Brain tissue sodium concentration in multiple sclerosis: a sodium imaging study at 3 tesla

Brain tissue sodium concentration in multiple sclerosis: a sodium imaging study at 3 tesla
复制标题

DOI:
10.1093/brain/awp334
复制
发表时间:
2010-03-01
期刊:
影响因子:
14.5
通讯作者:
Johnson, G.
Johnson, G.
中科院分区:
医学1区
文献类型:
--
作者:
Inglese, M.;Madelin, G.;Johnson, G.

文献摘要

被引文献

相似文献

神经轴突变性从多发性硬化症开始逐渐发生,被认为是增加临床残疾的一个重要原因。多发性硬化症和实验性自身免疫性脑脊髓炎的几项组织病理学研究表明,钠在轴突中的积累可以促进钠/钙交换剂的反向作用,从而导致轴突内钙的致命超载。我们假设钠磁共振成像可以提供多发性硬化症患者细胞和代谢完整性以及离子稳态的指标。利用短回声时间的三维径向梯度回波序列,我们对17例复发缓解型多发性硬化症患者和13例正常人进行了3 T的钠磁共振成像。测量了患者病变部位、正常白质和灰质的几个区域以及对照组白质和灰质相应区域的绝对总组织钠浓度。采用协方差混合模型分析比较患者和对照组的局部组织钠浓度水平。使用Spearman相关性来确定T(2)和T(1)加权病变区域组织钠浓度水平与标准化全脑、灰质和白质体积以及扩展的残疾状态量表评分之间的关系。在患者中,与正常白质区域相比,组织钠浓度水平在急性和慢性病变中均升高(P < 0.0001)。正常白质区域的组织钠浓度水平显著高于健康对照的相应白质区域(P < 0.0001)。组织钠浓度值在病变和正常白质和灰质区域上的平均值与T(2)加权(所有P < 0.001)和T(1)加权(所有P < 0.006)病变体积呈正相关。在患者中,只有正常灰质区域的组织钠浓度平均值与规范化灰质体积呈负相关(P = 0.0009)。最后,扩展残疾状态量表评分与慢性病变(P = 0.002)、正常白质区域(P = 0.004)和正常灰质区域(P = 0.002)的平均组织钠浓度值呈轻度正相关。本研究显示了在多发性硬化症患者体内使用3t钠磁共振成像的可行性。我们的研究结果表明,复发缓解型多发性硬化症患者组织钠浓度的异常值可能反映了病变细胞组成的变化和/或细胞和代谢完整性的变化。当与组织病理学相关时,钠磁共振成像有可能提供对组织损伤病理生理机制的深入了解。
Neuro-axonal degeneration occurs progressively from the onset of multiple sclerosis and is thought to be a significant cause of increasing clinical disability. Several histopathological studies of multiple sclerosis and experimental autoimmune encephalomyelitis have shown that the accumulation of sodium in axons can promote reverse action of the sodium/calcium exchanger that, in turn, leads to a lethal overload in intra-axonal calcium. We hypothesized that sodium magnetic resonance imaging would provide an indicator of cellular and metabolic integrity and ion homeostasis in patients with multiple sclerosis. Using a three-dimensional radial gradient-echo sequence with short echo time, we performed sodium magnetic resonance imaging at 3 T in 17 patients with relapsing-remitting multiple sclerosis and in 13 normal subjects. The absolute total tissue sodium concentration was measured in lesions and in several areas of normal-appearing white and grey matter in patients, and corresponding areas of white and grey matter in controls. A mixed model analysis of covariance was performed to compare regional tissue sodium concentration levels in patients and controls. Spearman correlations were used to determine the association of regional tissue sodium concentration levels in T(2)- and T(1)-weighted lesions with measures of normalized whole brain and grey and white matter volumes, and with expanded disability status scale scores. In patients, tissue sodium concentration levels were found to be elevated in acute and chronic lesions compared to areas of normal-appearing white matter (P < 0.0001). The tissue sodium concentration levels in areas of normal-appearing white matter were significantly higher than those in corresponding white matter regions in healthy controls (P < 0.0001). The tissue sodium concentration value averaged over lesions and over regions of normal-appearing white and grey matter was positively associated with T(2)-weighted (P < 0.001 for all) and T(1)-weighted (P < 0.006 for all) lesion volumes. In patients, only the tissue sodium concentration value averaged over regions of normal-appearing grey matter was negatively associated with the normalized grey matter volume (P = 0.0009). Finally, the expanded disability status scale score showed a mild, positive association with the mean tissue sodium concentration value in chronic lesions (P = 0.002), in regions of normal-appearing white matter (P = 0.004) and normal-appearing grey matter (P = 0.002). This study shows the feasibility of using in vivo sodium magnetic resonance imaging at 3 T in patients with multiple sclerosis. Our findings suggest that the abnormal values of the tissue sodium concentration in patients with relapsing-remitting multiple sclerosis might reflect changes in cellular composition of the lesions and/or changes in cellular and metabolic integrity. Sodium magnetic resonance imaging has the potential to provide insight into the pathophysiological mechanisms of tissue injury when correlation with histopathology becomes available.