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Brain injury-induced enhanced limbic epileptogenesis: Anatomical and physiological parallels to an animal model of temporal lobe epilepsy
Author(s): Coulter DA, Rafiq A, Shumate M, Gong QZ, DeLorenzo RJ, Lyeth BG
Source: EPILEPSY RESEARCH    Volume: 26    Issue: 1    Pages: 81-91    Published: DEC 1996  
Times Cited: 44     References: 34     
Abstract: Traumatic brain injury (TBI) is a leading cause of symptomatic epilepsy in young adults. This study examined physiological and anatomical epileptogenic consequences of a prior incident of TBI in rats. Rats were subjected to a fluid percussion brain injury one week prior to experimentation, and in vitro electrophysiological recording studies were conducted using combined hippocampal-entorhinal cortical slices (HEC slices). Results were compared to sham operated controls and rats in which a condition of chronic temporal lobe epilepsy was induced by a 2 h bout of pilocarpine-induced status epilepticus 2 months prior to recording (PILO). In field potential recordings, PILO HEC slices evidenced a greater degree of disinhibition in CAI than did TBI or control slices. TBI slices showed greater disinhibition in the dentate gyrus than did PILO or control rats. In in vitro kindling experiments, 86% of TBI HEC slices generated self-sustaining epileptic activity within 9 stimulus trains. This type of activity was never triggered in control slices. HEC slices prepared from PILO animals generated self-sustaining epileptic activity with fewer stimulus trains than did TBI slices. In anatomical studies, both TBI and PILO hippocampi evidenced significant loss of neurons within the hilar region. TBI induces a series of changes within the limbic system of rats, which are qualitatively similar in many aspects but quantitatively less severe than changes seen in rats with chronic temporal lobe epilepsy. These physiological and anatomical TBI-associated alterations in the limbic system may contribute to the development of epilepsy following head trauma.
Document Type: Proceedings Paper
Language: English
Reprint Address: Coulter, DA (reprint author), VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT NEUROL, RICHMOND, VA 23298 USA
Addresses:
1. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT PHYSIOL, RICHMOND, VA 23298 USA
2. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT NEUROSURG, RICHMOND, VA 23298 USA
3. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, COMPREHENS EPILEPSY INST, RICHMOND, VA 23298 USA
Publisher: ELSEVIER SCIENCE BV, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
Subject Category: Clinical Neurology
IDS Number: VX953
ISSN: 0920-1211
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