A model of posttraumatic epilepsy induced by lateral fluid percussion brain injury in rats

Kharatishvili, I., Nissinen, J. P., McIntosh, T. K. and Pitkänen, A. (2006) A model of posttraumatic epilepsy induced by lateral fluid percussion brain injury in rats. Neuroscience, 140 2: 685-697. doi:10.1016/j.neuroscience.2006.03.012


Author Kharatishvili, I.
Nissinen, J. P.
McIntosh, T. K.
Pitkänen, A.
Title A model of posttraumatic epilepsy induced by lateral fluid percussion brain injury in rats
Journal name Neuroscience   Check publisher's open access policy
ISSN 0306-4522
1873-7544
Publication date 2006-01-01
Sub-type Article (original research)
DOI 10.1016/j.neuroscience.2006.03.012
Volume 140
Issue 2
Start page 685
End page 697
Total pages 13
Place of publication Kidlington, Oxford, United Kingdom
Publisher Pergamon
Language eng
Abstract Although traumatic brain injury is a major cause of symptomatic epilepsy, the mechanism by which it leads to recurrent seizures is unknown. An animal model of posttraumatic epilepsy that reliably reproduces the clinical sequelae of human traumatic brain injury is essential to identify the molecular and cellular substrates of posttraumatic epileptogenesis, and perform preclinical screening of new antiepileptogenic compounds. We studied the electrophysiologic, behavioral, and structural features of posttraumatic epilepsy induced by severe, non-penetrating lateral fluid-percussion brain injury in rats. Data from two independent experiments indicated that 43% to 50% of injured animals developed epilepsy, with a latency period between 7 weeks to 1 year. Mean seizure frequency was 0.3±0.2 seizures per day and mean seizure duration was 113±46 s. Behavioral seizure severity increased over time in the majority of animals. Secondarily-generalized seizures comprised an average of 66±37% of all seizures. Mossy fiber sprouting was increased in the ipsilateral hippocampus of animals with posttraumatic epilepsy compared with those subjected to traumatic brain injury without epilepsy. Stereologic cell counts indicated a loss of dentate hilar neurons ipsilaterally following traumatic brain injury. Our data suggest that posttraumatic epilepsy occurs with a frequency of 40% to 50% after severe non-penetrating fluid-percussion brain injury in rats, and that the lateral fluid percussion model can serve as a clinically-relevant tool for pathophysiologic and preclinical studies. © 2006 IBRO.
Keyword Hippocampal damage
Recurrent seizures
Traumatic brain injury
Video-EEG
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Centre for Advanced Imaging Publications
 
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Created: Wed, 30 Mar 2011, 21:31:55 EST by Sandrine Ducrot on behalf of Centre for Advanced Imaging