Traumatic brain injury (TBI) frequently leads to epilepsy. The process of epileptogenesis - the development of that seizure state - is still poorly understood, and effective antiepileptogenic treatments have yet to be identified. The ketogenic diet (KD) has been shown to be effective as an antiepileptic therapy, but has not been extensively tested for its efficacy in preventing the development of the seizure state, and certainly not within the context of TBI-induced epileptogenesis. We have used a rat model of TBI - fluid percussion injury (FPI) - to test the hypothesis that KD treatment is antiepileptogenic and protects the brain from neuronal cell loss following TBI. Rats fed a KD had a higher seizure threshold (longer latency to flurothyl-induced seizure activity) than rats fed a standard diet (SD); this effect was seen when KD was in place at the time of seizure testing (3 and 6 weeks following FPI), but was absent when KD had been replaced by SD at time of testing. FPI caused significant hippocampal cell loss in both KD-fed and SD-fed rats; the degree of cell loss appeared to be reduced by KD treatment before FPI but not after FPI. These results are consistent with prior demonstrations that KD raises seizure threshold, but do not provide support for the hypothesis that KD administered for a limited time directly before or after FPI alters later seizure sensitivity; that is, within the limits of this model and protocol, there is no evidence for KD-induced antiepileptogenesis.
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