• Ashley Nemes, Imad M Najm, John T Gale, Zhong Ying, Matthew Johnson, and Jorge Gonzalez-Martinez.
• 1 Epilepsy Center, Neurological Institute, Cleveland Clinic , Cleveland, Ohio.
• J. Neurotrauma. 2016 Oct 15; 33 (20): 1883-1891.

AbstractTraumatic brain injury (TBI) is a significant risk factor for development of epilepsy in humans. It is unclear, however, why some persons are at an increased risk of becoming epileptic, while others recover from the TBI seizure-free. We previously showed that the presence of a proepileptic pathology increases the risk of epilepsy in an animal model of cortical dysplasia (CD) after a secondary insult, which we described as the "second hit". Here we sought to evaluate the prevalence of epileptic activity and seizures in CD after a moderate TBI to determine the influence of dysplastic pathology on TBI-induced epileptogenesis. CD was generated in rats through in utero irradiation (the "first hit"). Nondysplastic and CD rats were surgically implanted with EEG electrodes. Craniotomies were performed over the pre-central cortex, and rats were given a moderate TBI using the lateral fluid percussion injury device. Rats were monitored with chronic EEG and video. EEG data were analyzed for the occurrence of interictal spikes and epileptic EEG seizure patterns. Brains were harvested and evaluated histologically. Spontaneous seizures are more prominent and occur earlier in rats with CD after a moderate TBI compared with nondysplastic control rats. All of the CD animals exhibited interictal spiking after TBI, while only a portion of nondysplastic animals produced spikes. These results suggest that the presence of a proepileptic pathology may increase the risk for the development of epilepsy after TBI. Diagnosis and treatment of TBI may depend on underlying pathologies contributing to epilepsy after a brain injury.

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