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.

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