Brooks D J, Luthert P, Gadian D, Marsden C D
Institute of Neurology, National Hospital for Nervous Diseases, Queen Square, London, UK.
J Neurol Neurosurg Psychiatry. 1989 Jan;52(1):108-11. doi: 10.1136/jnnp.52.1.108.
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.
T2加权磁共振成像(MRI)显示基底神经节信号减弱,在1.5特斯拉(T)的高磁场强度下,这种信号衰减更为明显。基底神经节含有大量铁,有人认为这些铁沉积物通过一种机制导致大量水分子T2质子缩短,该机制涉及水通过铁产生的局部磁场梯度扩散。这种机制产生的弛豫贡献与外加静磁场B0的平方成正比,如果该贡献显著,则弛豫率1/T2应强烈依赖于B0。然后,T2加权MRI将提供一种潜在的方法,用于在足够高的磁场强度下对局部脑铁含量进行成像,此时该机制具有重要意义。已测量了来自四名死于非神经系统疾病的受试者以及一名帕金森病受试者的新鲜脑尸检材料中的尾状核、额叶皮质和白质样本的大量水分子质子自旋-自旋弛豫时间(T2)。将T2值与局部脑铁含量进行了比较。在高磁场强度(2.35 T和8.5 T)下,未发现局部脑水分子T2值有显著变化;尽管尾状核、皮质和白质的铁含量不同,但其水分子质子自旋-自旋弛豫时间相似。将磁场强度从2.35 T提高到8.5 T导致局部脑平均T2值普遍降低50%,而如果T2弛豫主要由依赖于B02的机制主导,则预期会降低13倍。因此,无法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信号减弱的原因。