Turtzo L Christine, Chapagain Nikita Y, Peterkin Nicole, Cota Martin R, Vorn Rany, Devoto Christina, O'Keefe Jessica, Emanuel Olivia M, Parikh Gunjan, Diaz-Arrastia Ramon, Butman John A, McGavern Dorian B, Chan Leighton, Latour Lawrence L
Acute Cerebrovascular Diagnostics Unit, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD.
MTBI2, formerly known as CNRM.
Neurology. 2025 Mar 25;104(6):e213448. doi: 10.1212/WNL.0000000000213448. Epub 2025 Feb 25.
Traumatic meningeal enhancement (TME) can be observed on MRI of patients with acute traumatic brain injury (TBI) and reflects abnormal contrast extravasation into the meninges. Resolution of TME occurs over time, but TME can persist for weeks, suggesting incomplete meningeal repair. This study's objectives were to describe TME's prevalence, severity, and evolution over time and to investigate TME's association with other imaging findings, blood-based biomarkers commonly associated with TBI, and incomplete recovery.
Patients with suspected TBI presenting within 48 hours of injury to Suburban Hospital or Washington Hospital Center were prospectively enrolled between 2010 and 2019, received MRI, and underwent optional blood collection at baseline and follow-up visits at 1 week, 30 days, 90 days, and 1 year. Independent trained raters blinded to patient details scored for the presence and severity of TME on postcontrast MRI. Neuroimaging findings on CT and MRI, other than TME, were extracted from neuroradiology reports. Plasma biomarker levels (total tau [t-tau]; neurofilament light chain [NfL]; glial fibrillary acidic protein [GFAP]; ubiquitin C-terminal hydrolase-1 [UCH-L1]) were assessed with single-molecule array kits. Incomplete recovery was defined as a Glasgow Outcome Scale-Extended (GOSE) score <7 at 30-90-day follow-up. Factors associated with recovery were assessed through multivariable logistic regression analysis controlled for confounding variables.
Of 675 patients (male/female/neither 68%/31%/1%; median [interquartile range] age: 45 [28-58] years; Glasgow Coma Scale score 15 [15-15]), 359 (53%) were positive for TME at baseline (16 [6-25] hours after injury). At 30-90-day follow-up, TME remained absent in 117 (37%), resolved in 139 (45%), and persisted in 56 (18%). Acute TME had a high positive predictive value (PPV) for acute TBI-related findings on CT (87.7%) and MRI (86.1%). One-way analysis of covariance demonstrated significant associations between baseline TME and CT for plasma biomarker levels ((): t-tau = 19.328 (2); NfL = 20.458 (2); GFAP = 78.662 (2); UCH-LI = 46.680 (2)). Patients with persistent TME were more likely (odds ratio 3.809; 95% CI 1.703-8.519; = 0.001) to have GOSE score <7.
TME was prevalent at baseline, with high PPV for other neuroimaging findings, but was not associated with recovery. TME's persistence was independently associated with incomplete recovery, suggesting that the meninges' failure to repair may be a mediator of recovery after TBI.
ClinicalTrials.gov NCT01132937.
急性创伤性脑损伤（TBI）患者的磁共振成像（MRI）上可观察到创伤性脑膜强化（TME），其反映了造影剂异常渗入脑膜。TME会随时间消退，但可能持续数周，提示脑膜修复不完全。本研究的目的是描述TME的患病率、严重程度及其随时间的演变，并调查TME与其他影像学表现、TBI常见的血液生物标志物以及恢复不完全之间的关联。
2010年至2019年期间，前瞻性纳入了在郊区医院或华盛顿医院中心受伤后48小时内就诊的疑似TBI患者，这些患者接受了MRI检查，并在基线以及1周、30天、90天和1年的随访时进行了选择性血液采集。对患者详细信息不知情的独立训练评分者对增强后MRI上TME的存在和严重程度进行评分。除TME外，CT和MRI上的神经影像学表现从神经放射学报告中提取。使用单分子阵列试剂盒评估血浆生物标志物水平（总tau蛋白[t-tau]；神经丝轻链[NfL]；胶质纤维酸性蛋白[GFAP]；泛素C末端水解酶-1[UCH-L1]）。恢复不完全定义为在30 - 90天随访时格拉斯哥预后量表扩展版（GOSE）评分<7。通过控制混杂变量的多变量逻辑回归分析评估与恢复相关的因素。
675例患者（男性/女性/其他性别分别占68%/31%/1%；年龄中位数[四分位间距]：45[28 - 58]岁；格拉斯哥昏迷量表评分15[15 - 15]）中，359例（5
