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Brain Advance Access originally published online on November 24, 2004
Brain 2005 128(1):174-188; doi:10.1093/brain/awh337
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Brain Vol. 128 No. 1 © Guarantors of Brain 2004; all rights reserved

Progression from frontal–parietal to mesial–temporal epilepsy after fluid percussion injury in the rat

Raimondo D'Ambrosio1,2,4, Jason S. Fender1, Jared P. Fairbanks1, Ednea A. Simon2, Donald E. Born3,4, Dana L. Doyle3 and John W. Miller1,2

1 Department of Neurological Surgery, 2 Department of Neurology and Regional Epilepsy Center, 3 Department of Pathology and 4 Center on Human Development and Disability, University of Washington, School of Medicine, Harborview Medical Center, Seattle, WA, USA

Correspondence to: Raimondo D'Ambrosio, PhD, Harborview Medical Center, Department of Neurosurgery, Box 359915, 325 Ninth Avenue, Seattle, WA 98104, USA E-mail: raid{at}u.washington.edu

We recently described an in vivo model of post-traumatic epilepsy (PTE) in the rat where chronic spontaneous recurrent seizures appear following a single episode of fluid percussion injury (FPI). PTE, studied during the first 2 months post-injury, was focal and seizures originated predominantly from the frontal–parietal neocortex at or around the injury site. However, rarer bilateral seizures originating from a different and undefined focus were also observed. To shed light on the Posttraumatic Epileptogenic mechanisms and on the generation of bilateral seizures, we studied rats up to 7 months post-injury. In vivo paired epidural and depth-electrode recordings indicated that the anterior hippocampus evolves into an epileptic focus which initiates bilateral seizures. The rate of frontal–parietal seizures remained constant over time after 2 weeks post-injury, while the rate of hippocampal seizures greatly increased over time, suggesting that different mechanisms mediate neocortical and hippocampal post-traumatic epileptogenesis. Because of different temporal evolution of these foci, the epileptic syndrome was characterized by predominant frontal–parietal seizures early after injury, but by predominant mesio-temporal seizures at later time points. Pathological analysis demonstrated progressive hippocampal and temporal cortex pathology that paralleled the increase in frequency and duration of bilateral seizures. These results demonstrate that FPI-induced frontal–parietal epilepsy (FPE) progresses to mesial–temporal lobe epilepsy (MTLE) with dual pathology. These observations establish numerous similarities between FPI-induced and human PTE and further validate it as a clinically relevant model of PTE.


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