Prognostic biomarkers for post-injury outcome are necessary for the development of neuroprotective and antiepileptogenic treatments for traumatic brain injury (TBI). We hypothesized that T₂ relaxation magnetic resonance imaging (MRI) predicts the progression of perilesional cortical pathology and epileptogenesis. The EPITARGET animal cohort used for MRI analysis included 120 adult male Sprague-Dawley rats with TBI induced by lateral fluid-percussion injury and 24 sham-operated controls. T₂ MRI was performed at days 2, 7, and 21 post-TBI. The lesioned cortex was outlined, and the T₂ value of each imaging voxel within the lesion area was scored using a five-grade pathology classification. Analysis of 1-month video-electroencephalography recordings initiated 5 months post-TBI indicated that 27% (31 of 114) of the animals with TBI developed epilepsy. Multiple linear regression analysis indicated that T₂-based classification of lesion volume at day 2 and day 7 post-TBI explained the necrotic lesion volume with greatly increased T₂ (>102 ms) at day 21 post-TBI (F_(13,103) = 52.5; p < 0.001; R² = 0.87; adjusted R² = 0.85). The volume of moderately increased (78–102 ms) T₂ at day 7 post-TBI predicted the evolution of large (>12 mm³) cortical lesions (area under the curve, 0.92; p < 0.001; cutoff, 1.9 mm³; false positive rate, 0.10; true positive rate, 0.62). Logistic regression analysis, however, showed that the different severities of T₂ lesion volumes at days 2, 7, and 21 post-TBI did not explain the development of epilepsy (χ²_(18,95) = 18.4; p = 0.427). In addition, the location of the T₂ abnormality within the cortex did not correlate with epileptogenesis. A single measurement of T₂ relaxation MRI in the acute post-TBI phase is useful for identifying post-TBI subjects at highest risk of developing large cortical lesions, and thus, in the greatest need of neuroprotective therapies after TBI, but not the development of post-traumatic epilepsy.

中文翻译：

---

在实验性创伤性脑损伤后，皮质 T2 松弛的早期增加是严重皮质损伤演变的预后生物标志物，但不是癫痫发生的预后生物标志物。

对于创伤性脑损伤 (TBI) 的神经保护和抗癫痫治疗的开发，损伤后结果的预后生物标志物是必要的。我们假设 T ₂弛豫磁共振成像 (MRI) 预测病灶周围皮层病理和癫痫发生的进展。用于 MRI 分析的 EPITARGET 动物队列包括 120 只因侧向液体冲击损伤引起的 TBI 成年雄性 Sprague-Dawley 大鼠和 24 只假手术对照。T ₂ MRI 在 TBI 后第 2、7 和 21 天进行。勾勒出受损皮层的轮廓，T ₂使用五级病理分类对病变区域内每个成像体素的值进行评分。对 TBI 后 5 个月开始的 1 个月视频脑电图记录的分析表明，27%（114 只中的 31 只）患有 TBI 的动物发生了癫痫。多元线性回归分析表明，在 TBI 后第 2 天和第 7 天，基于T ₂的病灶体积分类解释了坏死病灶体积在 TBI 后第 21 天大幅增加的 T ₂ (>102 ms) ( F _(13,103)  = 52.5；p  < 0.001；R ²  = 0.87；调整后的R ²  = 0.85）。中度增加 (78–102 ms) T ₂的音量在 TBI 后第 7 天预测大（> 12 mm ³）皮质病变的演变（曲线下面积，0.92；p  < 0.001；截断值，1.9 mm ³；假阳性率，0.10；真阳性率，0.62）。然而，逻辑回归分析显示，TBI 后第 2、7 和 21 天T ₂病变体积的不同严重程度并不能解释癫痫的发展（χ ² _(18,95)  = 18.4；p  = 0.427）。此外，皮层内T ₂异常的位置与癫痫发生无关。单次测量 T ₂ TBI 后急性期的松弛 MRI 可用于识别发生大皮层病变风险最高的 TBI 后受试者，因此，在 TBI 后最需要神经保护性治疗时，但不是外伤后癫痫的发展。