City University of New York (CUNY) School of Medicine, Townsend Harris Hall, 160 Convent Avenue, Convent Avenue, New York, NY 10031, United States; City University of New York (CUNY) Graduate Center, 365 5(th) Avenue, New York, NY 10016, United States.
University of Pennsylvania, Perelman School of Medicine, 3400 Civic Center Boulevard, Philadelphia, PA 19104, United States.
Neuroimage Clin. 2023;37:103344. doi: 10.1016/j.nicl.2023.103344. Epub 2023 Feb 11.
Traumatic brain injury (TBI) is associated with alterations in cerebral blood flow (CBF), which may underlie functional disability and precipitate TBI-induced neurodegeneration. Although it is known that chronic moderate-severe TBI (msTBI) causes decreases in CBF, the temporal dynamics during the early chronic phase of TBI remain unknown. Using arterial spin labeled (ASL) perfusion magnetic resonance imaging (MRI), we examined longitudinal CBF changes in 29 patients with msTBI at 3, 6, and 12 months post-injury in comparison to 35 demographically-matched healthy controls (HC). We investigated the difference between the two groups and the within-subject time effect in the TBI patients using whole-brain voxel-wise analysis. Mean CBF in gray matter (GM) was lower in the TBI group compared to HC at 6 and 12 months post-injury. Within the TBI group, we identified widespread regional decreases in CBF from 3 to 6 months post-injury. In contrast, there were no regions with decreasing CBF from 6 to 12 months post-injury, indicating stabilization of hypoperfusion. There was instead a small area of increase in CBF observed in the right precuneus. These CBF changes were not accompanied by cortical atrophy. The change in CBF was correlated with change in executive function from 3 to 6 months post-injury in TBI patients, suggesting functional relevance of CBF measures. Understanding the time course of TBI-induced hypoperfusion and its relationship with cognitive improvement could provide an optimal treatment window to benefit long-term outcome.
创伤性脑损伤 (TBI) 与脑血流 (CBF) 的改变有关,这可能是功能障碍的基础,并促使 TBI 诱导的神经退行性变。虽然已知慢性中重度 TBI (msTBI) 会导致 CBF 减少,但 TBI 早期慢性期的时间动态仍不清楚。我们使用动脉自旋标记 (ASL) 灌注磁共振成像 (MRI),在 3、6 和 12 个月时检查了 29 名 msTBI 患者的 CBF 变化与 35 名年龄匹配的健康对照组 (HC) 相比。我们使用全脑体素分析研究了 TBI 患者的两组之间的差异和组内时间效应。与 HC 相比,TBI 组在损伤后 6 个月和 12 个月时 GM 的 CBF 均较低。在 TBI 组中,我们发现从损伤后 3 个月到 6 个月 CBF 广泛下降。相比之下,从 6 个月到 12 个月 CBF 没有下降的区域,表明低灌注稳定。相反,在右侧楔前叶观察到一小部分 CBF 增加。这些 CBF 变化没有伴随皮质萎缩。从损伤后 3 个月到 6 个月,CBF 的变化与 TBI 患者执行功能的变化相关,表明 CBF 测量的功能相关性。了解 TBI 诱导的低灌注的时间过程及其与认知改善的关系,可能为受益于长期结果提供最佳治疗窗口。