From The Mind Research Network Lovelace Biomedical and Environmental Research Institute (J.M.L., S.K., T.T., A.R.M.), Albuquerque; Department of Psychology (A.R.M.), University of New Mexico, Albuquerque; and Neurology Department (A.R.M.), University of New Mexico School of Medicine, Albuquerque, NM.
Neurology. 2013 Dec 10;81(24):2121-7. doi: 10.1212/01.wnl.0000437302.36064.b1. Epub 2013 Nov 20.
To examine the underlying pathophysiology of mild traumatic brain injury through changes in gray matter diffusion and atrophy during the semiacute stage.
Fifty patients and 50 sex-, age-, and education-matched controls were evaluated with a clinical and neuroimaging battery approximately 14 days postinjury, with 26 patients returning for follow-up 4 months postinjury. Clinical measures included tests of attention, processing speed, executive function, working memory, memory, and self-reported postconcussive symptoms. Measures of diffusion (fractional anisotropy [FA], mean diffusivity) and atrophy were obtained for cortical and subcortical structures to characterize effects of injury as a function of time.
Patients reported more cognitive, somatic, and emotional complaints during the semiacute injury phase, which were significantly reduced 4 months postinjury. Patients showed evidence of increased FA in the bilateral superior frontal cortex during the semiacute phase, with the left superior frontal cortex remaining elevated 4 months postinjury. There were no significant differences between patients and matched controls on neuropsychological testing or measures of gray matter atrophy/mean diffusivity at either time point.
Increased cortical FA is largely consistent with an emerging animal literature of gray matter abnormalities after neuronal injury. Potential mechanistic explanations for increased FA include cytotoxic edema or reactive gliosis. In contrast, there was no evidence of cortical or subcortical atrophy in the current study, suggesting that frank neuronal or neuropil loss does not occur early in the chronic disease course for patients with typical mild traumatic brain injury.
通过在亚急性期内灰质扩散和萎缩的变化，研究轻度创伤性脑损伤的潜在病理生理学。
大约在损伤后 14 天，50 名患者和 50 名性别、年龄和教育程度匹配的对照组接受了临床和神经影像学检查，其中 26 名患者在 4 个月后进行了随访。临床评估包括注意力、处理速度、执行功能、工作记忆、记忆和自报告的脑震荡后症状测试。为了描述损伤随时间的影响，还获取了皮质和皮质下结构的扩散（各向异性分数[FA]、平均扩散率）和萎缩的测量值。
患者在亚急性损伤阶段报告了更多的认知、躯体和情绪主诉，这些主诉在 4 个月后明显减轻。在亚急性期，患者双侧额上回的 FA 增加，左侧额上回在 4 个月后仍保持升高。在神经心理学测试或灰质萎缩/平均扩散率测量方面，患者与匹配对照组在两个时间点均无显著差异。
皮质 FA 的增加与动物实验中神经元损伤后灰质异常的新兴文献大体一致。FA 增加的潜在机制解释包括细胞毒性水肿或反应性神经胶质增生。相比之下，在当前研究中没有发现皮质或皮质下萎缩的证据，这表明在典型轻度创伤性脑损伤患者的慢性病程早期，不会发生明显的神经元或神经胶质丢失。
