Diffusion Tensor Imaging in Late Posttraumatic Epilepsy


Address correspondence and reprint requests to Dr. R.K. Gupta at MR Section, Department of Radiodiagnosis, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, UP, India, 226014. E-mail: rakeshree@hotmail.com; rgupta@sgpgi.ac.in


Summary: Purpose: The main objective of this study was to use diffusion tensor imaging (DTI) to search and quantify the extent of abnormality beyond the obvious lesions seen on the T2 and fluid-attenuation inversion recovery (FLAIR) magnetic resonance images in patients with chronic traumatic brain injury (TBI) with and without epilepsy.

Methods: DTI was performed on 23 chronic TBI patients (with late posttraumatic epilepsy, n = 14; without epilepsy, n = 9) and 11 age-matched controls. The ratios of fractional anisotropy (FA) and mean diffusivity (MD) between the regions of interest beyond the T2/FLAIR-visualized abnormality and the corresponding contralateral normal-appearing region were calculated. FA and MD ratios were compared for relative changes in these parameters among the TBI subjects with and without epilepsy and controls. Tissue volumes exhibiting abnormalities on DTI also were measured in these patients.

Results: The mean regional FA ratio was significantly lower, whereas the mean regional MD value was higher in patients with TBI compared with controls. The mean regional FA ratio was significantly lower in TBI patients with epilepsy (0.57 ± 0.059) than in those without epilepsy (0.68 ± 0.039). Although the regional MD ratio was higher in TBI patients with epilepsy (1.15 ± 0.140) relative to those without epilepsy (1.09 ± 0.141), the difference did not reach statistical significance. The tissue volume with low FA value also was found to be higher in TBI patients with epilepsy than without.

Conclusions: Severity of injury as predicted by the DTI-derived increased volume of microstructure damage is associated with delayed posttraumatic epilepsy in TBI patients. These findings could be valuable in predicting epileptogenesis in patients with chronic TBI.