Epilepsy related to traumatic brain injury

Abstract

Post-traumatic epilepsy accounts for 10-20% of symptomatic epilepsy in the general population and 5% of all epilepsy. During the last decade, an increasing number of laboratories have investigated the molecular and cellular mechanisms of post-traumatic epileptogenesis in experimental models. However, identification of critical molecular, cellular, and network mechanisms that would be specific for post-traumatic epileptogenesis remains a challenge. Despite of that, 7 of 9 proof-of-concept antiepileptogenesis studies have demonstrated some effect on seizure susceptibility after experimental traumatic brain injury, even though none of them has progressed to clinic. Moreover, there has been some promise that new clinically translatable imaging approaches can identify biomarkers for post-traumatic epileptogenesis. Even though the progress in combating post-traumatic epileptogenesis happens in small steps, recent discoveries kindle hope for identification of treatment strategies to prevent post-traumatic epilepsy in at-risk patients.

Figures

Fig. 1

(a) Coronal T2-weighted image from a rat with lateral fluid-percussion-induced TBI 23 days earlier, demonstrating the regions of interests (dashed lines), from which T2 and T1σ (c) were analyzed. (b) Receiver–operating characteristics for parameters in (c). Note that including data from the hippocampus (HC) for the calculation of the area under curve (AUC) did not increase sensitivity. (c) Summary of parameters with the highest sensitivity at 90 % specificity 9 days after TBI regarding prediction of seizure susceptibility 12 months after TBI. *P ≤ 0.05, **P ≤ 0.01 AUC compared with the area under diagonal line. For details, see [68]. PrhCx = perirhinal cortex; S1 = somatosensory cortex 1, Th=thalamus