From the New York University Langone Medical Center, New York, New York.
AJNR Am J Neuroradiol. 2018 Dec;39(12):2200-2204. doi: 10.3174/ajnr.A5903. Epub 2018 Nov 29.
Mild traumatic brain injury is a leading cause of death and disability worldwide with 42 million cases reported annually, increasing the need to understand the underlying pathophysiology because this could help guide the development of targeted therapy. White matter, particularly the corpus callosum, is susceptible to injury. Animal models suggest stretch-induced mechanoporation of the axonal membrane resulting in ionic shifts and altered sodium ion distribution. The purpose of this study was to compare the distribution of total sodium concentration in the corpus callosum between patients with mild traumatic brain injury and controls using sodium (Na) MR imaging.
Eleven patients with a history of mild traumatic brain injury and 10 age- and sex-matched controls underwent sodium (Na) MR imaging using a 3T scanner. Total sodium concentration was measured in the genu, body, and splenium of the corpus callosum with 5-mm ROIs; total sodium concentration of the genu-to-splenium ratio was calculated and compared between patients and controls.
Higher total sodium concentration in the genu (49.28 versus 43.29 mmol/L, = .01) and lower total sodium concentration in the splenium (which was not statistically significant; 38.35 versus 44.06 mmol/L, = .08) was seen in patients with mild traumatic brain injury compared with controls. The ratio of genu total sodium concentration to splenium total sodium concentration was also higher in patients with mild traumatic brain injury (1.3 versus 1.01, = .001).
Complex differences are seen in callosal total sodium concentration in symptomatic patients with mild traumatic brain injury, supporting the notion of ionic dysfunction in the pathogenesis of mild traumatic brain injury. The total sodium concentration appears to be altered beyond the immediate postinjury phase, and further work is needed to understand the relationship to persistent symptoms and outcome.
轻度创伤性脑损伤是全球范围内导致死亡和残疾的主要原因，每年报告的病例有 4200 万例，因此需要深入了解其潜在病理生理学机制，这有助于指导靶向治疗的发展。白质，特别是胼胝体，容易受到损伤。动物模型表明，轴突膜的拉伸诱导机械穿孔导致离子转移和钠离子分布改变。本研究旨在使用钠（Na）磁共振成像比较轻度创伤性脑损伤患者和对照组胼胝体总钠浓度的分布。
11 例有轻度创伤性脑损伤病史的患者和 10 例年龄和性别匹配的对照组在 3T 扫描仪上进行 Na 磁共振成像。使用 5mm ROI 测量胼胝体膝部、体部和压部的总钠浓度；计算并比较患者和对照组的膝部-压部总钠浓度比值。
与对照组相比，轻度创伤性脑损伤患者的膝部（49.28 与 43.29mmol/L， =.01）总钠浓度较高，压部（虽无统计学意义；38.35 与 44.06mmol/L， =.08）总钠浓度较低。轻度创伤性脑损伤患者的膝部总钠浓度与压部总钠浓度比值也较高（1.3 与 1.01， =.001）。
在有症状的轻度创伤性脑损伤患者中，胼胝体总钠浓度存在复杂差异，支持离子功能障碍在轻度创伤性脑损伤发病机制中的作用。总钠浓度似乎在损伤后即刻阶段之外发生改变，需要进一步研究以了解其与持续症状和结局的关系。
