与所施加的静态场B0的平方成比例的松弛贡献,并且如果显着,松弛率1 / T2应该强烈依赖于Bo。然后,T2加权MRI将提供一种在场强下对局部脑铁水平进行成像的潜在手段,该场强对于这种机制很重要。取自四名非神经系统疾病死亡者和一名帕金森氏病患者的新鲜脑剖检材料中的尾状核,额叶皮层和白质样品的总水质子自旋自旋弛豫时间(T2) 。将T2值与局部脑铁含量进行比较。在高场强(2.35 T和8.5 T)下,区域脑水质子T2值没有显着变化。尽管铁含量变化,尾状,皮层和白质具有相似的水质子自旋自旋自旋弛豫时间。场强从2.35 T增加到8.5 T导致区域平均脑T2值普遍降低50%,而如果T2弛豫受依赖于B02的机制支配,则预期的降低13倍。因此,不可能提供证据表明铁沉积本身是T2加权MRI中从基底神经节获得的衰减信号的原因。

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